ATAR Notes: Forum
VCE Stuff => VCE Science => VCE Mathematics/Science/Technology => VCE Subjects + Help => VCE Biology => Topic started by: WhoTookMyUsername on January 24, 2011, 08:46:43 pm
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Thought we should gather all the kerfuffle (by me) and place it into one continuing post !
For discussion of the finer points of a great subject!
I'll start by posting some starter questions to get deep thinking rolling! (copied from my other thread)
(1) Where are non - essential amino acids synthesized ? In the nucleus? Mitchondria? Specialized cells?
(2) Is Freezing an enzyme so it no longer works at that temperature denaturing? or does denaturing refer to permanent, irreversible change?
(3) Does denaturing an enzyme imply it no longer works? or that it works at way less than optimal rate ( e.g. very cold but still works)
(4) Why does Pyruvate need to be further converted to lactic acid (in animals) in anaerobic respiration as lactic acid is harmful to animals but pyruvate not?
(5) When are plants pronounced 'dead?'
(6) Does anyone know exactly where in a cell hydrolysis of atp occurs to release energy?
(7) If substrate concentration is plotted against rate of reaction and there is a straight line 45 degree angle going north east, and at point Z in the middle,
is the rate of product formation increasing?
(8) If anyone has neap AOS1 part multiple choice 1.21 and 1.23 o.o
(9) Does anaerobic respiration involve the kreb's cycle ? and if not why not?
(10) Does glycolysis (more accurately) occur in the cytosol or cytoplasm of cells?
(11) Does kreb's cycle require oxygen?
(12) Are C3 plants more efficient in cooler climates because they take greater advantage of moisture and Co2?
(13) What is the difference between ectothermic and heterothermic? (also endothermic and homeothermic)
(14) Are neurotransmitter substances enzymes or hormones or both? (are all proteins?)
Cheers
Have *fun* :uglystupid2:
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Stickied. I also trimmed the title for simplicity's sake.
Please remember, new post for a new question and we'll try to help out as best we can :)
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Does an enzyme have only 1 active site, if yes, what is the point of some enzymes having more than one secondary coiling?
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Enzymes may have more than one active site
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Between the CNS and a receptor, are there many interneurons or 1 sensory neuron or many connected sensory neurons transmitting the one signal to the CNS?
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Varies. Sensory information can be sent directly, along a single afferent neuron pathway or can also involve an interneuron. Each pathway has a specific purpose, which escapes me right now, but you probably don't need to know it.
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What are the differences ( and functions of)
glycolipids, glycoproteins, carbohydrate, and proteins involved in facilitated diffusion ( and how do you tell the difference)
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I think in facilitated diffusion, only proteins are used... The proteins form channels and in fact facilitate the foreign material through the cell membrane. The role glycolipids, glycoproteins and carbohydrates play in facilitated diffusion are very minimal (I don't think they play any role in fact).
Glycoproteins, proteins on the cell membrane which have short carbohydrate chains protruding out from them, are sometimes used as receptor molecules. But this is more for hormones than in facilitated diffusion. Glycoproteins also from H-bonds with H2O molecules to maintain cell shape or something (I don't remember the details). Glycolipids, lipids with an attached carbohydrate, have a similar role as receptor molecules.
In terms of 'telling the difference', that probably depends on how they are drawn, but I doubt you would need to identify them separately on an exam or SAC.
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(4) Why does Pyruvate need to be further converted to lactic acid (in animals) in anaerobic respiration as lactic acid is harmful to animals but pyruvate not?
Correct me if im wrong...which is most likely...
Pyruvate needs to be converted to lactic acid because to continue glycolysis there must be a ready supply of NAD+, but without oxygen this cannot happen. So instead the NADH gives off its electrons to the pyruvate so NAD+ is regenerated and ready for glycolysis again. When the pyruvate receives the electrons from the NADH-> NAD+ it is reduced and lactic acid is formed.
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i have a question: What gives carbon the ability to form chains that are almost unlimited in length :)
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It's also the size of the atom. Silicon also has 4 valence electrons but is larger/heavier than carbon, so isn't as adept at forming chains/biomolecules. There have been a few theoretical approaches to constructing a silicon based lifeform but they're all predominantly inefficient and difficult to form.
This is really more of a chemistry question though
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It requires 4 bonds so can form polymers continuosly with a carbon backbone. The other 2 bonds usually are attached to other elements
What are the 4 bonds and why does the backbone have to be carbon in all biomolecules (this is probably a stupid q.)
Where did you get this info from? :O
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Uh the 4 bonds is basic chemistry. Carbon needs to form 4 covalent bonds to get a full outer shell, so it has 4 'bonds available'. Second one is actually a good question wouldn't mind the answer to that :)
Oh yeaaa. i remember that. So it can bond with any element in groups 15,16,17,18?
So basically it can join with A LOT of elements including other carbon elements, hydrogen, oxygen, sulphur ....
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Oh yeaaa. i remember that. So it can bond with any element in groups 15,16,17,18?
So basically it can join with A LOT of elements including other carbon elements, hydrogen, oxygen, sulphur ....
For bio, it can bond with other carbons, hydroxyl groups (OH-), oxygens and hydrogens...
Carbon-sulphur bonds are ones that I have not come across before...
AND carbon is able to form chains more easily than atoms of silicon (same group and valency), which tends to crystallise (ie no chains) instead.
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Is a Lipid a Macromolecule? ( i have a definition that does not include lipids as macromolecules??)
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Is a Lipid a Macromolecule? ( i have a definition that does not include lipids as macromolecules??)
Yes, but they are not polymers. That's the more important distinction to remember.
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A macromolecule is a very large molecule commonly created by some form of polymerization. In biochemistry, the term is applied to the four conventional biopolymers (nucleic acids, proteins, carbohydrates, and lipids)
...
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woludn't that be wrong becuase it just says that " biopolymers (lipids)"?
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woludn't that be wrong becuase it just says that " biopolymers (lipeds)"?
Appears so. Who wants to go and edit Wiki for us to fix that :P
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woludn't that be wrong becuase it just says that " biopolymers (lipids)"?
Its really a tough one. And it depends on how you take the definition of a polymer (hence, disagreement in some textbooks and websites).
A polymer is something that has repeated subunits, and those subunits have to be covalently (...intermolecular) attached. Thats the standard definition.
Why some textbooks classify them as polymers:
Lipids are groups of carbon atoms (the 'monomers') that are attached covalently, and so it fits the overall definition of a polymer. Plus, by doing so they don't need a new big heading for lipids and can make that neat table of the 4 'polymers'.
Why it shouldn't be a polymer:
The subunits for a polymer, the monomers, should not be atoms, but molecules; although this is not specified in the definition of a polymer (or a biopolymer -a polymer produced by living organisms).
My conclusion: as probably realised, this is pretty hazy and definitions are always changing and are accepted by some and not others. If on an exam (and it wouldn't be, so calm down!), I would say they aren't because of the definition of a monomer being a molecule (although this isn't in the definition of a polymer).
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Hmmm.... I would have just argued that lipids are not polymers since they do not
have repeated identical or similar units.
Though they are biomacromolecules since there are lots of lipids in our cells e.g
phospholipid bilayer and they are synthesized by biological organisms?
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Irrespective of whether they're polymers, they're certainly biomacromolecules.
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Hey guys,
What is meant by a reducing sugar?
Russ - merged topic
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Lipids are macromolecules but definitely not polymers cause theyre not a chain of identical/similar sub-units linking together
glycerol + fatty acid chains aint monomers. well, thats wat Douchy sed :D
BTW, do we have to know about condensation and hydrolysis reactions? do they appear in sacs/exam?
And do we have to know what specific proteins do?
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Lipids are macromolecules but definitely not polymers cause theyre not a chain of identical/similar sub-units linking together
glycerol + fatty acid chains aint monomers. well, thats wat Douchy sed :D
BTW, do we have to know about condensation and hydrolysis reactions? do they appear in sacs/exam?
And do we have to know what specific proteins do?
Their not hard really,
Just condensation to form a polymer and hydrolysis to break it down
Does condensation AlWAYS require energy, and hydrolysis ALways release energy?
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BTW, do we have to know about condensation and hydrolysis reactions? do they appear in sacs/exam?
And do we have to know what specific proteins do?
As said it's not hard, condensation produces water as it builds up a larger molecule (think peptide bond formation). Hydrolysis is the reverse, it splits a water molecule to add it across either side of a bond, thus breaking it.
It's chemistry so it won't be assessed directly but it's useful to know
I doubt you'll need to know specific proteins, this is only VCE but it can't hurt to know a couple of the major/common ones that come up through the year.
Hey guys,
What is meant by a reducing sugar?
This is chemistry not biology and has me trying to remember my 1st year classes...from memory it's a sugar with a functional group that can be oxidized (this subsequently reduces something else, hence the name). Page Mao for this, it's not really biology
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Does condensation AlWAYS require energy, and hydrolysis ALways release energy?
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Not necessarily. The products will be at a higher/lower energy state than the reactants (depending on which process) but it may not "release" energy.
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Where does the energy go then :S
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It's not my strength, but it's related to the entropy of the system (Gibbs Free Energy) and how "ordered" it is.
If you want, you can just think of it as always releasing/consuming energy because I don't think the distinction will ever be important
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What effect does Cholesterol have on the Cell membrane? Douchy said it was to add stability and rigidity but elsewhere it says to add fluidity?
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What effect does Cholesterol have on the Cell membrane? Douchy said it was to add stability and rigidity but elsewhere it says to add fluidity?
I would have said fluidity.
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At low temperatures it keeps the membranes fluid and prevents them from crystallizing but it also has other important structural functions
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At low temperatures it keeps the membranes fluid and prevents them from crystallizing but it also has other important structural functions
Such as?... :)
also
1 ) Do things like penicillin also prevent cell wall synthesis in plants? (are the enzymes they block common ?)
2 ) Are all poisons non - competitive inhibitors ? (poison must have permanent bond???)
3 ) Is Cysteine very common in proteins ? ( is it in most ? douchy said that i think )
4 ) IS a better defintion of a Organic compound Carbon and Hydrogen or Carbon containing excluding carbonides etc...
5 ) Are things like Oxygen Gas molecules ? (according to douchy must have more than one different element covalently bonded ) if not, what are they called
6 ) Does water soluble refer to the complete breakdown of the molecular compound / molecule structure (e.g. NaCl -> Na + Cl) and/or the tendency for substances to seperate into individual, unconnected parts in water (e.g. full glucose molecule). Does it depend on Ionic / Covalent bonds?
7 ) Does plasma membrane refer to any phospholipid bilayer?
8 ) NOB says some enzymes work by lock and key and others by induced fit, biozone states Induced fit is the current model, which is correct?
9) Are all Antibodies Proteins?
10) Can some RNA act as enzymes?
11 ) Does denaturation change Secondary and/or teritiary, or tertiary and/or quartenary structure?
Russ: Post new questions in a new post, only edit an old post if nobody has replied yet
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I'll help with the ones I remember:
3) Not on the course, there is no need to know this.
4) I would just say an organic compound is one that contains a 'backbone' of covalently bonded carbon atoms.
5) Oxygen gas is simply known as oxygen, and many consider it an 'element' and it is made up of only one type of atom (02). Like N2 (nitrogen gas), He (helium gas), C (diamond).
6) The first part of your question is wrong. NaCl is not a molecule. But the process described is dissociation of ionic compounds (not all are soluble). Water is hence, able to overcome ionic bonds in some ionic compounds. Solubility also refers to polar substances (molecules) that are able to form hydrogen bonds with the polar water molecules.
Don't remember 1) and 2)... ;D
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1 ) Do things like penicillin also prevent cell wall synthesis in plants? (are the enzymes they block common ?)
Penicillin targets peptidoglycan, which isn't present in plant cells.
2 ) Are all poisons non - competitive inhibitors ? (poison must have permanent bond???)
No (there are very few absolute statements in biology)
5 ) Are things like Oxygen Gas molecules ? (according to douchy must have more than one different element covalently bonded ) if not, what are they called
Yes (both by the chemistry definition and the biology definition)
7 ) Does plasma membrane refer to any phospholipid bilayer?
Yes, but I guess you could apply it to a monolayer/non phospholipid bilayer
8 ) NOB says some enzymes work by lock and key and others by induced fit, biozone states Induced fit is the current model, which is correct?
Induced fit is more correct than lock and key (at VCE it doesn't matter imo)
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9) Are all Antibodies Proteins?
Yes, they are those Y-shaped proteins
10) Can some RNA act as enzymes?
Yes, they are ribozymes (not in the course)
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11 ) Does denaturation change Secondary and/or teritiary, or tertiary and/or quartenary structure?
It denatures the secondary and tertiary structures (hence denaturing the quaternary structures if the protein has one).
Russ: Post new questions in a new post, only edit an old post if nobody has replied yet
+1, only saw the last few by luck
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What are the two major functions of monosaccharides:
1) Immediate energy source
2) ???? ( monomer of polysaccharides? )
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I would say that they are an immediate soruce of chemical energy for cellular functions/ respiration.
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Structural is the first thing that jumps to mind
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9) Are all Antibodies Proteins?
Yes, they are those Y-shaped proteins
10) Can some RNA act as enzymes?
Yes, they are ribozymes (not in the course)
pfft they arent all Y shaped lol
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Structural is the first thing that jumps to mind
Thought they have to be polysacchardies for structural?
9) Are all Antibodies Proteins?
Yes, they are those Y-shaped proteins
10) Can some RNA act as enzymes?
Yes, they are ribozymes (not in the course)
pfft they arent all Y shaped lol
What is an example of non Y shape?
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IgM, IgA
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Quote from: Russ on Today at 11:37:10 AM
At low temperatures it keeps the membranes fluid and prevents them from crystallizing but it also has other important structural functions
Such as?...
also
1 ) Do things like penicillin also prevent cell wall synthesis in plants? (are the enzymes they block common ?)
2 ) Are all poisons non - competitive inhibitors ? (poison must have permanent bond???)
3 ) Is Cysteine very common in proteins ? ( is it in most ? douchy said that i think )
4 ) IS a better defintion of a Organic compound Carbon and Hydrogen or Carbon containing excluding carbonides etc...
5 ) Are things like Oxygen Gas molecules ? (according to douchy must have more than one different element covalently bonded ) if not, what are they called
6 ) Does water soluble refer to the complete breakdown of the molecular compound / molecule structure (e.g. NaCl -> Na + Cl) and/or the tendency for substances to seperate into individual, unconnected parts in water (e.g. full glucose molecule). Does it depend on Ionic / Covalent bonds?
7 ) Does plasma membrane refer to any phospholipid bilayer?
8 ) NOB says some enzymes work by lock and key and others by induced fit, biozone states Induced fit is the current model, which is correct?
9) Are all Antibodies Proteins?
10) Can some RNA act as enzymes?
11 ) Does denaturation change Secondary and/or teritiary, or tertiary and/or quartenary structure?
What are the two major functions of monosaccharides:
1) Immediate energy source
2) ? ( monomer of polysaccharides? )
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pfft they arent all Y shaped lol
haha, I was going to say this but I figured it didn't actually matter
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Hmmm I would say that not all polysaccharides play a role in structural support,
infact in both heinemann and NOB only cellulose is mentioned, other than that I would say
they obviously are energy storage molecules. And in reference to Bazza's initial question
" two functions of monosaccharide" the first one i said before was obviously right, but maybe
another one could be building blocks for larger molecules such as polysaccharide (even though
this pertains more to disaccharide).
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pfft they arent all Y shaped lol
Shows how much I knew about Unit 3 bio...
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IgM, IgA
How are they shaped, are the individual molecules still Y shaped, just that their is multiple bodies that form a *ring* almost?
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IgM, IgA
How are they shaped, are the individual molecules still Y shaped, just that their is multiple bodies that form a *ring* almost?
Yeh, the individual antibody proteins are all Y-shaped. However they form complexes (IgG, IgA, IgM, IgE, IgD i.e. 'GAMED') of which G, E and D are monomers, A is a dimer and M is a pentamer. See here for an illustration.
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IgM
(http://upload.wikimedia.org/wikipedia/commons/thumb/7/77/IgM_scheme.svg/220px-IgM_scheme.svg.png)
IgA
(http://upload.wikimedia.org/wikipedia/commons/thumb/5/59/Immunglobulin_A_as_Dimer.png/220px-Immunglobulin_A_as_Dimer.png)
Wow, I never knew that...
EDIT: Beaten by better pics by shinny
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yep all the antibodies are in monomeric form when they are membrane bound but those two polymerize when secreted to form those structures^
pfft they arent all Y shaped lol
Shows how much I knew about Unit 3 bio...
no it doesnt mean that its probably that your teacher didn't think it was important for you to know as Russ said
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Incidentally, IgD seems to be the useless sibling of the Ig family and I've never seen it used
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Which ones? Most/all of them have been answered
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1 ) Do things like penicillin also prevent cell wall synthesis in plants? (are the enzymes they block common ?)
2 ) Are all poisons non - competitive inhibitors ? (poison must have permanent bond???)
3 ) Is Cysteine very common in proteins ? ( is it in most ? douchy said that i think )
4 ) IS a better defintion of a Organic compound Carbon and Hydrogen or Carbon containing excluding carbonides etc...
5 ) Are things like Oxygen Gas molecules ? (according to douchy must have more than one different element covalently bonded ) if not, what are they called
6 ) Does water soluble refer to the complete breakdown of the molecular compound / molecule structure (e.g. NaCl -> Na + Cl) and/or the tendency for substances to seperate into individual, unconnected parts in water (e.g. full glucose molecule). Does it depend on Ionic / Covalent bonds?
7 ) Does cell membrane refer to the outermost membrane of a cell, and plasma membrane as also to membrane bound organelle?
8 ) NOB says some enzymes work by lock and key and others by induced fit, biozone states Induced fit is the current model, which is correct?
What are the two major functions of monosaccharides:
1) Immediate energy source
2) ? ( monomer of polysaccharides? )
Still not 100% certain on these ones
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Incidentally, IgD seems to be the useless sibling of the Ig family and I've never seen it used
{warning: vce students, you do not need to know any of this below}
heh yeah not much is known about it compared to the others although heres some of them i found in one journal article
'used as marker of B-cell maturation'
'The importance of its function in the immune responses is considered enigmatic due to the fact that IgD-deficient mice have an intact immune development and a relatively normal humoral immune response to a variety of T-cell-dependent and -independent antigens.'
'mIgD can recognize and bind antigens through its variable region with same specificity and avidity as mIgM. Such bindings through mIgD can lead to activation and/or clonal deletion or anergy of B-cells in vivo.'
'Similarly, an antibody that cross-links mIgD(anti-IgD) can also elicit a pronounced and complex immune response through activation of B-cells in vitro and in vivo.'
'It can also modulate both T-helper (Th) cell-dependent and-independent polyclonal antibody responses in vivo.'
and the study also found that
'In summary,our study provided an evidence-based rationale for the therapeutic use of anti-IgD as a new method of selective depletion of mature B cells that can also induce immune tolerance through the augmentation of regulatory B-and T-cell populations, and possibly by promoting an anti-inflammatory Th2-biased response.'
so i guess there is a therapeutic use for using antibodies to target IgD
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Bazza16
1) already answered by Russ on page 3. no its specific to bacterial cell wall synthesis, plants do not have peptidoglycan in their cell wall
3) do you need to know that? i dunno but disulfide bonds form between side groups of cysteine residues and disulfide bonds give stability and strength to a protein, one example of this is a protein like IgG.
this is what wikipedia says
"In secreted proteins that do not spend time in the cytoplasm, disulfide bonds between cysteine residues help to maintain the protein's tertiary structure. "
"The disulfide bonds are extremely rare in cytosolic proteins, since the cytosol is generally a reducing environment."
7) interchangable like if your talking about eukaryotic cells, the one surrounding the entire cell i would use either, although cell membrane seems so generic lol but yeah if its the membrane surrounding organelles just say plasma membrane.
8) i would know both but enzymes do have some leeway they arent like stone, so they can move to some little degree.
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How is the cytosol a reducing environment and how does it affect disuplhide bonds? (adding back the Hydrongen?)
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all i know is that in an increasingly reducing environment, the disulfide bonds will break down
wiki to the rescue...
"The oxidation and reduction of protein disulfide bonds in vitro also generally occurs via thiol-disulfide exchange reactions. Typically, the thiolate of a redox reagent such as glutathione or dithiothreitol attacks the disulfide bond on a protein forming a mixed disulfide bond between the protein and the reagent. This mixed disulfide bond when attacked by another thiolate from the reagent, leaves the cysteine oxidised. In effect, the disulfide bond is transferred from the protein to the reagent in two steps, both thiol-disulfide exchange reactions."
"In eukaryotic cells, in general, disulfide bonds are formed in the lumen of the RER (rough endoplasmic reticulum) but not in the cytosol. This is due to the oxidative environment of the ER and the reducing environment of the cytosol (see glutathione). Thus disulfide bonds are mostly found in secretory proteins, lysosomal proteins, and the exoplasmic domains of membrane proteins."
http://en.wikipedia.org/wiki/Disulfide_bond
go learn some chemistry...na but seriously i dont think you need to know this
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If you're asking questions for VCE Bio which are pushing the limits of Me, Russ and Truelight, you know you're going too far :P Besides that, a lot of those questions in your last list have already been answered. If you want another explanation, expand on what you don't understand so we can give a proper explanation which corrects any misunderstandings. Right now I don't really know what to say without simply repeating what's already been said.
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RE: reducing environments, I'm thinking it's either the amount of water in the cytosol or the fact that physiological pH is ~7.4
Either way, you don't need to know it.
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Thanks for the help :) Even i'm not sure what i want to know exactly :S
1) I think i am confused about what dissolve actually entails.
Correct me if i'm wrong (i think i am)
For ionic compounds, dissolve means that it dissociates into its non - metal and metal parts, while for
Organic compounds (with covalent bonds) it entails splitting into individual monomers / molecules, not individual atoms (e.g. dissolving of glucose doesn't mean splitting into Carbon atoms).
OR (/and)
Does it mean:
E.g. glucose molecules being surrounded by water and hydrogen bonds but not breaking the covalent bonds?
So for instance: Why is the glycerol and/or phosphate on a lipid *water soluble* does it dissolve further? or just has an affinity to be surrounded by water molecules.
*original question* Does water soluble refer to the complete breakdown of the molecular compound / molecule structure (e.g. NaCl -> Na + Cl) and/or the tendency for substances to seperate into individual, unconnected parts in water (e.g. full glucose molecule). Does it depend on Ionic / Covalent bonds?
2)
Does a monosaccharide (in monomer form) have any functions other than immediate energy supply?
3)
I'm also still confused about cell membranes. Is a plasma membrane by definition any phospholipid bilayer?
(e.g. if there was a picture of a cell with an arrow pointing to outer membrane, do i say plasma membrane or cell membrane?)
4)
The elements of Proteins are defined as
(CHON(S,P)) Which (any?) amino acids contain phosphorus? (if not, why is P in proteins sometimes?)
5)
Are there any amino acids which are non - polar and are form peptide hormones?
If they are do they transfer signals like lipid based hormones?
6) How are thyroid hormones different to Steroid hormones?
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I'm not going to give a chemical definition of dissolve but if you put something in water and the water molecules can bind it (ie it's polar) then it is capable of dissolving. Whether or not it does dissolve depends upon how many bonds form/size of the molecule etc.
2. Anabolic pathways
3. A phospholipid bilayer is a plasma membrane but not all plasma membranes are phospholipid bilayers. (I would write cell membrane but either is OK)
4. Huh, I never thought about that. From memory none of the standard amino acids have P in them but there may be others that do, or it may be acquired from lipids/ATP/chaperone proteins that are intimately associated with the protein whilst it forms
5. Individual amino acids are generally polar (NH+/COO-) but the side chain may be non polar. I can't think of any examples of an amino acid acting as a hormone though. Hypothetically, something like Glycine might be able to get across the cell membrane because it's not particularly large and find a cytosolic receptor but that's really not relevant/I'm not sure how correct it is. Opinions from anyone else?
6. Thyroid hormones are just hormones from the thyroid gland, steroid hormones are hormones with a steroid ring structure
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5. Individual amino acids aren't hormones, but there are many amino acid derivatives which are. The most obvious example would be noradrenaline which is made from tyrosine, but there's some others such as serotonin and such too. That's not particularly relevant anyhow. Point is, they act similar to peptides in that they do not cross the cell membrane and act on extracellular receptors, and do not require assistance to travel in the bloodstream. As for amino acids being hormones, that wouldn't make any sense. If they could, then these receptors would be constitutively active within any cell given that these amino acids are pretty much floating around everywhere. Hence, that's why these amino acids are changed a little to give some derivatives which are a bit more specific.
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How are amino acids active in anabolic pathways?
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How are amino acids active in anabolic pathways?
You mean monosaccharides? AAs is pretty self-explanatory o.O
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Not too sure what Russ meant by it, but they can be used in anabolic pathways either through providing energy for them (i.e. same as the first answer we had), or through actually being a building block of them. For example, cellulose and chitin are both polymers made from monomers of glucose or derivatives of it. Overall I wouldn't worry too much about this question. All that's important is the main function.
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Can the act as NADH or carrier molecules or something?
Also: Does Chitin dissolve in water>/.
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Also: Does Chitin dissolve in water>/.
hm i think they dont, cause usually complex CHOs are insoluble in water
btw, do both polar and non-polar molecules have no overall charge?
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Neither have an overall charge - polar simply has ends that are slightly charged
Are all non - polar substances have a pH of 7?
and
What feature makes the protein of spider webs so elastic (how is this due to beta plating) and strong?
and
Is a promoter sequence just a Methionine?
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Polar molecules might have an overall charge, although I guess it depends how you define polar.
Are all non - polar substances have a pH of 7?
This doesn't make sense..?
Is a promoter sequence just a Methionine?
No, a promoter sequence controls expression of the gene. The first amino acid in the protein chain is Met.
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Polar molecules might have an overall charge, although I guess it depends how you define polar.
Are all non - polar substances have a pH of 7?
This doesn't make sense..?
I mean, e.g.
a polar molecule must be charged.
Acidic or Basic substances must have an excess of H or OH as charge?
So does that mean all acidic or basic substances are charged?
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Polar molecules might have an overall charge, although I guess it depends how you define polar.
Hm, polar molecules have no overall charge cause theyre made from covalent bonds? :/
... not made of charged ions? :O
What feature makes the protein of spider webs so elastic (how is this due to beta plating) and strong?
I think its the fact that beta pleated sheets are stronger structures than alpha helices. plus spider webs are fibrous proteins thus theyd be very tough and insoluble in water? (i got most of this from biozone ^^ )
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Well if you think about it, a web does still bend quite a bit, so i guess that's elasticity
But why does Beta plating lead to bending? (or is it just less relative to alpha?)
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Well if you think about it, a web does still bend quite a bit, so i guess that's elasticity
But why does Beta plating lead to bending? (or is it just less relative to alpha?)
wait...i read about something a bit like this in NOB...
o here it is:
The major protein of wool is alpha-keratin, a spiral molecule. If the fi bre is
stretched and the hydrogen bonds are broken the fi bre becomes extended. If
the fi bre is then ‘let go’, the hydrogen bonds reform and the fi bre returns to its
original length.
• The major protein of silk is fi broin that is fully extended and lacks the coiling
found in the structure of wool. The silk molecules form a beta-pleated sheet
(see fi gure 1.18b). The polypeptide chains of silk are already extended and
cannot be extended further.
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Yeah i saw that, but that doesn't say anything about beta elasticity though, but they ARE elastic?
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Do lipids need to be converted into glucose before their energy can be released?
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Do lipids need to be converted into glucose before their energy can be released?
No, lipids are mostly converted into acetyl-CoA which feeds directly into Krebs' cycle and hence by-passes glycolysis.
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Yeah i saw that, but that doesn't say anything about beta elasticity though, but they ARE elastic?
According to answer.yahoo.com they are incredibly elastic: http://answers.yahoo.com/question/index?qid=20101016151853AAZNper
:)
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RE: beta sheets, I don't think it's particularly important but at a guess, the extra elasticity is derived from the fact that they're aligned with H-bonds between them, which allows for sliding of the sheets relative to each other.
Or something like this I guess
Hm, polar molecules have no overall charge cause theyre made from covalent bonds? :/
... not made of charged ions? :O
Just because they contain covalent bonds, doesn't mean they can't have an overall charge?
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Wouldn't that be ionic AND covalent bonding though? (does that occur?)
How do water molecules get through the phospholipid bilayer (cos they are small, ? could they get in without aquaporins?)
Q
In eukaryotic cells the conversion of ADP and phosphate into ATP occurs:
A) Only in the mitochondria, and requires energy.
C) In both the mitochondria and the cytoplasm, and requires energy (i.e. draws energy from other exergonic reactions?)
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How do water molecules get through the phospholipid bilayer (cos they are small, ? could they get in without aquaporins?)
Q
In eukaryotic cells the conversion of ADP and phosphate into ATP occurs:
A) Only in the mitochondria, and requires energy.
C) In both the mitochondria and the cytoplasm, and requires energy (i.e. draws energy from other exergonic reactions?)
Predominately through aquaporins, although some can leak through the plasma membrane despite being charged given its size.
C. Glycolysis occurs in the cytoplasm, while the ETC is obviously in the mitochondria. Glycolysis also requires energy as stated in C. It actually produces 4 ATP, but consumes two, leading to a net production of 2 as you should be familiar with.
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Thanks :)
Another one (of an infinite amount :S)
I think the answer is D but not 100% sure
Process of anaerobic respiration is different in plants and animals because:
C) Contain Different organnelles
D) Contain different enzymes
Also shinny, can ADP + Pi form ATP by reactions such as the breaking of peptide or polysaccharide bonds (right name? :S)
Thirdly
Do Cyanobacteria have chlorophyll?
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It would be D. Anaerobic respiration doesn't really require any organelles.
Not sure if the catabolism of polypeptides themselves can create ATP, I don't think they can, but the individual AAs resulting can be metabolised in the liver into acetyl-CoA which once again feeds directly into Krebs' cycle. AAs can also be turned into glucose.
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Okay thankyou. In some TSFX notes i bought it says all catabolic reactions are exergonic and create ATp but that doesn't sound right..
Also i'm very confused about this whole naming system for WBC and all the names like leukocytes, lymphocytes etc.
Is there a flow chart anywhere on the site?
thankyou
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You should check out the biozone website. it has kool animation links. does anyone else know a good biology site? :)
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Also i'm very confused about this whole naming system for WBC and all the names like leukocytes, lymphocytes etc.
Is there a flow chart anywhere on the site?
thankyou
leukocytes are the same thing as white blood cells, its just the scientific way of saying it
just google 'Hematopoiesis', there should be a few around
eg: http://www.ncbi.nlm.nih.gov/books/NBK27092/figure/A40/?report=objectonly
also natural killer cells are part of the lymphoid lineage
or this one from wiki
http://en.wikipedia.org/wiki/File:Hematopoiesis_(human)_diagram.png
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lol does anyone know the answer to
whether all non - polar molecules have ph of 7 (or vice versa) thanks
a polar molecule must be charged.
Acidic or Basic substances must have an excess of H or OH as charge?
So does that mean all acidic or basic substances are charged?
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pH depends a lot on temperature. Just because something has a pH of 7, doesn't necessarily mean it is 'neutral'.
Polar molecules are not 'charged' but rather have uneven distribution of charge in certain covalent bonds creating polar region (due to differing electronegativities of O-H, N-H and F-H).
Acidic or Basic substances must have an excess of H or OH as charge?
Have no idea what you mean there.
So does that mean all acidic or basic substances are charged?
Ditto, but I am inclined to say 'no'.
You really need to know the meaning of 'charged' before posting these question...
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lol does anyone know the answer to
whether all non - polar molecules have ph of 7 (or vice versa) thanks
a polar molecule must be charged.
Acidic or Basic substances must have an excess of H or OH as charge?
So does that mean all acidic or basic substances are charged?
im not 100% sure on what you mean by these q.s, but i do know that:
* Water has a tendency to ionize, split into H+ and OH- ions
= pH is therefore the concentration of Hydrogen (H+) ions per litre of solution and hence is a measure of the acidity or alkalinity state of a solution
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Haha ,
That's the definition in the Heinemann book lol ;D
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My chemistry isn't the greatest anymore so I'm happy for anyone to make any corrections, but from what I remember...
whether all non - polar molecules have ph of 7 (or vice versa) thanks
Uh, if they're non-polar, then that means they can't dissolve in water (a polar but not charged substance). If it can't dissolve, how the heck are you going to measure the pH :P
a polar molecule must be charged.
Explained by Rohitpi above. Read your Chem textbook or my unit 1 notes that I've attached for further clarification though. Your foundations of Chemistry seem a bit weak and if you want to understand Biology to the depth that you seem to be wanting to, you need the principles of Chem unit 1 and some of 2 as well. It's hard for me to fully explain all of this since what I'm covering in this post involves knowledge from across pretty much all of unit 1, so it's best for you to just go back and revise.
