VCE Biology Question Thread

[PhoenixxFire]

Cheers
Thanks for the reply. Also how does swelling occur in the inflammation response? Is it because of the restricted blood flow from the source of infection?

Inflammation does not restrict blood flow. Histamine bind to capillary walls and cause vasodilation and increased permeability. This allows the fluid (lymph) and leukocytes to enter the surrounding tissue. This causes swelling (Permeability), heat (both), and redness (vasodilation).

[Seno72]

Thanks. So it is the lump fluid at the site of infection that causes swelling? At school I learned 'exudate'. Is that the same thing as lymph fluids?

Also change in subject, for the BMP 4 expressions in Darwins finches, does larger expressions lead to larger beak depth and width or larger beak length and width?

In BMP4 expressions of Cichlids, does higher levels of BMP4 lead to a more robust jaw structure and teeth spaced closely together?

Are cichlids and darwins finches an example of adaptive radiation?

What do we need to know about biogeography? Is it just that species living in close proximity tend to be more related to each other?

[PhoenixxFire]

Thanks. So it is the lump fluid at the site of infection that causes swelling? At school I learned 'exudate'. Is that the same thing as lymph fluids?

Had a quick look at Wikipedia, yes they appear to be the same.

Also change in subject, for the BMP 4 expressions in Darwins finches, does larger expressions lead to larger beak depth and width or larger beak length and width?

In BMP4 expressions of Cichlids, does higher levels of BMP4 lead to a more robust jaw structure and teeth spaced closely together?

Have no idea on this. I believe it has to do with the timing of BMP4 expression as much as the amount. If I have time tomorrow morning I'll try to make a poster on it.

Are cichlids and darwins finches an example of adaptive radiation?

Yes. Adaptive radiation is very rapid divergent evolution which they show.

What do we need to know about biogeography? Is it just that species living in close proximity tend to be more related to each other?

Yes. Basically if there are similar species that seem to have appeared around the same time some land split that indicates they had a common ancestor.

[Seno72]

Thanks for the reply. Also what do we need to know about the 'molecular clock' concept and why is mtDNA used in determining relatedness in species?

[areeb008]

Inflammation does not restrict blood flow. Histamine bind to capillary walks and cause vasodilation. This allows the fluid (lymph) and leukocytes to enter the surrounding tissue. This extra fluid is what causes the swelling and heat. The histamine also causes increased blood flow to the area which is what makes it red (also contributes to heat).

Pretty sure it's blood plasma that leaks out through capillaries rather than lymph.

[zxcvbnm18]

A definition: The formation of a new species as a result of the ancestral population becoming isolated by a geographical barrier.
For a scenario question:
GSD
G Geographical Isolation
S Selection Pressures - The groups face different selection pressures, causing them to evolve differently
D Differences accumulate to the point where, if brought back together they will not interbreed to produce fertile, viable offspring.

Thanx

[smamsmo22]

I understand that naive B cells and cytotoxic T cells can be activated into an effector cell by direct exposure to their specific antigens (whether it be on the surface of a pathogen or a free antigen, or on the MCH1 marker of an infected self cell), which is clonal selection, right? (Correct me if I'm wrong)
But I believe that they cannot undergo clonal expansion - rapid division and differentiation - unless they are stimulated by cytokines released by (specific) activated effector T helper cells.
In completing practice exams about the humoral or cell mediated response in terms of B cells and Tc cells, the suggested answers rarely mention that the rapid division of the cell is stimulated by Th cells specific to the same antigen; it usually just says the antigen activates the specific cell and it undergoes rapid proliferation etc.
As someone who often writes too much in exams and runs out of space, is it necessary that I mention the Th cytokines when describing the clonal expansion mechanism, in adaptive immune system or allergic response scenarios?
Thanks!

[PhoenixxFire]

I understand that naive B cells and cytotoxic T cells can be activated into an effector cell by direct exposure to their specific antigens (whether it be on the surface of a pathogen or a free antigen, or on the MCH1 marker of an infected self cell), which is clonal selection, right? (Correct me if I'm wrong)
But I believe that they cannot undergo clonal expansion - rapid division and differentiation - unless they are stimulated by cytokines released by (specific) activated effector T helper cells.
In completing practice exams about the humoral or cell mediated response in terms of B cells and Tc cells, the suggested answers rarely mention that the rapid division of the cell is stimulated by Th cells specific to the same antigen; it usually just says the antigen activates the specific cell and it undergoes rapid proliferation etc.
As someone who often writes too much in exams and runs out of space, is it necessary that I mention the Th cytokines when describing the clonal expansion mechanism, in adaptive immune system or allergic response scenarios?
Thanks!

