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July 20, 2019, 05:11:03 am

Author Topic: VCE Biology Question Thread  (Read 1264044 times)  Share 

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khadeejaatif

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Re: VCE Biology Question Thread
« Reply #11775 on: June 20, 2019, 08:17:33 pm »
0
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/

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« Last Edit: June 20, 2019, 08:28:53 pm by Calebark »
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laura_

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Re: VCE Biology Question Thread
« Reply #11776 on: June 20, 2019, 08:28:04 pm »
+3
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!!
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Re: VCE Biology Question Thread
« Reply #11777 on: June 20, 2019, 08:29:36 pm »
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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!!
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Erutepa

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Re: VCE Biology Question Thread
« Reply #11778 on: June 20, 2019, 09:20:49 pm »
+9
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. :)
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gary123

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Re: VCE Biology Question Thread
« Reply #11779 on: June 20, 2019, 10:35:34 pm »
+1
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 :D

« Last Edit: June 20, 2019, 10:41:34 pm by gary123 »
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Erutepa

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Re: VCE Biology Question Thread
« Reply #11780 on: June 20, 2019, 11:16:20 pm »
+14
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?

This is good! Although I would specify that dendritic cells present pathogenic/non self antigens on the mhc class 2 receptors. Realistically dendritic cells do present not just pathogenic antigens, but as far as our course is concerned, dendritic cells just present pathogenic antigens.
Realistically dendritic cells will bind to other cells like cytotoxic T cells and what not, but these specifics aren't relevant to the course. Just know that they bind to the t helper cell as you have mentioned.

Quote

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?

Yes. This sounds right!

Quote

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)

As a result of a primary immune response, memory b cells specific to the antigen illiciting this response are produced. These memory b cells exist in a greater number relative to that of the nieve cells in a primary infection such that secondary infections are characterised by a faster and greater antibody production.
Basically, because of memory b cells, there are more cells that can potentially bind to the antigen and be activated by t helper cells such that the immune response occurs faster and to a greater extent.
Does this help?
Quote

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.

The inflammation response involves many different aspects which all contribute to the immune response. It's not just the case that inflammation involves the release of cytokines which attract other immune cells to the region of infection, but this is certainly one major part of the inflammation response. You could use that as an answer. You could also talk about the vasodilation and adaptations to the local vasculature that enable the migration of immune cells.
Quote

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?

This is correct except mhc class 2 receptors are not antibodies. You might be thinking about b cell receptors which are surface bound antibodies.

Quote

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

Not entirely sure about this, but your reasoning seems quite sound. Remember that an immune response is illicited by the sensing of damage and/or danger from the immune system. If the virus is completely inactive it won't cause damage and thus has a much lower chance of Illiciting an immune response
Quote

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)

You are right. This is out of the study design and you do not need to know this.
Quote

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?

You don't need to know much. This content is usually examined through questions asking you to simply identify the pathogen from basic characteristics. So just know the key features of each one. You don't need the specifics of how they function. Hobestly worms, virions, prions and fungi are not all That prevelant, atleast from my own experience. The main thing is understanding and being able to differentiate between viruses and bacteria.
Quote
°
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 :D
Must be by mhc class 2 markers, thus must be by a macrophage or dendritic cell.
« Last Edit: June 20, 2019, 11:21:57 pm by Erutepa »
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FrankieDens

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Re: VCE Biology Question Thread
« Reply #11781 on: June 21, 2019, 02:37:09 pm »
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Hi everyone!

I just finished my Unit 3 Outcome 2 SAC (the cell communication one) and overall it was great but one question really stumped me. Basically a pregnant horse was vaccinated and a graph of the foal's antibody concentration is included. At the beginning, the concentration is pretty high but it decreases until at 3 months old where there are 0 antibodies left.

I don't remember the exact wording of the question but it basically asks why it would be ineffective to vaccinate the foal before 3 months old. Is it because it still relies on its naturally (acquired) passive immunity?