In a nutshell though, charged stuff are ions. Molecules (i.e. stuff joined by covalent bonds) are not charged. However, they can be polar if there is non-symmetrical electron distribution around an atom or molecule, resulting in a momentary and temporary dipole arrangement of charge. Therefore, think charge=permanent, polar=temporary charge.
Acidic or Basic substances must have an excess of H or OH as charge?
So does that mean all acidic or basic substances are charged?
Go back to your definitions of acids and bases, and to that of charge. Acids are proton donors; bases are proton receivers. Charge is due to the gain and loss of electrons. They're distinct concepts. So no, this means not all acids/bases are charged. For example, something as simple as ethanoic acid (CH3COOH) isn't charged, but it's an acid as the name implies. Pull simple examples to test any queries you have. That one shouldn't have been very difficult to disprove.
EDIT: Forgot you're only year 11 so you're doing Chem unit 1/2 now :P In that case, it'll progressively make more sense perhaps as you do Chemistry. A lot of this stuff should've been covered in previous years to some extent though?
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OHHHHHH. despite it being Bazza16 q.s that explanation helped clear things out a bit :)
Haha ,
That's the definition in the Heinemann book lol ;D
HEHE, it totes was :P
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A lot of this stuff should've been covered in previous years to some extent though?
'Charge' is definitely in VELS yr 10. Polarity might be new though, but is fairly simple once you get the basic idea of electronegativity.
-
Yah but the books dont explain it properly and if you went to a shitty school like me, the teacher didnt really teach us chem well... :(
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My chemistry isn't the greatest anymore so I'm happy for anyone to make any corrections, but from what I remember...
whether all non - polar molecules have ph of 7 (or vice versa) thanks
Uh, if they're non-polar, then that means they can't dissolve in water (a polar but not charged substance). If it can't dissolve, how the heck are you going to measure the pH :P
a polar molecule must be charged.
Explained by Rohitpi above. Read your Chem textbook or my unit 1 notes that I've attached for further clarification though. Your foundations of Chemistry seem a bit weak and if you want to understand Biology to the depth that you seem to be wanting to, you need the principles of Chem unit 1 and some of 2 as well. It's hard for me to fully explain all of this since what I'm covering in this post involves knowledge from across pretty much all of unit 1, so it's best for you to just go back and revise.
In a nutshell though, charged stuff are ions. Molecules (i.e. stuff joined by covalent bonds) are not charged. However, they can be polar if there is non-symmetrical electron distribution around an atom or molecule, resulting in a momentary and temporary dipole arrangement of charge. Therefore, think charge=permanent, polar=temporary charge.
Acidic or Basic substances must have an excess of H or OH as charge?
So does that mean all acidic or basic substances are charged?
Go back to your definitions of acids and bases, and to that of charge. Acids are proton donors; bases are proton receivers. Charge is due to the gain and loss of electrons. They're distinct concepts. So no, this means not all acids/bases are charged. For example, something as simple as ethanoic acid (CH3COOH) isn't charged, but it's an acid as the name implies. Pull simple examples to test any queries you have. That one shouldn't have been very difficult to disprove.
EDIT: Forgot you're only year 11 so you're doing Chem unit 1/2 now :P In that case, it'll progressively make more sense perhaps as you do Chemistry. A lot of this stuff should've been covered in previous years to some extent though?
Thanks a lot!
Does that mean though that non - polar don't affect ph of solution? By proton donors and revievers do you just mean H+ ?
I was confused because some of the TSFX notes i bought seemed to suggest only polar substances change ph :S
:D
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Non-polar stuff can't even be in the solution to begin with because it can't dissolve. Think of mixing oil and water. It just forms a separate layer on top. And yeh, H+ is essentially just a proton because the most common hydrogen isotope has no neutrons. Therefore a hydrogen atom missing an electron (H+) is just a proton.
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My bio teacher today said that to mix polar and non-polar substances, you'd need something that's both, like detergent or phospholipids.
I haven't really gotten my head around this concept yet - how would you apply this to the oil in water thing? Does it apply? Or am I just taking it out of context?
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Read here
The idea is that when you mix the two, polar clumps with polar and non-polar with non-polar. A detergent has areas that can bind polar substances and non-polar substances. That way, it can bind the oil on the plate you're washing as well as the water you're using, in order to pull it off.
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what is an amino acid?
-
Building block of polypeptides.
Consist of an amino group, a carboxyl group, a carbon 'centre', a hydrogen sticking out one side, and a variable R group the other side
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what is an amino acid?
Picture is worth a thousand words... (although it is a monomer of polypeptides and proteins)
(http://deadguyblog.files.wordpress.com/2010/01/amino_acid_structure_2.jpg)
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Don't need to know alpha carbon though? (+ wtf is it)
-
Just a designation of the central carbon
-
Just a designation of the central carbon
Yep, its just got an awesome name because every scientist wants to be famous for naming something.
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Well there's a naming system in chemistry that goes alpha/beta/etc. but it's got no relevance to the role of the atom
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Well there's a naming system in chemistry that goes alpha/beta/etc. but it's got no relevance to the role of the atom
Sort of relevant - but why do most elements end in IUM?
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Might sound like a stupid question, but why do ions have trouble getting through membranes? I probably would have heard the answer somewhere already, but it's completely slipped my mind at the moment.
Does it have to do with polarity or anything like that?
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Might sound like a stupid question, but why do ions have trouble getting through membranes? I probably would have heard the answer somewhere already, but it's completely slipped my mind at the moment.
Does it have to do with polarity or anything like that?
Yeh, kinda. Basically ions are charged (not polar - read my last post for the difference between them), so they can't get through the non-polar phospholipid bi-layer.
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Well there's a naming system in chemistry that goes alpha/beta/etc. but it's got no relevance to the role of the atom
Sort of relevant - but why do most elements end in IUM?
At a guess it's a latin suffix that means something relevant
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Yeh, kinda. Basically ions are charged (not polar - read my last post for the difference between them), so they can't get through the non-polar phospholipid bi-layer.
Right, but I was reading on Douchy's forum, and he said that the fatty acid tails of the phospholipids repel ions! Aren't the fatty acid tails supposed to be non-polar? If so, shouldn't it be that the phosphate heads are the ones that repel ions?
-
Oh haha,
Actually no, infact the non-polar fatty acid tails don't
interact with the ions, they move away from anything
charged like water and ions. Where as the phosphate
heads would be attracted to the charged ions and so
the ions would never be able to pass through the
membrane. :P
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Well there's a naming system in chemistry that goes alpha/beta/etc. but it's got no relevance to the role of the atom
Sort of relevant - but why do most elements end in IUM?
Its just tradition, but is is now part of the official naming system for new elements I think
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Well the latin root is apparently
Suffix used to form nouns, sometimes having the sense of bigger or more complicated.
which makes sense
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What is the difference between osmotic gradient and osmotic pressure? (can osmotic pressure simply refer to a change in osmotic gradient as there is more 'pressure' on 1 side of membrane after osmosis occurs?
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The osmotic gradient is the difference in concentration between two solutions on either side of a semipermeable membrane.
The osmotic pressure is the pressure which needs to be applied to a solution to prevent the inward flow of water across a semipermeable membrane (helps with turgidity).
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Given Substance A containing more solute than B, with a net movment of water into A initially, but gradually decreasing, can this pressure be referred to as osmotic pressure?
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Given Substance A containing more solute than B, with a net movment of water into A initially, but gradually decreasing, can this pressure be referred to as osmotic pressure?
I think so
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is it osmotic pressure or simply equilibrium of osmotic gradient or both? :DS
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I would say its simply equilibrium of osmotic gradient, Oh but it would depend on the
type of cell right?
I thought that if it was a plant cell then it would appropriate to use the term
osmotic pressure
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Osmotic pressure refers to the pressure on just one side of the semi-permeable membrane caused by water wanting to diffuse to the other side. However, unless there's nothing on the other side of the membrane, there's going to be a osmotic pressure on the other side as well which opposes that pressure and effectively cancels each other out to some extent. The remaining force is the osmotic gradient and can be seen to be the net force resulting.
For example, there might be 100 osmoles on one side, 90 on the other, and a osmotic gradient of 10 osm.
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Thanks that clears it up :)
So for example
If A and B are seperated by a semipermeable membrtane and both the membrane and substance enclosing the solutions is *invincible*, and solution A has an Infinitely higher solute concentration, then eventually as solution A filled, the net movement of water would stop *before* the gradient has reached equiligrium as the imprenatrable substance counters it with an osmotic gradient :?
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Thanks that clears it up :)
So for example
If A and B are seperated by a semipermeable membrtane and both the membrane and substance enclosing the solutions is *invincible*, and solution A has an Infinitely higher solute concentration, then eventually as solution A filled, the net movement of water would stop *before* the gradient has reached equiligrium as the imprenatrable substance counters it with an osmotic gradient :?
...whut? How can this invincible substance have an osmotic gradient itself? Only a solution can have an osmotic gradient. Maybe try explaining again what you mean with just a glass container, a semi-permeable membrane and tangible amounts of solution?
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lol. I meant solutions in invicible container :D
yeah i guuess it was probably not necessary
ok..
So
Solution A and Solution B are seperated in a glass contaner (with a lid) by a semipermeable membrane.
Solution A contains a much higher solute conc. than B
Water from solution B flows into solution A until Solution A has filled up and is stopped from filling more by the lid, but it still has a higher solute conc.
Is this an example of 'osmotic gradient'?
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lol. I meant solutions in invicible container :D
yeah i guuess it was probably not necessary
ok..
So
Solution A and Solution B are seperated in a glass contaner (with a lid) by a semipermeable membrane.
Solution A contains a much higher solute conc. than B
Water from solution B flows into solution A until Solution A has filled up and is stopped from filling more by the lid, but it still has a higher solute conc.
Is this an example of 'osmotic gradient'?
Yeh, I guess. I don't see why you need such an elaborate set-up though. An osmotic gradient doesn't need to be permanently there to count as one. It can just be a temporary thing until an equilibrium is established.
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m... does sheer 'mass of increasing water' count as osmotic pressure?
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m... does sheer 'mass of increasing water' count as osmotic pressure?
That would be hydrostatic pressure increasing due to an increased mass. Hydrostatic pressure in a basic sense refers to the weight of the water as affected by gravity creating pressure against the walls of its container. Osmotic pressure only refers to pressure resulting from differences in osmolarity. So by diluting the water, you'd probably create an osmotic pressure anyway. However, the 'mass' itself as you were asking doesn't (well, indirectly does). Hopefully you understand the distinction I'm trying to show here =/
Even if you don't, hydrostatic pressure isn't a concept covered in Biology 3/4 though, so don't worry about it. It is equally important as osmotic pressure when it comes to haemodynamics and such in the human body though.
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thanks :) i think i understand now
Does Globular and fibrous refer to tertiary or quaternary structure?
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Pretty sure it can be used for either, but usually tertiary as most proteins don't have a quaternary structure.
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lol. NOB got it wrong then, NOB said, globular and fibrous are quartnery structures, therfore suggesting all enzymes have a quaternary structure
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The spherical structure is induced by the protein's tertiary structure.
From here. Seems NoB may be wrong here
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Definitely tertiary though many fibrous 'proteins' band together to form a bigger fibrous 'protein' with other molecules holding it together thus giving it a quarternary structure..
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What exact term woudl you describe the capabilities of monsaccharides ?
-An immediate source of chemical energy
or
- The immediate precursor to useable ATP
-The most immediate chemical energy source?
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I think an immediate source of chemical energy would be okay
-
Almost definitely 'The immediate precursor to useable ATP'.
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lol should have made this clearer
*those were examples i thought of from different perspectives, any refinement possible ?
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Oh okay :)
In that case I would rid with the term 'precursor' (bio uni people please confirm that it's not ideal here) but keep something similar to that definition.
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Get up to 1000 posts :D
I looked up synonyms for precursor.
I don't think herald fits well ! :)
But yeah, i think there should be a better word (not sure what it is)
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I think it's not the correct term in that glucose doesn't in any way become ATP (again, I'm not 100% sure on this). You could just say it is used to resynthesise ATP.
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m... probably
The - add descriptive word descriping neccesity / order(fundamental?) source of energy to synthesise ATP?
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Umm yeah something like that. I think synthesise gives the wrong impression though...
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Pretty sure it can be used for either, but usually tertiary as most proteins don't have a quaternary structure.
i reckon most proteins form a quaternary structure because you get proteins forming complexes with other proteins in most of the cases i can think of
look here for eg
http://vce.atarnotes.com/forum/index.php/topic,26528.msg268958.html
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m... yeah i doubt they'll end up asking that, do you have a defintion for the role of Glucose as a source of energy?
(simply saying, glucose is a asource of energy, is not really great because starch, glycogen, fat are all sources of energy
the 'predominant' (precursor?) to ATP?
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Just call it a requirement for cellular respiration to occur
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Is glycogen water-soluble because it has more alpha -1,6 glycosidic links?
-
More links than what?
I'm trying to think of how that would affect solubility and can't think of anything. It's the OH groups that determine it.
-
hm im confused :buck2:
it says in my workbook that glycogen is more highly branched and water-soluble than starch cause it has more alpha-1,6 glycosidic links than alpha -1,4 ones.
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hm im confused :buck2:
it says in my workbook that glycogen is more highly branched and water-soluble than starch cause it has more alpha-1,6 glycosidic links than alpha -1,4 ones.
Glycogen is more soluble than starch (even though they both have 1,6 glycosidic links and alpha -1,4 ones) because starch exists in general as an alpha helix while glycogen is a more highly branched and random structure. In the alpha-helical conformation there are less exposed -OH (hydroxide) groups to the solution making the starch less hydrophilic than the glycogen. As there are less OH groups available to from hydrogen bonds with the polar water molecules, that is why starch is less soluble.
It is due to this 'extra' branching that glycogen has that enables it to be more soluble.
Hope that helps. :)
(this specific stuff will never come up in the exam btw)
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People I need help please!!! ASAP!!! My class is doing a SAC on osmosis right now and we are testing potato cylinders. Now we are putting the potato cylinders in different sucrose concentrations. Our control is potato cylinder in distlled water. However apparently it is not a 'true' or 'valid' control. why is that? Please reply ASAP!
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Because it is not truly isotonic
-
Can someone pls explain (possibly from a chemistry POV) why a substance such as glycogen or starch and only be hydrolysed at the end molecules? I know it has something to do with free OH groups, but am still confused
so if you have
monosaccharide - monosaccharide - monosaccharide etc...
do the "taken up" OH groups in the middle somehow prevent hydrolysis (HOW exacltly ) thanks
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do the "taken up" OH groups in the middle somehow prevent hydrolysis (HOW exacltly ;) ) thanks
If someone else wants to try and attempt to explain this to a year 11 chemistry level, they can, but at this point I think you're better served by just accepting it and not worrying.
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okay maybe not from a year 11 chemistry level. i think there was a simple explanation that i forgot :S
Something about simply a reason why Hydrolysis needs 1 free bond to work?
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People I need help please!!! ASAP!!! My class is doing a SAC on osmosis right now and we are testing potato cylinders. Now we are putting the potato cylinders in different sucrose concentrations. Our control is potato cylinder in distlled water. However apparently it is not a 'true' or 'valid' control. why is that? Please reply ASAP!
Well first you've got to define what a control group is. Simplest way to put it is a group which isn't exposed to the intervention that is being put in place. In this case, that intervention is the sucrose solution, and you're measuring the effect of this solution on the mass of the resultant cylinders. The control which is needed to verify that the cylinders aren't just changing their mass spontaneously or due to a factor other than the osmosis that's expected to occur is to have a potato which is given no solution at all. If the mass of a potato without the solution did change, then obviously there's something else going on here other than just the osmosis and that'd invalidate all your results. So pretty much, that's the ideal control. The 0% sucrose solution doesn't really work because distilled water itself is hypotonic to the potato cells, so obviously that's going to create some weight change.
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hm im confused :buck2:
it says in my workbook that glycogen is more highly branched and water-soluble than starch cause it has more alpha-1,6 glycosidic links than alpha -1,4 ones.
Glycogen is more soluble than starch (even though they both have 1,6 glycosidic links and alpha -1,4 ones) because starch exists in general as an alpha helix while glycogen is a more highly branched and random structure. In the alpha-helical conformation there are less exposed -OH (hydroxide) groups to the solution making the starch less hydrophilic than the glycogen. As there are less OH groups available to from hydrogen bonds with the polar water molecules, that is why starch is less soluble.
It is due to this 'extra' branching that glycogen has that enables it to be more soluble.
Hope that helps. :)
(this specific stuff will never come up in the exam btw)
oooooo but does this mean that its fully water-soluble? i thought that all polysaccharides were insoluble in water?
Out of curiosity, what is everyone's classes up to? We just started membranes today, would you say that we're behind? :/
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No. we're still halfway through chapter 1 :S (though our teacher was on camp for first week)
MHS rarely finishes the bio course (any teacher)
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Hey guys, can someone explain the events that take place in apoptosis in simple terms? NOB is confusing me -.- and how would you explain caspases? Thanks in advance :)
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Caspases are just a particular family of proteases, responsible for breaking down the internal structure of the cell during cell death/destruction.
In apoptosis, the cell receives a signal to self destruct or fails to suppress such a signal. This leads to activation of the relevant enzymes and destruction of the cell organelles. "blebbing" occurs, where the cell membrane forms random invaginations/bulges and apoptotic bodies are released (similar to vesicles). Eventually the cell membrane begins to lose its integrity and molecules can leak from the cell.
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this video is pretty awesome (as usual by wehi lol)
please dont remember all these steps lol
http://www.youtube.com/watch?v=9KTDz-ZisZ0
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Caspases are just a particular family of proteases, responsible for breaking down the internal structure of the cell during cell death/destruction.
In apoptosis, the cell receives a signal to self destruct or fails to suppress such a signal. This leads to activation of the relevant enzymes and destruction of the cell organelles. "blebbing" occurs, where the cell membrane forms random invaginations/bulges and apoptotic bodies are released (similar to vesicles). Eventually the cell membrane begins to lose its integrity and molecules can leak from the cell.
Thanks! That was a lot easier to understand :)
this video is pretty awesome (as usual by wehi lol)
please dont remember all these steps lol
http://www.youtube.com/watch?v=9KTDz-ZisZ0
LOL ! That was actually unnerving haha, the background music and stuff, but thanks guys, helped a lot.
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Heya Guys
Whats the difference between Peripheral Proteins and Integral Proteins, and what are examples of each
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Heya Guys
Whats the difference between Peripheral Proteins and Integral Proteins, and what are examples of each
Both are associated with the cell plasma membrane. Peripheral proteins (eg G-proteins) are attached to the membrane temporarily, whilst integral proteins (eg Insulin receptor) are attached to it permanently. Peripheral proteins can actually attach themselves to integral proteins.
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Can triglycerides etc. (not phospholipids) form micelles? They still have a hydrophillic head (glycerol)? If not why not?
-
iirc, yes they can
-
haha nice ;D
That would probably look weird though with the
3 fatty acid tails and all. :P
-
how do proteins stabilise pH?
-
Proteins are polar. When the pH of a solution around them changes, the amino acids in the proteins may either lose or gain a hydrogen ion (H+), to stabalise the pH of the solution.
-
Hi guys, just wondering, can proteins be stored? if so, how?
-
Hi guys, just wondering, can proteins be stored? if so, how?
Stored where?
-
in cells?
-
in cells?
They're often stored in vesicles (phospholipid membrane bubbles basically). This prevents them from reacting with anything else. A good example of this is lysosomes - basically vesicles within certain immune cells which are used to to digest pathogens. If the contents of these just floated around everywhere (lipases, proteases, nucleases etc.), the cell would practically eat itself.
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proteins can be used as storage i think --> eg. Ferritin (storage of iron in spleen)
And, what structure (primary/secondary/tertiary) determines the functionality of an enzyme's active site?
EDIT: woopsies, shinny is right, misread question. ignore my storage comment ^^
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proteins can be used as storage i think --> eg. Ferritin (storage of iron in spleen)
And, what structure (primary/secondary/tertiary) determines the functionality of an enzyme's active site?
Ultimately, the tertiary.
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tertiary :) and thanks for the help :)
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proteins can be used as storage i think --> eg. Ferritin (storage of iron in spleen)
And, what structure (primary/secondary/tertiary) determines the functionality of an enzyme's active site?
Ultimately, the tertiary.
ok i was thinking that it would be tertiary. but could it be secondary cause the random coils/loops make up the active site?
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proteins can be used as storage i think --> eg. Ferritin (storage of iron in spleen)
And, what structure (primary/secondary/tertiary) determines the functionality of an enzyme's active site?
Ultimately, the tertiary.
ok i was thinking that it would be tertiary. but could it be secondary cause the random coils/loops make up the active site?
But they don't. The tertiary makes the overall 3D structure.
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lol yea you dont get an alpha coil doing anything its the combined structure of alpha coils and beta sheets and the bonds that form between residues that make up the tertiary structure
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kool thanks guys. i get it now :)
btw does the unit 3 exam have more bio-macromolecule q.s on it or more plasma m-brane/diffusion q.s
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kool thanks guys. i get it now :)
btw does the unit 3 exam have more bio-macromolecule q.s on it or more plasma m-brane/diffusion q.s
It's pretty well balanced as far as I know. Biomacromolecules are generally MCQ questions though whereas diffusion and osmosis is basically a guaranteed short answer. That being said, try to understand the concepts of osmosis and such, whereas biomacromolecules is mostly rote learning.
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In the beetroot SAC, an error would be that the amount of leaked pigment couldn't be quantified. How could you improve this next time?
-
in cells?
They're often stored in vesicles (phospholipid membrane bubbles basically). This prevents them from reacting with anything else. A good example of this is lysosomes - basically vesicles within certain immune cells which are used to to digest pathogens. If the contents of these just floated around everywhere (lipases, proteases, nucleases etc.), the cell would practically eat itself.
Probably also worth mentioning that they can also be stored on the vesicle membranes and when needed, the vesicle fuses with the cell membrane to insert the protein (eg GLUT4 transporters + insulin)
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in cells?
They're often stored in vesicles (phospholipid membrane bubbles basically). This prevents them from reacting with anything else. A good example of this is lysosomes - basically vesicles within certain immune cells which are used to to digest pathogens. If the contents of these just floated around everywhere (lipases, proteases, nucleases etc.), the cell would practically eat itself.
Probably also worth mentioning that they can also be stored on the vesicle membranes and when needed, the vesicle fuses with the cell membrane to insert the protein (eg GLUT4 transporters + insulin)
so are they found as amino acids there? or do they needed to be converted to enzymes or hormones first before being stored? also do plants store protein? don't legumes like lentils have heaps of protein?
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in cells?
They're often stored in vesicles (phospholipid membrane bubbles basically). This prevents them from reacting with anything else. A good example of this is lysosomes - basically vesicles within certain immune cells which are used to to digest pathogens. If the contents of these just floated around everywhere (lipases, proteases, nucleases etc.), the cell would practically eat itself.
Probably also worth mentioning that they can also be stored on the vesicle membranes and when needed, the vesicle fuses with the cell membrane to insert the protein (eg GLUT4 transporters + insulin)
so are they found as amino acids there? or do they needed to be converted to enzymes or hormones first before being stored? also do plants store protein? don't legumes like lentils have heaps of protein?
They would have already been translated to their functional form. There's no point storing amino acids because when the cell needs that particular enzyme or hormone, it won't be readily available. The point of storage is so that such proteins can be released en masse at demand. And yeh, I'd assume plants would. Obviously my knowledge of botany isn't as good as my knowledge of the human body, but I can't see any reason why they wouldn't. Well more so, I see a necessity why they would need to.
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hey guys.
i was just wondering if there was a particular structure to answering a question in biology.
like, 3 marks = 3 points.
and do you answer it in a structure of like answer, explanation etc.
adding a structure to my answers i think would really help!!
-
also. what would a couple of errors be in an enzyme SAC.
liver cubes in a test tube, with added detergent and different concentrations of hydrogen peroxide.
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hey guys.
i was just wondering if there was a particular structure to answering a question in biology.
like, 3 marks = 3 points.
and do you answer it in a structure of like answer, explanation etc.
adding a structure to my answers i think would really help!!
Three marks = three points, yes. My structure is basically to make a statement answering the question (1mark) and then provide either examples or further reasoning for 1 mark each until I reach the required amount. If it's a broader discussion questions (eg for 10marks) then I write structured paragraphs rather than 10 individual points. If you post a question I'll give you an example answer.
also. what would a couple of errors be in an enzyme SAC.
liver cubes in a test tube, with added detergent and different concentrations of hydrogen peroxide.
Experimental error (always) and insufficient time for reactions to occur are the two biggest ones I can think of
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also. what would a couple of errors be in an enzyme SAC.
liver cubes in a test tube, with added detergent and different concentrations of hydrogen peroxide.
This is copied directly from my SAC, we did a similar/same SAC:
One of the major factors that contribute to the rate of reaction is the concentration of the enzyme and substrate in the solution. The concentration of the substrate, hydrogen peroxide, was measured fairly equally. However, the amount of enzyme (catalase) wasn’t controlled accurately. Some pieces of liver were bigger than others, corresponding to varying amounts of enzyme quantity. If I have a chance to redo this experiment, I will be more careful in cutting up my pieces of liver to exact sizes.
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thank you!
but...
how would you structure a question asking you to outline or describe an experiment you should design.
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What happens to the cell wall on a beetroot cell when the membrane gets damaged by an acidic solution? Pigment leaks out, so does that mean that the cell wall is penetrated as well?
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What happens to the cell wall on a beetroot cell when the membrane gets damaged by an acidic solution? Pigment leaks out, so does that mean that the cell wall is penetrated as well?
I'm pretty sure that the cell wall is quite porous. I know that the proteins will be denatured by the high acidity but i think that only affects its function, not its structure.
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By penetrated if you mean that the pigment leaks out
of the cell wall, then yes. Remember that the cell wall
is permeable to everything, including solutions carrying
solutes as well.
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Why is it that wen you put a potato strip in a solution thats 5 % sodium chloride for 30 minutes the potato ends up losing more mass than one that was put in a solution that was 20% sodium choloride? (both hypertonic solutions)
-
Experimental error perhaps?
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nah it wasnt. my teacher sed its suppose to happen. I was thinking of something along the lines of greater concentration gradient = increased rate of diffusion? o.o
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are all coenzymes (the temporarily bound cofactors) organic?
-
are all coenzymes (the temporarily bound cofactors) organic?
i believe they are.
edit, beaten..
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ok thanks guys.
'the apoenzyme is the protein portion of the functionally active enzyme' (biozone answers)
but i thought that the apoenzyme wouldnt work without its cofactor? so how can it be 'functionally active' :/
also, would it be right to say that; prosthetic group = inorganic cofactors and then coenzyme group = organic cofactors? (as well that one is permanent and the other temporary)
or can prosthetic be organic as well
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Why is it 36 or 38 ATP and not 37 produced during aerobic respiration?
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Why is it 36 or 38 ATP and not 37 produced during aerobic respiration?
Not particularly VCE level knowledge, but it's because in the brain, liver, heart and kidneys, a certain shuttle molecule exists which doesn't elsewhere which brings the NADH made in glycolysis from the cytoplasm into the mitochondria so it can be reduced in the electron transport chain. Therefore you get more ATP. Keep in mind that these are all theoretical maximums. Apparently you get nowhere near 36-38 ATP.
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ok thanks guys.
'the apoenzyme is the protein portion of the functionally active enzyme' (biozone answers)
but i thought that the apoenzyme wouldnt work without its cofactor? so how can it be 'functionally active' :/
also, would it be right to say that; prosthetic group = inorganic cofactors and then coenzyme group = organic cofactors? (as well that one is permanent and the other temporary)
or can prosthetic be organic as well
the terms you ask about are less to do with whether the compounds are organic or not and more to do with their function. Cofactors can (depending on whose definition you take) include both organic and inorganic compounds.
prosthetic groups and coenzymes are both types of cofactors and are both usually organic - prosthetic groups bind tightly (usually permanently) to the enzyme whereas coenzymes bind loosely to the enzyme - coenzymes enter the reaction as a cosubstrate, are changed by the reaction and released. examples of coenzymes include ATP, NAD, FAD and coenzyme A; examples of prosthetic groups (I don't think these are even on the VCE course just btw, but for interest's sake...) include the Heme group (e.g. Haemoglobin) and the Flavin group.
EDIT: also with regard to apoenzymes (Which I also think are not on the course), they are functionally active once they have their cofactor - without the cofactor they are inactive - just be careful how you interpret Biozone's terminology.
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Hey guys, one of the Checkpoints questions included:
"Why is it advantageous for starch and glycogen to be large and not soluble?
Both are needed as energy stores inside the cell. They are large and soluble and therefore form solid grains inside cells. These grains do not interfere with metabolic reactions taking place in cells and do not affect the osmotic gradient."
This is the first time I've come across 'starch/glycogen grains.' What are they made of exactly?
Also, I was looking over some Neap Smartstudy questions and they referred to microscopes a few times but I've read before that we don't need to know about them? Is Neap being vague, or should I actually learn about the electron etc. microscopes?
Thanks ! :)
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This is the first time I've come across 'starch/glycogen grains.' What are they made of exactly?
They're made of...starch/glycogen respectively :P
EDIT: Wait so did you understand the rest of Checkpoints' explanation? Basically since they're insoluble, they don't dissolve within the cytoplasm and will form solid masses i.e. the grains. The reasons for this occurring are pretty much as Checkpoints has said. As for the microscopes, they might get mentioned often as part of the stimulus material but I think all you need to know is what organelles are visible under a light and electron microscope.
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LOL, I know haha but are the grains like, covered in anything? Or is it just that since starch/glycogen is insoluble, it can just float around in the cytoplasm? Idk how to explain my question -.-
But thanks :)
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LOL, I know haha but are the grains like, covered in anything? Or is it just that since starch/glycogen is insoluble, it can just float around in the cytoplasm? Idk how to explain my question -.-
But thanks :)
Well yeh, they just float around I guess. They don't need to be covered in anything (such as a phospholipid bilayer vesicle etc.) because they're already soluble.
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Haha, thanks for that :)
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Would 'catalase will breakdown hydrogen peroxide at differing rates due to factors, such as temperature and pH, affecting the rate of reaction' be a suitable one mark hypothesis statement when experimenting the rates of reactions of catalase in liver with hydrogen peroxide?
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possibly. if your teacher is very harsh he would expect a more detailed explanation that enzyme action and reaction rates will decline as pH and temp vary away from the optimum, though if he is more lenient (or she) they will give you full mark
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hey guys I have a question,
" when plant and animal cells are placed in a saline solution why does the plant cell retain its shape
whilst the animal cell doesn't ?"
I thought that the plant cell wouldn't really retain its shape since the presence of the cellulose cell
wall merely maintains its shape whilst the plasma membrane shrivels.
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hm well wen the plant cell undergoes plasmolysis, the plama membrane may shrival but the cell wall doesnt shrink too with it. it stays the same in size and shape if you look at the wall, its only inside the contents are squished together and changed in shape.
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^That's it
Not a great question though, as the plant cell really doesn't retain its shape
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^That's it
Not a great question though, as the plant cell really doesn't retain its shape
Why are you doing bio at 7 (-ish) in the morning?
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Can you view vacuoles under LM?
-
Can you view vacuoles under LM?
light microscope?
We did an experiment where we could in a plant cell, some cells had the chloroplasts pushed against the cell wall because of a large bubble (vacuole) taking up so much room.
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Can you view vacuoles under LM?
ye i think you can for plants.
is chlorophyll a lipid?
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no chlorophyll is a pigment
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no chlorophyll is a pigment
That's y9! I actually understood one Q in this thread! :)
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no chlorophyll is a pigment
Pigment's more of a functional description. In terms of biochemical, a quick Google search suggests it's technically actually a lipid because it's lipid-soluble. Not exactly required knowledge though.
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Intriguing! A pigment is not a chemical description but a tendency to change wavelengths into selective wavelengths, so all colour has some pigment!
-
Exactly how does the amino acid sequence of a polypeptide determine the final shape of the protein?
-
well the amino acids each have an R group. an R group can determine wheter teh AA is polar, non-polar or charged. the bonds (disulfide bridge/ionic/H bonds) that form between the neighbouring AAs when they fold into its 3D structure are dependent on the R groups and their position in the sequence. for eg. a polar amino acid in one area of the sequence that formed a hydrogen bond with a another polar amino during the tertiary structure stage acid vs. a charged aa forming an ionic bond with another charged amino acid
--> the shape and function would totally be different!
Intriguing! A pigment is not a chemical description but a tendency to change wavelengths into selective wavelengths, so all colour has some pigment!
i didnt noe that too! :O
This is the chlorophylls structure: a porphyrin ring (the head of the molecule with a central mg ion) attached to a hydrocarbon tail (interacts with hydrophobic regions of proteins in the thylakoid membrane)
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lol and you DEFINATELY do not need to know that ;)
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are transition reactions part of the Krebs cycle?
