ATAR Notes: Forum
VCE Stuff => VCE Science => VCE Mathematics/Science/Technology => VCE Subjects + Help => VCE Biology => Topic started by: saheh on February 20, 2012, 07:19:42 pm
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I will undoubtedly have a million questions/confusions regarding bio so i may as well add them to a thread...like everyone else hehe
anyway I'll just start with one...
regarding membranes, specifically ions, one of my sources says ions can't pass through, yet the other says some can...
so how do ions pass through, via their polarity or something..?? also for 'lipid soluble molecules'?
or dont we need to be that specific??
thanks in advance guys :)
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wait I just found it; facilitated diffusion/active transport etcetc
as if i didnt think of that ><
'Explain how the following can affect the ability of a molecule to pass across a cell membrane: a.)size b.)charge c.) solubility (eg lipids) <<Thats the bit I'm confused on...
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a- smaller molecules can diffuse faster than larger molecules (which would need facilitated diffusion; or even active transport at times). This is because smaller molecules can fit easier than larger molecules.
b- charged molecules cannot readily diffuse through molecules because charged ions are polar and plasma membrane is non-polar (like dissolves like; but in this case they aren't the same)
c- lipid soluble (non-polar) molecules (e.g. chloroform) readily pass through plasma membrane (non-polar)- mainly because of that 'like dissolves like' rule
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thankyou! i totally get it now
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Ok so we had our sac today :) it was pretty straightforward; sultanas in a sucrose solutions of 0%,2%,5%,10%,20% and 30%
although we don't complete our discussion til next week because of camp
anyway, I've worked out my %change, and it's all over the place :/
we left them for about 40 minutes..
and yeah i expected there to be a stage where it (the osmosis rate) changed because of the sucrose content within the sultana
and this is what i got
0%= 17% + change in weight
2%= 18% + change in weight
5% = 22% + "" ""
10%= 16% +
20% = 9% +
30% = 15% +
(all gained weight, non lost it ><)
is the discrepancy most likely an error in the 30% jar?? i'd expect it to continue going down.....
any help would be appreciated!! thankyou!
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I guess i should try and make this work again instead of spamming the wall lol
What's the difference between Gibberellins and Cytokonins?
Where one promotes cell division, the other stimulates it.. umm?
I was doing a prac exam and a qn asking about Gibberellins was on it,
and yeahh
Thanks guys :)
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I think the best way to view them is that they are BOTH growth promoters.
Gibberellins- stimulates cell division/elongation; stimulate seed germination (i.e. via inducing amylase and protease biosynthesis and mobilising food reserves)
Cytokinin- stimulates lateral bud movement (antagonistic to auxin); slows down senescence; breaks seed dormancy; stimulate cell division (specifically, cytokinises); AND (posibly the major diff b/w the two) cytokinin is involved in TISSUE DIFFERENTIATION (as cytokinin:auxin ratio affects tissue differentiation)
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Hey again
Im going away for two weeks and just trying to catch up on my study
I have a sac that im missing out on
its the first for aos2
all i knw is that it's a 'summary report of a plant or animal response to a chemical/physical stimuli'
sooo basically id want to be studying endocrone/nervous system
it wouldnt have anything to do with pathogens and disease no?
Thanks again :)
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I doubt it would include disease. It will probably include a fair bit about signalling molecules, how they travel, signal transduction. etc.
I'd prepare for stimulus-response models too.
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Thanks!
What sort of sac is it do you know?
Like Prac etc?
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It'll vary between schools. For instance, my school goes to GTAC and does the prac, and then comes back to school and does a test.
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Heeeeeey everyone
I have a question for schoolwork
explain the immune system response , including the third level of defence and the step involved in eliminating it from the body, and any chemicals involved.
how would you go about answering this? would you do cell-mediated, and then how it links to antibody mediated?? with interleukins etc and cytotoxins??
also: What would be the similarities and differences between the second and third level?
And b-cells recognise the antigen right? so would they recognise the one on the antigen/mhc complex of APCs? or just mainly on viruses bacteria?
I know the t-cells bind to the antigen-mhc complex and are activated, but how/what do b-cells bind to/recognise mainly??
thanks!!!!
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also guys: adenovirus/retrovirus
was told that retro=rna with viral coat
adeno=dna
??
A tsfx qn says that HIV is caused by a retrovirus (so i think rna) and the qn is
retrovirsus:
a. must produce their own DNA inside host before they can reproduce
b. contain dna with protein coat
c. do not require host cell to reproduce
d. primarily attack bacteria in form of bacteriophages
answer is a, is that because the rna turns into dna in the cell????
i know c and d are wrong..
