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Reply 40
ro.
Can someone please help me!!

I'm stuck on:

Replication

Immune system




I'll help with what I think hasn't been answered:

Replication:

Occurs inside the nucleus. The process is as follows (I think it's more helpful in words, because sometimes books can be a little diagram heavy and it becomes hard to know how to phrase stuff):

1. Firstly, an enzyme called DNA Helicase "unzips" the double helix in DNA, by breaking the hydrogen bonds between bases.

2. a) Next, free floating nucleotides which are found in the nucleus line up next to the two poly-nucleotide strands we have from unzipping DNA.

2. b) Complementary base pairings line up next to each other - Cytosine to Guanine, and Adenine to Thymine (or simply, a purine next to a pyramidine)

3. Hydrogen bonds reform between the bases. 3 between C and G, 2 between A and T.

4. An enzyme called DNA Polymerase now forms covalent bonds between the free floating nucleotides, called PHOSPHODIESTER bonds.

5. We now have two identical strands of DNA!*

*This is called Semi-Conservative replication, because in each new strand of DNA, we have one strand from the original "Parent DNA".

Replication occurs before processes like MITOSIS.

Immune System:

Obviously there is more to it than what I am about to explain but this is the gist of it (some books go into great detail about things like monokines and interleukins but these aren't in our syllabus!):

1. Firstly, a pathogen enters the body. The pathogen has antigens on its surface which alert white blood cells to its presence.

2. White blood cells called MACROPHAGES approach the pathogen and engulf it, trapping it in a PHAGOSOME.

3. Inside the macrophage, the pathogen inside the phagosome is broken down by LYSINS (digestive enzymes), into harmless products.

4. The macrophage now PRESENTS the antigens of the pathogen on the surface of the cell. (This simply means they stick the antigens on their membrane).

5. White blood cells called T-lymphocytes approach the macrophages. They have receptors on their surface, and try to bind to the antigens on the surface of the MACROPHAGE.

6. When a COMPLEMENTARY receptor meets a SPECIFIC antigen on the macrophage surface, a response is triggered. This is called CLONAL SELECTION, where a specific shape of receptor/specific lymphocyte is chosen.

7. The T-lymphocytes now undergo CLONAL EXPANSION. This means they divide by mitosis and DIFFERENTIATE into T-plasma cells and T-memory cells (we'll come to these later)

8. There are two kinds of plasma cell: HELPER and KILLER. T-Killer cells kill pathogens by injecting them with HYDROGEN PEROXIDE (but you don't need to know this). T-helper cells release stuff called CYTOKINES (which are basically chemical hormones) to stimulate a response in specific B-lymphocytes.

9. The stimulated B-lymphocyte has ANTIBODIES on its surface, with a shape that is also complementary to the antigens on the surface of the pathogen. This, again, is clonal SELECTION.

10. The B-lymphocytes undergo CLONAL EXPANSION, dividing and differentiating into B-memory and B-plasma cells.

11. B-plasma cells have proteins on their surface, which they release, called ANTIBODIES. They have a specific complementary shape to the pathogen's antigens.

12. Antibodies serve several purposes, but I won't bore you with the details because it's more for you to read and for me to write.

13. Finally, after the pathogen is gone, the MEMORY cells which were produced from clonal expansion stay in the blood for a long time after infection. They grant the infected person with IMMUNOLOGICAL MEMORY, meaning next time they get infected, clonal expansion and selection is a million miles faster.

Phewph!!!
Reply 41
here is a summary of smoking:

nicotine -

nicotine causes the release of adrenaline which increases the heart, breathing rate and causes constriction of the arterioles. This increases the blood pressure which can damage the lining of the artieries. The damage attracts phagocytes which encourage the growth of smooth muscle and deposition of fatty substances. More fats are deposited in the wall of the artery. Artheromas form which can form plaques that restrict the lumen of the coronary arteries. This is atherosclerosis. This can lead to coronary heart disease as less blood flows to cardiac muscle and the cardiac muscle receives less oxygen for respiration.

