What are the modifying factors and toxic/therapeutic effects of cisplatin? Define all new terms and acronyms. Please don't put AI/GPT text, please make sure all text is 100% human written Please include at least 5 reliable apa references.
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What are the modifying factors and toxic/therapeutic effects of cisplatin?
Define all new terms and acronyms.
Please don't put AI/GPT text, please make sure all text is 100% human written
Please include at least 5 reliable apa references.
AI-generated content may present inaccurate or offensive content that does not represent bartleby’s views.
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- You are in charge of a new gene therapy clinic. Two cases have been referred to you for review and possible therapy. Case 1. A mutation in the promoter of a proto-oncogene causes the gene to make too much of its normal product, a receptor protein that promotes cell division. The uncontrolled cell division has caused cancer. Case 2. A mutation in an exon of a tumor-suppressor gene makes this gene nonfunctional. The product of this gene normally suppresses cell division. The mutant gene cannot suppress cell division, and this has led to cancer. What treatment options can you suggest for each case?The prospect of using gene therapy to alleviate genetic conditions is still a vision of the future. Gene therapy for adenosine deaminase deficiency has proved to be quite promising, but many obstacles remain to be overcome. Currently, the correction of human genetic defects is done using retroviruses as vectors. For this purpose, viral genes are removed from the retroviral genome, creating a vector capable of transferring human structural genes into sites on human chromosomes within target-tissue cells. Do you see any potential problems with inserting pieces of a retroviral genome into humans? If so, are there ways to combat or prevent these problems?Although it is well known that X-rays cause mutations, they are routinely used to diagnose medical problems, including potential tumors, broken bones, and dental cavities. Why is this done? What precautions need to be taken?
- The pre-mRNA transcript and protein made by several mutant genes were examined. The results are given below. Determine where in the gene a likely mutation lies: the promoter region, exon, intron, cap on mRNA, or ribosome binding site. a. normal-length transcript, normal-length nonfunctional protein b. normal-length transcript, no protein made c. normal-length transcript, normal-length mRNA, short nonfunctional protein d. normal-length transcript, longer mRNA, shorter nonfunctional protein e. transcript never madeIn selecting target cells to receive a transferred gene in gene therapy, what factors do you think would have to be taken into account?DNA Profiles as Tools for Identification STRs are: a. used for DNA profiles b. repeated sequences present in the human genome c. highly variable in copy number d. all of these e. none of these
- The following is a portion of a protein: met-trp-tyr-arg-gly-pro-thr-Various mutant forms of this protein have been recovered. Using the normal and mutant sequences, determine the DNA and mRNA sequences that code for this portion of the protein, and explain each of the mutations. a. met-trp- b. met-cys-ile-val-val-leu-gln- c. met-trp-tyr-arg-ser-pro-thr- d. met-trp-tyr-arg-gly-ala-val-ile-ser-pro-thr-The Adaptive Immune Response Is a Specific Defense Against Infection In cystic fibrosis gene therapy, scientists propose the use of viral vectors to deliver normal genes to cells in the lungs. What immunological risks are involved in this procedure?Antibiotics and Protein Synthesis Antibiotics are molecules produced by microorganisms as defense mechanisms. The most effective antibiotics work by interfering with essential biochemical or reproductive processes. Many antibiotics block or disrupt one or more stages in protein synthesis. Some of these are mentioned here. Tetracyclines are a family of chemically related compounds used to treat several types of bacterial infections. Tetracyclines interfere with the initiation of translation. The tetracycline molecule attaches to the small ribosomal subunit and prevents binding of the tRNA anticodon during initiation. Both eukaryotic and prokaryotic ribosomes are sensitive to the action of tetracycline, but this antibiotic cannot pass through the plasma membrane of eukaryotic cells. Because tetracycline can enter bacterial cells to inhibit protein synthesis, it will stop bacterial growth, helping the immune system fight the infection. Streptomycin is used in hospitals to treat serious bacterial infections. It binds to the small ribosomal subunit but does not prevent initiation or elongation; however, it does affect the efficiency of protein synthesis. Binding of streptomycin changes the way mRNA codons interact with the tRNA. As a result, incorrect amino acids are incorporated into the growing polypeptide chain, producing nonfunctional proteins. In addition, streptomycin causes the ribosome to randomly fall off the mRNA, preventing the synthesis of complete proteins. Puromycin is not used clinically but has played an important role in studying the mechanism of protein synthesis in the research laboratory. The puromycin molecule is the same size and shape as a tRNA/amino acid complex. When puromycin enters the ribosome, it can be incorporated into a growing polypeptide chain, stopping further synthesis because no peptide bond can be formed between puromycin and an amino acid, causing the shortened polypeptide to fall off the ribosome. Chloramphenicol was one of the first broadspectrum antibiotics introduced. Eukaryotic cells are resistant to its actions, and it was widely used to treat bacterial infections. However, its use is limited to external applications and serious infections. Chloramphenicol destroys cells in the bone marrow, the source of all blood cells. In bacteria, this antibiotic binds to the large ribosomal subunit and inhibits the formation of peptide bonds. Another antibiotic, erythromycin, also binds to the large ribosomal subunit and inhibits the movement of ribosomes along the mRNA. Almost every step of protein synthesis can be inhibited by one antibiotic or another. Work on designing new synthetic antibiotics to fight infections is based on our knowledge of how the nucleotide sequence of mRNA is converted into the amino acid sequence of a protein. Questions Why is targeting protein synthesis an effective strategy for preventing infection?
