One treatment for hyperuricemia is administration of xanthine oxidase inhibitors like allopurinol. Discuss the mechanism and show an illustration how this drug able to alleviate symptoms of hyperuricemia.
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One treatment for hyperuricemia is administration of xanthine oxidase inhibitors like
allopurinol. Discuss the
mechanism and show an illustration how this drug able to alleviate symptoms of
hyperuricemia.
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- In 2-page worth of words (around 500), discuss CYCLAMATE's regulation, allowable levels, and what group of people are at high risk for the side effects of CYCLAMATE in the body.One mechanism by which lead exerts its poisonous effect on enzymes can be stopped by chelation therapy with EDTA. Describe this type of lead poisoning and explain why it is reversible.One treatment for hyperuricemia is administration of xanthine oxidase inhibitors like allopurinol. What is the biochemical rationale for this treatment? Discuss the mechanism and show an illustration how this drug able to alleviate symptoms of hyperuricemia?
- Is monosodium glutamate (MSG) harmful? Please provide explanationIndividuals with hyperammonemia are given a-ketoacids as a treatment. Explain.Explain the role of L-tartrate in the determination of acid phosphatase . Differentiate thymolphthalein monophosphate method from alpha naphthyl phosphate method of prostatic acid phosphate determination. Why is acid phosphatase determination useful in establishing recent sexual intrusion as in the case of alleged rape? EXPLAIN 3-5 SENTENCES
- A series of novel phenadoxone derivatives without mu2 receptor activity (mu2 activity is responsible for physical dependence) proposed to be developed as analgesics is shown below. Addition of which heterocyclic substituent R to phenadoxone is LIKELY to cause the MOST binding of the corresponding derivative to plasma proteins? Use the additivity of approximate estimates of logP to answer this question. phenadoxone derivatives A. Azetidine B. Thiophene C. Oxetane D. Furan E. Pyrrole ترف لي تي في R= -NHThe plasma profiles of codeine (COD) and metabolites for 2 individuals (labeled A and B) are shown below. The X-axis is time in hours after an oral dose of codeine. [M=morphine; C6G=COD-6-glucuronide; M3G = morphine-3-glucuronide; NM (ignore)]. Note the data is shown on a log scale on the Y-axis. (A) Which individual is the poor metabolizer? Explain how you know this from the profiles? (B) Is this a problem for cough suppression? Explain. -CH HO Codeine COD 10 000 1000 C6G COD 100 M3G M6G NM 10 M 10 20 30 0 10 20 30 Plasma concentration (nmol I-)Explain using 2-3 sentences the biological significance of the following peptides . Glucagon Insulin Glutathione Ceruloplasmin Oxytocin
- In own words, give 5 or more reasons why most of the clinical features of the diseases a-ketoglutarate dehydrogenase deficiency, succinate dehydrogenase deficiency, and fumarase deficiency involve muscle and nerve tissue? and explain those reasons. Cite used references.Based on the image below, select the correct statements. Note: There may be more than 1 correct response. Ribose 5-phosphate ribose phosphate pyrophosphokinase (PRPP synthetase) glutamine-PRPP amidotransferase adenylosuccinate synthetase AMP -> PRPP 5-Phosphoribosylamine I adenylosuccinate lyase 9 steps Adenylosuccinate AMP IMP <-- ADP <- AMP <-- GMP <-- IMP IMP dehydrogenase <- GMP. XMP ADP ATP XMP-glutamine amidotransferase GMP يا Increased levels of ADP inhibit the production of PRPP. Increased levels of GMP inhibit the production of XMP. Increased ADP activates PRPP synthase to increase PRPP levels. Increased IMP activates glutamine-PRPP amidotransferase to further increase IMP levels.6-Mercaptopurine , after its conversion to the corresponding nucleotide through salvage reactions, is a potent competitive inhibitor of IMP in the pathways for AMP and GMP biosynthesis. It is therefore a clinically useful anticancer agent. The chemotherapeutic effectiveness of 6 mercaptopurine is enhanced when it is administered with allopurinol. Explain the mechanism of this enhancement.