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Author Topic: VCE Biology Question Thread  (Read 3570837 times)  Share 

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vox nihili

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Re: VCE Biology Question Thread
« Reply #11730 on: June 04, 2019, 11:47:08 pm »
+2
Ooo just quickly
difference between antibodies and complement proteins. I feel like they do pretty much the same thing except antibodies are specific and that antibodies also trigger  complement proteins. Someone explain pls <3

You're literally basically on the money. They have slightly different roles too, which you don't need to understand in VCE biology. Complement is innate, antibodies adaptive. That's really it.
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PhoenixxFire

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Re: VCE Biology Question Thread
« Reply #11731 on: June 04, 2019, 11:49:40 pm »
+2
Got ma Bio SAC on thursday gonna ask a shit ton of questions.
When talking about humoural response, what're the main points to go through?
Need to mention that the antigen is extracellular
-macrophage presents antigen on MHC II markers
The B cell does not bind to the antigen present on MHC2. The B cell binds to a free antigen, the T helper cell binds to the antigen on MHC2
-Naive B cell binds to antigen(sketchy I have no idea about how to shorten: macrophages are looking for a matching a naive B cell that matches with antigen structure) If the B cell can bind then its implied that it matched the antigen. If you want to be clear you can say that a B cell with a complementary shape binds to it.
-B cell proliferates and differentiates into plasma B cells and memory B cells
-Plasma B cells produce antibodies while memory B cells stay behind for secondary immune response remain in the body to defend against subsequent infection by a pathogen with the same antigen specificity.
-Antibodies cause: agglutination, neutralization, precipitation, cell lysis Complement proteins can cause lysis, antibodies do not
Should I include part about helper T cells deciding whether or not B cells can proliferate or not? Yes
In case I just made that a bit confusing, here's what I wrote in my notes. I essentially just repeated this in all my answers and adapted it a bit to whatever scenario was presented.
Spoiler
-A naïve B cell will bind to a free antigen.
-A Th cell will be presented with its antigen on a MHC2 molecule by a macrophage.
-The ‘selected’ B cell and Th cell will then find each other and if they have bound the same antigen, the Th cell will release cytokines.
-These cytokines cause the B cell to divide and differentiate into B memory cells and B plasma cells.
-These cytokines also cause the Th cell to divide and differentiate into Th memory cells and Th cells.
-The memory cells remain in the body to fight subsequent infection by a pathogen with the same antigen specificity and the B plasma and Th  cells fight off the current infection.

Neurotransmitters:
How tf do their ion channels work. Like I get the bit where theres a chemical imbalance between inside and outside of the cell membrane. But how is that stuff an electrical impulse.
Haven't got a clue. You don't need to know this anymore (it was in the old study design).

Signal transduction:
Hydrophillic signalling molecules: whatre the main points to mention when talking about hydrophillic signalling molecules?
-ligand binds to receptor on the surface say extracellular surface or outside of the cell membrane.
-ligand forms signalling molecule-receptor complex no need to include this line
-receptor changes shapes causing a cascade of events leading to release of secondary messengers
-Secondary messengers amplify the signal throughout the cell causing cellular response
Also other interesting question I have:
Is there any advantage between hydrophobic or hydrophillic signalling molecule? Do hydrophobic molecules cause a more long lasting response(since transcription is affected) than hydrophillic signalling molecules.
Neither is better than the other, they have different roles. Hydrophobic molecules tend to act as transcription factors. Hydrophobic last longer, but I don't know why and you don't need to either.

I know a lot of my points are sorta wrong, sorta wrong order, sorta non sense and all of you are pretty little angels but srly dont hold back. If I got an idea completely backwards, let me have it. Be sure to tell about how my non sense insulted the very core understanding of biology. :P Aight im off to sleep
Pretty sure I managed to make sense of it :p but please say something if any of my comments don't make sense.
« Last Edit: June 04, 2019, 11:51:43 pm by PhoenixxFire »
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vox nihili

