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Edexcel A2 Biology SNAB 6BI04 ~ 6BIO5 June 2016

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Do IAL papers contain the same spec for Unit 4&5? If so, i got more work to do then son!
Original post by .JC.
Just do all the previous past papers and you'll be fine. There may be some things that come up that haven't done previously, but just revising past questions is enough to get you an A/A* provided you get them spot on.


Typically I will just write as much relevant stuff as I can, I find that picks up the marks if I'm unsure on a question.
Original post by tayloryeah
- observing patterns by ecological studies


Whats this?

Original post by tayloryeah
- the effect of temperature on the hatching of brine shrimp/ germination of seeds


Do we need to learn both of these
Guys can someone please go over immunity. I know most of immunity but I don't get how B cells can act as macrophages etc? I thought only macrophages act as APC etc... Also I thought just T helper cells bind to the macrophage APC and produce cytokines which activate T killer cells and B cells. And I thought that was it? But I see things like B cells binding to APC and stuff like that...

Also in terms of viruses and HIV I thought they don't contain antigens. I've seen a question and answered it about specific immune response to HIV/Virus and it talks about it being engulfed by phagocytes etc and antibodies being produced? I thought for viruses this wasn't possible?
Original post by noctisff
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Can someone explain marking point 3? I'm not sure why the B-cell acts as an APC to itself rather than act as an APC to a T-helper cell as it releases cytokines to help the b-cell divide.
This is the June 2014 reserve paper btw


I THINK what it means is that the B cell presents the antigens as an APC, as in the humoral response the B cell can carry out phagocytosis and become an APC also, which then binds to a complementary t helper clone from the previous stage, to divide into B effector and B memory clones (using cytokines released by the T-helper)
Original post by fpmaniac
Whats this?



Do we need to learn both of these


ecological sampling = random sampling/ systemic sampling = to measure the abundance and distribution of organisms

Brine shrimp involves:
- setting up beakers at 5 different temperatures
- 0C, 10C, 20C, 30C,40C ( 0C minimum enzyme activity temperature, 40C = optimum)
- place an equal volume of saline solution in each beaker
- place an equal number of brine shrimp in each beaker
- regulate temperatures in a water bath
- control variables: salinity of solution, the number, source and type of brine shrimp, light intensity
- repeat the experiment to gather a mean to produce reliable results
- when recording how many brine shrimp have hatched take photo evidence, because organisms move, this will decrease the risk of miscounting the number of hatched brine shrimp and increase validity.

Seedling growth
- place seedlings in a petri dish
- place in an incubator at different temperatures each time
- controls: [CO2], availability of light and water
- control the type and source of seed
- measure the height of the seedling
- repeat investigation to collect a mean
(edited 7 years ago)
what is the hardest biology unit 4 paper in your opinion?
Reply 427
Does anyone know how many marks you have to score to get full ums?
Reply 428
can someone please tell me the exact definitions of GPP and NPP for the exam? my textbook is quite vague
With the synoptic stuff, can it be anything from Unit 1 or 2 or is it specific topics?
Original post by rp1997
can someone please tell me the exact definitions of GPP and NPP for the exam? my textbook is quite vague


GPP - the rate at which energy is incorporated into organic molecules
NPP - the rate at which energy is incorporated into new plant biomass
Original post by hellohello6
what is the hardest biology unit 4 paper in your opinion?


Try June 12 - quite tricky.
What is synoptic stuff that pops up again and again?
Original post by Susta1nz
Guys can someone please go over immunity. I know most of immunity but I don't get how B cells can act as macrophages etc? I thought only macrophages act as APC etc... Also I thought just T helper cells bind to the macrophage APC and produce cytokines which activate T killer cells and B cells. And I thought that was it? But I see things like B cells binding to APC and stuff like that...

Also in terms of viruses and HIV I thought they don't contain antigens. I've seen a question and answered it about specific immune response to HIV/Virus and it talks about it being engulfed by phagocytes etc and antibodies being produced? I thought for viruses this wasn't possible?


I also want to know this..?
Could anyone clear up to the carbon fixation thing for me please? Is carbon fixation when carbon dioxide and RuBP combine, or is it when GP is converted into GALP during the Calvin cycle? My teacher didn't know the answer.
@Susta1nz @ABeingOnEarth
B cells have antibodies on their surface and when they bind to the complementary antigen they become APCs. The T helper cell with the complementary receptor then binds to this APC which releases cytokines to trigger clonal selection of the specific B cells into memory cells and plasma cells.

With viruses, they invade the host cell and do present foreign antigens on the membrane, however in the case of HIV as there is a high rate of mutation within the gene that codes for the antigen the immune response isn't as effective as lots of T Helper cells are being digested by phagocytes and T killer cells and eventually HIV could go undetected.
I think you may be getting confused with TB, as this evades the immune system by preventing antigen presentation inside the phagocytes. That's why it can lie dormant.
Original post by PhysicsIP2016
@Susta1nz @ABeingOnEarth
B cells have antibodies on their surface and when they bind to the complementary antigen they become APCs. The T helper cell with the complementary receptor then binds to this APC which releases cytokines to trigger clonal selection of the specific B cells into memory cells and plasma cells.

With viruses, they invade the host cell and do present foreign antigens on the membrane, however in the case of HIV as there is a high rate of mutation within the gene that codes for the antigen the immune response isn't as effective as lots of T Helper cells are being digested by phagocytes and T killer cells and eventually HIV could go undetected.
I think you may be getting confused with TB, as this evades the immune system by preventing antigen presentation inside the phagocytes. That's why it can lie dormant.


Ohhh thanks! That's quite useful. So what's the difference between B cells acting as APCs? When does that happen compared to the macrophage acting as an APC. How do we know which one happens and when?
Original post by etherealinsanity
Could anyone clear up to the carbon fixation thing for me please? Is carbon fixation when carbon dioxide and RuBP combine, or is it when GP is converted into GALP during the Calvin cycle? My teacher didn't know the answer.


When Carbon Dioxide and RuBP combine. Technically GP is reduced to GALP using NADPH and phosphorylated using ATP so there is no transfer of carbon.
Do all retroviruses use reverse transcriptase?
Original post by Susta1nz
Ohhh thanks! That's quite useful. So what's the difference between B cells acting as APCs? When does that happen compared to the macrophage acting as an APC. How do we know which one happens and when?


Macrophages are the first cells to act as APCs because they function to activate the correct T helper cell with the complementary receptor upon infection.
When the B cell acts as an APC the now activated T helper cells stimulate clonal selection which produces the correct antibodies for the pathogen.

Think of macrophages turning into APCs being mainly present in primary infection. In the case of secondary infection the B memory cells recognise the same antigen so they can differentiate immediately (with the aid of T memory cells) without needing the macrophage to activate them.
(edited 7 years ago)

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