Nicotine can also increase the risk of coronary heart disease as it makes platelets sticky which increases the risk of blood clots forming. blood clots in the coronary arteries restricts the flow of blood in the arteries and restricts blood flow to cardiac muscle, so the cardiac muscle receives less oxygen for respiration, therefore death of the cardiac muscle.

carbon monoxide can also increase the risk of coronary heart disease
carbon monoxide damages the lining of the arteries which causes more fats to be deposited in the walls of the arteries and fatty deposits called artheromas form. This leads to atherosclerosis and reduces the lumen of the artery, restricting blood flow to cardiac muscle

also carbon monoxide enters red blood cells and combines with HB to form carboxyhaemoglobin which reduces oxygen carrying capaciy of blood so cardiac muscle recieves less oxygen.


nicotine and carbon monoxide also increases the risk of having a stroke
Reply 42
Cheers guys, you were all really helpful :smile:
Reply 43
I saw a question in a past paper and I don't have the markscheme.

Suggest why there is not a vaccine for malaria, TB and AIDS. (4)

Any help?
Jono300
I saw a question in a past paper and I don't have the markscheme.

Suggest why there is not a vaccine for malaria, TB and AIDS. (4)

Any help?


My answer is for Malaria, TB is
1/ There are MANY TYPES OF PATHOGENS so it's hard to delevope a general vaccine
2/ There are MANY SHAPES OF ANTIGENS as the pathogen have many stages in the body. The vaccine must incoperate all thes antigens to trigger the immunity
3/ ANTIGEN CONCEALMENT, pathogens are out of reaching of antibodies eg Plasmodium in RBC, Mycobacterium in lungs
I am not sure abt the HIV suggestions
1/ HIV are viruses which bring their genetic information into cells so antibodies cant reach them. I think it is kind of cell concealment
2/ They use our own cells to replicate their DNAs in fast rate
3/ They attack T helper cells which stimulate producing of antibodies

I hope it might help :smile:
I have really big problems with the last chaper : Biodiversity and somethings :frown:
Does anybody have any revision notes for these stuffs?
Thank u :biggrin:
Reply 46
benweil, thats a brilliant summary and really useful. Thanks :smile:

Also, does anyone have any past questions on sampling and measuring biodiversity? Or any mark scheme specific notes on these topics? I can't find any because its the new spec and in the textbook seems to over complecate the whole topic?

Stuff on conservation and maintaining biodiversity would also be really appreciated :smile:

Many thanks
Reply 47
BTW...not that it means anything to anyone: but i have a very strong feelin evolution and sampling will come up :biggrin:
Reply 48
Jono300
I saw a question in a past paper and I don't have the markscheme.

Suggest why there is not a vaccine for malaria, TB and AIDS. (4)

Any help?



I have seen a similar question, and the marks for these are deceptive. I think what they want you to talk about is firstly the phenomena known as ANTIGENIC SHIFT/DRIFT.

Antigens change constantly (especially in the case of HIV), due to random mutation.

This makes it hard to create specific vaccines for, similarly to influenza, but possible worse.

Next, you could talk about how Malaria is caused by more than one species of Plasmodium, so its difficult to vaccinate against all of them.

Also, I read an answer to a question like this specifically against Malaria, and it talked about how the plasmodium parasite is difficult to vaccinate against as inside the host it is constantly changing form (from zygote to gametes etc. etc.)

I think that may be enough for the marks.
Reply 49
larry000
benweil, thats a brilliant summary and really useful. Thanks :smile:

Also, does anyone have any past questions on sampling and measuring biodiversity? Or any mark scheme specific notes on these topics? I can't find any because its the new spec and in the textbook seems to over complecate the whole topic?

Stuff on conservation and maintaining biodiversity would also be really appreciated :smile:

Many thanks


There aren't many on the topic, which is really annoying.
I do remember them asking a question about sampling a field, and the only thing relevant to sampling they asked you was what the scientist would need to measure if he wanted to specifically calculate the biodiversity index of the field (and you just basically wrote out the calculation for Simpson's Biodiversity Index. It was only worth two marks). The rest of the question for that was on biodiversity in general. I think that was last year's paper.

I wouldn't worry about sampling too much. To be honest I'd just learn Simpson's Index, learn about how to exclude bias in results (e.g. use a random number generator) and learn about what techniques you can physically use. I wouldn't get too bogged down by details, as it's not a particularly scientifically detailed part of the course, so I think they'd ask you some pretty simple q's on it, along the lines of: "How could person X calculate the number of moles in the habitat using capture+recapture"/"How could he eliminate bias from his experiment."
I would be v. surprised/annoyed if they asked a massive question on it all. They are more likely to lead into long ex situ/in situ conservation questions with some two markers on the calculations.