-
are transition reactions part of the Krebs cycle?
by transition it indicates the reactions before Krebs and after glycolysis. so converting the products of glycolysis to the form used at the start krebs cycle (pretty sure its Acetyl CoA)
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The efficient folding of a protein molecule is ensured by the presence of other proteins known as protein chaperons in a cell. A likely result of defective chaperone is:
a)the production of a protein with a faulty primary structure
b)the production of proteins with incomplete tertiary structures
c)the production of a protein with a faulty secondary structure
d)the overproduction of the protein
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Answer is B
Doubt they would ask that on exam as it is very indepth knowledge, but it could be one of the harder MC on there
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Answer is B
Doubt they would ask that on exam as it is very indepth knowledge, but it could be one of the harder MC on there
Quite possible IMO. They gave you all the information you needed regarding chaperone proteins as you're not expected to know about them. What you were meant to know about was the word 'folding', which is essentially a tertiary structure process.
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okie. i got b too but i was quite tempted to choose a. this was on one of teh A+ practice tests on enzymes and proteins.
what is a reason for eliminating A?
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Because folding of proteins is a tertiary structure process as I said above. Primary structure is only dictated by the order of the amino acids which isn't affected if folding was faulty.
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i dont get it (sorry, im a bit slow in processing things)
are the chaperone proteins helping the protein fold into its tertiary structure. if so, wouldnt the folding part of the q. be irrelevant to how chaperone protein is defective.
thats why i sort of just thought of it as wat makes a protein not work. if the proteins amino sequence was altered it wouldnt even be able to become chaperone = defective chaperone
OH AND DOES ANYONE HAVE THE SOLUTIONS TO A+ PRACTICE TESTS?
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It's asking what the effect of defective chaperone proteins on other proteins being synthesised would be - not the chaperone protein itself. That is, if a cell didn't have chaperone proteins to ensure correct folding of other proteins being synthesised, then their tertiary structure wouldn't be correct.
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OHHHHHH ok i get it now! i must read q.s more carefully next time
its totally B then.
ok thanks shinny, cleared up that confusion for me a lot! :)
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for teh following graph,
The variable being investigated in these two samples was most probably
a)amount of substrate
b)amount of reactant
c)concentration of enzyme
d)pH
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I'd probably go for (a), amount of substrate.
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I think A is wrong since the concentration of product is the same for both haha the answer would most likely be C.
Because sample 1 arrives at its destnatino much quicker than sample 2.
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Secondary structures are nowhere near as variable as tertiary structures. Google "Ramachandran Plot" and you'll see what I mean. As such, they don't require chaperone proteins to control their folding.
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yeah oops it's C
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okie kewl thats wat i put down. :)
If ONE amino acid of haemoglobin changed due to mutation, wat structural level (primary/secondary/tertiary/quaternary) would definitely be changed and wat structural level MIGHT change? explain.
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OK, the primary structure definitely changed because the primary structure is the sequence of amino acids, and the amino acid has mutated meaning it is different.
Secondary structure MIGHT change, but I'm not really sure how to put that into words except for really saying that there is no longer the same type of bond? So an alpha helix MIGHT become a random coil due to the different bond.
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ok thanks.
i get the first part but for the second part of the q., could it be tertiary as well?
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Yeh, secondary, tertiary and quaternary consequently might change. Primary by definition must change.
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you know a polar R group can it for a hydrogen bond with a different polar R group then the polar one it usually bonds to?
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Yeh. Hence why those chaperone proteins referred to in your post a few questions ago are needed.
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Hey guys,
I was doing the TSSM 2010 exam when I came across this question.
Why would the answer be glycoprotein? Wouldn't molecule A be a
glycolipid sinceit isn' attached to a protein? If not how did they
decipher the answer to be glycoprotein?
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Hey guys,
I was doing th TSSM 2010 exam when I came cross this question.
Why would the answer b glycoprotein? Wouldn't molecule A be a
glycolipid?
It looks like glycolipid to me. it is obviously on the phospholipid bilayer rather than on the protein.
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a reason for it being more of a glycoprotein could be because glycolipids usually have more of it is suspended in the plasma membrane since the bottom bit it lipid soluble. whereas this picture indicates that the whole conjugated molecule is hydrophilic.
-
I would have said that it was a glycolipid also, as there is no obvious protein structure attached to it.
Maybe it is because glycolipids are generally shorter than glycoproteins (although that is relative anyway)?
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Someone do me a favour and tell me what are the things you've studied so far. Would I be correct in assuming that you've just finished Area of Study 1?
ie this
• the chemical nature of the cell
– synthesis of biomacromolecules: polysaccharides, nucleic acids and proteins
– the structure and function of lipids
– the structure and function of DNA and RNA
– the structure and functional diversity of proteins: the proteome;
• the role of organelles and plasma membranes in the packaging and transport of biomolecules;
• the nature of biochemical processes
– enzymes as organic catalysts
– energy requirements of cells; catabolic and anabolic reactions
– energy transformations, including main stages in and sites of photosynthesis and cellular
respiration; ATP-ADP cycle; factors affecting rate of energy transformations;
• applications of molecular biology in medicine including the design of drugs and in medical
diagnosis.
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Someone do me a favour and tell me what are the things you've studied so far. Would I be correct in assuming that you've just finished Area of Study 1?
ie this
• the chemical nature of the cell
– synthesis of biomacromolecules: polysaccharides, nucleic acids and proteins
– the structure and function of lipids
– the structure and function of DNA and RNA
– the structure and functional diversity of proteins: the proteome;
• the role of organelles and plasma membranes in the packaging and transport of biomolecules;
• the nature of biochemical processes
– enzymes as organic catalysts
– energy requirements of cells; catabolic and anabolic reactions
– energy transformations, including main stages in and sites of photosynthesis and cellular
respiration; ATP-ADP cycle; factors affecting rate of energy transformations;
• applications of molecular biology in medicine including the design of drugs and in medical
diagnosis.
Yeah finished all that... just started homeostasis, responses and feedback and I think we are meant to finish about half of AOS2 over the holidays...
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Cheers. I'll post a thread with questions / post sample questions in here next week.
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thanks Russ,
My teacher is a bit behind, so we've only covered up to photosynthesis in class :S
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Cheers. I'll post a thread with questions / post sample questions in here next week.
That would be great!! Thanks :D
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There will be no photosynthesis questions posted because I hate it and don't consider it important.
But yeah, probably no earlier than Tuesday because I'm still finishing exams
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this question is abit confusing :(:
Muscle cells respire using
a)aerobic respiration
b)anaerobic respiration
c)both aerobic and anaerobic respiration
d)fermentation
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this question is abit confusing :(:
Muscle cells respire using
a)aerobic respiration
b)anaerobic respiration
c)both aerobic and anaerobic respiration
d)fermentation
...C?
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this question is abit confusing :(:
Muscle cells respire using
a)aerobic respiration
b)anaerobic respiration
c)both aerobic and anaerobic respiration
d)fermentation
I would say c) both. Muscles are certainly capable of respiring aerobically (normal functioning) but when put under pressure (e.g. 100m sprint) can also undergo anaerobic respiration.
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correcto! :D
if the q. had sed yeast cells instead of muscle cells would it still be c too?
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correcto! :D
if the q. had sed yeast cells instead of muscle cells would it still be c too?
Yeh, yeast can do either as well.
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o really? does that mean no organisms only respire anaerobically? wat about organisms which only live in areas without O2 (or is there no such thing)
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There are a few select organisms which can live without oxygen such as obligate
anaerobes. In fact they would die if they had oxygen lol.
-
out of interest, would you say that obligate anaerobes respire anaerobically or is it more accurate to say they respire through fermentation? :/
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out of interest, would you say that obligate anaerobes respire anaerobically or is it more accurate to say they respire through fermentation? :/
There's a few distinctions that need to be made here. Obligate anaerobes are organisms that can only respire anaerobically - whether that be through true anaerobic respiration (similar to aerobic respiration, but using substances other than oxygen in the electron transport chain) or anaerobic fermentation (the correct name for what is commonly stated - even in academic circles - as anaerobic respiration). So they can do either; the bottom line is that they don't need oxygen (and as kaushik said, can die from it). So your first statement is kinda correct; that obligate anaerobes respire (only) anaerobically. If you're asking about the whole respiration vs. fermentation thing, then for a Bio 3/4 level, then it'd be fermentation which is more correct. I've never actually learnt about true anaerobic respiration formally. It's just something I've come across in Wiki, so you don't really need to know about it either. In an exam, I'm fairly sure that they'd accept either since many textbooks muddle up the terms as well.
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By use of a diagram/flow chart show why phototropism fits the stimulus/response model.
?? :O
help please!
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By use of a diagram/flow chart show why phototropism fits the stimulus/response model.
?? :O
help please!
Ask yourself these questions: What is the stimulus? What sort of receptors measure that change? What happens (for this example, think at a cellular level) when these sensors/receptors are triggered? what is the overall/end result of the plant's response to the change?
As an aside, you'll often be asked to consider then whether the response reduces (negative) or compounds (positive) the effect of the stimulus = what is the feedback mechanism.
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do enzymes denature in pH outside the optimal pH range because they act as buffers and donate Hyrdrogen ions to the pH environment, disrupting the Hydrgoen bonds in active site?
-
yes, though their not really buffers as that is not their aim (although sum amino acids are buffers)
-
By use of a diagram/flow chart show why phototropism fits the stimulus/response model.
?? :O
help please!
Ask yourself these questions: What is the stimulus? What sort of receptors measure that change? What happens (for this example, think at a cellular level) when these sensors/receptors are triggered? what is the overall/end result of the plant's response to the change?
As an aside, you'll often be asked to consider then whether the response reduces (negative) or compounds (positive) the effect of the stimulus = what is the feedback mechanism.
i'm not too sure what the receptor and control centre for this would be though?
-
By use of a diagram/flow chart show why phototropism fits the stimulus/response model.
?? :O
help please!
Ask yourself these questions: What is the stimulus? What sort of receptors measure that change? What happens (for this example, think at a cellular level) when these sensors/receptors are triggered? what is the overall/end result of the plant's response to the change?
As an aside, you'll often be asked to consider then whether the response reduces (negative) or compounds (positive) the effect of the stimulus = what is the feedback mechanism.
i'm not too sure what the receptor and control centre for this would be though?
ok - photoreceptors measure light - and as plants don't have a central nervous system there is a chemical response (movement of auxins to dark side of stem) which results in cellular changes...
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exaltly how do the stimulus trigger a chemical response in plants/
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You really don't need to know more details than that of the textbook with regard to tropisms - basically just that the receptors (photo, chemo, whatever) trigger the release / production / movement of a plant hormone (auxin, ABA, gibberellins etc).
If you want to learn more - read the third paragraph of this wiki entry http://en.wikipedia.org/wiki/Phototropism
but tbh- not really relevant.
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Hey Russ,
Could you possible upload the questions soon that is if you're not too busy.
Haha thanks in advance.
Kind regards,
Dooodyo
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I have written a few so far, things got busy.
I will try to get some more done over the weekend.
Protein A is responsible for catalysing the transformation of reactant B into product C. If A is bound by another protein (D), which of the following is not a possible outcome:
A. The rate of reaction decreases
B. The amount of product at completion decreases
C. The rate of reaction increases
D. Protein A is degraded
Lipids are comprised of:
A. Hydrophobic heads and hydrophobic tails
B. Hydrophobic heads and hydrophilic tails
C. Hydrophilic heads and hydrophobic tails
D. Hydrophilic heads and hydrophilic tails
Production of ATP during aerobic respiration:
A. Is the same as the amount of ATP produced anaerobic respiration
B. Always produces the same amount of ATP
C. Is slower than anaerobic respiration
D. Is less efficient than anaerobic respiration
Which of the following cell organelles contain hydrolytic enzymes:
A. Golgi apparatus
B. Lysosome
C. Mitochondrion
D. Endoplasmic reticulum
Where is the electron transport chain located:
A. mitochondrial outer membrane
B. mitochondrial matrix
C. mitochondrial inter membrane space (IMS)
D. mitochondrial inner membrane
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Thanks Russ
SPOILER ALERT:
Not sure by your first question if you mean they are inhibited but
C is the odd one out
2.C
3. C i think
4: B
5: B
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Haha lol I concur, I had the same solutions.
However q1 is a bit iffy ???
But C is probs the safest bet
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SPOILER ALERT TOO :D
hm i got slightly different answers:
1.d (can protein D be a co enzyme? i dont know wat degraded means. it sounds like it means falling apart and enzyme A can become disfunctional but i dont think it can actuall fall apart physically... :laugh:)
2. a (dont fats and oils have hydrophobic heads and tails - thought this was best answer cause phospholipids are conjugated lipids)
3. c (anaerobic respiration happens faster cause it doesnt need to undergo krebs cycle and ETC)
4. b (lysosomes contain enxymes that break down stuff... i rmb 'hydrolytic' = describing breaking bonds between molecules using water)
5.d (doesnt ETC happen in mitochondiral cristae which = inner membrane of mitochondria)
these q.s are a bit tricky. thanks Russ for making these q.s up for us :D
EDIT: waitttt changed my answer to 1. protein D cant be a coenzyme cause its a protein! so i choose c now)
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Hey PhilDunphy,
Haha q 5 would be D, haha silly me :)
And for 2 I think its C since fats and oils are lipids, and a usually have a triglyceride structure and hence the hydrophobic fatty acid tails and hydrophilic glyerol head.
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This thread has taught me I really need to proof read my questions. Never appreciated how hard it was for the VCAA lol
I did mean phospholipids (I think of them synonymously), so 2C
Everyone got 3C and 4B
5 could have been more specific and stated it was the proteins of the ETC I was asking about, but inner membrane was correct so 5D
And now for 1. Looking back, this is a slightly confusing question :P
I was intending for the answer to be B, on the principle that an enzyme won't change the final equilibrium (hence the at completion). Options A and C are both possible if protein D is an allosteric regulator, whilst option D is possible if protein D has some sort of proteolytic activity.
I was hoping people would be convinced that C couldn't be possible because we usually think of enzymes already being at the optimal efficiency.
Thoughts?
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I thought 1 implied it was an allosteric regulator but relooking at it that's not necessarily the case. I guess C is unlikely as all enzymes would have to be altered which usually does not occur so B is the best option.
5 ) :( i really need to cover the course before school starts, we are so far behind!
Thanks again russ
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Hydrolysis is the addition of a water molecule resulting in the release of energy (exergonic).
Why then is respiration, in which Water is a product, not a condensation reaction?
-
At a guess, because condensation is a specific subset of chemical reaction where you combine two small molecules into one large molecule and produce water as a byproduct, which isn't the case in respiration.
-
also cellular respiration is catabolic and condensation reactions are anabolic. you cant have a reaction that is both
hm i reviewed biomolecules again (specifically lipids). i dont get this:
do fats and oils have a hydrophilic head? then why isnt it amphipathic?
and wat does conjugated specifically mean? i made a mistake before, phospholipids arent conjugated xD
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also cellular respiration is catabolic and condensation reactions are anabolic. you cant have a reaction that is both
hm i reviewed biomolecules again (specifically lipids). i dont get this:
do fats and oils have a hydrophilic head? then why isnt it amphipathic?
and wat does conjugated specifically mean? i made a mistake before, phospholipids arent conjugated xD
Thanks Russ, again !
it seemed like they release water molecules and yet were hydrolytic which is also impossible
fats and oils do not have a hydrophilic head. Glycerol loses polarity when in a triglyceride an has only a small amount of polarity (insignificant to 3/4) when in a mono/di glyceride
Conjugated refers to 2 or more groups of biomacromolecules joined together , which a phosphate group IS NOT
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ahh i see :)
Russ can you plz please give us more q.s if you have time to
-
I looked in my text and i don't actually know where Kreb's cycle occurs.
Glycolysis is in the cytosol
and the
ETC is ? on or in? the cristae
but i don't know where Kreb's occurs :S
Somebody help :D
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The matrix of the mitochondrion, the products are passed straight to the ETC in the inner membrane
Russ can you plz please give us more q.s if you have time to
I'll pick some from my tutoring collection and post a holiday sample work thread tonight.
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I looked in my text and i don't actually know where Kreb's cycle occurs.
I think Biozone has some nice spreads on these details
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I looked in my text and i don't actually know where Kreb's cycle occurs.
I think Biozone has some nice spreads on these details
yup biozone is really good for c.respiration/photosynthesis. also nelson textbook is great at explaining the steps/processes, but it has nothing on limiting factors for photosynthesis! >:(
-
is the cell wall permeable to everything?
-
What is the name of the fine structure that can only be seen using an electron microscope where carbon fixation takes place?
-
ribosomes
-
What is the name of the fine structure that can only be seen using an electron microscope where carbon fixation takes place?
in photosynthesis, carbon fixation occurs in the chloroplast during the Calvin Cycle..
-
hm but i thought chloroplasts were visible under light microscopes.
and im not entirely sure about ribosomes. i noe that chloroplasts have their own ribosomes but i cant relate this to carbon fixation...
and the q. says fine structure - it sounds like thylakiod membranes but only light dependent state happens here :/
any other suggestions?
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Chloroplasts can be seen under a light microscope. I honestly don't know the answer.
-
o the question must be wrong or something. it was from the 2008 Lisachem topic test 1 :|
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happen to have a copy to post pleeeeaasse?
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i wrote on it already. but here is 2011 :D
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more
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last pages
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Can organisms compensate for the lack of enzymes in a biochemical pathway by using a different biochemical pathway?
This is a question from STAV 2008
Question 5
A section of nucleic acid taken from a human cell has the following base sequence
UCUUCAUAA
It is reasonable to conclude that:
B. This base sequence codes for 3 different amino acids
D. Template base sequence would be AGAAGTATT
i answered D, which is the answer,
but
is the reason it can't be B because, may not code for 3 different amino acids, or/and may be 'junk dna'?
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Can organisms compensate for the lack of enzymes in a biochemical pathway by using a different biochemical pathway?
Yep, of course. It's not really a case of 'can', but it's a natural thing that will be enforced. If A can be turned into B and C via certain enzymes, and the enzyme to catalyse the conversion to B is screwed up, then consequently A will naturally increase and the increase in substrate will be shunted into the C pathway, leading to more C.
As for Q5, note the presence of uracil. If there is uracil, it is a strand of mRNA. Hence, it cannot be junk DNA because it's already been transcribed. However, look in your databook and translate that strand; it actually becomes Ser-Ser-STOP. Hence, only two amino acids. However, if it was a DNA strand, then it could have been a non-coding sequence (hesitant to use the term 'junk DNA').
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ah okay thankyou, so STOP is not an amino acid? like methionine is a 'start?"
Also for chemical pathways if
A->B -> C is the reaction
but A - B enzyme is messed up, how does the body get past this? I'm not sure if in your answer you meant
A->B or A -> C
I'm not sure exactly how it works
is it just by chance that there is another enzyme that turns it into the product? or does every product have more than 1 possible pathway?
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Thaaaanks heaps ! :D
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ah okay thankyou, so STOP is not an amino acid? like methionine is a 'start?"
Also for chemical pathways if
A->B -> C is the reaction
but A - B enzyme is messed up, how does the body get past this? I'm not sure if in your answer you meant
A->B or A -> C
I'm not sure exactly how it works
is it just by chance that there is another enzyme that turns it into the product? or does every product have more than 1 possible pathway?
Yeh stop isn't one. And I meant A->B and A->C, so if A->B doesn't work, C will increase. Did you mean getting the same product through a different pathway? But if there was something like A->B1->C and A->B2->C, a decrease in one pathway will cause a compensatory increase in the other just by principle. A possible example would be something like the production of glucose in the body, where there's many possible sources (fats, glycogen, proteins etc) involved.
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The exact question is
The follwoing diagram represents a biochemical pathway in a living organism. The final product, substance T, is essential for the life of the organism
P -> (enzyme P) Q -> (enzyme q) R -> (enzyme r) S -> (enzyme s) T
The organism involved undergoes a mutation and is no longer able to produce enzyme r. It is reasonable to predict that:
A. The organism will be able to compensate for the lack of enzyme r by using an alternative pathway
B Substance Q will tend to accumulate
D the lack okf enzyme r will be fatal for this organism
I said D but the answer is A.
It seems to suggest alternative pathways are quite common in a case like this?
EDIT: Also, no proteins have no tertiary structure... right?
Engage Education exam says fibrin is a 'secondary protein' not a 'tertiary protein'
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i would have said d too :o
wat was option c btw
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I don't agree with that answer. Alternative pathways aren't really that common as far as I can tell. You also shouldn't be expected to know that in Bio 3/4 anyhow. It really isn't reasonable to assume that at all I would think - going from what they've given, D is far more justifiable.
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oh ok. my teacher sed STAV doesn't have good solutions, i havent done these ones yet.
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if there is a decrease in water concentration in the blood, what would be the receptor for this situation? Would it be the osmoregulator in the hypothalamus or the mechanorecpetors in the blood that detect blood pressure?
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osmoregulator, as change in water conc. may not result in change in BP
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Hey guys,
Whats the difference between glycocalyx and oligosaccharides?
From what I decipher it seems that oligosaccharides are short carbohydrate chains attached to proteins or
lipid molecules on the membrance and according to wikipedia they seem to have a similar function. ???
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oligo is part of the numbering/naming system:
mono = one
di = two
oligo = several
poly = many
So an oligosaccharide is just several sugar molecules linked together.
Glycocalyx is slightly more complicated. It's a layer around the outside of a cell, designed for adhesion and (to some extent) protection. Bacterial cells often use certain types of glycocalyces called "capsules" to hide from the immune system and stick to your cells (eg plaque deposits in your mouth)
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highly doubt that knowledge is necessary though
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What is the difference between Natural Killer Cells and Cytotoxic C Cells if they both kill virus infected cells?
Also, are all cells of the immune system, e.g. B cells, T cells WBC's?
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I would be fairly confident at VCE level that all cells are considered WBCs ("leucocytes").
There might be a bit of debate about dendritic cells but i don't think it's an important distinction.
RE: NK and Cytotoxic T Cells (typo?)
NK cells are basically highly specialized antiviral cells with some other functions. Cytotoxic T Lympocytes (CTLs) are a subset of T cells that are responsible for killing infected or abnormal cells. Cells can be infected by viruses but also by various other pathogens (eg Salmonella).
So CTLs have a much broader spectrum of action. There are a lot of fine more specific differences but they're definitely not going to be assessed.
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Thanks Russ! That makes sense C was a typo :D
This is a series of questionable questions and answers from TSFX 2010
Could someone please explain the answers.
1)
The roles of cholestrol include:
A) Acting as a a precurser molecule to steroid hormones such as testoseron and adrenalin.
D) Assisting in membrane stability at 37 C
2)
Rate of reaction could be further increased by
B) adding more substrate
C) adding more enzyme
3)
During photosynthesis, rubisco is the enzyme responsible for grabbing C02 in the atmosphere in
A) CAM
B) C3
C) C4
plants
Do we need to know this
?
4) A water soluble hormone includes
B) The thyroid amino acid derivate thyroxin
A) The peptide hormone insulin
D The neurotarnsmitter acetylcholine
15)
Endorphins are neurotransmitters which reduce the chances of impulses traveeling along pain pathways. Their effect ois to
A) Hyperpolarise the membrane of the post - synaptic cell (not even in textbook?)
C) Attach to excitatory neurotransmittors before the reach the post - synaptic membrane
20)
Unlike most proteins, prions
C) Do not denature when superheated
D) Contain nucleotide side chains
I got 18/25 in MC. In every other exam i've done so far i've gotten 23- 25 (8 exams) in MC, so i think possibly many of these things we don't need to know?
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1. Cholesterol plays an important role in membrane stability, not sure if it's important at 37 degrees though. Adrenaline also isn't a steroid hormone.
2. I would have thought either, based on circumstances. Hmmmm...
4. ACh at a guess, based on structure/size
15. Both plausible, no idea. Based on the question stem, A, since that will prevent all impulses.
20. C but if you weren't taught it I doubt it's going to be asked. One of the great virulence problems with prions is they're so resilient.
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let me attempt :
1)d (ive never heard of cholesterol doing a) )
2)c (adding more enzyme seems immediately more effective)
3)b (C3 because with C4 and CAM they grab C02 with a different enzyme i think that fixes it to a 4-carbon compund and not 3-carbon)
4)a (you either have steroid or protein hormones - lipid-soluble (travels straight into cell) or water-soluble (to surface of membrane) = peptide hormones would be water-soluble)
15) - havent covered this yet
20)d (all proteins can denature at high temperatures unless they already live in high temp. - i dont think prions can cause they enter our bodies)
wat are the answers :D
i havent tried tsfx yet, but it seems like you've gotten really good for MC with the other exams. have you done any VCAA ones yet? maybe then you can compare and see if these q.s are relevant.
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Thanks for the responses,
Hercules I'm doing VCAA 2009 in 20 minutes.
I haven't done that well in SA but i am improving
my scores in trial exams range from 60% - 90% so far which is alright as i haven't been taught and don't know half of the course that well
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I haven't done that well in SA but i am improving
me too. i just did the VCAA 2008 this morning, and i didnt do well in SA too. they are hard =(
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What is the difference between Natural Killer Cells and Cytotoxic C Cells if they both kill virus infected cells?
just to add...
NK cells are part of the innate immune system (therefore can work early on in infection before CTL's get activated)
CTLs part of the adaptive immune system
NK cells work in a completely different way in terms of how they kill infected or abnormal cells (they have different receptors both inhibitory and activating receptors and can detect changes in MHC 1 levels) whereas CTL's have T cell receptor that is highly specific)
but they both kill with their cytotoxic granules (perforin, granzymes...)
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I haven't done that well in SA but i am improving
me too. i just did the VCAA 2008 this morning, and i didnt do well in SA too. they are hard =(
I did 2009 and yes, the MC is MUCH easier, i got 25/25 for MC and 40/50 for SA 87%
I'm quite happy with that, and i learnt a lot which was great.
Made a few silly mistakes, and didn't know some of the stuff
I do have a few concerns though
I can't seem to spend long enough on practice exams, i'm always finished within an hour even though i'm trying to slow myself down. Is this the same for everybody?
This was an MC Q that i'm confused about a bit
Q 11) Human and plant hormones are similar in that all are :
C) Signalling molecules that act on receptor molecules
D) Transported around the organism by a circulating fluid.
I know that C is correct, but why is D wrong, i was of the belief that hormones in plants were circulated in the phloem?
Also , when writing a scientific experiment, is your hypothesis taken directly from the question? Are you not allowed to extrapolate so that, instead of testing the effect of an enzyme or substance in an animal, you aren't able to take it out and place it in a test tube?
(that's what answers seemed to suggest)
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Read every question carefully, the question states "all" and not all hormones will enter systemic circulation via some fluid
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how are chlororplasts involved in protein synthesis?
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at the end of photosynthesis glucose can sometimes be converted to amino acids --> protein synthesis?
can someone correct me if im wrong :|
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Are neurimindase and hameuglutinin on influenza antigens (according to text) or enzyme (according to Insight 2009)
Also
Do gylcoproteins, lipoproteins, glycolipids all perform a role as antigens? Are antibodies just normal proteins?
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Why can't they be both?
Conceivably, yes, anything specific to a pathogen can potentially serve as an antigen
Depends on the definition of "normal" but predominantly, yes.
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Thanks Russ
also
- Do amino acid derivates bind with receptors on the plasma membrane? Insight 2009 says they are hydrophobic and move through the plasma membrane while my textbook says otherwise.
Also , as neurons can recieve excitatory or inhibitarory charges, is an inhibitatory stimulus still considered a stimulus? (e.g. does -7 cause an action?) Thanks
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More questions
Is a G protien and secondary messenger or the instructor for precursor e.g. Cyclic AMP
What exactly is signal transduction?
One VCAA questions suggests neurotransmitters is a form of signal transduction ? or is it the signal is changed?
How are gene segments rearragend to form antibodies
Thanks!
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Do amino acid derivates bind with receptors on the plasma membrane? Insight 2009 says they are hydrophobic and move through the plasma membrane while my textbook says otherwise.
Would depend on the structure of whatever the product was
Also , as neurons can recieve excitatory or inhibitarory charges, is an inhibitatory stimulus still considered a stimulus? (e.g. does -7 cause an action?) Thanks
Inhibiting a neuron to hyperpolarise it won't cause an action potential. But in order to do that, you need to send an AP via an inhibitory neuron that synapses with the target neuron and secretes an inhibitory neurotransmitter.
Is a G protien and secondary messenger or the instructor for precursor e.g. Cyclic AMP
Rephrase, this makes no sense.
What exactly is signal transduction?
If a signalling molecule (eg hormone) can't cross the membrane then it can't have an intracellular effect. So it binds something on the plasma membrane (ie receptor), which will transduce the message across the membrane into the cell. It's often coupled with amplification, so 1 signal molecule will cause (say) 10 effector molecules to be produced within the cell.
One VCAA questions suggests neurotransmitters is a form of signal transduction ? or is it the signal is changed?
Rephrase the second bit. I'm not an neuro expert but some neurotransmitters (Ach) will undergo signal transduction, yes.
How are gene segments rearragend to form antibodies
Very complicated answer, the further you go the more detail there is. Long story short, the gene has lots (100s) of different segments. You only need a few segments to make a functional antibody, so there is random rearrangement of the gene to transcribe only a few of them. Since it's random, we get different antibodies with every B cell.
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Is a G protien and secondary messenger or the instructor for precursor e.g. Cyclic AMP
Translation :D
Is a G protein a secondary messenger or simply another chemical that aids the transmission of a message from the receptor to a true secondary messenger such as Cyclic AMP.
One VCAA questions suggests neurotransmitters is a form of signal transduction ? or is it the signal is changed?
Translation - Can signal transduction refer to the changing of the signal - e.g. from electrical to chemical etc.
Thanks again Russ
After i finish my holiday's practice Q's today or tomorrow the influx of questions will cease :)
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G proteins are membrane bound so they're not secondary messengers, they act to transduce signals.
Signal transduction refers to a signal being transduced across a membrane. This can be from electrical to chemical but you wouldn't use the term to refer specifically to that, it would refer to the overall process.
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Hey guys,
Just did a practice question and was wondering how many marks you guys would give this answer
out of a maximum of 2 I think.
Question: Different cell types have different sets of transport proteins. Explain.
My answer:
Transport proteins are very specific and only move certains solutes across the cell membrane. Since some cells can
be specialised to carry out particular functions they need to be able to exchange particular substances more so than
other cells.
Its a bit dodgy :P. So I wanted to know how you guys would set out your answers so as to achieve full marks?
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Anyone have VCAA 2001?
Any help much appreciated.
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Question: Different cell types have different sets of transport proteins. Explain.
My answer:
Transport proteins are very specific and only move certains solutes across the cell membrane. Since some cells can
be specialised to carry out particular functions they need to be able to exchange particular substances more so than
other cells.
Its a bit dodgy :P. So I wanted to know how you guys would set out your answers so as to achieve full marks?
i would give this full marks :D
maybe give an example to make your answer better?
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Hey,
What do you happen to mean by examples? Like cells in the respiratory
surfaces and etc ?
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hm well like
For example, liver cells would have large amounts of carrier proteins specifically pumping in glucose molecules?
...something like that :D
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i have a question about protein structure:
the beta sheets in the secondary structure - are the Hydrogen bonds between two polypeptide chains. and does this mean beta sheets only exist in proteins with quaternary structures?
im so confused :|
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yeah i saw that description somewhere. Its inaccurate, what it means is 'two portions of the same polypeptide chain' so its the same chain with a bend pressed against itself
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ohhh ok thanks for clearing that up! :D
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Question: Different cell types have different sets of transport proteins. Explain.
My answer:
Transport proteins are very specific and only move certains solutes across the cell membrane. Since some cells can
be specialised to carry out particular functions they need to be able to exchange particular substances more so than
other cells.
Its a bit dodgy :P. So I wanted to know how you guys would set out your answers so as to achieve full marks?
My answer would be:
Different cell types have different functions and, as such, have different requirements. Transport proteins exist to enable a cell to access the molecules required for its function and, for this reason, will differ between cell populations.
Your answer was good, just focus on fixing the wording because it was a little clunky :)
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Hey Russ,
I was wondering how would you structure your answers any guide as
of such ?
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can someone please explain the action of gravity and auxin on root cells? i'm not really understand it
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I haven't done that well in SA but i am improving
me too. i just did the VCAA 2008 this morning, and i didnt do well in SA too. they are hard =(
I did 2009 and yes, the MC is MUCH easier, i got 25/25 for MC and 40/50 for SA 87%
I'm quite happy with that, and i learnt a lot which was great.
Made a few silly mistakes, and didn't know some of the stuff
I do have a few concerns though
I can't seem to spend long enough on practice exams, i'm always finished within an hour even though i'm trying to slow myself down. Is this the same for everybody?
This was an MC Q that i'm confused about a bit
Q 11) Human and plant hormones are similar in that all are :
C) Signalling molecules that act on receptor molecules
D) Transported around the organism by a circulating fluid.
I know that C is correct, but why is D wrong, i was of the belief that hormones in plants were circulated in the phloem?
Also , when writing a scientific experiment, is your hypothesis taken directly from the question? Are you not allowed to extrapolate so that, instead of testing the effect of an enzyme or substance in an animal, you aren't able to take it out and place it in a test tube?
