VCE Biology Question Thread

[darkz]

feedback, how I can improve it to make it better

See the attached image for feedback. If you don't agree with anything, feel free to ask.

[xenx]

Could someone give give me a run down on the steps of both intrinsic and extrinsic pathways of apoptosis and also the stages of apoptosis?
thank you!

[YussifK]

See the attached image for feedback. If you don't agree with anything, feel free to ask.

OMG, this is what kind of feedback i wanted so my marks would improve..
This is the best birthday wish that came true.. (birthday October The 13th Sunday)

I completely agree with everything you have commented on my piece

[Chocolatemilkshake]

Could someone give give me a run down on the steps of both intrinsic and extrinsic pathways of apoptosis and also the stages of apoptosis?
thank you!

Here is my attempt...

INTRINSIC PATHWAY
1. Sensors recognise that the cell is under stress, causing the mitochondria to release Cytochrome C.
2. Cytochrome C forms aggregates with other compounds activating a caspase cascade, driving apoptosis.

EXTRINSIC PATHWAY
1. A death ligand in the extracellular environment binds to a death receptor on the cell surface.
2. Binding activates receptors which cleave caspases, leading to a caspase cascade, thus driving apoptosis.

STAGES OF APOPTOSIS
1. mRNA begins to decay, chromatin condenses and DNA fragments.
2. Caspases cleave cytoskeleton as well as other proteins in the cytoplasm & nucleus.
3. Cell blebs forming apopotic bodies

[Evolio]

Hi guys!
I just had a few questions I wanted to ask.

1. Explain how increasing body temperature can assist in the inflammatory response
 
I wrote: Increasing the temperature allows increased permeability of the capillaries, allowing the phagocytes to easily enter the site of infection.
I wasn't really sure about this question when answering it, so I sort of just gave it my best shot. I was wondering if this answer was valid and if my point was correct?

2. What is meant by the term immunodeficiency disease? The question stem talked about HIV and AIDS.

I wrote: There is an insufficient amount of immune cells, in this case, it is T helper cells where they are targeted and destroyed.

3. Describe the role of coenzymes in an enzymatic reaction

I wrote: A coenzyme speeds up the rate of enzymatic reactions
It provides energy for the reaction.
Is this correct?

[PhoenixxFire]

Here is my attempt...

INTRINSIC PATHWAY
1. Sensors recognise that the cell is under stress, causing the mitochondria to release Cytochrome C.  In a question, it'd probably be better to phrase this as "mitochondria releases Cytochrome C due to..." if they give you a reason in the stem, or as "damage to mitochondria results in the release of cytochrome C"
2. Cytochrome C forms aggregates with other compounds activating a caspase cascade, driving apoptosis.

EXTRINSIC PATHWAY
1. A death ligand in the extracellular environment binds to a death receptor on the cell surface.
2. Binding activates receptors (secondary messengers) which cleave caspases, leading to a caspase cascade, thus driving apoptosis.

STAGES OF APOPTOSIS
1. mRNA begins to decay, chromatin condenses and DNA fragments.
2. Caspases cleave cytoskeleton as well as other proteins in the cytoplasm & nucleus.
3. Cell blebs forming apopotic bodies

Your stages of apoptosis are correct, but VCAA has a few more of them - this is from the 2016 exam, from the way the suggested answers were phrased I don't think you would have had to mention all of them.

• enzymes; for example, caspases are activated within the cell
• digestion of cell contents (this is the cleaving of the cytoskeleton part)
• cell shrinkage
• cell blebbing
• cell breaks up
• cell signals macrophages

Also very important to note that VCAA does not consider macrophages engulfing the fragments of the cell after blebbing to be part of apoptosis, and you'll lose marks if you write about it.

Hi guys!
I just had a few questions I wanted to ask.

1. Explain how increasing body temperature can assist in the inflammatory response
 
I wrote: Increasing the temperature allows increased permeability of the capillaries, allowing the phagocytes to easily enter the site of infection.
I wasn't really sure about this question when answering it, so I sort of just gave it my best shot. I was wondering if this answer was valid and if my point was correct?

Local warmth is a side effect of the increased blood flow caused by vasodilation, not a cause of it. Increasing body temperature as a whole, not locally, is fever, which can help leukocytes do their thing (higher temp = increased function until it gets too hot) and can inhibit some pathogens as it's common for them to have a lower optimal temp than immune cells.

2. What is meant by the term immunodeficiency disease? The question stem talked about HIV and AIDS.

I wrote: There is an insufficient amount of immune cells, in this case, it is T helper cells where they are targeted and destroyed.

Immunodeficiency isn't about the number of cells, it's about how the immune system functions. An immonodeficiency disease causes the immune system to not work properly - HIV is an immunodeficiency disease because it infecting and killing T helper cells means that the immune system can't activate either of the humoral or cell mediated immune responses properly.