I really hate that part of the course.
Efoskjdfklsdjf
Reply 50
benweil
There aren't many on the topic, which is really annoying.
I do remember them asking a question about sampling a field, and the only thing relevant to sampling they asked you was what the scientist would need to measure if he wanted to specifically calculate the biodiversity index of the field (and you just basically wrote out the calculation for Simpson's Biodiversity Index. It was only worth two marks). The rest of the question for that was on biodiversity in general. I think that was last year's paper.

I wouldn't worry about sampling too much. To be honest I'd just learn Simpson's Index, learn about how to exclude bias in results (e.g. use a random number generator) and learn about what techniques you can physically use. I wouldn't get too bogged down by details, as it's not a particularly scientifically detailed part of the course, so I think they'd ask you some pretty simple q's on it, along the lines of: "How could person X calculate the number of moles in the habitat using capture+recapture"/"How could he eliminate bias from his experiment."
I would be v. surprised/annoyed if they asked a massive question on it all. They are more likely to lead into long ex situ/in situ conservation questions with some two markers on the calculations.

I really hate that part of the course.
Efoskjdfklsdjf



Yeh im glad I'm not the only one. I don't like these topics either. And thanks for the advice. Although I have just found some question
on the OCR website. There are some questions on sampling in the environmental biology papers so you may want to have a look :smile:
Reply 51
Am i right to say then CO and nicotine can cause atherosclerosis? Also can LDL's contribute to athermos and can they cause them too by attacking the lining of the arteries?
Reply 52
i think testing for biological molecules like lipids, proteins, starch, reducing sugars etc will come up. It hasn't come up in the previous exams and normally it is a common topic

also i think questions on active immunity/vaccination might come up as well as sampling
Ah I m resiting this damned module too.. gonna hang around later tonight.
Reply 54
i have seen this question a few times in past papers:

what is meant by epidemic

what is meant by pandemic.
Reply 55
TX22
i have seen this question a few times in past papers:

what is meant by epidemic

what is meant by pandemic.


Epi is widespread disease within a country, and pan is widespread disease worlwide, right? (Of a certain disease)

sc0307
Am i right to say then CO and nicotine can cause atherosclerosis? Also can LDL's contribute to athermos and can they cause them too by attacking the lining of the arteries?


Yes, both CO and nicotine damage the lining/endothelium of the arteries. CO damages it as it is, but nicotine damages the endothelium by encouraging the release of adrenaline, which raises blood pressure and therefore damaging the endothelium.

LDLs do contribute to atheromas as they do build up under the endothelium but it's also because they deposit cholesterol in the blood, which builds up under the lining of the artery. If you think of LDLs as "lazy" lipo-proteins, I find that helps. While HDLs carry cholesterol away from tissues to the liver, LDLs just dump cholesterol in the blood, for cells to absorb, which is why it is so dangerous.

I've never heard of LDLs actually causing any damage themselves. Where did you read that?
Reply 56
Has anyone had a look at the past paper questions on biodiversity/evolution and biological molecules that were in the old specification?
I find the mark schemes are really bizarre and difficult, I was doing a question today about selective breeding that was four marks.
I got two marks, because for some reason on the mark scheme you needed to say: "breed hemaphrodite/female resistant; with hemaphrodite/male resistant or reverse" for two marks.
Now I get that obviously that is how you do it, but since when is that kind of stuff on our syllabus? Like the specifics of selective breeding/knowing how plants reproduce.
Infuriating. And there loads of examples like that.

I hate that the new spec doesnt come with more than two/three past papers.
Reply 57
benweil
Epi is widespread disease within a country, and pan is widespread disease worlwide, right? (Of a certain disease)



Yes, both CO and nicotine damage the lining/endothelium of the arteries. CO damages it as it is, but nicotine damages the endothelium by encouraging the release of adrenaline, which raises blood pressure and therefore damaging the endothelium.

LDLs do contribute to atheromas as they do build up under the endothelium but it's also because they deposit cholesterol in the blood, which builds up under the lining of the artery. If you think of LDLs as "lazy" lipo-proteins, I find that helps. While HDLs carry cholesterol away from tissues to the liver, LDLs just dump cholesterol in the blood, for cells to absorb, which is why it is so dangerous.

I've never heard of LDLs actually causing any damage themselves. Where did you read that?

A YouTube animation actually said the LDL's directly attack the lining of the arteries.
Reply 58
^Weird! I've never heard that.
Well, it's certainly not on the syllabus, so you don't NEED to know it :biggrin:
Reply 59
Ok thanks.

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