(that's what answers seemed to suggest)
Hey Bazza16!
Option D is wrong because some plant hormones (e.g. auxin) undergo either apoplastic or symplastic transport - essentially being transported through the cell wall and the space between the cells, and through the cytoplasm of the cell, respectively.
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Hey Russ,
I was wondering how would you structure your answers any guide as
of such ?
I don't really have a guide for it but I tend to start by making a statement and then explaining that statement in subsequent sentences. I can get out some of my sample questions/answers if you want but *shrug*
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As endocrine cells/glands are 'ductless' does that mean the hormones are just released through diffusion etc. ?
Also, what exactly is a cellular/ organ duct
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It's an anatomical term/definition but it's just a channel leading to/from an organ.
Endocrine glands secrete directly to the blood but not necessarily through diffusion
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douchy explained it as hormones being secreted directly into the bloodstream and not into a tube.
duct = 'to lead'
EXOCRINE glands for example produce products delivered through tubes called 'ducts'
EDIT: go to http://answers.yahoo.com/question/index?qid=20080722100846AAz9qFt
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These organ ducts are also quite large structures - when Russ says channels, he doesn't just mean like an ion channel or something. Some are easily anatomically visible such as the biliary tree (connecting the liver, gallbladder and pancreas to the intestines), while others such as the tear ducts, mammary ducts and so on are a bit smaller. But basically, they're tubes lined by cells leading from one organ to another or to the surface.
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can someone please explain the action of gravity and auxin on root cells? i'm not really understand it
Auxin inhibits cell growth in roots. Therefore when auxin settles on the lower side of the root, cell growth is inhibited. However, the uppermost side of the root is still able to growth, resulting in the bending of the root towards gravity.
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Thankyou,
so does that mean hormones are secreted via normal cellular processes such as exocytosis, active transport, faciliated diffusion and diffusion?
Also, what exactly does humoral mean?
In terms of
a) immunity and
b) Describing homeostatic mechanisms such as Blood Glucose control
Edit: Are non - metallic ions such as chlorine minerals?
Edit 2: As trophic refers to the Carbon Source, why are prions and viruses 'non - trophic' if they get carbon from other organisms?
Edit 3: Can amino acids and glucose pass through the phospholipid bilayer by simple diffusion? Or are they too big / too polar
Edit 4: Are CAM plants C4 or C3, Neap says C4, teacher said C3
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Heinemann says that amino acids and simple sugars pass through protein channels. but insight 2007 exam says otherwise. i'm assuming you have already done that exam? :P
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also is there such thing as a "diuretic hormone"? or is less adh produced to combat a high water conc. in the blood?
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less adh is used
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so does that mean hormones are secreted via normal cellular processes such as exocytosis, active transport, faciliated diffusion and diffusion?
Mainly exocytosis as far as I know. Hence the need for large golgi and many mitochondria in most cases.
Also, what exactly does humoral mean?
Relating to the blood. So for immunity it refers to the antibody-based defenses rather than the cellular based ones. As for homeostasis, any mechanism which operates through the blood in some way.
also is there such thing as a "diuretic hormone"? or is less adh produced to combat a high water conc. in the blood?
Well there is atrial natriuretic peptide released by the heart, but it's not something you need to worry about. ADH is the main factor involved.
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The entire blood pressure regulation thing is a nightmare of acronyms :(
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The entire blood pressure regulation thing is a nightmare of acronyms :(
The hypothalamic-pituitary axis definitely takes the cake. TRH, GHRH, GnRH, CRH, ACTH, TSH, GH, LH, FSH, PRL to name a couple...
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I have repressed the hypothalamus from my memory of physiology and that's the way it should stay :(
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How can you reason whether an experiment has a control or not? For example, in an experiment with an egg in distilled water, an egg in a sucrose solution and an egg in an isotonic solution could you reason that the egg in the isotonic solution is the control (assuming that all other variables are kept constant)?
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The control is whichever experiment where the variable you're altering (tonicity) will not affect the variable you're measuring. A pure water solution or a pure sugar pill (for drug testing) is not always an appropriate placebo because it may have an effect
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Are CAM plants C4 or C3, Neap says C4, teacher said C3
i would say neither.
but since it was a question i think neap is right. CAM plants like C4 plants, form a 4-compound carbon ('malate' or 'malic acid') before it fixes it into a triose sugar. the only difference is that C4 plants transport this 4-carbon compound into the bundle sheath cells to be fixed whereas CAM plants store it overnight to be used in the calvin cycle during daytime (in the same mesophyll cells, not bundled-sheath cells).
but i also know that during rainfall CAM plants can convert back to the C3 pathway (maybe this is why your teacher thought they were more C3?)
Can amino acids and glucose pass through the phospholipid bilayer by simple diffusion? Or are they too big / too polar
I don't think so?
look at the diagram attached :D
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The control is whichever experiment where the variable you're altering (tonicity) will not affect the variable you're measuring. A pure water solution or a pure sugar pill (for drug testing) is not always an appropriate placebo because it may have an effect
so the egg placed in the isotonic solution has no effect on the variable (ie. increase or decrease in weight) and thus can be deemed a control?
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The control is whichever experiment where the variable you're altering (tonicity) will not affect the variable you're measuring. A pure water solution or a pure sugar pill (for drug testing) is not always an appropriate placebo because it may have an effect
so the egg placed in the isotonic solution has no effect on the variable (ie. increase or decrease in weight) and thus can be deemed a control?
basically - in that experiment, if you were to ask to name the control that would be it.
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As trophic refers to the Carbon Source, why are prions and viruses 'non - trophic' if they get carbon from other organisms?
Are CAM plants C4 or C3, Neap says C4, teacher said C3
Heterotroph and autotroph are applied to organisms, but prions and viruses technically aren't organisms - thus the 'non-trophic'.
I would agree with Hercules; CAM is another category, just like C3 and C4. But seriously, the VCAA never ask about CAM, and only ever occasionally about C3 and C4
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Thankyou,
A question i asked a while ago: Why does Pyruvate need to be converted into Lactic acid in humans when they are both toxic?
A response i recieve (that i thought was correct until today) was that it needed to recycle NAD, but because the body is simply rearranging the structure, and more NAD can be created, my teacher said that its due to 'concentration gradients' of pyruvate that are needed to ensure proper function of aerobic respiration when it resumes. Can anyone confirm or shed light upon this?
Thanks
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^ Oh good question. im also wondering why too now :)
yea why cant just the glycolysis part of anaerobic fermentation occur, cause thats the actual stage that produces the 2ATP :|
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I still stick by the need to recycle NADH. Wiki seems to agree with me. I have no idea about this pyruvate gradient thing your teacher is referring to. To me, the more pressing issue is the NAD+/NADH ratio which is required to be kept low in cells to drive redox reactions forward. Furthermore, simply 'creating more NAD' itself requires energy. Where's this energy coming from then?
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I still stick by the need to recycle NADH. Wiki seems to agree with me. I have no idea about this pyruvate gradient thing your teacher is referring to. To me, the more pressing issue is the NAD+/NADH ratio which is required to be kept low in cells to drive redox reactions forward. Furthermore, simply 'creating more NAD' itself requires energy. Where's this energy coming from then?
Yep I agree with Shinny. More specifically the NAD+/NADH ratio is required to enable glycolysis to continue and thus to allow continued production of ATP (in the short term), hence conversion to lactic acid.
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I still stick by the need to recycle NADH.
is this referring to how the NADH from glycolysis dumps the H onto the last electron acceptor (pryuvate) to form lactic acid = regenerating NAD
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I still stick by the need to recycle NADH.
is this referring to how the NADH from glycolysis dumps the H onto the last electron acceptor (pryuvate) to form lactic acid = regenerating NAD
Pretty much.
Also, you might want to be careful about NADH, NAD+ and H+ (technically H+ is just a proton) - the VCAA are really annoying and specific about always writing NAD+ and H+
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oh ok. whats the difference between NADPH+ and NADP + H.
i see this written in different ways - a bit confusing.
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could someone explain why people with short and stocky statures have a greater chance of
survival compared to people with taller and skinnier body shapes if they both were suffering
from hypothermia?
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could someone explain why people with short and stocky statures have a greater chance of
survival compared to people with taller and skinnier body shapes if they both were suffering
from hypothermia?
it has to do with the taller/skinnier person have a greater surface area to volume ratio than the short/stocky person, so loses more heat as more body surface is exposed.
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could someone explain why people with short and stocky statures have a greater chance of
survival compared to people with taller and skinnier body shapes if they both were suffering
from hypothermia?
It's a bit vague, but going by unit 3/4 knowledge, I'd assume the answer is SA:V ratio. i.e. they have less surface area to lose heat out of. I've said it many times; write out a list of all the common principles and refer to it whenever you get stuck. Almost everything in the unit 3 exam invariably comes back to these few simple principles.
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@ Shinny : apart from SA:V ratio what other common principles did you mean?
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@ Shinny : apart from SA:V ratio what other common principles did you mean?
Can't quite remember all of them, but diffusion and SA:V both inevitably come up in some strange form or manner often without people realising, then there's others which are a bit less abstract such as the stimulus-response model, all those enzyme rules regarding temperature, pH etc. Just flick through each chapter and identify them.
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1. No
and
2. I would say yes.
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arent all ions non-metallic?
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1. No
and
2. I would say yes.
Why aren't non -metal ions considered minerals?
what are they called (e.g. chlorine etc.)
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Why is it an advantage for hormones to be carried in the blood? :)
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Why is it an advantage for hormones to be carried in the blood? :)
it's the fastest way for them to be delivered in the body and so they can act on target cells while travelling in the blood :)
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Are non - metallic ions considered minerals?
More importantly,
Is it more accurate (at VCE level) to write NADPH + H+ Instead of just NADPH to more accurately reflect the nature of the transfer of electrons and protons?
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Are non - metallic ions considered minerals?
Be careful with the use of the word 'mineral'. I wouldn't use it it in the context of VCE bio if there was an alternative. But in response to your question, fluoride ions are considered to be minerals, so thats an example of a non-metallic ion.
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What do you mean be careful? in what situations is an alternative (and what alternatives) more accurate?
Also ;)
Is it more accurate (at VCE level) to write NADPH + H+ Instead of just NADPH to more accurately reflect the nature of the transfer of electrons and protons?
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What do you mean be careful? in what situations is an alternative (and what alternatives) more accurate?
Well, what I mean is that if you could specify the ions, that would be better than grouping them under 'mineral'. I'm pretty sure (need clarifying here though) that the term 'mineral' for context of ions is getting a bit out-dated too. Better to just specify the ions involved.
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Is it more accurate (at VCE level) to write NADPH + H+ Instead of just NADPH to more accurately reflect the nature of the transfer of electrons and protons?
Under what context? If you're writing an equation, then sure. But why would VCAA ever ask you about this equation? If you're just referring to NADPH in a short answer question, then there's no reason to specify the H+ as well.
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Ok thanks, should i refer to
NAD+ or just NAD?
I did mean normally when referring to cellular respiration.
Out of curiousity, how are the H+ protons transfered to the ETC/ Oxygen?
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Ok thanks, should i refer to
NAD+ or just NAD?
I did mean normally when referring to cellular respiration.
Out of curiousity, how are the H+ protons transfered to the ETC/ Oxygen?
It's NAD+ and NADH. Don't call it NAD. Regarding the second question, you don't need to know and it's quite a complicated process. On a basic level, the electron carriers dump off their electrons to the mitochondrial proteins to power active transport of H+ across the membrane. This process happens a few times making a big H+ gradient across this membrane. Finally this H+ gradient is cleared as the H+ is driven back to where it came from through a protein channel, ATP-synthase, which harnesses the energy from this osmotic drive to create ATP.
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so is it
NAD+ --> NADH
NADP+ --> NADPH
FAD+ --> FADH
why do they always write FAD2H instead of something like 2FADH
and what does the + indicate :D
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so is it
NAD+ --> NADH
NADP+ --> NADPH
FAD+ --> FADH
why do they always write FAD2H instead of something like 2FADH
and what does the + indicate :D



FADH2 refers to having two hydrogens bound to FAD and this is the form that is found in the body. 2FADH would mean having 2 FADs with one hydrogen bound to each. The + refers to the positive charge on the molecule. It's not particularly important anyway. My experience is that people dwell far too long on the trivial details of cellular respiration and such. It's seriously not tested to much detail. My advice is to start trial exams and you'll see what they ask about it.
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oh ok thanks for that shinny
just wanted to know to make my mind at ease
i have another question - with homoeostasis, different books give you different types of homoeostasis examples. Like i know that nelson (schools textbook) only looks at thyroxine, glucagon, insulin and growth hormones whereas other books provide a lot more examples such as those to do with stomata regulation. Will i be at a disadvantage?
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oh ok thanks for that shinny
just wanted to know to make my mind at ease
i have another question - with homoeostasis, different books give you different types of homoeostasis examples. Like i know that nelson (schools textbook) only looks at thyroxine, glucagon, insulin and growth hormones whereas other books provide a lot more examples such as those to do with stomata regulation. Will i be at a disadvantage?
You only need to understand the principles behind each. Specific examples aren't required. However, it is an advantage to vaguely know the common ones beforehand (e.g. blood sugar regulation) to save time in the exam. With enough practice exams, you'll learn them anyhow. You shouldn't need to make a conscious effort to learn any specific examples.
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oh ok thanks for that shinny
just wanted to know to make my mind at ease
i have another question - with homoeostasis, different books give you different types of homoeostasis examples. Like i know that nelson (schools textbook) only looks at thyroxine, glucagon, insulin and growth hormones whereas other books provide a lot more examples such as those to do with stomata regulation. Will i be at a disadvantage?
You only need to understand the principles behind each. Specific examples aren't required. However, it is an advantage to vaguely know the common ones beforehand (e.g. blood sugar regulation) to save time in the exam. With enough practice exams, you'll learn them anyhow. You shouldn't need to make a conscious effort to learn any specific examples.
You do need to know one specific example so you can fill in a feedback-response flow diagram if need be, with "stimulus", "receptor" etc... But apart from knowing one, I agree completely with Shinny. Familiarity is good, but if you do enough practice exams you should get the hang of it.
also from above; one of the main advantages of hormones travelling in the bloodstream is that they can act on many different parts of the body depending on where target cells are located. Also, they act in low concentrations and can provide an ongoing response. When you get to looking at the effects of adrenalin I think this will make more sense (especially compared to the advantages of nerves).
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what is threshold potential?
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The membrane potential that needs to be reached to trigger an action potential.
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so resting potential --> threshold potential --> action potential --> repeat?
how is threshold potential initiated?
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Yeah. Influx of ions changes the membrane potential, the threshold is just when a certain amount have entered - this triggers an action potential being sent
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so is it
first, you have normal resting potential.
Then a stimulus (?) causes the the ion channels for sodium to open.
Sodium ions flow in until enough has gone in (the threshold) to bring about a nerve impulse/action potential.
so is threshold potential more like a point in time right before the action potential rather than a period of time that ions flow in?
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The diagram I made over here might help. The labels are quite abbreviated so if there's a step you don't get, I can elaborate further.
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thanks
does 'ligand' mean that the ion pump is a two-way pump - it pumps sodium out but also pumps potassium in?
and does that mean that threshold potential is when the sodium ion channels open?
just say that you was looking at a specific section on a neurone. the section before it depolarized and now this section does; so the action potential has passed from that section to this section. what exactly stimluated the second section to open its channels/become permeable to sodium. is it the electrical impulse itself?
and can someone explain the "all our nothing effect" to me :)
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Ligand-gated refers to the fact that the ion channel opens when a ligand binds to the receptor on the channel. The ligand in this case would be the neurotransmitters sent from one neuron to another. So one neuron has an action potential going down it, it reaches the end of the nerve and the nerve then sends neurotransmitters across the synapse. These action potentials then bind to the start of the next neuron, activating these ligand-gated channels and allowing a small influx of sodium which brings the membrane potential above the threshold potential, allowing the voltage-gated channels to open and allowing a massive influx of sodium. This sodium then travels down the neuronal cell body and changes the membrane potential in the next section of nerve to be above threshold potential, thus perpetuating the cycle all along the nerve until it reaches the synapse.
So basically, the ligand-gated channels are only implicated in the very first section of nerve. From then on, that initial influx of sodium travels down the cell body to stimulate voltage-gated channels to perpetuate the rest of the neuron.
Regarding the 'all or nothing' effect, it refers to the fact that unless membrane potential reaches above the threshold, then nothing will happen. In addition, regardless of how much you reach above resting potential, there's no difference in the strength of the action potential. Basically, if you go above threshold, all of the voltage-gated channels will open to achieve a set membrane potential. If it doesn't go above threshold, no action potential is generated.
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Ohhhhhhhh i think ive got the gist of it now! :)
so ligand-gated channels at the dendrites are completely different to the voltage-gated channels along the neurone.
i thought they were the same cause they both send sodium ions into the cell.
From then on, that initial influx of sodium travels down the cell body to stimulate voltage-gated channels to perpetuate the rest of the neuron.
so the initial influx of sodium is from the ligand-gated channels and as these same sodium ions travel down the neurone, more threshold potentials are reached and the voltage-gated channels opens as a response to enough charge being changed--> then voltage-gated channels makes inside of cell even more positive (this is action potential)
PS. does anyone know a good link to a nerve impulse transmission animation :D
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Perhaps this one? Have a look around Youtube. There's heaps.
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found some moreeeeeeee:
http://outreach.mcb.harvard.edu/animations/actionpotential.swf
http://bcs.whfreeman.com/thelifewire/content/chp44/4402s.swf
http://www.biology4all.com/resources_library/source/63.swf
also this one for how neurotransmitters cross a synapse:
http://www.mind.ilstu.edu/curriculum/neurons_intro/neurons_intro.php (at the end of the page)
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How do antihistamines work? do they work by binding to the histamine receptor? or do they bind to mast cells to inhibit production of histamines???
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does a high concentration of auxin inhibit cell growth and low concentrations of auxin promote cell growth?
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How do antihistamines work? do they work by binding to the histamine receptor? or do they bind to mast cells to inhibit production of histamines???
They bind to the histamine receptors found throughout the body.
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how are osmoregulation and bloodpressssure closely related? WHY IS IT THAT WHEN YOU INCREASE WATER YOU INCREASE BLOOD P[RESSUREa?????????????/
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how are osmoregulation and bloodpressssure closely related? WHY IS IT THAT WHEN YOU INCREASE WATER YOU INCREASE BLOOD P[RESSUREa?????????????/
If you have a water balloon and you increase the volume by putting water into it, the balloon stretches and the pressure inside it increases. Same goes with blood vessels.
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is a nerve impulse the same thing as an action potential
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is a nerve impulse the same thing as an action potential
Yep.
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How exactly does bacteria cause diarrhea? lolwut.
Does the bacteria damage eptherial cells in the stomach?
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Some do. Common method is to prevent Na+ uptake by villi. That creates an osmotic gradient that draws water into the lumen of the GIT and causes diarrhoea
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oh i see thanks. haha
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Do excitatory neurons lead to positive feedback and with inhibitory neurons leading to negative feedback?
AND
Is a neurohormone a neurotransmitter?
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Douchy says chlrophyll is a protein, is that correcyt?
Also
Can someone please describe how to number carbons on DNA / RNA, numerous sources say different things
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Depends how you draw it but the carbon that links to the base is always carbon 1. From that you can work out the rest (phosphate = 5, free OH = 3)
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Douchy says chlrophyll is a protein, is that correcyt?
Also
Can someone please describe how to number carbons on DNA / RNA, numerous sources say different things
I don't think chlorophyll itself is a protein - it can certainly form protein complexes though.
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Douchy says chlrophyll is a protein, is that correcyt?
he said that you should just call it a porphyrin pigment i think. its chemically similar to a protein casue it contains nitrogen but its strucurally like a lipid cause it has a hydrocarbon tail that is hydrophobic and will suspend in the thylakoid membrane. :D
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What's the difference between bulk transport and active transport?
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What's the difference between bulk transport and active transport?
Bulk transport is endo/exocytosis.
Active transport is the movement of a substance against the concentration gradient, typically requiring ATP. Bulk Transport is actually a type of active transport.
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oh alright, thanks bud
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are second messengers the same as relay molecules?
AND
the definition of signal transduction says that signal amplification happens. but with lipid-soluble hormones how does this happen when second messengers are not used
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are 2nd messnegers relay molecules
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are second messengers the same as relay molecules?
AND
the definition of signal transduction says that signal amplification happens. but with lipid-soluble hormones how does this happen when second messengers are not used
Second messengers are a type of relay molecule. That definition is just trying to stay broad once again to avoid losing marks unnecessarily. Signal transduction is a very loosely defined term. With lipid hormones, this happens because although they directly cause the transcription of DNA, the protein product which results is itself a relay molecule because that protein will go on to cause other effects.
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is a g protein a 2nd messenger
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is a g protein a 2nd messenger
Yes.
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what does the term amplified mean
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but you know second messengers arent they non-protein. how does that work when relay molecules are proteins.
(sorry about all these questions ^^)
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but you know second messengers arent they non-protein. how does that work when relay molecules are proteins.
(sorry about all these questions ^^)
Relay molecules aren't necessarily proteins.
what does the term amplified mean
Are you serious? =/ Hopefully you meant in the context of all of this then. Basically it's referring to fact that a single relay molecule could interact with a cell to produce a second messenger, then this second messenger can interact with 100 relay molecules, with these 100 relay molecules then interacting with another 1000 different relay molecules and so on, leading to the production of exponentially increased numbers of protein relative to the initial signal.
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but you know second messengers arent they non-protein. how does that work when relay molecules are proteins.
(sorry about all these questions ^^)
Relay molecules aren't necessarily proteins.
what does the term amplified mean
Are you serious? =/ Hopefully you meant in the context of all of this then. Basically it's referring to fact that a single relay molecule could interact with a cell to produce a second messenger, then this second messenger can interact with 100 relay molecules, with these 100 relay molecules then interacting with another 1000 different relay molecules and so on, leading to the production of exponentially increased numbers of protein relative to the initial signal.
ok. so if you think about it, relay molecules are everything in the cell involved in signal transduction except for the hormone-receptor complex?
and with the signal being amplified, could you also say that it means many responses can be produced in cytosol form one signal
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but you know second messengers arent they non-protein. how does that work when relay molecules are proteins.
(sorry about all these questions ^^)
Relay molecules aren't necessarily proteins.
what does the term amplified mean
Are you serious? =/ Hopefully you meant in the context of all of this then. Basically it's referring to fact that a single relay molecule could interact with a cell to produce a second messenger, then this second messenger can interact with 100 relay molecules, with these 100 relay molecules then interacting with another 1000 different relay molecules and so on, leading to the production of exponentially increased numbers of protein relative to the initial signal.
ok. so if you think about it, relay molecules are everything in the cell involved in signal transduction except for the hormone-receptor complex?
and with the signal being amplified, could you also say that it means many responses can be produced in cytosol form one signal
You could possibly include that? I'm not sure. Once again, everything's fairly loosely defined here.
And yeh, you could probably interpret amplification that way as well.
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Would i be correct in saying that extracellular pathogens cause the humoral immune response and intracellular pathogens cause the cell-mediated response?
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Yes, but intracellular pathogens can also cause humoral response and extracellular pathogens can cause CMI responses
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oh i see, but generally, in exam questions can i follow that "rule"?
for example if i had a question like how would t cells and b cells be involved in and infected cut on a finger, i would explain the humoral response?
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well its not a set rule because both arms of the adaptive immune response are involved but if you were talking about extracellular bacteria for example, you would emphasise more the phagocytosis, inflammatory immune response, complement, DC activation, antibody response which would be the more predominant response... stuff like that
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In childbirth, is the effector the posterior pituitary or the uterus?
And how do you tell in general?
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Uterine muscles, because they're actually having the effect (contraction).
I just work out whatever is last in the pathway
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is the pituitary the control centre then? or are there such things as primary/secondary effectors
Also:
can someone please explain the connection between skin blood flow and temperature?
my understanding is the body dilates arteries near the skin to increase O2 supply and CO2 removal to skeletal muscles whilst removing excessive temperature from the inside of the body and releasing it via evaporation etc.?
does more skin blood flow = higher body temp?
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pretty sure that the hypothalumus is the control centre and the pituitary gland is the effector
and to the second question, yeah more blood flow = higher body temp
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Why are you guys going so in-depth into homeostasis =S Pretty sure I'd basically not even heard of the hypothalamus and pituitary in Bio 3/4. Exam questions will give you everything you need to know... Don't bother with memorising these details >_>
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It's because i have a SAC on it tommorrow, i just want to know in general, how to determine the effector or control centre,
why does blood flow = higher body temp?
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High blood flow to skin capillaries is a result of high body temperature, it doesn't cause it. It lets heat diffuse out to the environment, hence it can restore your normal temperature
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thankyou, do glands such as the pituaitary function as control centres or secondary effectors?
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http://bcs.whfreeman.com/thelifewire/content/chp42/4202s.swf
May all your questions be answered
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I'm more confused :(
If the control centre is they hypothalmus, and the effector is the different target organs, what effect does the pituitary have?
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Err, what? The hypothalamus is the control centre, which sends a signal to the pituitary to release oxytocin or whatever
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You're best to stop using the stimulus-response model so strictly. Most things in the body aren't as simple as that. Most things operate in a multi-tiered chain with multiple effectors and so on. The hypothalamic-pituitary-adrenal (HPA) axis basically involves the hypothalamus releasing 'releasing' hormones, leading to the pituitary releasing 'stimulating' hormones, which then leads to the relevant effector organs releasing their hormone, of which acts on a number of different tissues themselves. So it's not exactly a straight forward case of stimulus-response. For the case of the exam though, they generally choose a simple scenario which does actually fit the stimulus-response model.
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okay thankyou, that solves my problems :D
Does anyone have any good links on Co2 negative feedback regulation (for my sac tomorrow, in depth knowledge required), i google searched it a few times but was suprised by the lack of good, substantiated info, or can anyone just explain how it works?
thakns
in an unrelated question,
as humans cannot digest cellulose, how do we get energy from plants? do bacteria digest and release the plants cytoplamsic contents? or do we just 'squish' and squeeze things out of the cell wall?
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Extremely long, wordy and largely irrelevant intro from my prac on this many years ago:
In order to survive, organisms must maintain a relatively stable internal environment. The state of a relatively stable internal environment which is maintained with narrow limits is called homeostasis (Kinnear & Martin, 2006). Homeostasis is maintained within organisms by counteracting changes when deviations from a steady state occur. This is performed by a sequence of events known as the stimulus-response model. This model begins with a stimulus, a physical or chemical change in the environment, capable of provoking a response in an organism (Greenwood, Shepherd, & Allan, 2007). The stimulus is received by a receptor, which then transmits a message to the central nervous system (CNS). The CNS is composed of the brain and the spinal cord. The CNS then sends a message to an effector, which is capable of producing a response. This response acts to return a variable to its normal state (Canavan, 2006).
A clear example of homeostasis in action is the control of breathing in humans. Like all other organisms, humans must perform cellular respiration in order to survive. Because humans mostly perform aerobic respiration, a steady supply of oxygen in cells is required to maintain this process. However, because aerobic respiration produces carbon dioxide as a by-product, an increase in carbon dioxide levels would occur if homeostatic mechanisms did not act to reduce them. Increases in carbon dioxide cause a change of pH in the blood, and therefore must be regulated accordingly.
The exchange of respiratory gases is performed by the act of respiration, also known as breathing. Involuntary breathing is known as quiet breathing or tidal breathing, and consists of two main phases, inspiration and expiration, also known as inhalation and exhalation. Inhalation is achieved by increasing the available space within the lungs, by contracting the external intercostal muscles and diaphragm. This decreases the pressure within the lungs, and air flows into the lungs as a result of the pressure gradient (Greenwood, Shepherd, & Allan, 2007). The reverse of this process occurs in exhalation.
The above process of quiet breathing describes the involuntary action of breathing as a result of the autonomic nervous system. However, breathing can increase as a result of exercise or forced breathing, and is known as active breathing (Silverthorn, 2007). Active breathing changes the action in exhalation, to also include the contraction of the internal intercostals and abdominal muscles, to increase the force of exhalation (Greenwood, Shepherd, & Allan, 2007). This overall increases the rate of carbon dioxide expulsion.
As stated before, because oxygen and carbon dioxide concentrations must be kept within a certain level, mechanisms must act to regulate these respiratory gases. The concentrations of these gases are primarily maintained by the rate and depth of respiration, where as the rate and depth of respiration increases, the concentration of oxygen increases while the concentration of carbon dioxide decreases. This response is triggered by certain stimuli, which is mainly the carbon dioxide concentration within the blood. This is detected in central chemoreceptors. In addition, the rate of breathing may also be affected by oxygen concentration and blood pH. These stimuli are picked up by peripheral chemoreceptors which are located in the carotid and aortic arteries. However, oxygen receptors are unlikely to alter breathing rate because the oxygen receptor will only take effect if oxygen levels become extremely low, roughly equivalent to ascending to a height of 3000 metres (Silverthorn, 2007). In either case, a message is sent to the CNS, which then directs a message towards effectors such as the respiratory muscles mentioned before to adjust the rate and depth of respiration.
Through these mechanisms, a steady proportion of oxygen and carbon dioxide is maintained within the organism. In normal conditions, concentrations of oxygen and carbon dioxide in inhaled air are approximately 21.0% and 0.04% respectively, while the concentrations in exhaled air during tidal breathing are 16.4% and 3.6% respectively (Silverthorn, 2007). However, these concentrations can be changed, and this experiment tests the influence of possible changes to carbon dioxide concentrations. The level of carbon dioxide is altered by performing hyperventilation, and hypoventilation. Hyperventilation will involve taking very rapid, deep breaths in order to remove more carbon dioxide from the blood. Hypoventilation will be performed by breathing into a bag, which will gradually increase the carbon dioxide concentration of the surrounding air. Through both of these tests, conclusions can be made about the influence of carbon dioxide on breathing.
Only thing to add to that is that the central chemoceptors are found in the medulla oblongata (better known just as the medulla). If you've got any more specific questions, fire away.
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sweet, thanks alot shinny,
my unurgent question is
as humans cannot digest cellulose, how do we get energy from plants? do bacteria digest and release the plants cytoplamsic contents? or do we just 'squish' and squeeze things out of the cell wall?
:)
I think i'm ready for my sac tomorrow :S
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My intro (probably much n00ber than shinny's though):
Homeostasis, literally meaning ‘steady-state’, is the relative physiological consistency of the body, despite external fluctuations (Allan et al, 2010 p.55). Like many animals, humans exhibit homeostasis for a range of physical and chemical properties. For example, the human body maintains a fairly constant body temperature, pH of the blood and interstitial fluid, solute concentration of glucose in the bloodstream, respiration rate, and blood pressure (Kinnear and Martin, 2006 p. 136). An animal achieves homeostasis by maintaining a variable at or near a particular value (Figure 1). The most common homeostatic system is negative feedback. Fluctuations in a variable above or below the set point serve as the stimulus. A receptor, or sensor, detects the stimulus and triggers a response, a physiological activity that helps return the variable to the set point (Campbell et al, 2009 p. 861).
An example of negative feedback is thermoregulation, the maintaining of temperature within a certain range (Figure 2). For humans, this range is 36.1° to 37.8°. The sensors for thermoregulation are concentrated in a brain region called the hypothalamus (Campbell et al, 2009 p. 868). The hypothalamus contains a group of nerve cells that acts somewhat like a thermostat, responding to body temperatures outside a normal range by activating mechanisms that promote heat loss or gain. Warm receptors signal the hypothalamic thermostat when temperatures increase; cold receptors signal when temperatures decrease. When body temperatures are below the normal range, the thermostat inhibits heat loss mechanisms and activates heat-saving ones such as the constriction of certain blood vessels, known as vasoconstriction, and the raising of hairs, while stimulating heat-generating mechanisms such as shivering (Anon, 2000). In response to higher than normal body temperature, the hypothalamic thermostat shuts down heat retention mechanisms and promotes body cooling by dilating blood vessels close to the skin surface, known as vasodilation, sweating, or panting. Skin also possesses thermoreceptors, which can detect the temperature of the external environment. This information is then relayed to the hypothalamus, which in turn begins the corrective mechanisms (Anon, 2000).
Another homeostatic feedback system is positive feedback. Positive feedback is used to a lesser extent than negative feedback. Unlike negative feedback, positive feedback leads to a response escalating in the same direction. An example of this type of system is during labour (Figure 3), where the release of oxytocin is intensifies the contractions of the uterus so that labour proceeds to its conclusion. The system is restored by the birth, which removes the initiating stimulus (Allan et al, 2010 p.56).
The practical report aims to explain how a balance between heat gain and heat loss is achieved in the process of thermoregulation. We will be measuring breathing rates, core temperature in the ear and skin temperature from sweat. Breathing, or panting, as mentioned above, increases as a corrective mechanism to high temperatures. Core temperatures can be measured from the ear because the same blood vessel supplies the hypothalamus and ears, hence, an ear thermometer records the temperature detected by the hypothalmic thermostat (Campbell et al, 2009 p. 868). Sweat, similar to breathing rates, is secreted from sweat glands as a corrective measure to high temperatures.
