strikken

Hi! I'm currently studying immunology and am quite confused about how our body can eliminate an viral infection. As far as I've heard, the dendritic cells are important in this because they can present extracellular patogens as MHC class I and thereby activate CD8-T-cells. But how could that eliminate the intracellular viruses when the dendrittic cells reacted on an extracellular patogen in the first place? Or is the explanation that the extracellular fragment could be a viral particle? Furthermore, how could MHC class I activate B-cells to undergo differentiaton to plasma B-cells? Is it so that we don't have antibodies against virus, and that they are primarly killed by Natural Killer cells? I asked my professor, and he mentioned that B-cells can present viruses as MHC-class II, so that the B-cell could be activated by an CD4-T-helper cell. But how can a CD4-T-helper cell be complementary to this B-cell when CD4-T-cells are activated from MHCII presenting cells presenting MHCII only after taking up a extracellular patogen? Happy for all help, friendly regards "Strikken"

Thank you so much!

I'm new here..so hello everyone! *Smiling* I'm a first year student with some questions to biochemistry, trying to understand this to the spring exam. I'm from Scandinavia and not that good in English..but I'll hope this is somewhat understandable and clear. 1. Enzymes doesn't influence equibrilium, but they lower the activation energy. I wonder how this is possible? Isn't the activation energy expressed in free Gibbs energy? If so, how can the equibrilium be unchanged? I thought delta Gibbs was the same as the distance to equibrilium. Or are we maybe talking about different delta Gs? 2. Under ATP synthesis the enzym ATP synthase undergoes rotational catalysis. I understand that something is rotated, but I don't understand what. Is it a change in the seat themselves, or do they only change places among eachother? 3. Under starvation keton bodies can deliver energy to the brain. Ok enough that the brain can make AcCoA from the keton body acetoacetate, but how can AcCoA give energy further through oxidation in the citric acid cycle? I thought that there was a lack of intermediates in the citric acid cycle under starvation, to use the intermediates to build up as much sugar as possible, unless this situation only occurs in the liver. Comments appreciated. 4. How can insulin stimulate the degradation of proteins? I cannot see the logic in this statement, because, as far I can see, this will lead to a less effective removal of blood glucose as pyruvate and AcCoa from glucose will get competition from the same degradation products from proteins. 5. In a class the teacher mentioned something called telomers, important to prolong a DNA thread at the end of a DNA molecule so that a primer can be synthisized to complete the last part of the lagging strand. Fair enough that the laggging strand at the end of a DNA molecule lacks a place to attach a RNA primer, but I'm not totally sure where the telomer is attached. After my opinion, this has to be from the 5'-end of the "old" DNA strand (the template strand for the new lagging strand), is this right? I also wonder: is the only reason that we have thymine instead of uracil in DNA, that we can see if a deamination from cytosin has occurred?

Hi! I'm a girl from Scandinavia, studying my first year at the university in health science. This year I'm having biochemistry and chemistry, among other topics within health. Math and biology are my favorite topics. Besides this I at the moment feel a desire to make snowangels, here it's a lot of snow! Nice to meet you! *Smiles at you all*