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Re: VCE Biology Question Thread
« Reply #11782 on: June 21, 2019, 02:44:38 pm »
+4
Yeah thatís basically it, their immune system isnít developed at that point. If you give them a vaccination whilst they have antibodies, those antibodies will neutralise the antigenic fragments in the vaccine and the foals own immune system wonít have a chance to react to it, and therefore wonít generate memory cells and therefore no immunity.
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laura_

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Re: VCE Biology Question Thread
« Reply #11783 on: June 21, 2019, 03:08:14 pm »
0
Hey guys, just a couple of quick questions that I would appreciate some clarification with: (Unit 1)
1. How is information transmitted from the receptor to the control centre?

2. If someone has Type 1 diabetes will their blood glucose levels increase or decrease overnight. Why?
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Matthew_Whelan

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Re: VCE Biology Question Thread
« Reply #11784 on: June 21, 2019, 03:32:20 pm »
+4
Hey guys, just a couple of quick questions that I would appreciate some clarification with: (Unit 1)
1. How is information transmitted from the receptor to the control centre?

2. If someone has Type 1 diabetes will their blood glucose levels increase or decrease overnight. Why?

1. It depends on the pathway, eg  a external stimulus will be received at a receptor on the body which will transmit the info via neurons (electrochemical process) whereas other pathways could be a cell receiving a signal to elicit an intracellular response (encode RNA, undergo apoptosis); this is signal transduction.

2. Type 1 diabetes causes a deficiency of insulin production in the pancreas which causes the person's blood glucose levels to be abnormally high, so it would increase overnight I believe.

If I got something wrong pls point it out ;)

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Rom_Dog

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Re: VCE Biology Question Thread
« Reply #11785 on: June 22, 2019, 10:10:34 am »
+6
Hey guys, just a couple of quick questions that I would appreciate some clarification with: (Unit 1)
1. How is information transmitted from the receptor to the control centre?

2. If someone has Type 1 diabetes will their blood glucose levels increase or decrease overnight. Why?

Hey!

Matthew is right in saying type 1 diabetes is associated with a deficiency in insulin production however sugar levels remain abnormally high after meals as insulin is in low levels or absent, insulin lowers blood glucose by promoting the uptake of glucose by the body's cells (especially the liver and muscles where glycogen, the a highly branched polymer of glucose is produced and stored).

Over night blood glucose slowly decreases as it is metabolised by the body but blood glucose levels still remain elevated in comparison to a healthy individual which you can see on the graph here

Hope this helps!

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laura_

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Re: VCE Biology Question Thread
« Reply #11786 on: June 22, 2019, 06:33:35 pm »
0
Hey!

Matthew is right in saying type 1 diabetes is associated with a deficiency in insulin production however sugar levels remain abnormally high after meals as insulin is in low levels or absent, insulin lowers blood glucose by promoting the uptake of glucose by the body's cells (especially the liver and muscles where glycogen, the a highly branched polymer of glucose is produced and stored).

Over night blood glucose slowly decreases as it is metabolised by the body but blood glucose levels still remain elevated in comparison to a healthy individual which you can see on the graph here

Hope this helps!

Thank you!!
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Re: VCE Biology Question Thread
« Reply #11787 on: June 22, 2019, 10:03:17 pm »
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Why is it difficult to produce an effective influenza (or other disease) vaccine?

Also, what are the three major categories of vaccines and what are the advantages & disadvantages of each type?

Thanks!!
« Last Edit: June 22, 2019, 10:22:10 pm by f0od »
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vox nihili

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Re: VCE Biology Question Thread
« Reply #11788 on: June 22, 2019, 10:46:06 pm »
+1
Why is it difficult to produce an effective influenza (or other disease) vaccine?

Also, what are the three major categories of vaccines and what are the advantages & disadvantages of each type?

Thanks!!

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Re: VCE Biology Question Thread
« Reply #11789 on: June 23, 2019, 10:15:57 am »
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Quote
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.
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Hi guys.
Just had a few questions I wanted to ask.
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2. Assume a thylakoid is somehow punctured so that the interior of the thylakoid is no longer separated from the
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a. the splitting of water
b. the absorption of light energy by chlorophyll
c. the flow of electrons from photosystem II to photosystem I
d. the synthesis of ATP
e. the reduction of NADP+
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