The body’s ability to adapt to changes is crucial to the maintenance of life. The mechanisms mentioned and described above are capable of controlling variables within defined limits. This ability to control variables through homeostasis, whether negative or positive feedback mechanisms, gives us the ability to survive despite fluctuating or adverse environmental conditions, and is hence, is fundamental to our lives.
lol, I barely remember any of this :o
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as humans cannot digest cellulose, how do we get energy from plants? do bacteria digest and release the plants cytoplamsic contents? or do we just 'squish' and squeeze things out of the cell wall?
We get energy from other things within plants. Not all the carbohydrates are in the form of cellulose - not to mention the other nutrients available. The cellulose becomes what we know as dietary fibre.
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so humans can withdraw plant cellular substances without needing to break down the cell wall?
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so humans can withdraw plant cellular substances without needing to break down the cell wall?
Well it definitely gets broken down, but I'm not 100% on the main factor involved. There's other components in the cell wall that I'm fairly certain we can break down, and despite that, the mechanical process of chewing and the consequent digestion and stomach acid and whatnot would pretty much tear it apart.
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what does increased metabolic rate mean? :)
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Increased cellular activity producing ATP and heat. Giving that metabolism is the sum total of chemical reactions happening in the body, an increase in metabolic rate would simply mean more chemical reactions happening per unit of time
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Increased cellular activity producing ATP and heat. Giving that metabolism is the sum total of chemical reactions happening in the body, an increase in metabolic rate would simply mean more chemical reactions happening per unit of time
ohh ok thanks, this makes sense now :)
Oh, if your metabolic rate increases too much can their be a fatal build up of products? wat are the consequences of a too fast metabolic rate
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hey guys.
exam question, i don't really agree with the answer.
Evidence that molecule (aquaporin) was a component of cellular water channels came in an experiment with frogs' legs bathed in water solution. One group of eggs were injected with aquaporin RNA while the other group were not. Write a hypothesis based on what you think would happen to the two different groups of eggs.
ANSWER: THAT THE EGGS EXPRESSING AN AQUAPORINE, FOLLOWING INJECTION OG AQUAPORINS RNA, WILL ABSORB WATER, SWELL AND BURST, BUT THE EGGS WITHOUT THE AQUAPORINS WILL NOT BURST.
i thought more aquaporins would enhance water regulation?
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hey guys.
exam question, i don't really agree with the answer.
Evidence that molecule (aquaporin) was a component of cellular water channels came in an experiment with frogs' legs bathed in water solution. One group of eggs were injected with aquaporin RNA while the other group were not. Write a hypothesis based on what you think would happen to the two different groups of eggs.
ANSWER: THAT THE EGGS EXPRESSING AN AQUAPORINE, FOLLOWING INJECTION OG AQUAPORINS RNA, WILL ABSORB WATER, SWELL AND BURST, BUT THE EGGS WITHOUT THE AQUAPORINS WILL NOT BURST.
i thought more aquaporins would enhance water regulation?
Yes aquaporins will make the membrane more permeable to water.
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hey guys.
exam question, i don't really agree with the answer.
Evidence that molecule (aquaporin) was a component of cellular water channels came in an experiment with frogs' legs bathed in water solution. One group of eggs were injected with aquaporin RNA while the other group were not. Write a hypothesis based on what you think would happen to the two different groups of eggs.
ANSWER: THAT THE EGGS EXPRESSING AN AQUAPORINE, FOLLOWING INJECTION OG AQUAPORINS RNA, WILL ABSORB WATER, SWELL AND BURST, BUT THE EGGS WITHOUT THE AQUAPORINS WILL NOT BURST.
i thought more aquaporins would enhance water regulation?
Pure water is hypotonic to the cell, so if aquaporins are present, water will rush into the cell and lyse it. Cells which don't have aquaporins will only have water enter by osmosis across the lipid bi-layer itself - a fairly slow and negligible process - meaning that the cell will probably take a long time or never lyse. Not too sure how effectively water crosses a pure membrane. What exactly are they teaching in Bio 3/4 nowadays though? In '07, we were still being taught that water is freely permeable via simple diffusion without any mention of the need for aquaporins o_o
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so osmosis is a relatively slow process in comparison to if aquaporins were present?
eh this was just in an exam paper, never learned anything about aquaporins at school.
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so osmosis is a relatively slow process in comparison to if aquaporins were present?
That's my understanding, yes. Perhaps the Biomed students could elaborate. I didn't go very in-depth into biology in first year, and knowledge of aquaporins was quite limited back when I did Bio 3/4.
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so osmosis is a relatively slow process in comparison to if aquaporins were present?
That's my understanding, yes. Perhaps the Biomed students could elaborate. I didn't go very in-depth into biology in first year, and knowledge of aquaporins was quite limited back when I did Bio 3/4.
Didn't you cover this in kidney function? I recall something about aquaporins being stimulated by vasopressin release for fluid reabsorption by the collecting duct. So I'm not sure if this process is any different to frogs legs.
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so osmosis is a relatively slow process in comparison to if aquaporins were present?
That's my understanding, yes. Perhaps the Biomed students could elaborate. I didn't go very in-depth into biology in first year, and knowledge of aquaporins was quite limited back when I did Bio 3/4.
Didn't you cover this in kidney function? I recall something about aquaporins being stimulated by vasopressin release for fluid reabsorption by the collecting duct. So I'm not sure if this process is any different to frogs legs.
Kidney physiology and kidneys in general are the death of me. But yeh, I know aquaporins increase the rate of diffusion, but I'm not sure to what extent water can diffuse through the lipid bi-layer, that's all.
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so osmosis is a relatively slow process in comparison to if aquaporins were present?
That's my understanding, yes. Perhaps the Biomed students could elaborate. I didn't go very in-depth into biology in first year, and knowledge of aquaporins was quite limited back when I did Bio 3/4.
Didn't you cover this in kidney function? I recall something about aquaporins being stimulated by vasopressin release for fluid reabsorption by the collecting duct. So I'm not sure if this process is any different to frogs legs.
i only learned about the kidney in 1/2 and in not much depth. and what frog legs?
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another question, in cell mediated immunity, do the macrophages release cytokines that act on t lymphocytes to develop and proliferate into t cytotoxic cells and t helper cells?
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afaik, water diffuses through the membrane but also must use channels (presumably aquaporins) to achieve the measured rate of osmosis.
Naive T lymphocytes differentiate into Helper/Cytotoxic cells in the Lymph Nodes (technically in the thymus I guess but they acquire their actual effector function in the lymph nodes). They're usually activated by interaction with Dendritic Cells and subsequent stimulation by cytokines.
Macrophages can act to activate them but it's much less common
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CD4+ T cells (Helper T cell)
CD8+ T cells (CTL)
well yea naive CD4+ T cells, CD8+ T cells get activated and differentiate into effector CTL's or Th lymphocytes in the periphery (doesn't have to be lymph nodes, its in the peripheral lymphoid organs like spleen) but yes what Russ said DC's are the cells that initiation the primary adaptive immune response. But the cytokines produced by the DC's or macrophages does help to activate the T cells (like IL-2) and certain cytokines can help to differentiate T helper cells into certain types of Th cells (ie: Th1, Th2, Th17 etc) for example IL-12 produced by DC's or macrophages help to turn CD4+T cell into Th1 phenotype.
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After excercise, should amount of CO2 exhaled increase or decrease? we just did a praac where everyone got CO2 exhaled decreases after excercise, should i try and validatet this, or say it's wrong and attribute it to an error?
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After excercise, should amount of CO2 exhaled increase or decrease? we just did a praac where everyone got CO2 exhaled decreases after excercise, should i try and validatet this, or say it's wrong and attribute it to an error?
sounds like a PE question haha, im guessing its decrease.. simply because there is limited time to convert oxygen to co2, hence small amounts of co2 is exhaled? but i recommend you msg lexitu :)
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i'm getting annoying but i got another question.
I am having trouble finding a solid description on the process of cell mediated immunity, there seems to be some discrepancies between text books such as heinemann and other texts. heinemann says that a naive t cell will recognise an antigen on the mhc 1 marker on the antigen displaying cell. the t cell will then develop and proliferate into t cytotoxic cells and t helper cells. The t helper cells then release cytokines (interleukin-1) to activate natural killer cells. Cytotoxic cells and natural killer cells then directly kill virus infected cell. Other texts say that a t helper cell recognises the antigen, rather than a naive t cell.
Which is correct?
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After excercise, should amount of CO2 exhaled increase or decrease? we just did a praac where everyone got CO2 exhaled decreases after excercise, should i try and validatet this, or say it's wrong and attribute it to an error?
sounds like a PE question haha, im guessing its decrease.. simply because there is limited time to convert oxygen to co2, hence small amounts of co2 is exhaled? but i recommend you msg lexitu :)
Just about to leave for work, will answer this later - short answer it will decrease gradually.
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i'm getting annoying but i got another question.
I am having trouble finding a solid description on the process of cell mediated immunity, there seems to be some discrepancies between text books such as heinemann and other texts. heinemann says that a naive t cell will recognise an antigen on the mhc 1 marker on the antigen displaying cell. the t cell will then develop and proliferate into t cytotoxic cells and t helper cells. The t helper cells then release cytokines (interleukin-1) to activate natural killer cells. Cytotoxic cells and natural killer cells then directly kill virus infected cell. Other texts say that a t helper cell recognises the antigen, rather than a naive t cell.
Which is correct?
Our uni lecturer taught that naive T cells are activated by antigens, which causes them to specialise and proliferate.
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After excercise, should amount of CO2 exhaled increase or decrease? we just did a praac where everyone got CO2 exhaled decreases after excercise, should i try and validatet this, or say it's wrong and attribute it to an error?
sounds like a PE question haha, im guessing its decrease.. simply because there is limited time to convert oxygen to co2, hence small amounts of co2 is exhaled? but i recommend you msg lexitu :)
Just about to leave for work, will answer this later - short answer it will decrease gradually.
YES! that's what my results / class results show :) I'm excited ! Woudl love if you could do this by tomorow, as that's when my sac is to be finished :D
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@CO2, if lexitu is going to answer it in depth then I won't bother, but from a purely biochemical standpoint I presume it's related to decreased ATP production from the TCA cycle (and thus reduced CO2 production)
i'm getting annoying but i got another question.
I am having trouble finding a solid description on the process of cell mediated immunity, there seems to be some discrepancies between text books such as heinemann and other texts. heinemann says that a naive t cell will recognise an antigen on the mhc 1 marker on the antigen displaying cell. the t cell will then develop and proliferate into t cytotoxic cells and t helper cells. The t helper cells then release cytokines (interleukin-1) to activate natural killer cells. Cytotoxic cells and natural killer cells then directly kill virus infected cell. Other texts say that a t helper cell recognises the antigen, rather than a naive t cell.
Which is correct?
A naive T cell will recognise an antigen on MHC (MHC1=CD4, MHC2=CD8). This will cause proliferation and differentiation. CD4 cells will become T helper (Th) cells and CD8 cells will become cytotoxic T lymphocytes (CTLs).
Th cells will produce multiple cytokines, some of which will activate NK cells. NK cells do not absolutely require activation, they can have effects without T cell help. CTLs and NK cells will then target intracellular pathogens (NK cells are predominantly for antiviral functions, CTLs can target all many of intracellular pathogens).
The confusion may stem from the fact that a naive T cell can be either a Th cell or a CTL. By the time they reach the periphery and encounter Ag, they've already determined whether or not they will become Th or CTLs. As such, sometimes people say "naive cells encounter Ag" and sometimes they say "T Helper cells encouter Ag".
Our uni lecturer taught that naive T cells are activated by antigens, which causes them to specialise and proliferate.
fwiw, Ag signalling isn't enough for specialisation, they need cytokine stimulation as well
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i'm getting annoying but i got another question.
I am having trouble finding a solid description on the process of cell mediated immunity, there seems to be some discrepancies between text books such as heinemann and other texts. heinemann says that a naive t cell will recognise an antigen on the mhc 1 marker on the antigen displaying cell. the t cell will then develop and proliferate into t cytotoxic cells and t helper cells. The t helper cells then release cytokines (interleukin-1) to activate natural killer cells. Cytotoxic cells and natural killer cells then directly kill virus infected cell. Other texts say that a t helper cell recognises the antigen, rather than a naive t cell.
Which is correct?
A naive T cell will recognise an antigen on MHC (MHC1=CD4, MHC2=CD8). This will cause proliferation and differentiation. CD4 cells will become T helper (Th) cells and CD8 cells will become cytotoxic T lymphocytes (CTLs).
Th cells will produce multiple cytokines, some of which will activate NK cells. NK cells do not absolutely require activation, they can have effects without T cell help. CTLs and NK cells will then target intracellular pathogens (NK cells are predominantly for antiviral functions, CTLs can target all many of intracellular pathogens).
The confusion may stem from the fact that a naive T cell can be either a Th cell or a CTL. By the time they reach the periphery and encounter Ag, they've already determined whether or not they will become Th or CTLs. As such, sometimes people say "naive cells encounter Ag" and sometimes they say "T Helper cells encouter Ag".
Our uni lecturer taught that naive T cells are activated by antigens, which causes them to specialise and proliferate.
fwiw, Ag signalling isn't enough for specialisation, they need cytokine stimulation as well
Oh i see, so i could say either the t helper cell or naive t cell? thanks for the help.
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T cells during development in the thymus already develop into CD4+ (helper) or CD8+ (cytotoxic) T cells... so that is already determined by the time they are in circulation
when they are exit the thymus and enter circulation they are all naive since they have not encountereed their antigen... once they encounter their antigen and are activated they become effector CD4+ T cells or effector CD8+ T cells
this may help you depending how much you know the terms already http://vce.atarnotes.com/forum/index.php/topic,25843.0.html
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True light if you kjnow the answer to my question, could you please ask it ? I'm not sure what time Lexitu gets baclk and i realy need an answer tonight :)
Thanks!
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Simplest explanation I can think of is that anaerobic respiration will be producing lactic acid, which has the unfortunate side effect of being an acid. That means it'll dump protons and drop the physiological pH. CO2 will be consumed by the body to buffer against this via hydrogen carbonate (H2CO3) production.
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how does h2cO3 buffer against acids? thought it could only buffer basic solutions
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As H2Co3 splits into
HCO3 + H, this would raise the acidity of the blood???
or does the body have some way of ridding the protons, so HCO3 can acept other hydrogen ?
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As H2Co3 splits into
HCO3 + H, this would raise the acidity of the blood???
or does the body have some way of ridding the protons, so HCO3 can acept other hydrogen ?
The body produces HCO3. Carbonic acid is the result when it binds to CO2.
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sorry guys, another question,
why can there be two different codons for one amino acid?
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As H2Co3 splits into
HCO3 + H, this would raise the acidity of the blood???
or does the body have some way of ridding the protons, so HCO3 can acept other hydrogen ?
The body produces HCO3. Carbonic acid is the result when it binds to CO2.
Is Russ's whole answer correct then?
In. Co2 absorbtion is necessary after strenous excersice to form HCO3 to bond with H + produced?
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sorry guys, another question,
why can there be two different codons for one amino acid?
Why is the sky blue; answer, it turned out that way. It's just one of the ways that the body evolved. Because there were 64 codons and only 20 essential amino acids, some of the codons had to code for more than 1.
In terms of function though, it's a very important mechanism for suppressing mutations
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As H2Co3 splits into
HCO3 + H, this would raise the acidity of the blood???
or does the body have some way of ridding the protons, so HCO3 can acept other hydrogen ?
The body produces HCO3. Carbonic acid is the result when it binds to CO2.
Is Russ's whole answer correct then?
In. Co2 absorbtion is necessary after strenous excersice to form HCO3 to bond with H + produced?
The body compensates for decreased pH (in this case, due to increased CO2 and thus carbonic acid) in two ways - increasing available HCO3 via the kidneys, or by increasing ventilation in the lungs to expel more CO2. However, increasing HCO3 via the kidneys is a process which takes days. In a fit and healthy person, the decrease in pH following exercise will be quickly corrected by the increase in ventilation (hence why you puff when you exercise). Thus, since the body has to expel all that excess CO2, then the CO2 in the exhaled air will be increased.
On the other hand, to explain your results, perhaps the increase in ventilation overcompensates and leads to hyperventilation, leading to a decrease in CO2 concentration soon after exercise. This might explain why you feel light headed during severe exercise, similar to how you do when you purposefully hyperventilate. I've doubts about this answer but it's the only way I can think of to explain your results. Lets hope lex has some clearer answers :P
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hey guys just have a few questions:
How does CoQ10 enhance muscle function and also reduce lipid oxidation?
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hey guys just have a few questions:
How does CoQ10 enhance muscle function and also reduce lipid oxidation?
Uhh...do you really need to know this?
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yeah kinda for a SAC :P
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hey guys just have a few questions:
How does CoQ10 enhance muscle function and also reduce lipid oxidation?
CoQ10 is the only lipid-soluble antioxidant that is synthesized in the human body. Antioxidants prevent tissue damage by inhibiting oxidative reactions that cause damage to cells. That explains why lipid oxidation is reduced.
As humans age, the number of mitochondria per cell declines therefore the ability to produce ATP declines right... the level of CoQ10 also declines with age. Coenzyme 10 is a co-enzyme in mitochondrial actions that produce ATP, don't ask me how/where/why because it's "beyond the scope of the 3/4 course" LOL, but I know it is =P. Anyways, as such current research shows that heart tissue in people with cardiovascular diseaser = lower then avg. CoQ 10 concentrations. Essentially the reason why it enhances muscle function is because it's a co-enzyme in ATP producing reactions in the mitochondria.
NOTE: My source for this is NOB book 2, page 61, I think your SAC wouldn't expect you to go into more depth than that on something that technically isn't really part of the course? (It's sorta just an example).
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yeah kinda for a SAC :P
Urgh, what's with schools setting these amazingly detailed SACs. This isn't even stuff I go into much detail for in uni...
Basically CoQ10 is one of the proteins involved in the electron transport chain. Because muscles have high energy requirements, increased concentrations of CoQ10 allows more ATP production, and thus greater muscle stamina.
CoQ10's function in the ETC is only possible because it is easily reduced and oxidised between its two forms. The CoQ10 found in the blood stream can thus reduce any free radicals floating around which would normally otherwise oxidise other things, such as lipids, which can then lead to clogging of arteries.
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Russ or anyone else if you can answer it, or link me to an appropriate page by 1130 am that would be hugely appreciated!
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Sorry sorry sorry. Didn't realise this was for a SAC so I left it for today to answer.
Oxygen consumption is high during exercise because high amounts of aerobic respiration take place. This means that venous blood has a high concentration of carbon dioxide especially in high-intensity exercise (because it's the end=product of respiration). As soon as an athlete finishes exercise the amount of oxygen being consumed will begin to decrease (although it remains elevated somewhat in order to reverse the effects of metabolic processes such as lactic acid accumulation).
Does that answer your question. Anything that you want clarified, let me know, I have all morning.
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Just realised that this didn't fully answer the question. So, if the amount of carbon dioxide being produced by muscle cells decreases, as I said the concentration in the veins carrying blood back to the heart will also decrease. When the blood is taken to the membranes where gaseous exchange takes place, there will be less of a concentration gradient for the net diffusion of carbon dioxide from the capillaries to the alveoli. This means less carbon dioxide will be exhaled.
During exercise, because so much oxygen is being consumed there is a high concentration of carbon dioxide in the blood returning to the heart and eventually the lungs. This means there will be more diffusion for both gases. Carbon dioxide will be exhaled in higher concentrations and oxygen will be inhaled in higher concentrations.
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Thankyou very much, class results showed that CO2 exhalation immediatly after excercise was LESS than before excercise, i think it is just class results are wrong :|
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Oh, less than BEFORE EXERCISE. That does seem odd. Class results must have been wrong. Also, a possibility would have been an anticipatory response to exercise causing increased oxygen consumption (due to hormonal changes, etc.), but still you'd expect CO2 exhalation immediately after to be still quite high, even though on the decline.
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i know i'm being pendantic. i'm fussing over a MHC question.
so there are tumour cells in tasmanian devils that can be transmitted to other uninfected tasmanian devils and go unoticed as they are accepted as self cells.
Should i say that the protein displayed on the MHC 1 marker is similar, therefore they are not identified as non self cells, or should i say that the MHC 1 marker is similar.
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That's not pedantic, that's an important difference. Cells are defined as self if they have the same (or similar enough) MHC marker
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so what if the mhc marker is the same, but display a non self protein? wouldn't this occur in viral cells?
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I don't understand your question but I hope this answers it:
T cells are trained by the body to not target "self" MHC - if they did, they'd spontaneously target every cell in your body. If you get a foreign cell transplanted with non-self MHC, you get a response to it (transplant rejection). If it is the same, your body will respond to it as normal - ie only when it has a foreign peptide displayed.
When a cell is infected with a virus, viral components are expressed on MHCI...this obviously leads to recognition and immune response.
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hah. i see, thanks for the help
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was just looking around and here this might also make things clear what Russ said is correct
http://chickenoreggblog.wordpress.com/2010/04/13/tasmanian-devil-facial-tumour-disease-too-good-a-match-for-the-immune-system/
"Devil populations in eastern Tasmania have low levels of genetic diversity due to reductions in population size over the last 150 years. DFTD is so virulent in these populations because the tumours have the same MHC type as healthy devil cells. Being an infectious cancer, transmission of DFTD between individuals is a bit like a skin graft or organ transplant. If the tissue’s MHC type matches, the transplant is accepted, if not it is rejected. Because the MHC types of the tumour and the devil match, DFTD cells are not recognised as foreign so no immune response is mounted. And because of the low genetic diversity, all devils in the population have similar MHC types meaning the disease can easily spread from one individual to another...
Here the story gets a little (more) complicated: Tasmanian devils have multiple MHC genes (up to 7 genes each), which fall into two groups on the basis of their DNA sequence. The tumour cells have both group 1 and group 2 variants, as do the individuals from the susceptible eastern populations. However the northwestern populations harbour a greater diversity of MHC types, and many individuals from these populations have MHC types which have only either group 1 or group 2 sequences. None of these individuals have succumbed to DFTD, suggesting they are resistant to the disease. Belov’s group proposes that in individuals with only group 1 sequences, the immune system will recognise the group 2 sequences on the tumour as foreign and resist it (and vice versa for individuals with only group 2 sequences). This has yet to be tested in practice, as it is obviously difficult to get permission to infect an endangered species with a deadly disease. However, these findings are promising for the continued survival of the species and may have a significant impact on their conservation management."
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:) thanks truelight, you didn't have to go to so much trouble. yeah it was this question that tripped me up.
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haha na it was nothing just a google search .... mmm trifle...who watched masterchef lol
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ahaha hells yeyahh. ah i digress.
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how do memory B cells work? i know they remember the certain pathogen so that the next time they come, the immune response is quicker but i was wondering how it actually works.. like to they divide or like activate stuff or something? :S LOL
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yes your right in that memory B cells respond much faster in a secondary immune response but there are some differences...like they are long lived, circulate in the periphery, hardly divide with no antigen stimulation...also
memory b cells have differentiated from b cells that have been primed and activated so they have already gone through the various stages of b cell development. So their antibodies are of much higher affinity. Also memory B cells in a secondary immune response produce large amounts of the effector antibody ie: IgG... not IgM...
they also have larger amount of MHC on their surface and CD80/86 therefore there is less of a requirement for costimulation and you don't need as much antigen to stimulate the memory b cell and therefore the response is quicker.
they also have different molecules (or different levels) on their surface that help memory b cells with adhesion, activation threshold, cell survival etc...
but the way in which of memory b cells are activated is the same as naive b cells in that it recognises antigen, uptake, process, present to Th cells, activate, proliferate, differentiate and go along to do their thing but the response in doing all these is much faster and greater.
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are cysts like spores? can they exist on childrens toys etc?
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What context?
A cyst in the body is not a spore, no
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oh hang on, wrote something completely stupid. just ignore.
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After the Calvin Cycle finishes, and PGAL is produced, do 2 molecules combine to form fructose (as NOB says) , and then into glucose, or into glucose directly?
Also, can someone please explain how electrons in chloroplasts absorb energy and transfer this to the water molecule?
cheers
3)
Does negative feedback work by simply causing a change in the variable being detected, or does it act directly on the gland (i'm sure its the first one but some sources imply otherwise) i.e. when drawing a negative feedback diagram, should i draw the feedback arrow to the stimulus, or the gland producing the hormone?
4) Is a protein glycolipid just a protein + carb attached to an already present lipid in plamsa membrane and
is a glycolipid just a carb molecule attached to an already present phospholipid?
5) Do leukocytes phagocytose eukaroyttc pathogens? Neap says they do but Campbells says otherwise
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I don't do plant biology, but electrons will move to higher energy levels/subshells in order to "absorb" energy
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bump added a Q thanks russ
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why does the humoral response involve the MHC 2 marker, while the cell mediated response involves the MHC 1 marker?
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why does the humoral response involve the MHC 2 marker, while the cell mediated response involves the MHC 1 marker?
MHCI is recognised by CD8 cells, which then destroy the cell they bind. That makes it directly cell mediated.
MHCII is recognised by CD4 cells, which are responsible for activating B cells, which produce antibodies. That makes it "humoral" because the antibodies are soluble in the serum etc.
Does negative feedback work by simply causing a change in the variable being detected, or does it act directly on the gland (i'm sure its the first one but some sources imply otherwise) i.e. when drawing a negative feedback diagram, should i draw the feedback arrow to the stimulus, or the gland producing the hormone?
How does it cause a change in the variable/stimulus without affecting the gland? If there's too much sugar in the blood, you can't just magically reduce it, you have to stimulate the pancreas to produce insulin to insert GLUT4 into cell membranes to transport sugar out of the blood.
5) Do leukocytes phagocytose eukaroyttc pathogens? Neap says they do but Campbells says otherwise
Depends what you mean by leucocytes and phagocytose. Eukaroytic pathogens generally aren't phagocytosed because they're too big...but phagocytes are involved in their clearance, as are other cells. Degranulation and oxidative burst to produce various toxic molecules are important clearance mechanisms.
q4 is biochem and i can't remember it clearly enough right now. google and wikipedia might help you out
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Thankyou
another question :S in addition to the remaining ^ ones :D
- i remember someone talking about this before, but i couldn't find the exact page -
is it better to define an autoimmune disease as
the body is unable to distngush between self and non self
or
the body recognises self AS non - self cells
thanks
EDIT:
This may sound stupid
What does water do for the body, from a VCE biological standpoint?
Is it mainly just to provide solvent etc.
?
or does it directly participate in reactions (in addition to hydrolysis etc. ) integral to VCE Biology? (except photosynthesis)
thanks
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Thankyou
another question :S in addition to the remaining ^ ones :D
- i remember someone talking about this before, but i couldn't find the exact page -
is it better to define an autoimmune disease as
the body is unable to distngush between self and non self
or
the body recognises self AS non - self cells
thanks
EDIT:
This may sound stupid
What does water do for the body, from a VCE biological standpoint?
Is it mainly just to provide solvent etc.
?
or does it directly participate in reactions (in addition to hydrolysis etc. ) integral to VCE Biology? (except photosynthesis)
thanks
Autoimmune disease is where the body attacks its own cells as it is unable to distinguish self from non-self. also be aware of the difference between immunodeficiency and autoimmunity.
Water acts as a solvent, transport and reaction medium, and also (occasionally but still significantly) as a reactant in some metabolic processes. Osmotic regulation is also a vital part of homeostasis because we lose control of everything if we become too dehydrated.
Just be careful - the body is not quite as black and white as your questions seem to make it out to be.
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hehe thanks :)
I often ask questions in that format just so i can get a more direct idea and more direct response
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is it better to define an autoimmune disease as
the body is unable to distngush between self and non self
or
the body recognises self AS non - self cells
Both. The body recognises self as non-self because it is unable to distinguish between them. Worth bearing in mind that simply saying "the body cannot distinguish between self and non self" isn't correct (although VCE might let it slide). It is extremely rare that the immune system will simply target all self molecules as non-self...it's almost always a specific antigen or class of antigens
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is it better to define an autoimmune disease as
the body is unable to distngush between self and non self
or
the body recognises self AS non - self cells
Although it's often said in the former way - that the body is unable to distinguish self and non-self - I think it's better said in the latter way. That's because the former could also be interpreted to not only mean that the body recognises self as non-self, but also vice versa. This would lead to an immunodeficiency of sorts where the body recognises foreign antigens as self. However, auto-immune diseases aren't associated with that, and it's purely a one way thing. So yeh, it's probably best to specify that the body recognises self as non-self.
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As always thanks for your great help :)
At VCE level , how is water produced in light independent reactions of photosynthesis?
I looked at both NOB and Campbells, and neither has water leaving the calvin cycle :S
EDIT:
Wiki says Natural Killer cells are lymphocytes, shoudl we describe as such or just avoid
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Yes, they're one of the three types (T/B cells just get more press)
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As always thanks for your great help :)
At VCE level , how is water produced in light independent reactions of photosynthesis?
I looked at both NOB and Campbells, and neither has water leaving the calvin cycle :S
Pretty sure water's a reactant, isn't it?
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i suggest you look at this :) http://vce.atarnotes.com/forum/index.php/topic,40044.15.html
but dont think you need to really know how, just the fact that its both a reactant and a product in photosynthesis, i havent come across any questions that have asked
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Is a single amino acid considered a biomacromolecule? I thought not... but apparently it is? ???
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hmmm i think its an organic molecule but i wouldnt call it a biomacromolecule cause its not a big molecules like a protein.
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hmmm i think its an organic molecule but i wouldnt call it a biomacromolecule cause its not a big molecules like a protein.
That's what I thought... but Neap 2007 MC:
2. Which of the following biomacromolecules contains smallest number of atoms?
A. phospholipid
B. an amino acid
C. a protein
D. a starch molecule
Answer is B ???
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:S
sorry, no idea then
i would have chosen (semi guess) and gone with A
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:S
sorry, no idea then
i would have chosen (semi guess) and gone with A
That's what I put... Hate these company exams! :(
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I wouldn't categorize an amino acid as a biomacromolecule but the answer to that question is definitely B.
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Would an amino acid coded for a jelly fish that glows in the dark be the same code in perhaps a mice? If so, would that make the mice glow in the dark?
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Would an amino acid coded for a jelly fish that glows in the dark be the same code in perhaps a mice? If so, would that make the mice glow in the dark?
Pretty sure that experiment's been done, but it wasn't an amino acid/protein, it was the code for the glow-in-the-dark gene that they transferred into the mice.
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This one?
And yes, it's basically a tag that they can attach to other proteins etc.
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This one?
And yes, it's basically a tag that they can attach to other proteins etc.
Yeah that's it, just wanted to clarify something. Thanks!
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how to phagocytes detect pathogens if they do not have specific antibodies?
Is it due to the lack of 'self' receptors or the clear differences (e.g. cell walle tc.)
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They have receptors to what are called Pathogen Associated Molecular Patterns (PAMPS). Things like flagellin, that are never found in the human body, trigger uptake by phagocytes. They also have a couple of other tricks, like receptors for antibodies; so once an Ab has bound a pathogen it can be bound by a macrophage for destruction
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Thanks again Russ , another immunity questinon:
Can viruses floating in interstitial fluid trigger a B cell? or does the virus HAVE to be attached to a host cell?
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What do you mean by interstitial fluid? If a B cell is in the blood it will bind a free virion but B cells don't really go into the tissues.
Viruses also don't really attach to host cells, it's a very temporary arrangement whilst they either merge with the membrane or are endocytosed.
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sorry didn't make it clear
by interstitial fluid i just meant extracellular fluid circulating through lymphatic system at points
*also, by attach to host cell i mean protein coat left on surface which acts an antigen i believe
so B cells can attach to free viruses?
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B cells just have an Ig molecule on their cell surface. If they're exposed to an antigen they will bind it, regardless of where it is etc.
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i don't entirely agree with this answer, I went with c.
Question 16
Thyroxine is a hormone which is released from the thyroid gland into the bloodstream. It is
transported through the circulatory system until reaching target cell receptors around the body.
Thyroxine is synthesised from the amino acid tyrosine and
A. can move through the plasma membrane of the cell because it is small and
hydrophobic.
B. can move through the plasma membrane of the cell because it is small and hydrophilic.
C. binds with a receptor protein on the plasma membrane.
D. binds with a target protein on the plasma membrane.
Answer is A
• A is correct – for an amine-based molecule, thyroxine is small and also hydrophobic so
can therefore move through the plasma membrane.
I thought all protein or amino acid hormones required receptors...and dont amino acids need protein channels to enter the cell anyways?
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Maybe i should just put 'thanks Russ and all answers in bio q megathread '
1 more question
i am confused as to the terms adenovirus, retrovirus etc.
i know adenovirus have dna
retrovirus have rna
but i don't think all rna / dna are retro/adeno
so what is the difference and how do you tell?
EDIT: Do all bacteriophages have DNA or do some have RNA
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i don't entirely agree with this answer, I went with c.