I generally write something along the lines of 'a Tc cell binds to its antigen, causing it to divide and differentiate, this is further stimulated by cytokines released from activated Th cells.' So I mention Th cells without having to write too much. For humoral immunity I describe both B cells and Th cells in detail.

[vox nihili]

Cheers
Thanks for the reply. Also how does swelling occur in the inflammation response? Is it because of the restricted blood flow from the source of infection?

I’m not really convinced that you need to know about inflammation in the detail that’s been described here, but to deal with a couple of misconceptions in various spots:

-the fluid that causes swelling in inflammation comes from the blood. It leaks out of the blood vessels (hence exudate). Calling it lymph is kind of accurate, insofar as all fluid in tissues eventually becomes lymphatic fluid, as it enters the lymphatics to be returned to the blood
-dead neutrophils also contribute to swelling (pus)
-vasodilation itself does not cause swelling. It merely brings more blood into the area. What causes the swelling is the fast that cytokines make the blood vessels more leaky, so that that extra blood brought in by the vasodilation can leak out and become extracellular fluid and contribute to the swelling

[smamsmo22]

2 more questions/confirmations (:

1. In an autoimmune response, are B cells or Tc cells activated by the self cells? i.e.; the antigens on the self cells on which an immune attack is stimulated are viewed as non-self antigens like those found on a pathogen (that would stimulate a humora/antibody-mediated response), not altered self markers that display a foreign antigen that would activate a Tc cell?
2. Seeking more of a confirmation than an answer, but am I right in believing;
Generally, active transport is used to move ions and glucose across the PM, whereas bulk transport/endocytosis and exocytosis moves bacteria/pathogens, polysaccharides or other (very) large polar molecules or large amounts of a particular molecule/substance.
And do these (or some of them) molecules that use bulk transport ever use facilitated diffusion via protein channels, or are they also too large for those?

Thanks

[PhoenixxFire]

1. In an autoimmune response, are B cells or Tc cells activated by the self cells? i.e.; the antigens on the self cells on which an immune attack is stimulated are viewed as non-self antigens like those found on a pathogen (that would stimulate a humora/antibody-mediated response), not altered self markers that display a foreign antigen that would activate a Tc cell?

Now this is an interesting question. I believe it can be either. Tc cells may be able to incorrectly bind to a peptide fragment being presented, which would trigger an autoimmune response. However I recently did a 2017 practice exam that asked about how antibodies may prevent insulin from being in the bloodstream and the answer was that the antibodies bind to the beta cells, attracting phagocytes to the area to engulf them. My teacher said that a humoral immune response may be stimulated by chemicals that happen to have the same specificity as the cells and that is why there is a humoral response like this.

2. Seeking more of a confirmation than an answer, but am I right in believing;
Generally, active transport is used to move ions and glucose across the PM, whereas bulk transport/endocytosis and exocytosis moves bacteria/pathogens, polysaccharides or other (very) large polar molecules or large amounts of a particular molecule/substance.
And do these (or some of them) molecules that use bulk transport ever use facilitated diffusion via protein channels, or are they also too large for those?

Glucose definitly uses facilitated diffusion. Unsure on ions, I don't think so? The molecules that use bulk transport definitly don't.

[dimenc]

Check out PhoenixxFire's resource 
https://atarnotes.com/forum/index.php?topic=174693.0

Hi,
I am unsure about the reliability of this recourse as I did a practice exam which stated that Angiosperms first arose in the Cretaceous period

[PhoenixxFire]

Hi,
I am unsure about the reliability of this recourse as I did a practice exam which stated that Angiosperms first arose in the Cretaceous period

My source for 200 mya is http://www.bbc.com/earth/story/20141017-how-flowers-conquered-the-world
It states that they first appeared 200mya ago (after the Triassic-Jurassic Mass extinction) and became widespread throughout the cretaceous period.

Darwin did suggest a solution, however. Angiosperms, he said, may have evolved gradually in a remote region of the world as yet unexplored by scientists. By the middle of the Cretaceous, something caused them to spill out of their homeland and rapidly spread across the world. This, reasoned Darwin, would give the misleading impression to researchers working in Europe and North America that a wide variety of flowering plant species had all evolved at the same time. Aware of the lack of evidence to back up his theory, Darwin described it as "wretchedly poor".

