VCE Biology Question Thread

[GodNifty]

- Does clonal expansion mean all progenies are the same, or all progenies have the same antigen specificity, and can be of any type (like plasma cell and memory cell)
- In humoral response, when one Helper T cell is selected and clonal expands, can they differentiate into Memory T cells or just more Helper T Cells?
- Are second line defense leukocytes involved in the cell mediated or just normal cells?
- Do Cytotoxic T cells act as death ligands or do they secrete molecules (like cytokines) as death ligands?

Thanks all

[PhoenixxFire]

- Does clonal expansion mean all progenies are the same, or all progenies have the same antigen specificity, and can be of any type (like plasma cell and memory cell)

Same antigen specificity

- In humoral response, when one Helper T cell is selected and clonal expands, can they differentiate into Memory T cells or just more Helper T Cells?

Both. There's probably a more scientific name for each of the types, but some of the Th cells will fight the current infection, and some will be memory cells.

- Are second line defense leukocytes involved in the cell mediated or just normal cells?

Which leukocytes do you mean? (leukocyte is a very broad term and includes everything from neutrophils and basophils to B and T cells). If you're referring to phagocytes they'll eat the apoptotic fragments formed as a result of cell-mediated immunity, but that's it.

- Do Cytotoxic T cells act as death ligands or do they secrete molecules (like cytokines) as death ligands?

Thanks all

Cytotoxic T cells release perforin (a protein that can make holes in membranes), and granzymes (an enzyme that enters the cell and activates caspases, inducing apoptosis).

[Zacm]

How can I access the 2019 unit 1 neap exam answers?

[jack.cameron]

Does anybody have any u3 aos 2 practise sacs or any online practise questions. I've done all my schools practise sacs and every other resource I've bought or have been given. cheers

[PhoenixxFire]

Does anybody have any u3 aos 2 practise sacs or any online practise questions. I've done all my schools practise sacs and every other resource I've bought or have been given. cheers

There's some practice questions I wrote a couple of years ago here, but they're not really the sorts of questions you'll get on SACs, so probably not very helpful outside of checking you haven't missed any content.

From the sounds of things you've already done quite a lot of practice questions - if so, it'll probably be more useful to go back and redo the ones you didn't get full marks on, there's no point doing copious amounts of questions if they're not helping you improve your answers.

[jack.cameron]

There's some practice questions I wrote a couple of years ago here, but they're not really the sorts of questions you'll get on SACs, so probably not very helpful outside of checking you haven't missed any content.

From the sounds of things you've already done quite a lot of practice questions - if so, it'll probably be more useful to go back and redo the ones you didn't get full marks on, there's no point doing copious amounts of questions if they're not helping you improve your answers.

I'm getting full marks on practically everything I do, it's more just I'm trying to expose myself to as many variations of questions so on the day I don't get confused by any questions. Thank you for the resource though

[Evolio]

Hello guys.
I just wanted someone to check my response to this question and give me any constructive feedback. It is worth 2 marks.

Describe how hydrophilic hormones, such as glucagon, stimulate a metabolic process, such as glycogenolysis, inside a cell
Response:
Hydrophilic hormones(signalling molecules) such as glucagon bind to a cell surface receptor. Then second messengers are produced, causing a chain of relay molecules to be produced. The signal is amplified until it reaches the nucleus of the cell, where the chemical message is received. Then genes can be expressed to allow for a metabolic process, such as glycogenolysis to occur inside the cell.

Are second messengers produced, activated or stimulated?

[FrankieDens]

Hey everyone!

If any of you have the time can you please answer some of my 'confusions'? (hehe Kansas vs Arkansas):

• Where are complement proteins produced and how is it activated?
• What is the purpose of complement proteins?
• What are the steps of monoclonal antibody production?
• Does anyone have a good definition for herd immunity?
• Why are booster shots needed?
• (Exam 1, 2013) VCAA stated that booster shots are needed to produce more memory cells because they are short-lived... but I thought memory cells are produced for long-term memory?
  

Thank you! 

[DBA-144]

Hey everyone!

If any of you have the time can you please answer some of my 'confusions'? (hehe Kansas vs Arkansas):

• Where are complement proteins produced and how is it activated?
• What is the purpose of complement proteins?
• What are the steps of monoclonal antibody production?
• Does anyone have a good definition for herd immunity?
• Why are booster shots needed?
• (Exam 1, 2013) VCAA stated that booster shots are needed to produce more memory cells because they are short-lived... but I thought memory cells are produced for long-term memory?
  

Thank you! 

All proteins are produced at a ribosome, complement proteins produced in the liver specifically. Purpose is just to adhere to any non self antigen (they're non specific) and will lyse bacterial cells, opsonise antigens/pathogens and are involved in the clearance of antigen antibody complexes.

Imo steps of the production of monoclonal antibodies is not needed for the course, only the uses.

Hello guys.
I just wanted someone to check my response to this question and give me any constructive feedback. It is worth 2 marks.

Describe how hydrophilic hormones, such as glucagon, stimulate a metabolic process, such as glycogenolysis, inside a cell
Response:
Hydrophilic hormones(signalling molecules) such as glucagon bind to a cell surface receptor. Then second messengers are produced, causing a chain of relay molecules to be produced. The signal is amplified until it reaches the nucleus of the cell, where the chemical message is received. Then genes can be expressed to allow for a metabolic process, such as glycogenolysis to occur inside the cell.