3. Describe the role of coenzymes in an enzymatic reaction

I wrote: A coenzyme speeds up the rate of enzymatic reactions
It provides energy for the reaction.
Is this correct?

How many marks was this out of? If it's one mark, I'd just stick with the first part. ATP isn't the only coenzyme, however it's the only molecule that you're really taught provides energy (other molecules can also provide energy but that doesn't come up in vce).

[Evolio]

How many marks was this out of? If it's one mark, I'd just stick with the first part. ATP isn't the only coenzyme, however it's the only molecule that you're really taught provides energy (other molecules can also provide energy but that doesn't come up in vce).

This was 2 marks.

Thank you for your help!
 

[darkz]

This was 2 marks.
Thank you for your help!
 

While your response was okay, for a two marker you'll want to be slightly more detailed. Here's what I would've written:
In enzymatic reactions, coenzymes assist the binding of the substrate with the active site [by increasing the affinity of the active site for the substrate], thereby leading to both the activation of the enzyme and an increase in reaction rate.
[ ] denotes what you could probably do without.

[Evolio]

While your response was okay, for a two marker you'll want to be slightly more detailed. Here's what I would've written:
In enzymatic reactions, coenzymes assist the binding of the substrate with the active site [by increasing the affinity of the active site for the substrate], thereby leading to both the activation of the enzyme and an increase in reaction rate.
[ ] denotes what you could probably do without.

Cool, thank you, darkz!
I was wondering how the coenzyme increases the affinity of the active site of the substrate?
Also, did you do all the VCAA biology exams, from 2002 all the way until 2017?

[BitcoinEagle]

Cool, thank you, darkz!
I was wondering how the coenzyme increases the affinity of the active site of the substrate?
Also, did you do all the VCAA biology exams, from 2002 all the way until 2017?

So, from what I know, a coenzyme has a shape that when used together with a substrate allows the combination to bind better to the active site of an enzyme.
I have some questions of my own actually:
1. What is the idea/theory of monoclonal antibodies and to what extent do we need to discuss these?
2. To what extent are the lymphatic system knowledge needed. (ie what do we need to know about it)
3. What do we need to know about dates that groups of species emerged in geological history? Like specific dates or orders or...
Thanks guys!

Mod edit (PF): Merged post. Please edit your post rather than posting twice in quick succession

[Erutepa]

I have some questions of my own actually:
1. What is the idea/theory of monoclonal antibodies and to what extent do we need to discuss these?
2. To what extent are the lymphatic system knowledge needed. (ie what do we need to know about it)
3. What do we need to know about dates that groups of species emerged in geological history? Like specific dates or orders or...
Thanks guys!

The study design states that you need to know about monoclonal antibodies interms of treating cancer.
For this you should know how they are synthesised:
1. extract a plasma B cell that produces antibodies specific to your target antigen
2. Fuse this plasma B cells with a tumour cell, producing a hybridoma. This is done because plasma cells have a finite lifespan and thus cannot be harnessed to produce large quantities of an antibody. These hybridoma cells, however, produce the specific desired antibody essentially indefinitely.
3. Monoclonal antibodies are produced and extracted to be used as a therapeutic.

Ways in which these monoclonal antibodies may be used against cancer include
1. To deliver a cytotoxic compound to cancer-specific antigens, thus killing the cells
2. Stimulating the action of immune cells to destroy the cancer cells
3. Bind to and block receptors that may, for example, prevent the cancer cells from receiving grown signals, thus inhibiting the proliferation of the cancer.

In regards to the lymphatic system you should be able to explain:
1. where in the lymphatic system B and T cell are produced and where they mature
2. Its role to circulate APCs and antigens
3. The role of secondary lymphoid tissue (emphasis on lymph nodes) as the site of antigen recognition of these antigens by lymphocytes (th cells)

In regards to major dates of evolution, I personally just memorised a fairly basic timeline of what evolved when (not specific dates but rather eras) however I am not sure about to what extent you can be examined.

While your response was okay, for a two marker you'll want to be slightly more detailed. Here's what I would've written:
In enzymatic reactions, coenzymes assist the binding of the substrate with the active site [by increasing the affinity of the active site for the substrate], thereby leading to both the activation of the enzyme and an increase in reaction rate.
[ ] denotes what you could probably do without.

While I have found some research on coenzymes altering the stability of an enzyme in a range of temperatures, I haven't really been able to find any resource mentioning the role of coenzymes to increase binding affinity as such.
I have found resources stating that coenzymes are small non-protein organic molecules that bind to the active site of an enzyme and function to enable its catalytic action, potentially doing this through the transfer of electrons or energy and, in doing so, are cycled between loaded and unloaded forms.