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Re: VCE Biology Question Thread
« Reply #11732 on: June 04, 2019, 11:51:18 pm »
+6
In case I just made that a bit confusing, here's what I wrote in my notes. I essentially just repeated this in all my answers and adapted it a bit to whatever scenario was presented.
Spoiler
-A naïve B cell will bind to a free antigen.
-A Th cell will be presented with its antigen on a MHC2 molecule by a macrophage.
-The ‘selected’ B cell and Th cell will then find each other and if they have bound the same antigen, the Th cell will release cytokines.
-These cytokines cause the B cell to divide and differentiate into B memory cells and B plasma cells.
-These cytokines also cause the Th cell to divide and differentiate into Th memory cells and Th cells.
-The memory cells remain in the body to fight subsequent infection by a pathogen with the same antigen specificity and the B plasma and Th  cells fight off the current infection.
Haven't got a clue. You don't need to know this anymore (it was in the old study design).
Neither is better than the other, they have different roles. Hydrophobic molecules tend to act as transcription factors. Hydrophobic last longer, but I don't know why and you don't need to either.
Pretty sure I managed to make sense of it :p but please say something if any of my comments don't make sense.

Extra points to you for knowing the difference between complementary and complimentary. This was a compliment from me that complements your post well.
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Comet striker

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Re: VCE Biology Question Thread
« Reply #11733 on: June 05, 2019, 07:39:59 pm »
0
Thank you both for this. I'd appreciate if you can keep giving me more help ;-;

Starting with inflammatory response heres what I have got:
-First line of defence(eg: intact skin) is breached.
-Damaged mast cells release histamine
-Histamine causes blood vessel's to dilate causing vassodilation and inflammation
-Neutrophils are white blood cells found all over the body are attracted to the inflammatory site.
-Neutrophils engulf pathogens and release cytokines that attract Macrophages
-Macrophages also engulf bacteria through phagocytosis and present antigens on their MHC II markers. (not needed?)
- Inflammatory response continues until pathogen dies

Do I need to mention:
-Interleukins(I think?) raising body temperarure
-Dead plasma cells used to cover up(clot?) site of infection to prevent entry to more pathogens
Is this detail good/bad? what more do I need to say? Do I need to cut off some stuff? Whatre the specific words when describing it.
edit: while we are at the topic: what is the body's strat with heating up everything. Is it heat normalling outside of the pathogen's tolerance zone so it's proteins degrade while body cells can hold on?
« Last Edit: June 05, 2019, 08:00:09 pm by Comet striker »
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PhoenixxFire

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Re: VCE Biology Question Thread
« Reply #11734 on: June 05, 2019, 09:49:07 pm »
+2
You've gone a bit too far into the immune response here - If the question is just about the inflammatory response then I'd stop at the point about phagocytes eating the pathogens.
Thank you both for this. I'd appreciate if you can keep giving me more help ;-;

Starting with inflammatory response heres what I have got:
-First line of defence(eg: intact skin) is breached. correct, but not really necessary, I would just skip this line
-Damaged mast cells release histamine
-Histamine causes blood vessel's to dilate causing vassodilation Blood vessels dilating is called vasodilation - you've repeated yourself here and increased permeability inflammation Just saying inflammation isn't specific enough to really answer this.
This increased permeability and dilation of blood vessels increases local blood supply, leading to localised heat, redness, and swelling.
-Neutrophils are white blood cells found all over the body are attracted to the inflammatory site. The first half of this sentence is unnecessary - you can assume your teacher knows what neutrophils are. You need to link the presence of the neutrophils to the vasodilation - increased blood flow and permeability assists their migration to the area
-Neutrophils engulf and destroy pathogens and that's where you stop (assuming the question is just asking about the inflammatory response)
and release cytokines that attract Macrophages
-Macrophages also engulf bacteria through phagocytosis and present antigens on their MHC II markers. (not needed?)
- Inflammatory response continues until pathogen dies

Do I need to mention:
-Interleukins(I think?) raising body temperarure
-Dead plasma cells used to cover up(clot?) site of infection to prevent entry to more pathogens
Is this detail good/bad? what more do I need to say? Do I need to cut off some stuff? Whatre the specific words when describing it.
Don't need to talk about either of those first two points, think I butchered your answer above enough to answer the rest of them

edit: while we are at the topic: what is the body's strat with heating up everything. Is it heat normalling outside of the pathogen's tolerance zone so it's proteins degrade while body cells can hold on?
I don't know heaps about how this works exactly, but yeah that's the idea, I'd imagine it doesn't denature the proteins - to do that would probably cause a bit too much damage to our own cells, but if you remember what the effectiveness of proteins against temperature graph looks like, it's a really steep dropoff at high temperatures, so even a small increase in temperature will hinder the ability of that pathogen to carry out cellular functions and reproduce.
« Last Edit: June 05, 2019, 09:50:54 pm by PhoenixxFire »
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Comet striker