Are second messengers produced, activated or stimulated?

Second messengers are activated. Look at a diagram of signal transduction and note that the reception of the ligand by its specific protein receptor on the taget cell's surface induces a conformational change in the receptor. This shape change is what leads to the activation of second messengers. THese are present in inactive forms in the cell. I suspect there will be cases were these are produced, but this isn't really required info.

There might be cases where a second messenger activates a molecule which then splits into 2 parts, one of which is used later in the pathway, for example. Again, this is not required knowledge.

Your response is ok. Perhaps you might like to say that the cell responds by >>>sythesising proteins that allow... to occur<<<. This is not essential, from what I have seen, but it might be something you want to include.

[jack.cameron]

does anyone have a definition for natural immunity only (not tagged on with active or passive) that doesn't involve the word natural or naturally. cheers xx

[kjistsehrtot]

perhaps someone's already answered this but there are so many pages on this forum so im just gonna ask anyway haha:

"How do blood glucose levels regulate when the levels are too high/low?"

does anyone have a definition for natural immunity only (not tagged on with active or passive) that doesn't involve the word natural or naturally. cheers xx

when a human is exposed to a live pathogen and develops that disease and if they become immune afterwards (primary immune response), this would classify as natural immunity

very simple definition: occurs when exposed to live pathogen, develops disease, and becomes immune as a result of the primary immune response

i honestly dont know if this helped and i had to google this to make sure i was right https://courses.lumenlearning.com/boundless-microbiology/chapter/classifying-immunities/

Mod edit: I've merged your posts. If you need to add new information, rathe than posting again right after, please click the 'modify' button, which you can find next to the quote button

[caffinatedloz]

Hello! As you probably know it's a form of negative feedback where the body is working to maintain homeostasis by reversing the direction of the change.

For high blood glucose:
High blood glucose levels will be detected by receptors in the pancreas.
They will release insulin which will target the liver.
Consequently, more glucose in the blood will be converted to it's stored form, glycogen.
Blood glucose levels will return to normal and homeostasis is maintained.

For low blood glucose:
Low blood glucose levels will be detected by receptors in the pancreas.
They will release glucagon which will target the liver.
This stimulates the conversion of more glycogen to glucose.
The blood glucose levels return to normal.

Hope this helps!!

[caffinatedloz]

Hi guys!
Does anyone know what the control centre in negative feedback is and have examples from how this is different from the receptors/effectors in osmoregulation, thermoregulation and the regulation of blood glucose levels.

Thank you!!

[Erutepa]

does anyone have a definition for natural immunity only (not tagged on with active or passive) that doesn't involve the word natural or naturally. cheers xx

I wouldn't think you'll ever have to define natural immunity by itself - it'll always be either natural passive, or natural active immunity.
Defining natural immunity itself is a bit hard, but it will be either immunity obtained through regular exposure to the live pathogen and subsequent activation of the adaptive immune response, or through the acquisition of antibodies from a mother as a fetus and newborn.

when a human is exposed to a live pathogen and develops that disease and if they become immune afterwards (primary immune response), this would classify as natural immunity

very simple definition: occurs when exposed to live pathogen, develops disease, and becomes immune as a result of the primary immune response

I don't think this definition is quite right for natural immunity in general, remembering that as stated above, natural immunity can be passive where the individual simply receives antibodies from the mother and is not necessarily exposed to the pathogen itself. This definition is, of course, correct for natural active immunity though.

[gary123]

Couple of questions for immunity:
Would I be correct in saying dendritic cells process antigenic material and display their antigens on their MHC 2 markers for T helper cells to recognise, thus providing a link to the adaptive immune response. Is it specifically targeting T helper cells or other leukocytes as well?

Am I right in saying MHC 1 markers displays antigens produced by the presenting cell whereas MHC 2 markers displays nonself antigens outside the presenting cell?

How would one describe how a person produces more antibodies during secondary exposure to specific antigen than the first exposure (basically how would I explain memory B cells and how they develop immunological memory - just looking for a more concise explanation than the one I have)

How specifically does inflammation response benefit the immune response? Do I just need to say it attracts phagocytes and large molecules to site of infection helping develop a rapid innate response via physiological changes
MHC 1 and 2 markers are all proteins, all antibodies are proteins, not all antigens are proteins, all MHC 2 markers are made of antibodies - is my understanding correct?

Why would a vaccine that contains the pathogen in an inactivated form be less effective than one where it is in an weakened form? I'd assume because since its dead it elicits a weaker adaptive immune response and weaker immunological memory but need someone to expand on this please

In multiple sclerosis, the B and T cells are involved in targeting the myelin sheathe of neurons as a result of failure of self-tolerance. Is it also due to mitochondria in oligodendrocytes breaking down that leads to destruction of myelin sheathe? If the second part is true do I have to mention this?(just feels like its out of the study design and not required)

How much do we need to know about types of pathogens such as prions and worms, I know their names but what features should I know about them?

Are T helper cells activated by antigen presenting cells specifically macrophages and dendritic cells or can they be activated by cells that display nonself antigens on their MHC 1 markers?
Thanks in advance