It does require you to know something about Thyroxine, so I guess it's not the best question. A quick glance at the thyroxine structure should indicate that it's pretty non polar (two aromatic rings...). As such A is correct but the only way to know it is by knowing the structure. As well as that, in the question they state that it binds target cell receptors which is probably also true so...bad question.
Maybe i should just put 'thanks Russ and all answers in bio q megathread '
I'm majoring in microbiology and immunology, this section of the course is fun revision for me :P
but i don't think all rna / dna are retro/adeno
so what is the difference and how do you tell?
There are a ton of taxonomic families (retroviridae etc.) and the only way to know whether or not it's DNA/RNA is to be told by your teacher. You don't need to know why or how they're categorized for VCE. Retroviruses, however, are also defined by the ability to convert RNA to DNA and integrate it back into the host genome (i've said this before in this thread, it breaks the crick central dogma)
Do all bacteriophages have DNA or do some have RNA
Either.
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i don't entirely agree with this answer, I went with c.
It does require you to know something about Thyroxine, so I guess it's not the best question. A quick glance at the thyroxine structure should indicate that it's pretty non polar (two aromatic rings...). As such A is correct but the only way to know it is by knowing the structure. As well as that, in the question they state that it binds target cell receptors which is probably also true so...bad question.
Maybe i should just put 'thanks Russ and all answers in bio q megathread '
I'm majoring in microbiology and immunology, this section of the course is fun revision for me :P
but i don't think all rna / dna are retro/adeno
so what is the difference and how do you tell?
There are a ton of taxonomic families (retroviridae etc.) and the only way to know whether or not it's DNA/RNA is to be told by your teacher. You don't need to know why or how they're categorized for VCE. Retroviruses, however, are also defined by the ability to convert RNA to DNA and integrate it back into the host genome (i've said this before in this thread, it breaks the crick central dogma)
Do all bacteriophages have DNA or do some have RNA
Either.
Thanks again :)
i thought all amino acids had to go through protein channels / cell membrane / hydrophilic?? due to carboxyl??
quick search on line indicates all thyroid hormones are lipophilic ?
what are hydrophilic amino acid derivitative hormones/?
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i don't entirely agree with this answer, I went with c.
It does require you to know something about Thyroxine, so I guess it's not the best question. A quick glance at the thyroxine structure should indicate that it's pretty non polar (two aromatic rings...). As such A is correct but the only way to know it is by knowing the structure. As well as that, in the question they state that it binds target cell receptors which is probably also true so...bad question.
Maybe i should just put 'thanks Russ and all answers in bio q megathread '
I'm majoring in microbiology and immunology, this section of the course is fun revision for me :P
but i don't think all rna / dna are retro/adeno
so what is the difference and how do you tell?
There are a ton of taxonomic families (retroviridae etc.) and the only way to know whether or not it's DNA/RNA is to be told by your teacher. You don't need to know why or how they're categorized for VCE. Retroviruses, however, are also defined by the ability to convert RNA to DNA and integrate it back into the host genome (i've said this before in this thread, it breaks the crick central dogma)
Do all bacteriophages have DNA or do some have RNA
Either.
Thanks again :)
i thought all amino acids had to go through protein channels / cell membrane / hydrophilic?? due to carboxyl??
quick search on line indicates all thyroid hormones are lipophilic ?
what are hydrophilic amino acid derivitative hormones/?
Thanks russ
Ohmygosh i never knew why amino acids had to go through protein channels before you told they had a carboxyl group !! thanks bazza16 :)
Hydrophilic Amino acid derivative hormones are derived from amino acids. They leave cells via diffusion exocytosis and have a short life span and they tral in the blood stream. Hydrophilic refers to its inability to cross the cell membrane as it is water soluble, however there are some exceptions, such as thyroxine.
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Also, am i right in saying that a retrovirus has RNA as its genetic material which produces viral DNA from viral RNA. This DNA is then integrated into the host's chromasomes which causes a change in gene transcription?
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What type of phagocytic cells can eat cells infected by viruses?
-
What type of phagocytic cells can eat cells infected by viruses?
None I'm pretty sure..? Or at least the main mechanism is Cytotoxic T cell destruction.
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m... my teacher and a few videos said some macrophages ingest whole virus infected cells, but i couldn't find any examples of this,
i think your right, can anyone confirm?
thanks lexitu
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With experimental design involving a group of humans, would you want a mix of age, ethnicity, weight etc or all those factors kept the same? Otherwise the result might just be the effect of the age group etc?
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You don't really need to be that specific - it would depend entirely on the type of experiment. Oftentimes the group is kept very similar - e.g. healthy caucasian males between 25-30. The main thing is to acknowledge that you are controlling these factors.
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I don't agree with this answer either. if ribosomes are membrane bound, why are they found in bacteria?
Unless they mean attached to endoplasmic reticulum...
Cells are involved in the production of many different biomacromolecules, many of which must be packaged and transported out of the cell. Polypeptides that require such transport are synthesised by
A. the smooth endoplasmic reticulum.
B. the Golgi apparatus.
C. free ribosomes found in the cytosol.
D. membrane-bound ribosomes.
D is the answer
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I don't agree with this answer either. if ribosomes are membrane bound, why are they found in bacteria?
Unless they mean attached to endoplasmic reticulum...
Cells are involved in the production of many different biomacromolecules, many of which must be packaged and transported out of the cell. Polypeptides that require such transport are synthesised by
A. the smooth endoplasmic reticulum.
B. the Golgi apparatus.
C. free ribosomes found in the cytosol.
D. membrane-bound ribosomes.
D is the answer
The ribosomes on the rough endoplasmic reticulum are membrane-bound, but there are ones that are found in the cytosol as well, hence why they're in prokaryotic cells.
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I don't agree with this answer either. if ribosomes are membrane bound, why are they found in bacteria?
Unless they mean attached to endoplasmic reticulum...
Cells are involved in the production of many different biomacromolecules, many of which must be packaged and transported out of the cell. Polypeptides that require such transport are synthesised by
A. the smooth endoplasmic reticulum.
B. the Golgi apparatus.
C. free ribosomes found in the cytosol.
D. membrane-bound ribosomes.
D is the answer
The ribosomes on the rough endoplasmic reticulum are membrane-bound, but there are ones that are found in the cytosol as well, hence why they're in prokaryotic cells.
so you're saying that the ribosomes found in the cytosol are not membrane bound?
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can anyone confirm whether macrophages can / cannot ingest whole virus infected cells? or is it just Tc / NK that kill viruses ?
Also
My textbook says that Th cells are 100% neccessary to stimulate ploliferation of B cells, but it also says T cells can only detect antigens on antigen presenting cells,
Does this mean that lone antigens / pathogens cannot cause B cells to ploliferate ?
EDIT:
Immunity is confusing me!
another 2 questions
1) exactly how are viruses destroyed and completely eradicated from body, is it by forming antibody virus complexes or by NK / Tc cells stopping them from reproducing or both
2) B cell has a similar (exactly the same) T cell, does this mean if an antigen binds with a B cell, they have to present this to the one correct Th cell and then the Th cell instructs the B cell to proliferate?
-
I don't agree with this answer either. if ribosomes are membrane bound, why are they found in bacteria?
Unless they mean attached to endoplasmic reticulum...
Cells are involved in the production of many different biomacromolecules, many of which must be packaged and transported out of the cell. Polypeptides that require such transport are synthesised by
A. the smooth endoplasmic reticulum.
B. the Golgi apparatus.
C. free ribosomes found in the cytosol.
D. membrane-bound ribosomes.
D is the answer
The ribosomes on the rough endoplasmic reticulum are membrane-bound, but there are ones that are found in the cytosol as well, hence why they're in prokaryotic cells.
so you're saying that the ribosomes found in the cytosol are not membrane bound?
Yeah, they're not membrane bound. Even the ones found at rough endoplasmic reticula aren't exactly membrane-bound: http://en.wikipedia.org/wiki/Ribosome#Membrane-bound_ribosomes.
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If I remember last year correctly (that's a huge assumption) cytosolic ribosomes are translocated to the ER when they are needed to translate a mRNA
can anyone confirm whether macrophages can / cannot ingest whole virus infected cells? or is it just Tc / NK that kill viruses ?
Macrophages would have a role in clearance of viruses but I am loathe to say they phagocytose the entire cell. They definitely phagocytose it after breakdown/apoptosis.
My textbook says that Th cells are 100% neccessary to stimulate ploliferation of B cells, but it also says T cells can only detect antigens on antigen presenting cells,
Does this mean that lone antigens / pathogens cannot cause B cells to ploliferate ?
1. B cells are antigen presenting cells
2. Yes, if a B cell encounters an antigen and does not receive T Cell help it won't proliferate.
1) exactly how are viruses destroyed and completely eradicated from body, is it by forming antibody virus complexes or by NK / Tc cells stopping them from reproducing or both
Assuming the virus can be eradicated it's both. There are other pathways that are important as well though.
2) B cell has a similar (exactly the same) T cell, does this mean if an antigen binds with a B cell, they have to present this to the one correct Th cell and then the Th cell instructs the B cell to proliferate?
B cells do not have "exactly the same" T cells, they're very different cells. If a B cell is presenting peptide via MHCII then it needs to find any Th (there will be more than one in the body) cell that has a TCR capable of binding the MHC+peptide complex. At this point, the T cell will trigger proliferation and differentiation.
Immunity is confusing me!
Join the club lol
-
haha thanks russ,
so B cells if they bind with an antigen, have to find a T cell specific for the antigen before proliferation (what does TCR stand for - something something receptor :D )
EDIT:
Are T cells as highly specific as B cells ?
2)
If a phagocyte presents an antigen to a T cell, how does the T cell transmit the message to a B cell (does the T cell attach to phagocyte and try to find B cell?)
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TCR = T-cell Receptors :D
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Are T cells as highly specific as B cells ?
They are also antigen specific, yes.
2)
If a phagocyte presents an antigen to a T cell, how does the T cell transmit the message to a B cell (does the T cell attach to phagocyte and try to find B cell?)
If a macrophage/DC is presenting a peptide via MHCII, it will migrate to the lymph nodes. It will then bind a Th cell specific for that peptide and activate it. The activated T cell is now capable of activating B cells in the same lymph node.
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why would you remove lymph nodes from the armpit areas if you have breast cancer?
-
If the breast cancer is metastatic (i.e. has invaded into the lymphatic system and can travel through it), then you'd need to take out the primary tumour as well as the nodes to prevent existing cancer cells inside the nodes from travelling from the nodes to elsewhere and starting up the cancer again.
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If the breast cancer is metastatic (i.e. has invaded into the lymphatic system and can travel through it), then you'd need to take out the primary tumour as well as the nodes to prevent existing cancer cells inside the nodes from travelling from the nodes to elsewhere and starting up the cancer again.
Why would this lead to a build up of tissue fluid containing leucocytes in the arm?
Also, am i right in saying that a retrovirus has RNA as its genetic material which produces viral DNA from viral RNA. This DNA is then integrated into the host's chromasomes which causes a change in gene transcription?
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What would i ever do without you Russ !
+ thanks Hercules
is the reason tyrosine is non - polar because the large variable group outways the slight polar COOH group?
Edit: I fail with acronyms, is DC dendritic cell?
Edit 2: If a B cell comes into contact with a different APC, does the B cell 'steal ' an antigen and take it to a T cell?
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If the breast cancer is metastatic (i.e. has invaded into the lymphatic system and can travel through it), then you'd need to take out the primary tumour as well as the nodes to prevent existing cancer cells inside the nodes from travelling from the nodes to elsewhere and starting up the cancer again.
Why would this lead to a build up of tissue fluid containing leucocytes in the arm?
Also, am i right in saying that a retrovirus has RNA as its genetic material which produces viral DNA from viral RNA. This DNA is then integrated into the host's chromasomes which causes a change in gene transcription?
If you remove most of the lymph nodes from that arm, the lymphatics in that arm all have to drain through just the few remaining ones, leading to fluid congestion and accumulation. Imagine closing off all the lanes except one on a freeway - same principle here really.
And regarding retroviruses, yep, pretty much. Only other important fact to know is that this is done via reverse transcriptase, and as Russ has said many times, is basically the only exception to the Crick Central Dogma.
What would i ever do without you Russ !
+ thanks Hercules
is the reason tyrosine is non - polar because the large variable group outways the slight polar COOH group?
Edit: I fail with acronyms, is DC dendritic cell?
Edit 2: If a B cell comes into contact with a different APC, does the B cell 'steal ' an antigen and take it to a T cell?
Re: edit 1, yes
Re: edit 2, why would it need to steal it? The APC can just present it to a T cell itself.
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Thanks Shinny
is the reason tyrosine is non - polar because the large variable group outways the slight polar COOH group?
Re: Re 2: if an B cell takes an antigen, then there is an increased likelyhood of one of them finding a T cell- does this occur?
Another question:
Do viruses ever go into phagocytes? How would this occur if it does? would they ingest single floating viruses?
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is the reason tyrosine is non - polar because the large variable group outways the slight polar COOH group?
Is chemistry, but yes.
Re: Re 2: if an B cell takes an antigen, then there is an increased likelyhood of one of them finding a T cell- does this occur?
The B cell won't "steal" an antigen from an APC, no, because of the fact that APCs present degraded, linear peptides whilst the BCR doesn't bind those peptides. The BCR is just an antibody expressed on the cell membrane, so it binds a specific conformation rather than an AA sequence.
I doubt you have to know that for VCE.
Another question:
Do viruses ever go into phagocytes? How would this occur if it does? would they ingest single floating viruses?
Viruses can infect phagocytes but phagocytes don't deliberately phagocytose them
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If I remember last year correctly (that's a huge assumption) cytosolic ribosomes are translocated to the ER when they are needed to translate a mRNA
can anyone confirm whether macrophages can / cannot ingest whole virus infected cells? or is it just Tc / NK that kill viruses ?
Macrophages would have a role in clearance of viruses but I am loathe to say they phagocytose the entire cell. They definitely phagocytose it after breakdown/apoptosis.
My textbook says that Th cells are 100% neccessary to stimulate ploliferation of B cells, but it also says T cells can only detect antigens on antigen presenting cells,
Does this mean that lone antigens / pathogens cannot cause B cells to ploliferate ?
1. B cells are antigen presenting cells
2. Yes, if a B cell encounters an antigen and does not receive T Cell help it won't proliferate.
1) exactly how are viruses destroyed and completely eradicated from body, is it by forming antibody virus complexes or by NK / Tc cells stopping them from reproducing or both
Assuming the virus can be eradicated it's both. There are other pathways that are important as well though.
2) B cell has a similar (exactly the same) T cell, does this mean if an antigen binds with a B cell, they have to present this to the one correct Th cell and then the Th cell instructs the B cell to proliferate?
B cells do not have "exactly the same" T cells, they're very different cells. If a B cell is presenting peptide via MHCII then it needs to find any Th (there will be more than one in the body) cell that has a TCR capable of binding the MHC+peptide complex. At this point, the T cell will trigger proliferation and differentiation.
Immunity is confusing me!
Join the club lol
yea i would say the immune mechanisms for clearing virus infection would be NK cells, type 1 and 2 interferons, complement, CTL's and antibody protection and macrophages would play a role like Russ said either clearing dead cells or engulfing some virion particles.
you prob dont need to know this cause most antigens (the protein ones) need Th help but.... B cells ARE able to proliferate without Th cytokine help but it depends on the type of antigen that it recognises and the amount. they are called thymus independent antigens (TI-antigens). for example LPS on gram negative bacteria, bacterial capsule polysaccharides and flagellin can induce B cell division... because the structure is repetitive it can crosslink many b cell receptors thus providing a strong enough signal to induce their proliferation.
russ answered it and i think i also answered one of your questions here http://vce.atarnotes.com/forum/index.php/topic,25843.0.html 4th post...
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i get real confused in graphs is their a particular way to understand them
-
If I remember last year correctly (that's a huge assumption) cytosolic ribosomes are translocated to the ER when they are needed to translate a mRNA
can anyone confirm whether macrophages can / cannot ingest whole virus infected cells? or is it just Tc / NK that kill viruses ?
Macrophages would have a role in clearance of viruses but I am loathe to say they phagocytose the entire cell. They definitely phagocytose it after breakdown/apoptosis.
My textbook says that Th cells are 100% neccessary to stimulate ploliferation of B cells, but it also says T cells can only detect antigens on antigen presenting cells,
Does this mean that lone antigens / pathogens cannot cause B cells to ploliferate ?
1. B cells are antigen presenting cells
2. Yes, if a B cell encounters an antigen and does not receive T Cell help it won't proliferate.
1) exactly how are viruses destroyed and completely eradicated from body, is it by forming antibody virus complexes or by NK / Tc cells stopping them from reproducing or both
Assuming the virus can be eradicated it's both. There are other pathways that are important as well though.
2) B cell has a similar (exactly the same) T cell, does this mean if an antigen binds with a B cell, they have to present this to the one correct Th cell and then the Th cell instructs the B cell to proliferate?
B cells do not have "exactly the same" T cells, they're very different cells. If a B cell is presenting peptide via MHCII then it needs to find any Th (there will be more than one in the body) cell that has a TCR capable of binding the MHC+peptide complex. At this point, the T cell will trigger proliferation and differentiation.
Immunity is confusing me!
Join the club lol
yea i would say the immune mechanisms for clearing virus infection would be NK cells, type 1 and 2 interferons, complement, CTL's and antibody protection and macrophages would play a role like Russ said either clearing dead cells or engulfing some virion particles.
you prob dont need to know this cause most antigens (the protein ones) need Th help but.... B cells ARE able to proliferate without Th cytokine help but it depends on the type of antigen that it recognises and the amount. they are called thymus independent antigens (TI-antigens). for example LPS on gram negative bacteria, bacterial capsule polysaccharides and flagellin can induce B cell division... because the structure is repetitive it can crosslink many b cell receptors thus providing a strong enough signal to induce their proliferation.
russ answered it and i think i also answered one of your questions here http://vce.atarnotes.com/forum/index.php/topic,25843.0.html 4th post...
haha just read through that its so long -=,-= thanks tl and russ
- just to clear some things up
do T cells proliferate as soon as they come into contact with an APC or do they find a B cell first
also can Th cells proliferate into Tc cells? if a Th cell detects an antigen on an APC, do they need to come into contact with Tc cells as well?
EDIT: IN VCAA 2010 in question 6 SA part c)
http://www.vcaa.vic.edu.au/vcaa/vce/studies/biology/pastexams/2010/2010biol1-w.pdf
Is the diagram inaccurate? Compound R almost appears to be an enzyme catalysising the reaction of Q into S, but the answers suggest Compound R can be turned INTO S as in an alternative metabolc pathway, is the diagram incorrect, or is this always how metabolic pathways are drawn?
Can someone please expain or linnk to a site expalining metabolic pathway diagrams / alternative metabolic pathway diagrams, i looked through my texts and notes, as well as online but i couldn't find anything :'(
Thanks
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"professional" antigen presenting cells - dendritic cell, macrophages, B cell
so b cells are APCs...but if the appropriate peptide is displayed on MHC and the T cell recognises it and it has appropriate co-stimulation then yes they will proliferate....DC's are the best at activating naive T cells
CD4+ T cells do not differentiate into CD8+ T cells! they are seperate types of cells
no they don't need to come into contact with Tc
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Can anyone provide some sort of a "formula" that can be applied to design an experiment questions?
-
Hey guys,
I need some help on this question. Any help would be much appreciated.
If asked to write down the balanced equation of photosynthesis would it be
correct to write:
light
1. 6CO2 + 6H20 -------------> C6H12O6 + 602
chlorophyll
or
light
2. 6CO2 + 12H20 -------------> C6H12O6 + 602 + 6H20 ?
chlorophyll
Oh and also why does the nature of biology textbook say that photosynthesis is most efficient in
light of blue and red wavelengths when it also says that in T.W Engelmann's experiment that violet was
where most oxygen was released (i.e. the highest rate of photosynthesis) ?
Thanks heaps in advance.
-
second one :)
a picky examiner will more likely take points off the 1st one (i think)
-
Haha yeah thats what I thought aswell, thanks for that Hercules :D
Do you happen to know the answer to my second question?
Thanks in advance.
-
do T cells proliferate as soon as they come into contact with an APC or do they find a B cell first (is this costimulation?)
how do cytotoxic T cells proliferate if they don't come into contact with antigen?
EDIT: IN VCAA 2010 in question 6 SA part c)
http://www.vcaa.vic.edu.au/vcaa/vce/studies/biology/pastexams/2010/2010biol1-w.pdf
Is the diagram inaccurate? Compound R almost appears to be an enzyme catalysising the reaction of Q into S, but the answers suggest Compound R can be turned INTO S as in an alternative metabolc pathway, is the diagram incorrect, or is this always how metabolic pathways are drawn?
Can someone please expain or linnk to a site expalining metabolic pathway diagrams / alternative metabolic pathway diagrams, i looked through my texts and notes, as well as online but i couldn't find anything
Thanks
-
Haha yeah thats what I thought aswell, thanks for that Hercules :D
Do you happen to know the answer to my second question?
Thanks in advance.
Because violet is essentially a sub-section of blue, and is the specific wavelength which is best absorbed. The first statement is just a bit of an oversimplification by breaking colour down into red, green and blue, and its saying that largely, red and blue are most absorbed, leaving green behind which gives plants their green colour.
-
VCAA 2010 says red is better absorbed than blue
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do T cells proliferate as soon as they come into contact with an APC or do they find a B cell first (is this costimulation?)
They don't proliferate "as soon as" they meet their Ag but they don't need to find a B cell first. Costimulation is just signals provided by an APC to trigger proliferation.
how do cytotoxic T cells proliferate if they don't come into contact with antigen?
What makes you think they don't...? How else would they be activated?
Is the diagram inaccurate? Compound R almost appears to be an enzyme catalysising the reaction of Q into S, but the answers suggest Compound R can be turned INTO S as in an alternative metabolc pathway, is the diagram incorrect, or is this always how metabolic pathways are drawn?
Diagram is accurate. Compound R is not an enzyme, it's a compound. It can be converted to S, just like Q can (but presumably a different mechanism).
Enzymes are written next to arrows, they don't get their own box.
-
VCAA 2010 says red is better absorbed than blue
I think it is for chlorophyll a. Chlorophyll b however has blue being absorbed better. Doesn't matter too much, they tend to give you the absorption spectra you need anyway.
-
Thanks heaps Shinny.
Oh and do we have to know those specific details about which chlorophyll absorbs which
wavelength of light better?
-
Thanks heaps Shinny.
Oh and do we have to know those specific details about which chlorophyll absorbs which
wavelength of light better?
Not specifically (as in the exact wavelength) but just know that it absorbs blue and red light best (and sub-sections like violet etc), and reflects green.
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Freshwater plants were put in test tubes. Would the CO2 levels in the test tubes be high or low in the absence of light (night time)??
-
Photosynthetic rate should be lower hence less CO2 consumption hence high CO2 concentration unless I'm missing something (which I almost definitely am).
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Photosynthetic rate should be lower hence less CO2 consumption hence high CO2 concentration unless I'm missing something (which I almost definitely am).
Yeah that's right according to the answers.
I just thought that since CO2 is required for the light-independent (usually dark) stage, levels would be lower...
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Yep, you're right in saying that about CO2 playing a role in the light-independent stage but the "dark stage" is a bit misleading - it doesn't have to occur at night, it's just that those reactions are not reliant on light as an energy input. So both light dependent and independent reactions would be occurring at much higher rates during daylights and therefore more carbon dioxide would be consumed.
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Yep, you're right in saying that about CO2 playing a role in the light-independent stage but the "dark stage" is a bit misleading - it doesn't have to occur at night, it's just that those reactions are not reliant on light as an energy input. So both light dependent and independent reactions would be occurring at much higher rates during daylights and therefore more carbon dioxide would be consumed.
Ah okay, thanks :D
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do T cells proliferate as soon as they come into contact with an APC or do they find a B cell first (is this costimulation?)
They don't proliferate "as soon as" they meet their Ag but they don't need to find a B cell first. Costimulation is just signals provided by an APC to trigger proliferation.
how do cytotoxic T cells proliferate if they don't come into contact with antigen?
What makes you think they don't...? How else would they be activated?
Is the diagram inaccurate? Compound R almost appears to be an enzyme catalysising the reaction of Q into S, but the answers suggest Compound R can be turned INTO S as in an alternative metabolc pathway, is the diagram incorrect, or is this always how metabolic pathways are drawn?
Diagram is accurate. Compound R is not an enzyme, it's a compound. It can be converted to S, just like Q can (but presumably a different mechanism).
Enzymes are written next to arrows, they don't get their own box.
ahk, thanks a lot russ
so to activate t h, tc and b cells - an antigen has to come into contact with all 3 to stimulateall 3?
+ sorry if this question has been answered already ( i couldn't find it last few pages) but can Th cells activate B / T cells without being attached to antigen? (like find antigen, proliferate, then seperate from pathogen and find B cell?)
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so to activate t h, tc and b cells - an antigen has to come into contact with all 3 to stimulateall 3?
B cells must come into contact with the antigen.
T cells must come into contact with a degraded peptide of the antigen
(there is a really poorly used naming convention)
A B cell must encounter the correct confirmation and then receive T cell help to activate
A T cell (whether Tc or Th) must encounter the presented peptide on an APC to activate (it receives help from the APC, Tc cells also get Th help)
+ sorry if this question has been answered already ( i couldn't find it last few pages) but can Th cells activate B / T cells without being attached to antigen? (like find antigen, proliferate, then seperate from pathogen and find B cell?)
As above, Th cells activate by presentation of peptides by an APC - they don't see the pathogen directly. Once activated they do not need to remain attached to the APC.
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Thanks so much Russ for answering my constant (6 pages or so) of immunity questions :)
I don't know what i would have done without you :D
This line of immunity questions will (possibly) cease for a short period of time (if your lucky until the weekend :P)
EDIT: :D - Do T cells differentiate (into Tc, Th etc. ) in the thymus or in the lymph?
(same with B cells, do they become memory in bone or lymmph?)
-
2 Questions:
What is the difference between an action potential and a nerve impulse?
Heinemann says they are the same; The Penguin Dictionary of Biology (1980 edition, lol) says they are different, yet I'm finding it hard to wrap my head around the way it is described there; and practice exam companies seem to be as confused as me.
Do facilitated diffusion and active transport occur solely through 'protein channels', and if not, do they occur also through 'protein pumps' and 'carrier proteins'?
Heinemann defines the two processes as occuring through 'protein channels' and makes no mention of the other two membrane proteins.
Thanks in advance!
-
2 Questions:
What is the difference between an action potential and a nerve impulse?
As far as I'm aware, the nerve impulse is the movement of the action potential along the axon.
Heinemann says they are the same; The Penguin Dictionary of Biology (1980 edition, lol) says they are different, yet I'm finding it hard to wrap my head around the way it is described there; and practice exam companies seem to be as confused as me.
Do facilitated diffusion and active transport occur solely through 'protein channels', and if not, do they occur also through 'protein pumps' and 'carrier proteins'?
Heinemann defines the two processes as occuring through 'protein channels' and makes no mention of the other two membrane proteins.
Protein pumps is a deceptive term which to me seems to imply that they require energy, which would rule them out of facilitated diffusion. I wouldn't use this term on an exam.
Facilitated diffusion can, however, occur through protein channels and carrier proteins, the fundamental difference being that carrier proteins change shape when the ion/substrate enters them.
see: http://bcs.whfreeman.com/thelifewire8e/pages/bcs-main.asp?v=&s=05000&n=00010&i=05010.01&o=|00510|00520|00530|00540|00550|00560|00570|00010|00020|00030|00040|00050|00060|00070|00080|00090|00100|00110|00120|00130|00140|00150|00160|00170|01000|02000|03000|04000|05000|06000|07000|08000|09000|10000|11000|12000|13000|14000|15000|16000|17000|18000|19000|20000|21000|22000|23000|24000|25000|26000|27000|28000|29000|30000|31000|32000|33000|34000|35000|36000|37000|38000|39000|40000|41000|42000|43000|44000|45000|46000|47000|48000|49000|50000|51000|52000|53000|54000|55000|56000|57000|99000| and
http://bcs.whfreeman.com/thelifewire8e/pages/bcs-main.asp?v=&s=05000&n=00010&i=05010.01&o=|00510|00520|00530|00540|00550|00560|00570|00010|00020|00030|00040|00050|00060|00070|00080|00090|00100|00110|00120|00130|00140|00150|00160|00170|01000|02000|03000|04000|05000|06000|07000|08000|09000|10000|11000|12000|13000|14000|15000|16000|17000|18000|19000|20000|21000|22000|23000|24000|25000|26000|27000|28000|29000|30000|31000|32000|33000|34000|35000|36000|37000|38000|39000|40000|41000|42000|43000|44000|45000|46000|47000|48000|49000|50000|51000|52000|53000|54000|55000|56000|57000|99000| for diagrams
Thanks in advance!
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Thanks so much Russ for answering my constant (6 pages or so) of immunity questions :)
I don't know what i would have done without you :D
This line of immunity questions will (possibly) cease for a short period of time (if your lucky until the weekend :P)
EDIT: :D - Do T cells differentiate (into Tc, Th etc. ) in the thymus or in the lymph?
(same with B cells, do they become memory in bone or lymmph?)
My impression is that T and B cells both differentiate upon activation, usually following contact with an antigen. This is most likely to occur in the lymph nodes.
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1) would 1 non - specific T cell coming into contact with antigen be able to give rise to a Tc and Th cell?
2) do we need to redifine (e.g. Red Blood cell (RBC)) for every part of question (e.g. 1 a , 2a?)
3) Does cellular respiration refer to any respiration in a cell, or the overall aerobic respiration chain, also can cellular respiration refer to anaerobic respiration?
4)Do yeast prefer to use oxygen / aerobic respiration
can they use ethanol to produce energy?
5) is it more accurate to call polymer of aminno acids poolypeptide or protein (VCAA says protein i think)
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T cells do NOT differentiate to Tc/Th cells on contact with an antigen. That's already predetermined. When Th cells contact an antigen they will differentiate to form a specific subset of Th cell, each with a specific cytokine/receptor/protein/transcription factor etc. profile. So you have Th1, Th2, Th17 etc. cells, each fulfilling a different role.
In my exams I wouldn't need to define RBC at all, it's a recognised abbreviation. In VCE I'd say write "Red Blood Cell (RBC)" in the first part then use RBC from then on. Or just use erythrocyte if you want to sound fancy.
Depends what the person using it means, it just refers to the production of ATP. Most of the time it's used to mean aerobic though.
Yeast can use oxygen, ethanol is a byproduct and i'm reasonably sure it would be toxic to some extent
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which book explains immunity the best? especially 3rd line of defence
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I've only glanced through Nelson and Heinemann, but NOB does a pretty good job of it
Thanks Russ,
one of the teachers today said (dodgy q on STAV) that ethanol can be metablolised further to release more energy i guess this must be wrong? (there was no indication that oxygen was 'introduced' at a certain point in time - if oxygen is present, do yeast prefer to repire aerobically
EDIT: Are Th cells need to stimulate Tc? (i'm still a bit confused :) )
EDIT 2: Is the output of the calvin cycle PGAL or Glucose more accurately?
VCAA seems to say glucose
also NOB says the first step to convert 5 C -> 2 3C with the addition of Co2 AND h20 but i cant find water as an input on any diagrams?
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isnt the H20 split in light dependent reactions already. the Hydrogen ions from water are carried to the calvin cycle in the form of ATP and NADPH. and the Os were released as oxygen gas in light dependent reaction.
i think PGAL is more accurately but on exam i would only say that along with the fact that it would be converted into glucose later on or other sugars.
Bazza16, do u have a copy of the STAV papers (i only have the 04 and 06 ones)
EDIT: dw, i found some more on VN :D
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yeah does anyone have ths stav paper for 2011
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For the 2007 VCAA exam for Question 5a), it asks for you to name one well-recognised allergen. In the examiner's report, it states that fur and dust are incorrect answers. So why can't fur and dust be allergens? ???
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EDIT: dw, i found some more on VN :D
:)
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Are Th cells need to stimulate Tc? (i'm still a bit confused)
Is the output of the calvin cycle PGAL or Glucose more accurately?
VCAA seems to say glucose
If bacteria cells such as C. Jejuni invade stomach cells, how does the immune system cope with this? Do the invaded cells display C. Jejuni antigens?
(please respond ASAP , for a SAC i'm currently writing up :) )
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Yes Th activate Tc
lolplants
Intracellular bacterial infection is targeted by CMI; MHC1 display of degraded peptides and subsequent CTL targeting (+ others)
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thanks russ
- lol can anyone else help with plants question :P
Do NK cells act against bacteria ?
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dumb question but can donated blood "attack" or agglutinate the recipient's blood? e.g. blood type O is given to a person with blood type A. Since blood type O has antibodies against A and B antigens, could it agglutinate the red blood cells in blood type A with the A antigen?
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if there was a previous exposure recently, possibly, if not no as no antibodies present in blood, but basically no under normal circumstances (if blood was given in suffiecient quantites to invoke immune response, this would cause damage to person)
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oh yeah that sounds right. Just clarifying, so the donated blood type O will have no antibodies as it has not been exposed to the Blood type A that has red blood cells with the A antigen. But if a lot of type O blood was given, a lot of antibodies against the blood type A would be produced, thus causing damage.
right? :P
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okay, just forget what i said, its just confusing.