[BitcoinEagle]

The study design states that you need to know about monoclonal antibodies interms of treating cancer.
For this you should know how they are synthesised:
1. extract a plasma B cell that produces antibodies specific to your target antigen
2. Fuse this plasma B cells with a tumour cell, producing a hybridoma. This is done because plasma cells have a finite lifespan and thus cannot be harnessed to produce large quantities of an antibody. These hybridoma cells, however, produce the specific desired antibody essentially indefinitely.
3. Monoclonal antibodies are produced and extracted to be used as a therapeutic.

Ways in which these monoclonal antibodies may be used against cancer include
1. To deliver a cytotoxic compound to cancer-specific antigens, thus killing the cells
2. Stimulating the action of immune cells to destroy the cancer cells
3. Bind to and block receptors that may, for example, prevent the cancer cells from receiving grown signals, thus inhibiting the proliferation of the cancer.

In regards to the lymphatic system you should be able to explain:
1. where in the lymphatic system B and T cell are produced and where they mature
2. Its role to circulate APCs and antigens
3. The role of secondary lymphoid tissue (emphasis on lymph nodes) as the site of antigen recognition of these antigens by lymphocytes (th cells)

In regards to major dates of evolution, I personally just memorised a fairly basic timeline of what evolved when (not specific dates but rather eras) however I am not sure about to what extent you can be examined.
While I have found some research on coenzymes altering the stability of an enzyme in a range of temperatures, I haven't really been able to find any resource mentioning the role of coenzymes to increase binding affinity as such.
I have found resources stating that coenzymes are small non-protein organic molecules that bind to the active site of an enzyme and function to enable its catalytic action, potentially doing this through the transfer of electrons or energy and, in doing so, are cycled between loaded and unloaded forms.

Thanks so much, the detail helped a lot!
If you don't mind me asking, what were those general events for the timeline?

[caqiu]

does the activation of cytotoxic T cells include binding to APCs and T helper cells releasing cytokines or can it be that it binds the infected cells and T helper cells release cytokines.

Is this definition correct?
- APCs engulf pathogen and place the foreign antigens on its MHC-1 and 2 marker.
- Cytotoxic T cells binds to corresponding antigen on the MHC-1 marker using their T cell receptor
- Cytokines are secreted by activated T helper cells that actives the cytotoxic T cell and cause it to differentiate and proliferate into active cytotoxic cells and memory cytotoxic T cells.
-The active cytotoxic T cells travels around the bodies and recognise specific antigen presented on the MHC -1 makers of infected cells
- When it bind to the antigen, it recognise it as foreign and secretes granzymes and perforins that rupture the plasma membrane causing it lysis and die.
 

[IThinkIFailed]

does the activation of cytotoxic T cells include binding to APCs and T helper cells releasing cytokines or can it be that it binds the infected cells and T helper cells release cytokines.

Is this definition correct?
- APCs engulf pathogen and place the foreign antigens on its MHC-1 and 2 marker.
- Cytotoxic T cells binds to corresponding antigen on the MHC-1 marker using their T cell receptor
- Cytokines are secreted by activated T helper cells that actives the cytotoxic T cell and cause it to differentiate and proliferate into active cytotoxic cells and memory cytotoxic T cells.
-The active cytotoxic T cells travels around the bodies and recognise specific antigen presented on the MHC -1 makers of infected cells
- When it bind to the antigen, it recognise it as foreign and secretes granzymes and perforins that rupture the plasma membrane causing it lysis and die.

For your first question, I reckon either can happen, but I think the lymph node response is the safest one to go with in an exam, where a naive T-Helper cell has an antigen presented to it, such that it undergoes clonal expansion into effector T helper cells and memory cells, releasing cytokines to activate specific Tc cells which seek out infected self cells presenting the specific antigen upon their MHC 1 markers

For your “definition”, correct me if this is wrong, but I learnt that APCs present the antigen on their MHC 2 markers?

Also, Tc cell’s stimulate apoptosis within their target self cells, not lysis. Lysis and apoptosis are different.

[caqiu]

For your first question, I reckon either can happen, but I think the lymph node response is the safest one to go with in an exam, where a naive T-Helper cell has an antigen presented to it, such that it undergoes clonal expansion into effector T helper cells and memory cells, releasing cytokines to activate specific Tc cells which seek out infected self cells presenting the specific antigen upon their MHC 1 markers

For your “definition”, correct me if this is wrong, but I learnt that APCs present the antigen on their MHC 2 markers?

Also, Tc cell’s stimulate apoptosis within their target self cells, not lysis. Lysis and apoptosis are different.

Thank you!
I just notice infected cells can't travel to the lymph nodes. Yep, APC place them on both markers but cytotoxic T cells bind to MHC-1 makers.

But does this mean could the cytototic cells react against the APC since it is also displaying a foreign marker?