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also guys: adenovirus/retrovirus
was told that retro=rna with viral coat
adeno=dna
??
A tsfx qn says that HIV is caused by a retrovirus (so i think rna) and the qn is
retrovirsus:
a. must produce their own DNA inside host before they can reproduce
b. contain dna with protein coat
c. do not require host cell to reproduce
d. primarily attack bacteria in form of bacteriophages
answer is a, is that because the rna turns into dna in the cell????
i know c and d are wrong..
Retroviruses contain RNA and the enzyme "reverse transcriptase" which will catalyse the reaction of RNA to DNA. They DO NOT contain DNA. The easiest way to remember I guess is R for RNA and Retrovirus.
To answer the question, this means they have to convert their RNA to DNA and include it into the host cell's DNA in order to code for its own proteins and reproduce.
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hey all
so I know B cells chill out in the lymph nodes after maturing in bone marrow,
and T cells Mature in the thymus after developing in bone marrow,
where do T Cells hang out?
In the lymph nodes? or just floating around everywhere?
thanks!
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yeah, i think after they have matured they just sit around in the lymph nodes and do their stuff.
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ok so i need a little clarification on primary/secondary hosts?
Teacher told us that the primary host is the one in which the parasite is 'born'.. or becomes a gamete or something,, im not too sure
could someone please explain?
Question from A+ practise exams (my attempt at doing a flowchart)
Life cycle of canine heartworm
Microfilariae found in dogs blood <<<<<<<<<<<< Adult female produce microfilariae
V ^
V ^
Mosquito ingests microfilariae whilst feeding Juveniles migrate to heart
V ^
V ^
Microfilariae mature into infective juveniles>>>>>>>Introduced to dog when mosquito feeds on dog
Is the primary host the dog?? because thats when the heartworm produces the 'microfilariae'??
and therefore vector is mosquito?
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In STAV 07 MC there was a question about radioactively labelling 02 to see where it goes, and the answer is that the O2 would be present in that given off by photosynthesis,
my question is, for aerobic cellular resp. where does the plant get the o2 from? my guess is partly from that from photosynth? does it give off soem into atmosphere, and some into plant??
Thanks!!!
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In STAV 07 MC there was a question about radioactively labelling 02 to see where it goes, and the answer is that the O2 would be present in that given off by photosynthesis,
my question is, for aerobic cellular resp. where does the plant get the o2 from? my guess is partly from that from photosynth? does it give off soem into atmosphere, and some into plant??
Thanks!!!
Yes you're right! It uses some for the plant and some to atmosphre for other organisms to use.
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Thanks!
The answer was though that it would be detected in co2 given off by the plant?
another question: what are positive and negative contorls?
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What would be a suitable definition of Signal transduction?
i have two and i dont know what is more appropriate:
The process by which a cell converts on kind of signal into another
or (off VCAA 07) Signal transduction refers to the series of events that occur after the receipt of a specific signal, which results in a response.
The word specific is what throws me off. :p thanks all!
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that because, the receptors that receive the stimulus is specific to that signal.
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so the second? thanks :) makes sense
Next question! haha
How do sodium/potassium move into neuron? I have written down (from tsfx 2010) that it is via facilitated diffusion, as they go through channels? (charged ions)
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yeah, facilitated diffusion, they use protein channels.
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Thanks :) yeah makes sense now
Ok another one hehe:
TSFX 2010 mc 15
Endorphins are neurotransmitters which reduce the chances of impuleses travelling along pain pathways to the brain. The ultimate effect of endorphins would be to:
Answer is A Hyperpolarise the membrane of the post-synaptic cell..
Could you or someone explain that, hyperpolarise, ?? Is it like a super action potential?
and then takes longer to come back down?
how does it work in reference to the pain pathways aspect?
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What ive got written in my notes:
The K+ ions leaves the cell and bring the potential back to negative there is an overshot of K+ leaving and this makes the potential more negative than usual. (the dip on the grapgh thing after the high peak). This is called Hyperpolarisation
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okeydokey awesome,
so any idea how this would stop pain?
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Can phopholipids have saturated+unsaturated tails?
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Sorry im totally spamming this
how are prions not denatured when superheated? if they are protein?
(TSFX multiple choice, that was answer)
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prions are heat resistant, apparently don't even get denatured or anything in autoclaving
they're just special and hardcore infectious agents like that
+ sidenote: that's why the prion diseases can be transmitted by usage of surgical instruments because prions aren't going to be destroyed by heat
someone correct me if I'm wrong :)
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okeydokey awesome,
so any idea how this would stop pain?