The short and correct answers is no reaction will occur as there are no specific antibodies present in blood
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dumb question but can donated blood "attack" or agglutinate the recipient's blood? e.g. blood type O is given to a person with blood type A. Since blood type O has antibodies against A and B antigens, could it agglutinate the red blood cells in blood type A with the A antigen?
if there was a previous exposure recently, possibly, if not no as no antibodies present in blood, but basically no under normal circumstances (if blood was given in suffiecient quantites to invoke immune response, this would cause damage to person)
Giving a mismatched ABO donation will cause a very serious reaction. It doesn't have to be a "lot" but that depends on what you consider to be a large donation. Getting a blood transfusion of AB blood if you're type O will probably kill you. You do not need to have been exposed to the antigen recently because your serum has constantly circulating antibodies to the sugars (A or B) that you don't have. No need to go into why because it's irrelevant to VCE.
oh yeah that sounds right. Just clarifying, so the donated blood type O will have no antibodies as it has not been exposed to the Blood type A that has red blood cells with the A antigen. But if a lot of type O blood was given, a lot of antibodies against the blood type A would be produced, thus causing damage.
No, I think you've confused yourself here :P How is transfusing blood without any antigens to a patient going to harm them?
The way it works is basically like this:
Type A = have A antigen (self) and B antibodies
Type B = have B antigen (self) and A antibodies
Type AB = have AB antigens (self) and no antibodies
Type O = have no antigens and AB antibodies
Thus you can put no antigens into anyone. But you can't put AB antigens into someone with A or B or AB antibodies.
Hence Type O is universal donor (can be given to any blood type) and Type AB is universal recipient (can receive any blood type).
ABO system is horribly annoying to get sorted in your head :P
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shiz i have got this all wrong !
ok, i'll try an rephrase it. why is blood type O known as the universal donor? Doesn't it have anibodies against A and B blood types? So if blood type O was donated to a person with blood type A, wouldn't the antibodies (A and B) from blood type O agglutinate the blood type A red blood cells as they have the A antigen?
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Blood type O contains NO A OR B Antigens. Therefore it can donate to anyone, as NO HUMAN can create antibodies against antigens which do not exist...
I'm not sure what Russ is talking about with respect to already present antigens, but for VCE i'm pretty sure you can just assume there are no antibodies present in the blood as antibodies are produced IN RESPONSE to an infection... and the donor has not been infected with group A or B or AB blood, or else he would probably be dead
hehe i meant like if you injected a tiny bit of blood into lymph node it may trigger a response without killing the person
oh wait what? blood group antigens already present in blood :O
Do NK cells act against bacteria ?
also if anyone knows (not russ ) whether the output of the calvin cycle PGAL or Glucose more accurately?
VCAA seems to say glucose
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one go around the calvin cycle gives PGAL - two rounds give glucose
at a VCE level, knowing that ultimately glucose comes out of the calvin cycle would be efficient and obviously vcaa agrees
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is all gooood. wiki is god.
from wikipedia:
By way of example: considering the transfusion of O Rh D negative blood (universal donor blood) into a recipient of blood group A Rh D positive, an immune reaction between the recipient's anti-B antibodies and the transfused RBCs is not anticipated. However, the relatively small amount of plasma in the transfused blood contains anti-A antibodies, which could react with the A antigens on the surface of the recipients RBCs, but a significant reaction is unlikely because of the dilution factors. Rh D sensitization is not anticipated.
haha my question must have made noo sense.
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ok, i'll try an rephrase it. why is blood type O known as the universal donor?
Has no antigens to stimulate an immune response, regardless of recipient
Doesn't it have anibodies against A and B blood types? So if blood type O was donated to a person with blood type A, wouldn't the antibodies (A and B) from blood type O agglutinate the blood type A red blood cells as they have the A antigen?
Yes, but these are part of the serum. Blood transfusions aim to remove the serum and give just the RBCs alongside other things (dextrose etc.). Depending on what it will be used for the companies often use different preparation techniques.
I'm not sure what Russ is talking about with respect to already present antigens, but for VCE i'm pretty sure you can just assume there are no antibodies present in the blood as antibodies are produced IN RESPONSE to an infection... and the donor has not been infected with group A or B or AB blood, or else he would probably be dead
Don't assume that; it's wrong. If you want the explanation, it's because your normal flora that you acquire from your mother during birth have antigens extremely similar to the ABO sugars. Your immune system can produce antibodies to all of them, but is stopped from targeting the ones on your cells by tolerance. Therefore, you have circulating Ab to the antigens prior to "infection" with foreign blood.
Do NK cells act against bacteria ?
They would have the potential to target intracellular bacteria but they're primarily concerned with anti-viral functions
haha my question must have made noo sense.
:P
Blood typing is incredibly confusing when you learn it, it still confuses me sometimes (and half my classmates)
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Doesn't it have anibodies against A and B blood types? So if blood type O was donated to a person with blood type A, wouldn't the antibodies (A and B) from blood type O agglutinate the blood type A red blood cells as they have the A antigen?
Yes, but these are part of the serum. Blood transfusions aim to remove the serum and give just the RBCs alongside other things (dextrose etc.). Depending on what it will be used for the companies often use different preparation techniques.
this helped heaps!!! even without understanding my no sense question. thanks :)
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Why do many people infected with HIV develop opportunistic infections? And why is it not possible to develop a live , attenuated vaccine for HIV?
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HIV kills Th cells, thus reducing immune function. That means that it's much easier for infections to take hold and things that wouldn't otherwise cause disease do.
HIV is incredibly error prone. A live vaccine would inevitable spontaneously revert to a virulent form (ie we'd be giving HIV to people)
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thanx and is the chemical communication between helpter t-cells and b-cells autocrine,paracrine or endocrine ?
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it'd be paracrine, because the helper t-cells and b-cells would be attached to an APC or free antigen, making them right next to each other
how does a virus, like influenza, give you diarrhea?
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it calls cells in the bladder to die, thus causing diarhea
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is this right: B cells find an antigen which binds to its receptors (or is it antibodies that it binds to?). It waits to get activated by a T helper cell (which has binded to the same antigen) and then undergoes clonal selection?
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it calls cells in the bladder to die, thus causing diarhea
Uh? Wrong end? :P
With influenza giving diarrhoea, it's not a typical presentation, but if it does occur as diarrhoea can in a wide range of illnesses, it's probably just a result of an in-built defense mechanism that causes expulsion of any foreign material in the body upon feeling sick. Basically, the body knows it sick but it doesn't know exactly where, so it just starts removing everything it can through any orifice it can.
EDIT: The above is really just a gross oversimplification and the mechanisms at hand are obviously more complex. The pathology's outlined in this article but I doubt any of that will make sense to you (barely makes sense to me). Basically though, infections which infect the entire body often lead to widespread release of cytokines which are chemicals secreted by the immune system to act on an infection. These cytokines have widespread effects throughout the body and one of these happens to be diarrhoea. But yeh, it's not well understood and there might be other mechanisms at hand.
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do T cells and B cells communicate through chemical means other than cytokines ?
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how many turns of the calvin cycle is needed to produce one glucose molecule. is it 6
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YEs six! 3 turns will produce 6 pgal...where 5 go back to form RuDP...and the 6th one waits....
then u have another 3 turns...5 go back and 6th one remains...
those two 6th ones join to form glucose :)
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Oh...and is the cell membrane an organelle?
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yes it is.
QUestion: Is a basophil a type of phagocyte? (it doenst engulf anything)
And is a mast cell a type of white blood cell?
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Oh...and is the cell membrane an organelle?
Actually I don't think it is. Organelles are specialised subunits within cells, whereas the cell membrane surrounds the entire cell and basically defines the cell to begin with.
QUestion: Is a basophil a type of phagocyte? (it doenst engulf anything)
And is a mast cell a type of white blood cell?
Basophils aren't really specialised phagocytes so I wouldn't consider them a phagocyte relaly. Mast cells aren't white blood cells because they're found in the tissues rather than the blood.
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RE: diarrhoea, the most common pathogenic reason for diarrhoea is affecting the Na/Cl export pumps and creating an osmotic gradient for water movement to the GIT
do T cells and B cells communicate through chemical means other than cytokines ?
Yes, they have several cell surface receptor/ligand pairs
Is a basophil a type of phagocyte? (it doenst engulf anything)
And is a mast cell a type of white blood cell?
Basophil = granulocyte
Mast cells are leucocytes (WBCs), yes, they're just tissue resident.
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is a granucolye a macrophage?
and is a dendritic cell also a macrophage
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Granulocyte is a class of cell that release granules. Macrophages are not. The most common granulocyte is a neutrophil.
DCs...depends. It's still up for debate. In VCE your answer will probably be "no".
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is a granulocyte a phagocyte
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They're classes of cell, you can't make comparisons like that.
Some granulocytes are phagocytes.
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handy diagram in my textbook that is pretty clear with classifying leukocytes:
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how do phagocytes recognise that a virus-infected cell is non-self?
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When a virus infects a cell, it leaves an antigen on the cell's surface that the T-cell can recognise as foreign.
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so do phagocytes engulf any virus infected cells at all? or does is jst engulf bacteria and viruses that haven not infected the cell? SO what happens to the virus infected cell? does it travel to the lymph node and attach itself to a T helper cell? Im confused :S
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Just checking do the antibodies bind to the antigens on cells when they agglutinate pathogens?
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I came across an MC q in insight 2007 and it said ribosomes, mitochondria and chloroplasts are directly responsible for the assembly of proteins - what do chloroplasts have anything to do with it?
I picked ribosomes, mitochondria and the nucleus ..
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In cell mediated immunity, should i say that t helper cells recognise antigens on MHC 2 markers and then stimulate cytotoxic t cell? or am i better off saying that cytotoxic t cells recognise antigens on MHC 1 markers? Can i say that t helper cells recognise antigens on MHC 1 markers and then stimulate cytotoxtic t cells?
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In cell mediated immunity, should i say that t helper cells recognise antigens on MHC 2 markers and then stimulate cytotoxic t cell? or am i better off saying that cytotoxic t cells recognise antigens on MHC 1 markers? Can i say that t helper cells recognise antigens on MHC 1 markers and then stimulate cytotoxtic t cells?
Th cells recognise antigens on MHC II markers, Tc cells are stimulated by them and then bind to MHC I markers to release their cytotoxins in cells.
Pretty sure Th recognise MHC II, not MHC I...
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Thanks!!!
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If a T helper cell is involved in activating B cells to produce antibodies, is it cell mediated immunity or the humoral response?
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If a T helper cell is involved in activating B cells to produce antibodies, is it cell mediated immunity or the humoral response?
T helper activating B cells = cell mediated
B cell producing antibodies = humoral
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omgosh thanks so much !!
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so do phagocytes engulf any virus infected cells at all? or does is jst engulf bacteria and viruses that haven not infected the cell? SO what happens to the virus infected cell? does it travel to the lymph node and attach itself to a T helper cell? Im confused :S
Phagocytes don't engulf the entire cell, it's too big.
The virus infected cell is recognised as such and destroyed by NK cells, granulocytes, Tc cells etc.
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Do B plasma cells secrete antibodies into lymph fluid or do they move to site of infection before they secrete?
Also
does 1 b lympocyte have the ability to secrete all classes ( or more than 1 ) class of antibodies ? ( e.g. IgA IgG)
thanks
Urgent response for SAC please :)
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im pretty sure the B cells release the anitbodies directly into the lymph fluid and each B cell and anitbody is specific... so im assuming that they react specifically to the antigen- so can only release one specific antibody
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do neutrophils only work on bacteria?
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are t helper cells part of the humoral response?
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Neutrophils don't work *only* on bacteria but that would be their main target.
Th cells aren't humoral but they aid the humoral response. They span humoral and CMI (IMO)
Do B plasma cells secrete antibodies into lymph fluid or do they move to site of infection before they secrete?
Into circulation, they don't head to the site of infection, they migrate to the bone marrow and reside there.
does 1 b lympocyte have the ability to secrete all classes ( or more than 1 ) class of antibodies ? ( e.g. IgA IgG)
thanks
All B cells initially secrete IgM and have the potential to switch to other types. Once they switch (IgM -> IgG) they can't switch back
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are t helper cells part of the humoral response?
i think they are because they are needed to activate the B cells by secreting interleukin 2 so that the B cell can proliferate in memory and plasma B cells
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whats the difference between the cytosol and the cytoplasm?
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Cytosol = fluid inside cells excluding nucleus
Cytoplasm = whole cell except nucleus
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how are primary hosts different to secondary hosts.
is it primary host = parasite reproduces sexually, secondary host = reproduces asexually or the other way around? the lifecycle diagrams confuse me
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Primary host simple means a host that is used to carry the adult stage of the parasite, which can obviously reproduce sexually
whereas the secondary host refers to the host that carries the larval stage of the parasite - so reproduces asexually.
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oh thanks :)
but how does this work with malaria. if the mosquito is the secondary host why does sexual reproduction occur within it (the zygote forms as a result)
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What makes you think the mosquito is the secondary host?
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isnt it?
it says in my book that it is
EDIT: google just confirmed that im wrong. ok, now i get it :D
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Mosquitoes aren't a host for plasmodium are they? Aren't they just the vector? Because plasmodium doesn't harm the mosquito?
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They are primary hosts and (I'm pretty sure) they are also vectors. "Host" status doesn't mean they have to be harmed, this can be seen in mutually beneficial relationships.
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They are primary hosts and (I'm pretty sure) they are also vectors. "Host" status doesn't mean they have to be harmed, this can be seen in mutually beneficial relationships.
When we talk about primary and secondary hosts we are often referring to parasitic lifecycles - because they are often in different forms throughout that cycle.
Mosquitoes are vectors - they help transfer the plasmodium (protozoan) - but, as Lex said, they are also the primary host, because that's where the protist matures.
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am i right in saying that little development occurs in the intermediate host?
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Yep generally that's correct :) because the parasite usually spends less time in the intermediate host although as Eddie (scocliffe09) mentioned the main thing that defines a host as primary or secondary/intermediate is whether the parasite matures while being hosted by them.
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(http://img862.imageshack.us/img862/9406/unledvah.png)
apparently the answer's B
whaaaattt
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(http://img862.imageshack.us/img862/9406/unledvah.png)
apparently the answer's B
whaaaattt
N is the only one that doesn't have antigens complementary to any of the antibodies already present in her body. Therefore no antibodies are present in her body that can recognise the bacterium. This means it will take longer to kill the virus, resulting in a more severe infection.
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OHHHHH that totally makes sense
Thanks!
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Neap says the proteome is the complete array of proteins in a cell produced in its lifetime
i thought proteome was under specific conditions at a specific time, and wiki (best source i know :|) confirms this
can anyone else? thanks
EDIT :
Do non - pathogenic material e.g. toxin, nicotine usually just small fragements that are completely bound by the variable region of an antibody (e.g. 1 binding site is fully occuped by 1 fragment, fragment cannot bond to otther antibodies) or is it more like a bacterium, where the antigens are on the outside of a circular shaped fragment?
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Neap says the proteome is the complete array of proteins in a cell produced in its lifetime
i thought proteome was under specific conditions at a specific time, and wiki (best source i know :|) confirms this
can anyone else? thanks
EDIT :
Do non - pathogenic material e.g. toxin, nicotine usually just small fragements that are completely bound by the variable region of an antibody (e.g. 1 binding site is fully occuped by 1 fragment, fragment cannot bond to otther antibodies) or is it more like a bacterium, where the antigens are on the outside of a circular shaped fragment?
The proteome is normally under specific conditions / at a specific time in the cell's life cycle, but I don't see why you couldn't define it as being of a cell's entire life. It's often used to analyse the gene expression of a cell.
The other question, I can assure you, is far beyond what you'll need to know for VCE - I don't quite know what your question is either. I think you need to be careful not to rely on simplified diagrams too much and remember that everything, such as antigen-toxin binding, is far more complex than VCE will tell you. That said, as far as I know, other material released by pathogens is bound by antibodies, and I don't see why more than one ab couldn't bind to it if there were more binding sites.
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thanks scocliffe
yeah i don't really know how to expalin the second question without diagram well, just in one of the NEAP exams, we had to draw nictotine binding to an antibody, and i drew the nicotine as more resembling a bacterium instead of just a small fragment that is enclosed fully by one actibody binding sites
in VCE level, should i draw toxins resembling the basic shape of a bacterium, with antigens on its surface, or just small fragments (e.g. 1 triangle representing 1 nictoine molecule?) thanks
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I never considered proteome = at a single time, I always likened it to genome, to be the total protein complement of the cell.
A toxin may have multiple binding sites (epitopes), so there's nothing to say it can't be bound by multiple Ab at any one time. Protein toxins are generally quite large relative to other (lipid) toxins, so they have a relatively large amount of conformational determinants.
I wouldn't draw toxins resembling a bacterium because they're not cells. I'd draw a squiggly line then an antibody with an Fab specific for one part of my line
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Describe how ATP acts as a supplier of energy to power metabolic reactions ?
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Describe how ATP acts as a supplier of energy to power metabolic reactions ?
The enzyme ATPase causes ATP to be hydrolysed to produce ADP and a free phosphate, thus releasing stored potential energy in the process.
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1. Do histamines cause fever as part of the inflammatory repsonse?
2. Attached below.
I said D because they look like channels to me, but the answers say B.
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its because the neurotransmitter needs a receptor to trigger a response in the next nerve cell, and I'm pretty sure neurons don't have receptors for neurotransmitters inside the cells themselves
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its because the neurotransmitter needs a receptor to trigger a response in the next nerve cell, and I'm pretty sure neurons don't have receptors for neurotransmitters inside the cells themselves
Yeah but they bind to a receptor in order to open the channels which are also on the postsynaptic membrane... and it looked like a channel to me :S
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its because the neurotransmitter needs a receptor to trigger a response in the next nerve cell, and I'm pretty sure neurons don't have receptors for neurotransmitters inside the cells themselves
Yeah but they bind to a receptor in order to open the channels which are also on the postsynaptic membrane... and it looked like a channel to me :S
Bit of a silly question =S Neurotransmitters open ligand-gated ion channels i.e. ion channels linked to a receptor. You can clearly see that they're defined as both receptors and ion channels within that Wiki page. Unless Russ can shed more light on this, I'd say it could go either way.
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its because the neurotransmitter needs a receptor to trigger a response in the next nerve cell, and I'm pretty sure neurons don't have receptors for neurotransmitters inside the cells themselves
Yeah but they bind to a receptor in order to open the channels which are also on the postsynaptic membrane... and it looked like a channel to me :S
Bit of a silly question =S Neurotransmitters open ligand-gated ion channels i.e. ion channels linked to a receptor. You can clearly see that they're defined as both receptors and ion channels within that Wiki page. Unless Russ can shed more light on this, I'd say it could go either way.
Couldn't agree more with Shinny - I was studying this today myself. Stupid question.
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when atp donates its phosphate group to induce a conformational change, does the energy power this exchange?
also when ATP simply releases stored energy to aid enzymes, can it be called a coenzyme?
What type of molecule is a prostglandin that triggers a fever?
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their is a question that I don't think I 'm answering properly . can u guys please help.
When a material such a pollen, snake venom,inactive agents or transplanted tissue from a donor enters a persons body and is recognised as non-self , it will usually cause an immune response. A developing foetus could also be considered an invader or none self , especially if it is developing inside a surrgate mother.
How are foreign cells recognised as non self by a persons body?
I said foreign cells are recognised by t cells receptors located on the surface of cells.
Is that wrong ?
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Question: What is the bond for lipids and nucleic acids?
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when atp donates its phosphate group to induce a conformational change, does the energy power this exchange?
also when ATP simply releases stored energy to aid enzymes, can it be called a coenzyme?
What type of molecule is a prostglandin that triggers a fever?
- I'm not too sure about the actual mechanism there, but yes, ATP-splitting powers most energy-requiring processes
- Nope, coenzymes assist structurally; they're actually bound to the enzyme.
- Prostaglandins are fatty acid molecules (which I really doubt you need to know about). Not sure about them triggering fever though. They have a similar role to histamine. Pyrogens are more the fever-trigerring molecules.
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How are foreign cells recognised as non self by a persons body?
Foreign cells are generally recognised by absence of "self" receptors or by specific pathogen antigens. You're right, T cells are an important response but the detail you'd need depends on how many marks are assigned
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Hey guys,
This is my first post so I don't really know how this works but could someone please explain
this question.
STAV 2006
Another disease of the Thyroid gland is Graves Disease. The sufferer of this condition produces antibodies that bind to the TSH receptor site mimicking the effect of TSH binding.
(i) Would this condition increase or decrease the production of thyroxin? Explain your answer.
their answer: (i) If these antibodies bind to the TSH receptor site and mimic what would happen if TSH itself bound then the result would be an increase in production of thyroxin (1) as the negative feedback of thyroxin resulting gin less TSH would not result in lowering thyroxin production. (1)
I don't really understand the second part of their answer.
Any help would be much appreciated.
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Antibodies mimic TSH -> thyroid hormones (eg thyroxine) produced
Hormones acts in negative feedback -> Decrease pituitary producing TSH
Decreased TSH would NORMALLY cause decreased hormone production but the auto-Ab are not affected by that feedback loop
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Thank you :)
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1. What is the actual function of rRNA aside from making up the main component of ribosomes?
2. Is the sequence on DNA (e.g. AAT CGC) the one that codes for the amino acids, or is it the complementary sequence on mRNA (e.g. UUA GCG) - when reading off those silly tables...
3. The photosynthetic rate of plants drops when they do not recieve enough water. This is due to the fact that:
A. water is a reactant in the light independent reaction
B. water provides oxygen for the light dependent stage.
C. the stomata close, lowering CO2 intake for the light independent stage.
D. hydrogen ions from water are not available for the light dependent stage.
^^ I understand why C is correct (which was the answer they had) but why is D wrong (what I put)? ???
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1. What is the actual function of rRNA aside from making up the main component of ribosomes?
2. Is the sequence on DNA (e.g. AAT CGC) the one that codes for the amino acids, or is it the complementary sequence on mRNA (e.g. UUA GCG) - when reading off those silly tables...
3. The photosynthetic rate of plants drops when they do not recieve enough water. This is due to the fact that:
A. water is a reactant in the light independent reaction
B. water provides oxygen for the light dependent stage.
C. the stomata close, lowering CO2 intake for the light independent stage.
D. hydrogen ions from water are not available for the light dependent stage.
^^ I understand why C is correct (which was the answer they had) but why is D wrong (what I put)? ???
hydrogen ions are not needed for the light DEpendent reaction, only the light independent. if it had said that hydrogen ions from water are not available for the light INdependent stage then it would've been correct :D
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oh and, when writing the formula for cellular respiration, do we need to include 36/38 ADP + 36/38 Pi?
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1. What is the actual function of rRNA aside from making up the main component of ribosomes?
2. Is the sequence on DNA (e.g. AAT CGC) the one that codes for the amino acids, or is it the complementary sequence on mRNA (e.g. UUA GCG) - when reading off those silly tables...
3. The photosynthetic rate of plants drops when they do not recieve enough water. This is due to the fact that:
A. water is a reactant in the light independent reaction
B. water provides oxygen for the light dependent stage.
C. the stomata close, lowering CO2 intake for the light independent stage.
D. hydrogen ions from water are not available for the light dependent stage.
^^ I understand why C is correct (which was the answer they had) but why is D wrong (what I put)? ???
hydrogen ions are not needed for the light DEpendent reaction, only the light independent. if it had said that hydrogen ions from water are not available for the light INdependent stage then it would've been correct :D
But they are split in the light dependent reaction? And the H+ ions join with the NADP+ in the light dependent stage... so how are they not "needed" when if you didn't have the H+ ions in the light dependent stage you wouldn't have the carrier molecules (NADPH) needed for the independent?
EDIT: In answer to your question, I'd put it in just in case.
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2. Is the sequence on DNA (e.g. AAT CGC) the one that codes for the amino acids, or is it the complementary sequence on mRNA (e.g. UUA GCG) - when reading off those silly tables...
Could be either; simply just look whether the table has U's in it or not to know which one to read off =T
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How do antibodies work? I know that plasma cells produce them in response to being activated, but how do the antbodies work?
And do antibodies work on free-floating pathogens or do they also affect infected cells?
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They're more for things within extracellular fluid - an antibody, when colliding with its specific antigen, will form an antibody-antigen complex and this inactivates the pathogen. This 'flags' it for removal by phagocytes. Infected cells are targeted by T cells.
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Thanks alot russ , And also how much of the action potential do we need to know and the nerve impulse do we need to know in detail like refractory period and hyperpolarization ?
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Thanks alot russ , And also how much of the action potential do we need to know and the nerve impulse do we need to know in detail like refractory period and hyperpolarization ?
You don't need that much detail.
Understand that resting membrane potential is negative inside and positive outside and that as the AP moves along, K+ flow out and Na+ flow in. Understand that myelin helps insulation and conduction and that the nodes of ranvier (between myelin) allow for the AP to move along the axon. Know the structures of sensory, inter and effector neurons. Understand the concept of reflex arcs. Don't know that there's that much more to it!
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Oh okay thanks alot and do we need to know the C4 and C3 in photosynthesis or only up to the light dependent and independent reacts that what i only know and the inputs and outs .
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I have some info that says some lipids contain nitrogen, is this correct and can anyone give me an example of this? Thanks
EDIT: Also, should i state on the exam that the polymer of amino acids is a protein or polypeptide?
I'm pretty sure polypeptide is more accurate, but i get the feeling that VCAA like protein
or should i give an answer such as
the polymer of amino acids is a polypeptide (or polypeptides, inc. func proteins?)
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Reasonably sure there are nitrogenous lipids.
Polypeptide = many amino acids, more so than an oligopeptide. It's reasonably interchangeable with protein, I usually use polypeptide to mean an unfinished or linear chain.
RE: antibodies, they can fix complement on the surface of infected cells, which obvious allows a response. they don't necessarily have to neutralise, they can simply bind and act as markers etc.
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Could someone please explain how the answer to this question is A, since I initially thought that it would be C
Question 16
The human thyroid gland is controlled by a negative feedback mechanism. The hypothalamus secretes
thyrotropin-releasing hormone (TRH). TRH stimulates the anterior pituitary to secrete thyroid stimulating
hormone (TSH). TSH induces the thyroid gland to secrete thyroxine.
The next step in the control system is
A. thyroxine will inhibit the secretion of TRH by the hypothalamus.
B. the hypothalamus will secrete a thyroid-inhibiting hormone that slows down production of thyroxine.
C. thyroxine will stimulate the increased production of TSH.
D. the rising level of thyroxine will act on the pituitary gland to slow down the production of TSH.
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It's not C because that would be positive feedback, seeing as it would be increasing production of TSH
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A due to negative feedback
Thanks Russ
Are transplanted organs rejected due to eosinophil action or cytotoxic T action , and how exactly does this work, as in, do phagocytes still e ngluf antigens somehow, and how does the body 'kill' the new organ
2) what should i call the membrane of mitochondria etc. plasma membrane / cell membrane / unit membrane / membrane?
Is a vector defined as a carrier of infectious disease that transmits it from one organsim to another without getting harmed itself? if it does get harmed, why is the mosquito instead of the human termed the 'vector'?
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Transplanted organs have different HLAs so they thus stimulate an immune response via Th cells because they haven't been educated to not react to the non-self HLA. Then it's a normal CMI
Vectors are organisms that transmit disease, just because they're affected doesn't mean they're not a vector. Infectious disease is human-centric so we talk about zoonotic infections as those that will be transmitted TO humans. If you did vet science, it'd be the other way round
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Transplanted organs have different HLAs so they thus stimulate an immune response via Th cells because they haven't been educated to not react to the non-self HLA. Then it's a normal CMI
Vectors are organisms that transmit disease, just because they're affected doesn't mean they're not a vector. Infectious disease is human-centric so we talk about zoonotic infections as those that will be transmitted TO humans. If you did vet science, it'd be the other way round
thanks russ, would NK cells attack the organs as well?
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Yes
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Why do lymph nodes swell up?
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Why do lymph nodes swell up?
I'm guessing that due to an infection the node will have more macrophages and lymphocytes, so they'd need get larger to accommodate them all. Also as another guess, they could be infected themselves and inflammation could occur in the node?
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Why do lymph nodes swell up?
I'm guessing that due to an infection the node will have more macrophages and lymphocytes, so they'd need get larger to accommodate them all. Also as another guess, they could be infected themselves and inflammation could occur in the node?
Hmm, well it's in response to a question from 2006 VCAA - there was a graph showing, between a specific time period, an increasing HIV concentration, with decreasing T-cell concentration and it asked to explain the swelling of the lymph node during this time period
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what is the difference between lymph gland and lymph node, does lymph gland have some sort of duct? what is an example of lymph gland?>
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Same thing.
Swollen nodes are caused because you get an infection and you get excess transport to the LNs and cell migration. It's only really a problem with serious overinfection (ie HIV). It won't happen from just a cold or similar
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Why do lymph nodes swell up?
I'm guessing that due to an infection the node will have more macrophages and lymphocytes, so they'd need get larger to accommodate them all. Also as another guess, they could be infected themselves and inflammation could occur in the node?
Hmm, well it's in response to a question from 2006 VCAA - there was a graph showing, between a specific time period, an increasing HIV concentration, with decreasing T-cell concentration and it asked to explain the swelling of the lymph node during this time period
I just checked the '06 assessment report and it just says 'answer needs to relate to their role within defense mechanisms against infective agents'... so I think my first answer was right as the lymph node is where macrophages go to present the pathogens they've ingested etc.... and bazza, afaik lymph gland is the same thing as lymph node.
edit: russ beat me to it =D
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Could someone please explain the difference between MHC 1 and 2 markers and do
B and T cells recognise other cells with the same MHC 2 markers ? I'm still a bit
confused ???
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Could someone please explain the difference between MHC 1 and 2 markers and do
B and T cells recognise other cells with the same MHC 2 markers ? I'm still a bit
confused ???
MHC I proteins are found on all/most body cells and are unique to that person so can be classified as self. Fragments of proteins synthesised within the cell are constantly being attached to these MHC proteins - so these MHC I proteins are able to display self-antigens. If a pathogen is to enter that cell and start producing substances then fragments of these substances will be displayed on the MHC I proteins of that cell - i.e. the MHC I proteins are displaying non-self antigens. This allows cytoxic T cells to bind to both the self-MHC I protein and the non-self antigen that it is displaying - there has to be double recognition - recognition of a self-protein (but not antigen) and recognition of a non-self antigen.
So, don't let MHC proteins confuse you. Cells have MHC class I proteins. When these are loaded they either display self-antigens or non-self antigens. If a cytotoxic T cell recognises the non-self antigen bound to an MHC class 1 marker then an immune response is initiated.
Class II MHC proteins are found only on surfaces of antigen presenting cells - the proteins loaded onto these MHC proteins are not produced within the cell but rather are phagocytosed, broken down, and then fragments are displayed on the MHC II proteins. Helper T cells are generally the only cells to bind to MHC II proteins and the non-self antigens that they are displaying. It's not the B cells that recognise these proteins and the antigens because they themselves are professional antigen presenting cells.
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EDIT: i just realised i don't really know much about the non - specific (e.g. non IgE) inflammatory response and how this occures, can someone elaborate?
histamines cytokines?
and how do general inflammation of the body occur (e.g. non - specific) is this just due to serotonin and histamine release from macrophages / basophil cells?
EDIT
1) can mast cells release histmanine without specific activation and how/
2) wtf is serotonin lol, i saw it mentioned as being released by mast / basophils, but i looked it up and there doesnt' seem to be info about serotonin / inflammatory response
EDIT 2: Is DNA present in nucleolus as well, and does the nucleolus hold tRNA and mRNA?
Thanks
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^ I'll get back to you on this (or let one of the VN experts answer this) but I think you might have confused yourself here - the vast majority of inflammatory responses are non-specific. I think it's just contact that promotes histamine release.
DNA isn't present in the nucleolus (at a simple level) and no, talk about rRNA not the others.
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Inflammatory responses aren't specific to a pathogen, bacterium X (s. aureus) can cause the same response as bacterium Y (s. pneumoniae). You get cytokine mediated vasodilation and upregulation of specific receptors/ligands on the blood vessels to allow leucocytes to stick. When they stick they migrate into the tissue. That causes the 4 typical inflammation signs (heat/swelling/soreness/redness).
The cytokines tend to originate from tissue resident macrophages.
RE: mast cells, depends what you mean by specific activation. They have IgE on the cell surface, which is obviously specific, but a mast cell isn't specific for a single pathogen. On activation, they secrete preformed histamine and start synthesizing lipid mediators (prostaglandins) and cytokines (TNFa, IL1 etc.).
I don't think you need to know any of that though.
Never heard of serotonin as a major inflammatory mediator, a quick look at the wiki article says it will affect blood vessels and a quick google says that inflammation decreases serotonin levels but not the other way around
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do all WBCs (e.g. macrophages) release the cytokines to cause inflammation?
