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.
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?
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)
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
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?
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.
@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?
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.
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.