why does covid 19 cause tissue factor and plasminogen activator inhibitors rise, whereas tissue factor inhibitors fall and the lung-blood barrier integrity deteriorates, and epithelial-derived substances promote coagulation by interacting with endothelial cells or circulating cells
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why does covid 19 cause tissue factor and plasminogen activator inhibitors rise, whereas tissue factor inhibitors fall and the lung-blood barrier integrity deteriorates, and epithelial-derived substances promote coagulation by interacting with endothelial cells or circulating cells
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- In covid-19 myocarditis happened, and endothelial cell is in charge of inhibiting the inflammation, what will happen to the endocardium? It will be affected?Therapeutic agents are currently being investigated that block the action of selectins in order to prevent the pathological effects resulting from leukocyte entry into sites of inflammation. These agents are molecules that inhibit selectin. Describe molecules that might be effective. (Information: Glycoproteins are an important class of proteins. There are many families of glycoproteins: lectins and selectins are examples.)One strategy for preventing type 1hypersensitivity is to induce plasma cells tosecrete lgG instead of IgE. Why would this blockallergy symptoms?
- Explain how expression of a dominant-negative mutant of JAK blocks the erythropoietin (Epo)-cytokine signaling pathway.The entry of naive T cells from the blood into lymph nodes and mucosal lymphoid tissues occurs by a process that involves similar steps and similar adhesion molecules to the process by which leukocytes are recruited into sites of inflammation. Yet naive T cells do not enter tissues at sites of inflammation, but rather, home to lymphoid tissues. Which class of adhesion molecules direct the specific homing of naive T cells to lymphoid tissues?For the PDHC, generally what goes on in each active site, what is the role of lipoamide, and what are the products of the overall process?
- c) State some of the features that cross the cell membrane and make "porin proteins" specific. d) Briefly clarify the concepts of "acylation", "prenylation" and "GPI stabilizer" in the context of membrane protein interactions. e) When determining ABO Blood Groups, give information about which blood group data can be obtained depending on the interaction of which antigens in the red blood cell and which antibodies in the serum.The production of antimicrobial peptides is one of the most evolutionarily ancient mechanisms of defense for multicellular organisms, and most eukaryotic species make many different forms of these proteins. For instance, human paneth cells in the gastrointestinal epithelium make 21 different defensins. The reason for this diversity of antimicrobial peptides is: Epithelial cells make different forms than those made by neutrophils. Neutrophils make many different defensins and store them as inactive proteins in their secretory granules. Most of them are produced only in response to infection. The production of different peptides is induced following a bacterial infection versus a fungal infection. Each one has distinct activities against Gram-negative bacteria, Gram-positive bacteria, or fungi.Cyclosporin A and rapamycin are each used as T cell immunosuppressants. They share the property of binding to immunophilin molecules in T cells as the initial step in their mechanisms of action. However, in the case of cyclosporin A, the drug:immunophilin complex binds to and inhibits the protein phosphatase calcineurin, whereas the rapamycin:immunophilin complex binds to and inhibitors mTOR. As a consequence, Cyclosporin A, but not rapamycin, blocks cytokine production by T cells. Both cyclosporin A and rapamycin block cytokine production by T cells. Rapamycin, but not cyclosporin A, blocks T cell proliferation. Neither rapamycin nor cyclosporin A block T cell proliferation. Both cyclosporin A and rapamycin inhibit co-stimulatory signaling through CD28 on T cells.