Histmaine is not involved in non - specific activated response?
still a bit confused :(
okay, this is what i think is happening
infection occurs, macrophages and other phagocytes engulf pathogen, these release cytokines that include various interleukins which promote inflammation, pyrogens that raise temperature, but NO histamine ? ( or is histmaine released in small amounts by phagocytes etc. as well? )
This then causes vasodilation, permeabiliyt etc.
and Mast cells are activated by a specific antigen, and each mast cell has many of the SAME receptors
?
lol
thanks!
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Its actually that the bacteria crosses your first line of defence causing mast cells to release histamine which cause the capillaries to dilate and this causes phagocytes to diapedise through the capillary and engulf foreign bacteria. Cytokines are released from the area where the activity is happening. The Khanacademy dude explains it exceptionally well.
http://www.khanacademy.org/video/inflammatory-response?playlist=Biology
Histamine are a part of the non-specific immune system as well as mast cells. They are activated by the substances released by the pathogen or from the chemokines released by the skin cells.
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sweet, so mast cells can be activated by cytokines + chemicals from bacteria, not only IgE activation!
Do basophils release histamine as a result of the same stimulus?
Do macrohpages release any cytokines?
http://img32.imageshack.us/img32/2793/gfdgfd.png
can anyone confirm the logic behind B - is it because the signal PASSEs to the interneuron, but does not initiated an action potential?
thanks
if vcaa
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Hmmm.....I thought that it would generate an AP in the sensory neuron and as a result passes to
the interneuron but is not able to reach the threshold for the motor neuron. Thus you could
definetly eliminate D,C and A as B is simply the best answer ;)
Hope that helps
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and Mast cells are activated by a specific antigen, and each mast cell has many of the SAME receptors
Mast cells have multiple receptors.
Do basophils release histamine as a result of the same stimulus?
Do macrohpages release any cytokines?
Yes/Yes.
can anyone confirm the logic behind B - is it because the signal PASSEs to the interneuron, but does not initiated an action potential?
Yes, if neuron X activates it will release neurotransmitters regardless of whether it's sufficient to activate the subsequent neuron
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how does a fever occur?
Heinemann says the infected cells release pyrogens that cause the hypothalamus to increase the set temperature but other texts, biozone in think says that the infected cells release interleukin 1 that travel to the brain causing it produce prostoglandins resulting in the hypothalamus increasing the set temp...
which is more correct?
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Pretty sure both are correct.
And can anyone explain buffers. I got the answer somewhere but I can't remember. A lot of practice papers mention them.
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Simple, they are substances that combine with or release hydrogen ions in a solution as required to
prevent a change in the pH of the solution.
Theres different kinds, e.g. protein buffers such as haemoglobin which can act as a buffer, and some
are intracellular buffers such as phosphate buffers. Oh and there are also bicarbonate buffers (act in blood).
Thats just off the top of my head but in saying that I don't think we would be required to know to really
in depth. Perhaps its good to just have a grasp of how they work. :)
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And can anyone explain buffers. I got the answer somewhere but I can't remember. A lot of practice papers mention them.
You mean amino acids acting as buffers?
If so: an alpha amino acid (the normal ones that make proteins, alpha for the central carbon) have three main groups, the amine (-NH2), the carboxylic acid (-COOH) and the Z group attached to the alpha carbon. If we take glycine (the simplest amino acid -I think), the Z group is a H. In a pH of 7, glycine, instead of having the amine and carboxilic groups as they are, from a zwitterion (don't need to know that word for bio). Basically, a zwitterion has a neutral overall charge but has charged areas. IN the case of amino acid at ph 7, it donates and accepts a proton and forms N+H3 and COO-. In a basic solution (pH>7), it will only donate a proton (only the COO-). In an acidic environment (pH<7), it will accept a proton (only N+H3). Hence, an amino acid (only by itself, not when in a polypeptide/protein) can accept and donate protons depending on the surrounding pH, effectively neutralising the solution, therefore acting as a pH buffer.
Thats just my chem 3+4 knowledge plus my ex-bio 3+4 knowledge chucked in a para :P Hope that makes sense
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And can anyone explain buffers. I got the answer somewhere but I can't remember. A lot of practice papers mention them.
You mean amino acids acting as buffers?
If so: an alpha amino acid (the normal ones that make proteins, alpha for the central carbon) have three main groups, the amine (-NH2), the carboxylic acid (-COOH) and the Z group attached to the alpha carbon. If we take glycine (the simplest amino acid -I think), the Z group is a H. In a pH of 7, glycine, instead of having the amine and carboxilic groups as they are, from a zwitterion (don't need to know that word for bio). Basically, a zwitterion has a neutral overall charge but has charged areas. IN the case of amino acid at ph 7, it donates and accepts a proton and forms N+H3 and COO-. In a basic solution (pH>7), it will only donate a proton (only the COO-). In an acidic environment (pH<7), it will accept a proton (only N+H3). Hence, an amino acid (only by itself, not when in a polypeptide/protein) can accept and donate protons depending on the surrounding pH, effectively neutralising the solution, therefore acting as a pH buffer.
Thats just my chem 3+4 knowledge plus my ex-bio 3+4 knowledge chucked in a para :P Hope that makes sense
Is there a more simple way of putting it. :S
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Is there a more simple way of putting it. :S
Basically, an amino acid is a pH buffer in that it can donate or accept a proton depending on the environment it is in. If in acidic env, it will accept. If in basic env, it will donate.
I think that amount of knowledge will suffice. :)
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Hey do you guys reckon we should know all of the homeostatic mechanisms?
such as the action of ADH, thyroxine etc?
Or is it best to just know the general principles behind feedback mechanisms,
since when I checked in the VCAA exams they gave information in their
questions for most, well obviously except for stuff about glucose regulation,
yet the trial exam companies ask about the intricate details pertaining to the
regulation of each and every variable :P
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If a neurotransmitter is NOT broken down (i.e. the enzyme that breaks it down is denatured) will this result in continual stimulation of the postsynaptic nerve, or no impulse as the neurotransmitter can't be broken down and reused? On most exams it's the former, but TSSM just said it's the latter... :idiot2:
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I think its the former, I don't really like TSSM exams since they usually have something
wrong in their exams. :P
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Just watch the video and all your doubts will be cleared up. As for chemokines, you don't need to know it. It's just extra information if you are interested.
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If a neurotransmitter is NOT broken down (i.e. the enzyme that breaks it down is denatured) will this result in continual stimulation of the postsynaptic nerve, or no impulse as the neurotransmitter can't be broken down and reused? On most exams it's the former, but TSSM just said it's the latter... :idiot2:
See VCAA 2009 Q6 (this is the most important stuff you need to know re neurotransmitters)
overstimulation is the main problem. If for some reason, neurotransmitter synthesis were being impeded, then i suppose breakdown would cause issues with regard to not having enough - but this is less likely methinks.
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Hey do you guys reckon we should know all of the homeostatic mechanisms?
such as the action of ADH, thyroxine etc?
Or is it best to just know the general principles behind feedback mechanisms,
since when I checked in the VCAA exams they gave information in their
questions for most, well obviously except for stuff about glucose regulation,
yet the trial exam companies ask about the intricate details pertaining to the
regulation of each and every variable
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Is it just me or does it seem like VCAA loves students to give comparative statements?
They've made a remark about this in most of the past exams that I've taken a look at. Well
I guess at times it appeared as though the question was not asking for a comparison whereas the
answer supplied suggested otherwise ??? So what do you guys reckon would it be safe to give a
comparison for some questions just in case and how are you guys able to decipher if the question
is asking us to make a comparative statement?
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Hey do you guys reckon we should know all of the homeostatic mechanisms?
such as the action of ADH, thyroxine etc?
Or is it best to just know the general principles behind feedback mechanisms,
since when I checked in the VCAA exams they gave information in their
questions for most, well obviously except for stuff about glucose regulation,
yet the trial exam companies ask about the intricate details pertaining to the
regulation of each and every variable
No way, exactly as you said. It's only other companies that mislead you into thinking that you need to know everything. You will be given enough information. You will need to know at least one example though if you are given an open-ended question and are required to show a pathway.
Sometimes VCAA exams are a bit ambiguous but overall they're very diligent and excellent at testing concepts in a holistic way. Yeah, they love comparisons :) I f you are genuinely unsure, go for it. There's nothing wrong with giving more information as long as you are addressing the question and not adding incorrect information. Obviously it would be inefficient to do so, though.
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How much chemistry do we have to know for the exam?
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Pure basics, don't let companies fool you in thinking you need to know complex molecular structures or anything like that :)
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do i need to know the nervous system in detail because im sure heinemann doesnt have alot of info on it and sensory neurons and stuff?
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Thanks you Lexitu :)
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Yep :) You should understand things like action potentials, basic structures of different neurons, reflex arcs, etc.
And no worries adrenaline :)
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if B cells mature in the Bone marrow does that mean they poliferate into B memory cells and plasma cells there? what does 'mature' mean.
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I think they would proliferate in the lymph nodes where they encounter the foreign antigen...
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Mature means they gain the ability to a) bind a specific antigen b) be tolerant of self-antigens.
As far as proliferation and differentiation goes, I think that is in the site of activation (in most cases the lymph nodes as Kaille said), but double check this :)
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oh ok. thanks kaille adn lexitu, that makes sense now :)
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does the electron transport chain require oxygen? its only the krebs cycle right? I know you need to go through the krebs before electron though.
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Yeah, the ETC needs oxygen so that it can bind to the hydrogen ions to make water
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Oxygen isnt actually used in krebs cycle but its presence is required for the krebs cycle to occur!
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Oxygen isnt actually used in krebs cycle but its presence is required for the krebs cycle to occur!
yep, its needed for the oxidation of pyruvate to acetyl CoA that enters the cycle.
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:uglystupid2: looks like i still have a lot of revision to do :/
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what are the difference between chemokines and cytokines - are chemokines released by any cell while cytokines are released by immune system cells? - are pyrogens cytokines? or does their classification depend on the target cells?
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Chemokines are a subgroup of cytokines. Chemokines are chemotactic for certain cell receptors, which makes the cell travel along the concentration gradient and thus migrate within the body.
Cytokine and chemokines can be released by more than just leucocytes.
Pyrogens are not necessarily cytokines.
Classification doesn't depend on target cells, it depends on the structure of the molecule (cyto/chemo) and the effect it has (pyrogen)
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Thanks Russ.
2 more questions
1) why do injected antibodies not trigger the immune response as they are foreign particles?
Is it because the body would then attack all antibodies?
2) do ige antibodies bind to allergens before or after binding to mast cells?
Edit: are single celled Protista engulfed by phagocytes?
Douchy said lone antigens can trigger t helper cells, is that wrong?
What does Pr stand for ? (as in something red light, Pr and Pfr)(can someone explain the shade avoidance response?)
Thanks!~
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Thanks Russ.
2 more questions
1) why do injected antibodies not trigger the immune response as they are foreign particles?
Is it because the body would then attack all antibodies?
Douchy said lone antigens can trigger t helper cells, is that wrong?
antibodies are more like 'self' i guess. If anitbodies were treated like antigens, then there would be nothing to kill the free antigens!
O, and antibodies aren't cells, so i guess they wouln't need the MHC markers? not sure :|
yea i dont think lone antigens can trigger helper T cells cause helper T cells can only bind to an antigen presented by a macrophage.
Oxygen isnt actually used in krebs cycle but its presence is required for the krebs cycle to occur!
yep, its needed for the oxidation of pyruvate to acetyl CoA that enters the cycle.
i thought it was solely needed for the ETC, to form water?
my teacher said that cytochrome = always the last electron acceptor in the ETC and then the rest in the ETC were different proteins. can anyone else confirm this?
And helper T cells, do they activate cytotoxic T cells, other helper T cells and B cells? When they activate cytotoxic T cells does it mean cytotoxic T cells start undergoign clonal expansion or does this only happen to Helper T cells. Or are they just activated to move to lymph nodes and meet with the infect cell and kill it.
also, are all T cells that come from the thymus gland, helper T cells?
Thanks :)
EDIT: are dendritic cells part of 2nd line of defence and are lymphokines a type of cytokine
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Oxygen isnt actually used in krebs cycle but its presence is required for the krebs cycle to occur!
yep, its needed for the oxidation of pyruvate to acetyl CoA that enters the cycle.
i thought it was solely needed for the ETC, to form water?
my teacher said that cytochrome = always the last electron acceptor in the ETC and then the rest in the ETC were different proteins. can anyone else confirm this?
And helper T cells, do they activate cytotoxic T cells, other helper T cells and B cells? When they activate cytotoxic T cells does it mean cytotoxic T cells start undergoign clonal expansion or does this only happen to Helper T cells. Or are they just activated to move to lymph nodes and meet with the infect cell and kill it.
also, are all T cells that come from the thymus gland, helper T cells?
Thanks :)
EDIT: are dendritic cells part of 2nd line of defence and are lymphokines a type of cytokine
The oxygen in the krebs cycle doesn't necessarily come from atmospheric oxygen, it comes from lysis of water molecules but that's way too, complicated you don't need to know that. Oxygen is ONLY an input in electron transport. The last electron acceptor is oxygen as far as I know... You don't need to know anything about the cytochrome complex other than that is a group of proteins that transfer H+ ions and electrons (and that you need to know this is unlikely)
Helper T cells activate everything, generally. The other cells need co-stimulation before they can proliferate. A VN pro can expand on this :)
Dendritic cells are definitely 2nd line. Lymphokines are cytokines but slow down there's NO WAY you need to know that!
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RE: helper cells, they don't activate other helper cells, they lack MHCII. thymus produces several types of T cell, the only ones you need to know are CD4 and CD8 though
1) why do injected antibodies not trigger the immune response as they are foreign particles?
They're self molecules. Every Ab has two regions, the Fab for antigen binding and the Fc for host recognition. All human Ab have the same Fc regions, so you can transfer them. Mouse Ab are different, you'll eventually get an immune response if you try it.
2) do ige antibodies bind to allergens before or after binding to mast cells?
Potentially both, but predominantly after. The concentration of serum IgE is something like 10 million times less than IgG.
Edit: are single celled Protista engulfed by phagocytes?
Doubt it, they're pretty big, but i suppose degranulation could chip away at them.
Douchy said lone antigens can trigger t helper cells, is that wrong?
Why would it be wrong? Anything presented on MHCII will trigger a Th response, regardless of where it came from
What does Pr stand for ? (as in something red light, Pr and Pfr)(can someone explain the shade avoidance response?)
Polyrefringence at a guess?
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RE: helper cells, they don't activate other helper cells, they lack MHCII. thymus produces several types of T cell, the only ones you need to know are CD4 and CD8 though
Oh thanks lexitu and russ :D
ok, but i read that the interleukin-2 released by Helper T cells activate other Helper T cells (tsfx bklets). what do they mean by this
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Oh, my bad, I thought you meant by direct TCR/MHCII binding. Yeah they secrete all sorts of cytokines that are responsible for causing other Th cells to differentiate etc.
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RE: helper cells, they don't activate other helper cells, they lack MHCII. thymus produces several types of T cell, the only ones you need to know are CD4 and CD8 though
1) why do injected antibodies not trigger the immune response as they are foreign particles?
They're self molecules. Every Ab has two regions, the Fab for antigen binding and the Fc for host recognition. All human Ab have the same Fc regions, so you can transfer them. Mouse Ab are different, you'll eventually get an immune response if you try it.
2) do ige antibodies bind to allergens before or after binding to mast cells?
Potentially both, but predominantly after. The concentration of serum IgE is something like 10 million times less than IgG.
Edit: are single celled Protista engulfed by phagocytes?
Doubt it, they're pretty big, but i suppose degranulation could chip away at them.
Douchy said lone antigens can trigger t helper cells, is that wrong?
Why would it be wrong? Anything presented on MHCII will trigger a Th response, regardless of where it came from
What does Pr stand for ? (as in something red light, Pr and Pfr)(can someone explain the shade avoidance response?)
Polyrefringence at a guess?
Thanks russ, i thought i read somewhere that T helper cells could only read antigens off macrophages?
Do horse antibodies (for snakevenom) trigger the immune response?
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Thanks russ, i thought i read somewhere that T helper cells could only read antigens off macrophages?
No way, any antigen presenting cell can be read by a T cell, the importance of macrophages is often overstated.
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*eep edit sorry :S
1) i meant can T helper cells only read antigens of APCs :O
Campbell's bio says - while B cell receptors recognize intact antigens, receptors on T cells recognize small fragments of antigens bound to normal cell - surface proteins called MHC molecues
(i think i meant off cells such as macrophages)
2)
Do horse antibodies (for snakevenom) trigger the immune response?
3) STAV '08 says
(in resposne to a question about growth by plants under shade)
"Chlorophyll absorbs red light for photosynthesis but not far red. the shaded plant will therefore be exposed to more far red light than red light. this will have the effect of the active Pfr
being converted to the inactive Pr.
The result will be stem elongation as Pfr prevents stem elongation"
can someone please explain this and what the P means (sorry i didn't make it clear before Russ)
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Ah, okay, in that case, as I understand it, the antigen fragments must be displayed on the MHC II proteins of antigen-presenting cells which is what Russ said, I think.
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1. Yes, the vast majority of antigens must be presented on MHCII in order to stimulate Th activation and production. Those that don't are irrelevant to VCE.
2. Yes, but it requires several exposures until the response is significant. The Ab Fc region is the immunogenic bit, but it's not particularly so.
3. lolplants
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what is a calcium influx in relation to synaptic transmission?
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influx of calcium ions causes the synaptic vesicles to migrate to the pre synaptic membrane and secrete neurotransmitter molecules into synaptic cleft.
i still dont fully get cell mediated immunity. is it:
APC releases a cytokine which attracts the helper T cell. Helper T cell then nids to the antigen fragment presented by the APC'S MHC 2 marker.
helper T cell is stimulated to release another cytokine which in turn activates B cells and also helper T cells to differentiate into clones including: cytotoxic T cells, more helper T cells, suppressor T cells, and memory T cells?
cytotoxic T cells kill infected cells. After they kill, what happens to Tc cells?
and is there anything else im missing
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Thanks russ
you understand it quite well it appears.
the cytotoxic T cells will naturally degrade and die just as other WBCs do.
cytotoxic T memory cells will remian though
STAV '08 says
(in resposne to a question about growth by plants under shade)
"Chlorophyll absorbs red light for photosynthesis but not far red. the shaded plant will therefore be exposed to more far red light than red light. this will have the effect of the active Pfr
being converted to the inactive Pr.
The result will be stem elongation as Pfr prevents stem elongation"
can someone please explain this and what the P means (sorry i didn't make it clear before Russ)
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P=phytochrome
its a type of phytoprotein that acts as a receptor to light (red or far red light) for plants
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why will the phytocrome change?
STAV '08 says
(in resposne to a question about growth by plants under shade)
"Chlorophyll absorbs red light for photosynthesis but not far red. the shaded plant will therefore be exposed to more far red light than red light. this will have the effect of the active Pfr
being converted to the inactive Pr.
The result will be stem elongation as Pfr prevents stem elongation"
can someone please explain this and what the P means (sorry i didn't make it clear before Russ)
-
ummmm well Pr = inactive form. so when it meets red light (natural light) it becomes activated into Pfr. as an enzyme triggers synthesis or activation of specific proteins in specific cells or altering transcription of genes, eventually causing a response. The amount of phytochrome in each form will enable plant to measure daylenght/nightlength = involved in photoperiodism.
And when Pfr meets with far red light (in the dark), it become inactivated again and is now Pr.
EDIT: just read q. again. ok, so when it absorbs red light it becomes activated in Pfr. When the enzyme did things to lead to a response i think this could have included stem elongation.
but with "The result will be stem elongation as Pfr prevents stem elongation" - i dont think that makes sense? :o
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But what does Pfr and Pr mean?, that one phytochrome can be converted into another?
What are bacterial cell wall composed of, I thought it was mainly complex polysaccharides but nob says lipid compounds or teichoic acid ( gram -,+) and amino acids and di saccahridrs?
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peptidoglycan. but gram positive have a thicker cell wall (this includes teichoid acid + more amino acids + disaccharides) and gram negative has a multilayered cell wall, having an additional outer membrane layer of lipids (without teichoic acid + less amino acids and disaccharides). this helps determine what type of antibiotics would work on the bacteria. For example gram positive bacterias are more susceptible to penicillin than gram negative.
With cell mediated immunity, when interleukin-2 activates cytotoxic T cell to proliferate does it mean it devides rapidly into same cytotoxic T cells or does it mean it differentiates into those 4 type of T cells through clonal expansion
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do loaded acceptor molecules carry electrons or hydrogen ions? cuz in the electron transport stage it says the electrons and hydrogen ions are passed into cytochromes..but i dont know where the electrons come from D=
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the electrons are from the Hydrogen ions. Ions have protons and then electrons orbiting around nucleus.
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whats the difference between hypolgycamemia and hyperglycameia ?
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Hypoglycaemia = low blood glucose levels
Hyperglycaemia = high blood glucose levels
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whats the difference between glucagon and glucogen?
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glucagon hormone which promotes glucose release into bloodstream, glycogen stored form of CHO in animals
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oh ok thanks , how much of hormones do we need to know ? am i wasting my time learning them into the detail?
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Just to clear things up.
Does a protein have a quaternary structure when it has two or more polypetide chains?
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Or is it one?
Two different sources are telling me two different things! :|
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I think it would be beneficial to know one hormone really well. Eg. Insulin. They might ask you to name one then describe how it causes a change in a cell (signal transduction) or draw a negative feedback model.
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Quaternary structures = two or more polypeptide chains
What are the lymphocytes that undergo clonal expansion/selection theory?
is it B cells and helper T cells
or
B cells, helper T cells and cytotoxic T cells?
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Quaternary structures = two or more polypeptide chains
What are the lymphocytes that undergo clonal expansion/selection theory?
is it B cells and helper T cells
or
B cells, helper T cells and cytotoxic T cells?
i think b lymphocytes, t helper and cytotoxic t cells undergo clonal expansion because they all have memory cells i think.....
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Quaternary structures = two or more polypeptide chains
What are the lymphocytes that undergo clonal expansion/selection theory?
is it B cells and helper T cells
or
B cells, helper T cells and cytotoxic T cells?
B-cells undergo clonal expansion; this then produces plasma cells and b-memory cells. These plasma cells produce antibodies specifically for the presented antigen :)
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OKay guys how much of parasympathetic and sympathetic do we need to know ???
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the electrons are from the Hydrogen ions. Ions have protons and then electrons orbiting around nucleus.
what whoaaa? LOL which molecules are carrying the electrons? and the hydrogen ions cant have a electron orbiting around them because the hydrogen ions being carried are positive so the carry molecules are only carrying protons... D=?
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the electrons are from the Hydrogen ions. Ions have protons and then electrons orbiting around nucleus.
what whoaaa? LOL which molecules are carrying the electrons? and the hydrogen ions cant have a electron orbiting around them because the hydrogen ions being carried are positive so the carry molecules are only carrying protons... D=?
i think the electrons are released when the hydrogen ions are split from the electron carriers, since now there is no pairing ofthe ions with the carriers to hold onto the electrons...as a result, those electrons will kind of be free to roam....but yes, hydrogen ions are not electrons coz they dnt have that electron!
also, is tissue rejection done by t cells only? no humoral response?
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On tissue rejection (from something I've posted elsewhere)
Transplants are pretty interesting. Even though it is not the person's self-MHC I proteins that exist on the transplanted tissue cell surfaces, sometimes cytotoxic T cells are able to bind to the MHC I proteins and the foreign antigens that they are displaying and "kill" the cell in the same way that they would if it was the person's own body cell that was infected. Here's a chunk from my uni textbook:
Before the onslaught can begin, the cytotoxic T cell must "dock" on the target cell by binding to a self-nonself complex. Remember, all body cells dis- play class I MHC antigens, so all infected or abnormal body cells can be destroyed by these T cells. The attack on foreign human cells, such as those of a graft, is more difficult to explain because here all of the antigens are nonself. However, apparently the Tc cells sometimes "see" the foreign class I MHC antigens as a combination of self class I MHC protein bound to foreign antigen. Once· cytotoxic T cells recognize their targets, there are two major mechanisms by which they can deliver a lethal hit.
So as you can see, T cells are pretty important - both cytoxic, and T helper (which are needed for activation). Also important are NK cells, phagocytes, and antibodies (so B cells). Both humoral and cell-mediated responses are important.
----
And guys, let's not let Chemistry override Biology :)
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OKay guys how much of parasympathetic and sympathetic do we need to know ???
Basic level stuff, unlikely it would come up, but definitely possible.
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dumb question but can bacteria like yersinia pestis (black death) be tramsmitted by sharing needles with contaminated blood?
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Don't know about that particular bacterium but yes of course, generally. If it inhabits the blood then don't see why not.
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uh oh, what's the effector part of a stimulus-response model again? just clarifiying, it's the target organ, not the hormone or signal because they're just the signalling molecules? therefore, in the case of say glucose regulation, the effector is the pancreas? which then effects liver cells to do its stuff?
:P
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On tissue rejection (from something I've posted elsewhere)
Transplants are pretty interesting. Even though it is not the person's self-MHC I proteins that exist on the transplanted tissue cell surfaces, sometimes cytotoxic T cells are able to bind to the MHC I proteins and the foreign antigens that they are displaying and "kill" the cell in the same way that they would if it was the person's own body cell that was infected. Here's a chunk from my uni textbook:
Before the onslaught can begin, the cytotoxic T cell must "dock" on the target cell by binding to a self-nonself complex. Remember, all body cells dis- play class I MHC antigens, so all infected or abnormal body cells can be destroyed by these T cells. The attack on foreign human cells, such as those of a graft, is more difficult to explain because here all of the antigens are nonself. However, apparently the Tc cells sometimes "see" the foreign class I MHC antigens as a combination of self class I MHC protein bound to foreign antigen. Once· cytotoxic T cells recognize their targets, there are two major mechanisms by which they can deliver a lethal hit.
So as you can see, T cells are pretty important - both cytoxic, and T helper (which are needed for activation). Also important are NK cells, phagocytes, and antibodies (so B cells). Both humoral and cell-mediated responses are important.
----
And guys, let's not let Chemistry override Biology :)
Do 2nd line of defence always fail in organ tranplants?
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What do you mean by fail? :S Both the second and third line work together to remove the transplant. It's a long process...
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hm well
However, apparently the Tc cells sometimes "see" the foreign class I MHC antigens as a combination of self class I MHC protein bound to foreign antigen. Once· cytotoxic T cells recognize their targets, there are two major mechanisms by which they can deliver a lethal hit.
as well as doing the above, do the cytotoxic T cells bind to antigen fragments presented on a phagocyte in second line of defence like normal immune responses?
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Ah okay, I see what you mean :) Cytotoxic T cells (in all immune responses) bind to MHC I proteins and the antigens they present so this usually means normal body cells not part of the immune system.
Helper T cells bind to class II MHC proteins that display foreign antigens - these antigens have been engulfed and then presented on the MHC II markers
Cytotoxic T cells bind to class I MHC proteins that display foreign antigens - these antigens are being produced inside the cell
Does that help?
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The only time a cytotoxic T cell will bind a macrophage is to destroy it, if it's infected.
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does the blood regulatory pathway have a 'control center' per se?
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What is a way of preventing bananas from ripening?
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Freeze the crap out of them so their metabolic rate goes down?
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What is a way of preventing bananas from ripening?
inhibit the production of the gas hormone ethylene..
i guess a way of preventing it to ripen is putting it in a colder environment as gases diffuse slower in the cold.
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does the blood regulatory pathway have a 'control center' per se?
What did you mean by this? :S
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like, e.g. stimulus response model,
temp control center = hypothalmus
does blood regulatory control centre just pancreas? or is that not necessary in diagram,
also
should the negative feedback arrow go directly to the gland / receptor? (e.g. for BG, straight to islets?)
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I'm still not following, control centre that regulates what? There are many components to blood.. Check the VCAA assessment reports for a suggested way to draw negative feedback models.
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Is it true that phagocytes are only within the bloodstream and macrophages are only outside the bloodstream?
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Freeze the crap out of them so their metabolic rate goes down?
Haha thank you, and I thought that you could like put them in a vacuum like bag with a
compound that absorbs ethylene and then make that bag impermeable to oxygen
to so no respiration would occur, that work as well?
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I know that an allergic reaction is stimulated by the overproduction of igE antibodies that bind to mast cells; but in a normal inflamation response do antibodies have anything to do with it or are the histamines produced without any antibodys binding to the mast cell?
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I'm still not following, control centre that regulates what? There are many components to blood.. Check the VCAA assessment reports for a suggested way to draw negative feedback models.
omg, if my communication systems are this bad tomorrow... :(
Blood GLUCOSE
regulatory system
:S
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Freeze the crap out of them so their metabolic rate goes down?
Haha thank you, and I thought that you could like put them in a vacuum like bag with a
compound that absorbs ethylene and then make that bag impermeable to oxygen
to so no respiration would occur, that work as well?
Yeah perfect mate, that's another thing that they use. By that sort of an answer you are demonstrating knowledge of quite a few concepts, good stuff.
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I'm still not following, control centre that regulates what? There are many components to blood.. Check the VCAA assessment reports for a suggested way to draw negative feedback models.
omg, if my communication systems are this bad tomorrow... :(
Blood GLUCOSE
regulatory system
:S
Oh haha :) Well check the VCAA exam report, I think it was 06-08 - the model is perfectly displayed there.
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"Cholesterol makes the cell membrane decrease the permeability of the bilayer to create small water-soluble molecules"
What does that mean? Does it mean that the membrane can form vesicles?
-
I'm still not following, control centre that regulates what? There are many components to blood.. Check the VCAA assessment reports for a suggested way to draw negative feedback models.
omg, if my communication systems are this bad tomorrow... :(
Blood GLUCOSE
regulatory system
:S
Oh haha :) Well check the VCAA exam report, I think it was 06-08 - the model is perfectly displayed there.
yeah no control centre
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Does it mean that the membrane can form vesicles?
How else would endocytosis happen?
Is it true that phagocytes are only within the bloodstream and macrophages are only outside the bloodstream?
Macrophages are phagocytes, so those two statements are mutually exclusive. Macrophages, however, are ONLY found in tissues (it's a great trick question)
I know that an allergic reaction is stimulated by the overproduction of igE antibodies that bind to mast cells; but in a normal inflamation response do antibodies have anything to do with it or are the histamines produced without any antibodys binding to the mast cell?
Doesn't have to be overproduction for mast cell binding. Normal inflammatory responses can cross link the IgE coating, yes. A normal inflammatory response, however, usually focus on other areas of the immune system
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Really basic question but ions require protein channels to diffuse into a cell?
Also, Complement proteins stimulate inflammation and inflammation increases access for complement proteins
to the infected area right? So which one comes first?
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Yes
Neither is dependent on the other, so it's down to chance
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my teacher says complement proteins are both in the second and third lines of defense...how is that so?
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hey im kinda freaking out about tomorrow can u guyys please tell me what are the important things we need to know from homestasis and nervous system aand endocrine and main things on immunity please ?
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is glucose predominantly absorbed from the stomach by faciliated diffusion?
Also, can disaccarides be absorbed from the stomach?
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This has probably been asked before, but I cbs looking through 50 pages for it:
VCAA 2010 MC 17...
Which plant has highest rate of photosynthesis; the one in red, blue, green or yellow light?
The answer is red light but all the absorption graphs I've seen show that blue light gives the highest rate...??
??? Confused... ???
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This has probably been asked before, but I cbs looking through 50 pages for it:
VCAA 2010 MC 17...
Which plant has highest rate of photosynthesis; the one in red, blue, green or yellow light?
The answer is red light but all the absorption graphs I've seen show that blue light gives the highest rate...??
??? Confused... ???
I was under the impression that photosystem II (p680) had the highest rate at 680mm which corresponds to absorption of red light.
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Hmm... well overall... I don't know.
Let's just go with VCAA because they mark the exams :)
Also, can someone explain how if less energy is retained from food it means that they will weigh more?
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That's a mistake in the suggested responses, ignore it :)
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That's a mistake in the suggested responses, ignore it :)
You mean if less energy is retained they will weigh less?
EDIT: Haha just read the other thread. Think I'm right and they're wrong because more energy retained = more stored = more weight :) Yay I can put those marks back on :)
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Yep. Just think about it logically - you eat a lot and you don't use much of energy then you put on weight. You eat a lot and you use heaps of that energy then you don't put on weight. Same idea here.
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But if your hypothesis WAS wrong, would they take marks off for it?
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If they outline what the researchers thought, then yes, I think they would. If they didn't give you enough information about what the researchers were hypothesising, then I think no - I hypothesis is exactly that - it can be supported or unsupported in the findings.
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Unit 3 // end
Unit 4 // Start
MY FIRST SAC IS IN UNDER 2 WEEKS ????
- is there experimental design for U4 as well?
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Perhaps we should start a Unit 4 Question Megathread?
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Do you want two different megathreads or just one? I can either make and sticky a new one or just rename this one
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New one please. It'd be so much easier to find things.
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Agree :)