In fact, his speculation has since proved to be partly correct. Angiosperms that predate the middle Cretaceous specimens by tens of millions of years have begun to turn up in rocks from China. But Darwin didn't get the details entirely right because very rare early angiosperms have been found in Europe and the US too.

"Our knowledge has greatly increased since the end of the 19th century," says Laurent Augusto at the National Institute for Agricultural Research in Bordeaux, France. Palaeobotanists may not yet agree on precisely where and when flowering plants first evolved, but their appearance in the fossil record much earlier than was previously known means they are no longer a problem for Darwin's theory of gradual evolution. Other debates about them, especially concerning their spectacular diversity, remain active, however.

"Our world is an angiosperm world," says Augusto. "In many ecosystems they dominate in species and in biomass – this angiosperm ecological dominance remains unexplained."

Clues to the ultimate origins of flowering plants are to be found on New Caledonia, a small island about 1,600 kilometres east of Australia. Here, around the time that Darwin was agonising over his angiosperm problem, botanists discovered a plant called Amborella. Careful study over the last century has shown it to be the sole survivor of one of the very earliest branches of the angiosperm evolutionary tree. This means its relationship to all living flowers is bit like that of the duck-billed platypus to all living mammals: it might look unassuming, but Amborella can tell us more than even the most elaborate orchid about how the angiosperms first evolved.

Last year, the plant finally spilled some of its secrets. The Amborella Genome Project unveiled a draft version of the plant's genome. The first angiosperms must have evolved from one of the gymnosperm species that dominated the world at the time. The Amborella genome suggests that the first angiosperms probably appeared when the ancestral gymnosperm underwent a 'whole genome doubling' event about 200 million years ago.

[smamsmo22]

Now this is an interesting question. I believe it can be either. Tc cells may be able to incorrectly bind to a peptide fragment being presented, which would trigger an autoimmune response. However I recently did a 2017 practice exam that asked about how antibodies may prevent insulin from being in the bloodstream and the answer was that the antibodies bind to the beta cells, attracting phagocytes to the area to engulf them. My teacher said that a humoral immune response may be stimulated by chemicals that happen to have the same specificity as the cells and that is why there is a humoral response like this.

Thank you for this. My understanding was that it triggered humoral response because as the cell antigens are identified as non self, antibodies will be produced as if it were any other cell that was not identified as the body’s own (eg: bacteria). Hence, production of autoantibodies is stimulated. But in knowing that Tc cells are the ones that usually mount attacks on self cells (That have been infected), I thought the autoimmune response might be cell mediated. But I think it is humoral…

Thanks for your second answer!

[vox nihili]

Now this is an interesting question. I believe it can be either. Tc cells may be able to incorrectly bind to a peptide fragment being presented, which would trigger an autoimmune response. However I recently did a 2017 practice exam that asked about how antibodies may prevent insulin from being in the bloodstream and the answer was that the antibodies bind to the beta cells, attracting phagocytes to the area to engulf them. My teacher said that a humoral immune response may be stimulated by chemicals that happen to have the same specificity as the cells and that is why there is a humoral response like this.
Glucose definitly uses facilitated diffusion. Unsure on ions, I don't think so? The molecules that use bulk transport definitly don't.

More important point: ions ALWAYS use facilitated diffusion. They need channels to get through (or in some cases carriers). They can't move directly through the plasma membrane.


You're absolutely right about autoimmune diseases potentially involving either arm of the adaptive immune system. Most autoimmune diseases involve a component of B-cells and T-cells, with one of the types of cells being more dominant. Indeed, MS for example only really involves T-helper cells (they do the majority of the damage!).

Thank you for this. My understanding was that it triggered humoral response because as the cell antigens are identified as non self, antibodies will be produced as if it were any other cell that was not identified as the body’s own (eg: bacteria). Hence, production of autoantibodies is stimulated. But in knowing that Tc cells are the ones that usually mount attacks on self cells (That have been infected), I thought the autoimmune response might be cell mediated. But I think it is humoral…

Thanks for your second answer!

As above it's actually both T-cells and B-cells that can do it, with some involving more than others. If you take autoimmune thyroid diseases as an example (you don't need to know the details), Graves disease mainly involves B-cells producing autoantibodies, whereas Hashimoto's thyroiditis is mainly a T-cell disease.