Solution-How antibodies help to destroy invading bacterial | Quick Homework Help
Part I.
1. Name the cytokines that regulate growth and maturation in erythrocytes, leukocytes, and megakaryocytes.
2. Distinguish between heme and hemoglobin, and between ferritin and transferrin
3. If you injured your finger by the cut with knife, what mechanisms will act to stop the bleeding?
4. Distinguish between the intrinsic, extrinsic, and common pathways of the coagulation cascade.
5. Describe the role of calcium in the intrinsic and extrinsic pathways.
6. Once platelets are activated to aggregate, what factors halt their activity?
7. Explain the mechanism of activation of fibrinolytic system.
8. Why heparin is a very powerful anticoagulant?
9. Explain why von Willebrand’s disease cause prolonged bleeding after a dental or surgical procedure.
10. A person with O blood type is transfused with type A blood. What happens? Why?
11. What constitutes a universal donor and a universal recipient? What happens when blood from a universal recipient is transfused to universal donor?
12. Why there is no universal donor or universal recipient anymore?
Part II.
1. Explain how antibodies help to destroy invading bacterial cells.
2. Describe the role of macrophages in activating the specific immune response to antigens.
3. Explain how tolerance to self-antigens may be produced. Also, give two examples of autoimmune diseases and explain their possible causes.
4. A child is stung by a bee for the first time. Why should the parents be particularly alert when the child is stung a second time?
5. Because antibodies are proteins, they are too large to cross cell membranes on transport proteins or through channels. How then do IgA and other antibodies become part of external secretions such as saliva, tears, and mucus?
6. Name the three main types of lymphocytes and their subtypes. Explain the functions and interactions of each group.
7. Why do lymph nodes often swell and become tender or even painful when you are sick?
8. What is meant by the term neuromodulation?
9. HIV is a retrovirus that uses an enzyme called reverse transcriptase to reproduce. New antiretroviral drugs are used to treat pts with AIDS. Why can’t retroviruses reproduce without reverse transcriptase?
10. What correlation can be made between T-cell count and the viral load of HIV in patients with AIDS?
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Biochemically Heparin is a socioeconomically that is secrets in the granules of mast cells. Pharmacological heparin acts a potential anticoagulant that catalyzes the coagulation of pro tease by antilogarithm. During the clot formation process, antilogarithm uses to trigger the inhibition of activated coagulation factors. The common pathway in the said process involves factors like thrombi, IXa, Xa and to some extent VIIa, which is inhibited by the antilogarithm. Owing to these process antilogarithm is also popularly substrate for suicide, which executes the mechanism with inhibition of protean activity over particular bond (Arg-Ser). The function of heparin in this context is mediated through the increase in rate of thrombi-antilogarithm reaction. In other words, heparin as a catalytic platform, where both pro tease and inhibitor can bind; and hence the reaction between them can be increased to thousand fold (Leung, Mannucci & Landaw, 2014).
Conformation change in protein is also an important phenomenon that leads to execution of several important pharmacological and signaling related actions. Heparin, upon binding also induces a conformation change in antilogarithm, which in turn leads to more exposure of the reactive binding site to the protean. Furthermore, in the catalysis process of reaction between thrombi and antilogarithm, the heparin molecule will be released from the complex. This molecule is further potent to increase the response rate among other bio molecules. Chemically, heparin molecules contain 200 to 300 Saccharomyces units, which are alternating sequence of D-glucagon acid and N-acetyl-D-glucose. The 3-O-sulfates glucose residues (a specific pentasaccharide) present in heparin, act as one of the specific binding site for antilogarithm. The heparin molecule is containing less than 18 Saccharomyces units does not include such specific binding site and thus are not potent to catalyze the inhibition of thrombi by antilogarithm molecule.