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Re: VCE Biology Question Thread
« Reply #11735 on: June 05, 2019, 10:21:37 pm »
0
Thnx Im feeling ready for the test but I still want to keep asking questions right before the SAC <3 r
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GodNifty

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Re: VCE Biology Question Thread
« Reply #11736 on: June 09, 2019, 02:06:15 pm »
0
Help please!

1. Describe the features of a target cell that makes it receptive to a particular signalling molecule
2. How do secondary messengers and G-Proteins affect signal transduction within the cell?
3. Insulin is a hydrophilic signalling molecule. It creates secondary messenger Tyroxin kinase. How does this protein amplify the response within the cell by initiating phosphorylation of protein?
4. What is the difference between antigen and immunogen (so confusing...)

Cheers everyone

PhoenixxFire

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Re: VCE Biology Question Thread
« Reply #11737 on: June 09, 2019, 02:16:52 pm »
+2
Help please!

1. Describe the features of a target cell that makes it receptive to a particular signalling molecule
2. How do secondary messengers and G-Proteins affect signal transduction within the cell?
3. Insulin is a hydrophilic signalling molecule. It creates secondary messenger Tyroxin kinase. How does this protein amplify the response within the cell by initiating phosphorylation of protein?
4. What is the difference between antigen and immunogen (so confusing...)

Cheers everyone
Hey!
What specifically about these questions are you struggling with? Us answering them for you won't really help you unless we know what you already know about the topic and where you're stuck.
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GodNifty

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Re: VCE Biology Question Thread
« Reply #11738 on: June 09, 2019, 02:20:14 pm »
0
Hey!
What specifically about these questions are you struggling with? Us answering them for you won't really help you unless we know what you already know about the topic and where you're stuck.
The questions are a bit iffy to understand 

Matthew_Whelan

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Re: VCE Biology Question Thread
« Reply #11739 on: June 09, 2019, 03:08:01 pm »
+1
Help please!

1. Describe the features of a target cell that makes it receptive to a particular signalling molecule
2. How do secondary messengers and G-Proteins affect signal transduction within the cell?
3. Insulin is a hydrophilic signalling molecule. It creates secondary messenger Tyroxin kinase. How does this protein amplify the response within the cell by initiating phosphorylation of protein?
4. What is the difference between antigen and immunogen (so confusing...)

Cheers everyone
Hey it might be good to know that specific details of the G-protein and secondary messenger pathways are not necessary according to the study design.
1. The necessary information to know is that signalling molecules (like most you study) are specific,hence the molecule must have the complementary structure to bind to the target cell's receptors.
3. I'd simply state that because insulin is hydrophilic, it cannot pass through the semi-permeable cell membrane (phospholipid bilayer), so the insulin receptors are on the membrane. When the ligand binds to the extracellular recpetor, it triggers a cascade of reactions (don't have to know reactions) which amplifies the response(usually to open ion channels ect).
4. Immunogens are antigens that elicit an immune response within an organism's immune system. Antigens aren't necessarily immunogens though, they are molecules (protein) that can bind to a product of an immune response (antibody).

I think the fourth question is a bit irrelevant as the difference is very little, and the second and third questions are not really within the range of the study design, although I'm not really sure.

I hope this correctly answers your queries, also if I made a mistake then pls point it out  ;D
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DBA-144

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Re: VCE Biology Question Thread
« Reply #11740 on: June 09, 2019, 03:18:53 pm »
+5
Help please!

1. Describe the features of a target cell that makes it receptive to a particular signalling molecule
2. How do secondary messengers and G-Proteins affect signal transduction within the cell?
3. Insulin is a hydrophilic signalling molecule. It creates secondary messenger Tyroxin kinase. How does this protein amplify the response within the cell by initiating phosphorylation of protein?
4. What is the difference between antigen and immunogen (so confusing...)

Cheers everyone


Some of these are quite irrelevant to the course, to be honest.

