(e) Two ADP agonists (drugs) were also found to bind to platelets: 2-methylthio-ADP bound with a Kp of 7 µM and 2-(3-aminopropylthio)-ADP bound with a Kp of 200 µM. Can these drugs effectively compete with ADP for binding to platelets? Explain your answer.
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- 2B. S. aureus hemolysin B attacks the RBC cell membrane by hydrolyzing the sphingomyelin headgroup: ОН HN .R hemolysin B cuts this bond i) Draw a plausible mechanism of hydrolysis for this lipid headgroup. Let B- and BH be general base and general acid. 00-P-O LOR2 OR, ii) Why is this damaging to the overall membrane architecture of the RBC?1. Researchers isolated a monomeric protein from platelets that has 2 binding sites (A and B) for ADP; Site A's Ka is 157 μM, and Site B's Kd is 2.2 μM. 1.1. A) Which binding site has higher affinity for ADP? B) Briefly justify your answer. C) For this higher affinity site, calculate the standard free energy change for ADP binding. Show your work. 1.2. What concentration of ADP is required to get site A filled in 20% of the proteins? 1.3. Based on this information, sketch a graph of the fraction of site B filled as a function of [ADP].Serum blood of a patient with dislipoproteinemia type 1 has milky appearance even in fasting. If serum stays at low temperature (40) for several hours fatty layer appears on its surface. What are the possible causes of these symptoms? To explain this, answer the questions and do the following tasks: a) what compounds of serum must be tested for that patient in biochemical lab? b) write the reaction which does not occur properly in patient’s blood; c) write down the schemes, explaining how the products of the previous reaction are used in adipose tissue and heart in healthy person 2 hours after a meal.
- ABC is an oral medicine and is a co-formulation containing Drug X and Drug Z. When administered alone, Drug X which is the active ingredient, exhibits poor bioavailability. Drug X is known to be metabolised by hepatic CYP enzymes. Studies have shown that addition of Drug Z results in higher blood levels of Drug X. 1) How this might be possible ? 2) Predict possible changes to the pharmacokinetic parameters of Drug X when co-administered with Drug Z ? 3) Clinical outcomes brought about by using this co-formulation ABC ?The anticlotting property of heparin is partly the result of the negative charges it carries. ( Q.) Which type of heparin is a better anticoagulant, one with a high or a low degree of polymerization?Amoeboid cells that migrate through our tissues, such as the class of white blood cells known as neutrophils, often do so in a directed manner, triggered, for instance, by chemical signals released by pathogens such as bacteria. Directed migration in response to a chemical stimulus is known as chemotaxis. Part of an efficient chemotactic response is the ability of cells to polarize. As is the case with our structurally-polar polymers like F-actin or microtubules, polarization here refers to an asymmetry in the cells, rather than an electrical charge. In this case, it involves one part of the cell becoming the “front” (or leading edge) and another the rear. In a well-polarized, migrating cell, it’s been observed that an active form of Rac (which, in turn, can activate ARP 2/3) is concentrated towards the front of the cell, whereas an active form of Rho (which, in turn, can activate formin, inhibit ADP, and activate myosin II) is found toward the rear of the cell. Based on your…
- Amoeboid cells that migrate through our tissues, such as the class of white blood cells known as neutrophils, often do so in a directed manner, triggered, for instance, by chemical signals released by pathogens such as bacteria. Directed migration in response to a chemical stimulus is known as chemotaxis. Part of an efficient chemotactic response is the ability of cells to polarize. As is the case with our structurally-polar polymers like F-actin or microtubules, polarization here refers to an asymmetry in the cells, rather than an electrical charge. In this case, it involves one part of the cell becoming the “front” (or leading edge) and another the rear. In a well-polarized, migrating cell, it’s been observed that an active form of Rac (which, in turn, can activate ARP 2/3) is concentrated towards the front of the cell, whereas an active form of Rho (which, in turn, can activate formin, inhibit cofilin/ADP, and activate myosin II) is found toward the rear of the cell. Based on your…a) Calculate the weight (in gram/ml) of tumour cells in each vial. Show your workings. b) Calculate the glucose concentration in each vial (in mol/ml). Show your workings. c) Based on Table 1, calculate the glucose concentration / 1 gram tumour cells in conditions A, B and C. Show your workings.Biomedical Engineering: An equilibrium dialysis experiment was performed to characterize the binding affinity of a mouse IgG or human IgG antibody for an antigen, GAD65. (The association constant for the monoclonal mouse IgG is 4.75 x 10^8 M-1 and for a human IgG is 1.3 x 10^10 M-1) a- calculate the dissociation constant for each antibody and explain which antibody has a higher binding affinity for GAD65? b-calculate the fraction of free Ab sites for each antibody for a For a GAD65 concentration of 0.7 nM
- List 4 different actiated carrier molecules, for each one, list both the oxided and reduced formsYour friend's genetic test revealed that they have a rare mutation - they lack the glycotransferase responsible for adding the terminal fucose molecule to the oligosaccharide on the surface of red blood cells. What is the consequence for a blood transfusion - which blood groups can they receive donations from, if any? Why? Although they lack the terminal fucose normally found on the surface of red blood cells, can you make any predictions as to wheter they also have or lack the Galactose or GalNAc found on A or B blood types? Your friend suggested a simpler way to test for this type of mutation. They have suggested taking a Fucosidase (a type of glycosidase) and mutating it so that the active site was no longer functional - they claim this would endow the protein with the properties of a lectin. Does their claim make any sense?One of the blocking solutions that is traditionally used is non-fat milk, but this is not recommended for studies of phosphoproteins. Why?