About 10% of lung cancer patients are cured of the disease, i.e., they survive 5 years after diagnosis with no evidence that the cancer has returned. Only 14% of lung cancer patients survive 5 yearsafter diagnosis. Assume that the fraction of incurable lung cancer patients that survives a time t after diagnosis is given by exp(-kt).Find an expression for the fraction S(t) of lung cancer patients who survive a time t after being diagnosed with the disease. Be sure to determine the values of all of the constants in your answer.(Round k to four decimal places.)S(t) =What fraction of lung cancer patients survives 8 years with the disease? (Round your answer to four decimal places.)12

The question asks for two things: an expression for the fraction of lung cancer patients who survive…

Answered: About 10% of lung cancer patients are…

Phlebotomy Essentials

6th Edition

ISBN:9781451194524

Author:Ruth McCall, Cathee M. Tankersley MT(ASCP)

Publisher:Ruth McCall, Cathee M. Tankersley MT(ASCP)

Chapter1: Phlebotomy: Past And Present And The Healthcare Setting

Section: Chapter Questions

Problem 1SRQ

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With age, somatic cells are thought to accumulategenomic “scars” as a result of the inaccurate repair of dou-ble-strand breaks by nonhomologous end joining (NHEJ).Estimates based on the frequency of breaks in primaryhuman fibroblasts suggest that by age 70, each humansomatic cell may carry some 2000 NHEJ-induced muta-tions due to inaccurate repair. If these mutations weredistributed randomly around the genome, how many pro-tein-coding genes would you expect to be affected? Wouldyou expect cell function to be compromised? Why or whynot? (Assume that 2% of the genome—1.5% protein-cod-ing and 0.5% regulatory—is crucial information.)
The genetic alteration responsible for sickle-cell anemia in humans involves: a transition mutation from A to G, substituting glutamic acid for valine in a-globin a transversion mutation from T to A, substituting valine for glutamic acid in b-globin a transition mutation from T to C, substituting valine for glutamic acid in b-globin a transversion mutation from G to C, substituting glutamic acid for valine in a-globin a frameshift mutation of one ATC codon, removing glutamic acid from b-globin
Mutation in the fibroblast growth factor receptor (FGFR) gene results in achondroplasia (dwarfism), which is a dominant condition caused by a single base substitution (GGG>AGG) that changes the amino acid glycine at position 480 to arginine (G480R) in the FGFR protein. Normally, FGFR is active when FGF binds to it and inhibits excessive bone growth, but the mutant FGFR is constantly active even when FGF is not bound to it. o How can you create a mouse model for achondroplasia? Select all that apply. OPronuclear injection of a mutant copy (G48OR) of the gene to a mouse zygote V CRISPR that knocks in a mutant copy (G480R) of the gene to a mouse genome O CRISPR that knocks out the wild-type gene in a mouse genome O RNAI that knocks down the wild-type gene expression in a mouse genome O FGFR gene inactivated by a marker gene is introduced to embryonic stem cells
A) 43 14 When Friend erythroleukemic cells are incubated with sodium butyrate, they differentiate into nondividing, hemoglobin-synthesizing cells. Butyrate-induced differentiation is accompanied by accumulation of acety- lated forms of H3 and H4 histones, as can be seen most clearly for H4 in Fig- ure 4-16A. In principle, butyrate treatment could increase the activity of his- tone acetyl transferases (HATS) or decrease the activity of histone deacety- lase complexes (HDACs). To distinguish between these alternatives, HAT and HDAC activities were measured in the presence and absence of butyrate (Figure 4-16B and C). From these results decide how butyrate treatment causes accumulation of acetylated histones. butyrate (B) H-acetylated histone (cpm, thousands) N -butyrate + butyrate boiled 9 30 10 20 time (minutes) (C) C free 'H-acetate (cpm, thousands) S43210 boiled -butyrate +butyrate,