Pain is a nerve signal. To send nerve signals you need to depolarise the membrane to produce an action potential. If your membrane is hyperpolarised then its gone the other way, and its even harder than usual to generate an AP. Thus, less pain
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that makes sense :) thanks
What do cell-mediated and humoral mediated mainly target??
so is humoral mainly extracellular pathogens?
and cell mediated for infected cells? (apcs would come under this part?)
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also, is it only self cells with MHC markers? and the just APC cells have MHC II? Is it suffice to say that it is the antigen of foreign tissue that is identified as non-self?
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also, is it only self cells with MHC markers? and the just APC cells have MHC II? Is it suffice to say that it is the antigen of foreign tissue that is identified as non-self?
All cells except RBC's have MHC 1 marker, immune cells have MHC 2. Yeah the antigen presented by the APC's are identified as nonself
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Ahhk
So if there's a question, how does the body recognise foreign/non-self cells? you'd say, the antigen is detected that does not match the body's self cells ?
and then is engulfed and antigen placed on MHCII marker?
Also:
what are plant defences, specifically the chemical ones?
I know things like waxy-cuticle and thick bark,
but there's nothing in the textbook.
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Ahhk
So if there's a question, how does the body recognise foreign/non-self cells? you'd say, the antigen is detected that does not match the body's self cells ?
and then is engulfed and antigen placed on MHCII marker?
Also:
what are plant defences, specifically the chemical ones?
I know things like waxy-cuticle and thick bark,
but there's nothing in the textbook.
Well macrophages just engulf the foreign pathogen, and then they display an antigen that is foreign onto the MHC 2 marker. T-cells will recognise the antigen on the APC as foreign and will go do the appropriate response
Plant defences
- Produce enzymes that digest pathogenic fungi walls
-Seal off infected areas (or dropping of the leaf if the infected area is there)
-Production of toxic chemicals in response to an insect bite leading to providing a barrier to the entry of foreign pathogen or just deterring the insect from biting more.
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You can use MHC as a self marker as well, it's a major part of what causes transplant rejection. T cells can recognize non self MHC and target it, which results in normal immune activation targeted against the cell with the non self MHC
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ahh you two are awesome!
thanks!!
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Can someone explain the similarities and differences between AIDS and HIV?
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HIV is the virus that causes AIDS, which attacks Th cells and leads to a weakened immune system
thats alll i know, may want to clarify :p
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HIV is a retrovirus (RNA instead of DNA) and therefore also contains reverse transcriptase to convert its DNA to RNA.
It also mutates which is why they can't produce an effective vaccine.
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HIV is a retrovirus (RNA instead of DNA) and therefore also contains reverse transcriptase to convert its DNA to RNA.
It also mutates which is why they can't produce an effective vaccine.
Other way round, be careful not to mix the two up by mistake
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In anaerobic respiration, do animal cells produce Co2?
I know they produce lactic acid
In plants it's ethanol and co2
Plus 2 ATP per glucose
Considering humans Breathe out co2? :p
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no they dont, only lactic acid and the ATP
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Ok thankyou!!
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hey all
so I know B cells chill out in the lymph nodes after maturing in bone marrow,
and T cells Mature in the thymus after developing in bone marrow,
where do T Cells hang out?
In the lymph nodes? or just floating around everywhere?
thanks!
In the nodes
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Thanks!
Ok couple of qns I found:
What cells recognise non-self cells?
Is it cells the macrophages/dendritic cells
In 2nd line,
And t and b cells in third?
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Thanks!
Ok couple of qns I found:
What cells recognise non-self cells?
Is it cells the macrophages/dendritic cells
In 2nd line,
And t and b cells in third?
Recognised by professional APCs - ie macrophages, dendritic cells (and B cells)
T and B cells are primarily in the 3rd line of defense - ie. acquired immunity
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Ok thanks!
So a macrophage will engulf material detected as foreign, and preset this on their MHC, and then trigger action of t/b cells?
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Mainly just activate T cells. CD4 T cells can then activate B cells (to become memory or plasma cells) which can then activate more CD8 T cells. Or, the macrophage can activate the CD8 T cells directly too :)
edit: CD4 T cells = T helper, CD8 T cells = cytotoxic T
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Can someone explain the terms:
fungi, protozoa, vectors, primary host and intermediate host?
Cheers.
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Do we need to know mitosis and meiosis in depth?
(like each stage etc? I haven't done unit 1/2))
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Do we need to know mitosis and meiosis in depth?
(like each stage etc? I haven't done unit 1/2))
Know it well enough to be able to draw it