1. To be able to respond to a signalling molecule, a cell has to have the specific receptor.
2. These molecules amplify the signal throughout the signal, via the signal cascade.
3. By phosphorylating the protein, the second messenger Tyroxin Kinase is amplifying the signal by activating other second messengers, which then activate other second messengers, via the signal cascade mechanism.
4. Don't need this for VCE, I think. Antigens are any chemical markers that are either self or non self and can initiate an immune response. Immunogens are molecules of the immune system's cells. 

Edit: Might also be worth noting that antigens are not simply proteins and that they are not simply going to be those molecules that can bind to the products of the immune system. For example, consider the nucleic acid of viruses. These won't really be binding to the products of the immune system, from what I know. However, I am not really so sure what a good definition of the word antigen would be. Matthew_Whelan's is otherwise pretty good! :)
« Last Edit: June 09, 2019, 03:24:38 pm by DBA-144 »
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Re: VCE Biology Question Thread
« Reply #11741 on: June 10, 2019, 01:49:28 pm »
+1
Would someone be able to please check these notes on transcription? I've had conflicting comments (specifically about RNA polymerase and transcription factors) so I'm not really sure what's correct anymore.

---

template strand - strand that gets copied - 3' TO 5' DIRECTION
coding strand - copy of the template strand - 5' TO 3' DIRECTION

promoter region - region at beginning of DNA strand where transcription starts
RNA polymerase - the enzyme that produces pre-mRNA by copying a strand of DNA
transcription factors - DNA binding proteins that affect the extent of transcription

exons - parts of pre-mRNA that are joined together to form mRNA and do get translated
introns - sections of pre-mRNA that are removed during splicing

free ribonucleotides - nucleotides that haven't been used to make RNA yet

   1. Transcription factors bind to promotor region of the gene and the strand of DNA unzips (template strand)

   2. RNA polymerase copies this gene (the DNA template strand) by joining complementary nucleotides thereby producing a coding strand of pre-mRNA. It stops at the terminator.

   3. The pre-mRNA undergoes post-transcriptional modifications to become mRNA:
      a. splicing - introns are removed and stay in the nucleus while the remaining exons recombine in a specific order
      b. poly-A tail attached to 3 prime end (aka 3')
         poly-A tail protects from enzyme damage while in cytosol
      c. methyl cap attached to 5 prime end (aka 5')

---

Thank you!

vox nihili

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Re: VCE Biology Question Thread
« Reply #11742 on: June 10, 2019, 01:56:17 pm »
0
Would someone be able to please check these notes on transcription? I've had conflicting comments (specifically about RNA polymerase and transcription factors) so I'm not really sure what's correct anymore.

---

template strand - strand that gets copied - 3' TO 5' DIRECTION
coding strand - copy of the template strand - 5' TO 3' DIRECTION

promoter region - region at beginning of DNA strand where transcription starts
RNA polymerase - the enzyme that produces pre-mRNA by copying a strand of DNA
transcription factors - DNA binding proteins that affect the extent of transcription

exons - parts of pre-mRNA that are joined together to form mRNA and do get translated
introns - sections of pre-mRNA that are removed during splicing

free ribonucleotides - nucleotides that haven't been used to make RNA yet

   1. Transcription factors bind to promotor region of the gene and the strand of DNA unzips (template strand)

   2. RNA polymerase copies this gene (the DNA template strand) by joining complementary nucleotides thereby producing a coding strand of pre-mRNA. It stops at the terminator.

   3. The pre-mRNA undergoes post-transcriptional modifications to become mRNA:
      a. splicing - introns are removed and stay in the nucleus while the remaining exons recombine in a specific order
      b. poly-A tail attached to 3 prime end (aka 3')
         poly-A tail protects from enzyme damage while in cytosol
      c. methyl cap attached to 5 prime end (aka 5')

---

Thank you!


Perfect. Excellent work.
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antigony

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Re: VCE Biology Question Thread
« Reply #11743 on: June 10, 2019, 02:39:33 pm »
0
Perfect. Excellent work.

Thank you very much!

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Re: VCE Biology Question Thread
« Reply #11744 on: June 10, 2019, 09:33:01 pm »
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similarities between photosynthetic autotrophs, chemosynthetic autotrophs?