Acatalasemia is a rare autosomal recessive condition that results in no expression of the enzyme catalase; however, persons with this condition are usually only mildly affected. The enzyme catalase is found in most organisms and is a protection against oxidative damage, specifically breaking down the highly reactive oxygen species, hydrogen peroxide. Symptoms may include mouth ulcers that disappear with good dental hygiene; with poor dental hygiene, the ulcers can lead to gangrene in the mouth soft tissues. Persons with this condition usually do not know they are affected unless a family member is tested for the mutation. Dejah recently learned that her Uncle Malik had a dental surgery that was complicated by mouth ulcers and gangrenous tissue that had to be removed. The oral surgeon had learned about genetic conditions that affect oral hygiene and recognized that this could be acatalasemia, and ordered genetic testing. Uncle Malik was positive for this recessive condition, having…
Give only typing answer with explanation and conclusion A healthy asymptomatic 27 year old female, Susan, presents to your clinic with known family history of Spastic Paraplegia 4 caused by pathogenic SPAST mutation identified in her mother. She wants to know the risk that she will develop symptoms eventually based on this information. the penetrance of SPAST mutation is approximately 85% for women and 96% for men.
The seed of the castor bean (Ricinus communis) contains large amounts of ricin, a deadly poison for animals, including humans. One of the two subunits of this toxin is a lectin that binds terminal N-acetylgalactosamine residues on glycoproteins on the surface of eukaryotic cells, allowing the other subunit to enter the cell and kill it by preventing proteins from being made. Select the possible antidotes that could prevent or reverse ricin-mediated entry of the toxin. a high concentration of N-acetylgalactosamine an oligosaccharide with the same structure as that recognized by ricin a compound that prevents synthesis of extracellular glycoproteins a compound that activates enzymes that break down glycogen into glucose an enzyme that degrades lipopolysaccharides
Which of the following mutations would produce a form of the Ras protein that would be more difficult to inactivate than normal Ras? Briefly explain your reasoning.(i) A mutation that allows Ras to cleave (hydrolyze) GTP more rapidly than usual(ii) A mutation that causes Ras to bind Ras-GAP more tightly than usual(iii) A mutation that causes Ras to cleave (hydrolyze) GTP more slowly than usual
Cystic fibrosis (CF) is a genetic disorder affecting a number of organs, including the lung airways, pancreas, and sweat glands. Mutations in both copies of the CFTR gene causes cystic fibrosis. Imagine that you have sweat gland samples from several Cystic Fibrosis patients (A-C) with unknown mutations in CFTR. You also have normal (+) sweat gland sample to use as a positive control. А В С А В С Choose which mutation would explain the RNA and protein results in A, B, & C: 1. Promoter/Regulatory mutation 2. Silent mutation 3. Missense mutation 4. Deletion mutation 5. Splice site mutation 6. Nonsense mutation RNA gel Protein gel
Considerable effort has been directed toward determining the genes in which sequence variation contributes to the development of type 2 diabetes. Approximately 800 genes have been implicated. Propose an explanation for this observation.
A genetic disease called glucose-6-phosphate dehydrogenase deficiency is inherited in a manner similar to that of sickle-cell anemia except that it occurs most frequently in males. The defective enzyme cannot keep erythrocytes supplied with sufficient amounts of the antioxidant molecule NADPH NADPH protects cell membranes and other cellular structures from oxidation. Describe in general terms the inheritance pattern of this molecular disease. Why do you think that the antimalarial drug primaquine, which stimulates peroxide formation, results in devastating cases of hemolytic anemia in carriers of the defective gene? Does it surprise you that this genetic anomaly is commonly found in African and Mediterranean populations?
An experiment was conducted with two groups of genetically identical female agouti mice (Avy/a) that were mated with normal (a/a) male mice . Both female groups ate lab chow with bisphenol A (BPA) (50mg/Kg). (BPA, used in the manufacture of polycarbonate plastics, has estrogenic effects that include decreased CpG methylation.) The lab chow of one group was supplemented with methyl donors (e.g., folate, choline, and vitamin B12). The effects of BPA were abolished in the Avya offspring of the mice fed with the methyl donor–supplemented chow (i.e., the coat color distribution observed was shifted toward brown). Explain.

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