The results shown in the accompanying graph support the hypothesis that Toll protein is necessary for protection from death by fungal infection O after fungal infection, wild-type flies die more rapidly than mutants lacking the Toll protein flies lacking the Toll protein die within one day of a fungal infection O Toll proteins have a delayed affect in killing flies
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- Bruce Ames and his colleagues have pointed out that although detailed toxicological analysis has been conducted on synthetic chemicals, almost no information is available about the mutagenic or carcinogenic effects of the toxins produced by plants as a natural defense against fungi, insects, and animal predators. Tens of thousands of such compounds have been discovered, and he estimates that in the United States adults eat about 1.5 g of these compounds each daylevels that are approximately 10,000 times higher than those of the synthetic pesticides present in the diet. For example, cabbage contains 49 natural pesticides and metabolites, and only a few of these have been tested for their carcinogenic and mutagenic effects. a. With the introduction of new foods into the U.S. diet over the last 200 years (mangoes, kiwi fruit, tomatoes, and so forth), has there been enough time for humans to develop resistance to the mutagenic effects of the toxins present in those foods? b. The natural pesticides present in plants constitute more than 99% of the toxins we eat. Should diet planning, especially for vegetarians, take into account the doses of toxins present in the diet?Last week when I mutated the SSA1 gene in yeast it made cells grow faster, but made them sensitive to temperature. SSA1 can be said to display what? a. Antagonistic hypertrophy b. Agonistic pleiotropy c. Agonistic hypertrophy d. Antagonistic pleiotropy e. Reductive pleiotropy f. Modular pleiotropyIncidence Computation The sum of the years "at-risk" of these 12 courses is 102 students-years and there were 3 occurrences of the disease. We can now compute the incidence rate. (One decimal place only, no need to include "%" sign)
- Link: Lack of RAC1 in macrophages protects against atherosclerosis - PMC (nih.gov) Could somone explain exactly what this means below? NOT HW just trying to get a better understanding on what this experiment is about. To produce mice that are deficient for RAC1 in macrophages, female C57BL/6 mice homozygously expressing the floxed Rac1 gene (Rac1fl/fl) [6] were crossbred with male mice homozygously expressing Cre under the monocyte-specific lysozyme M promoter (LC) [12]. Mice were genotyped for Rac1 deficiency as previously describedOne important role of Fas and Fas ligand is to medi-ate the elimination of tumor cells by killer lymphocytes.In a study of 35 primary lung and colon tumors, half thetumors were found to have amplified and overexpressed agene for a secreted protein that binds to Fas ligand. How doyou suppose that overexpression of this protein might con-tribute to the survival of these tumor cells? Explain yourreasoning.8. The Covid-19 pandemic started with the alpha variant that had an R0 of ~2 and a lethality rate of ~2%. What might things look like if we have a future pandemic caused by a pathogen that has an R0 of 5 and a lethality rate of 10%?
- Using the substrate Ac-Ser-Gln-Asn-Tyr*Pro-Val-Val-NH2 and 10 nM HIV-1 protease, an inhibitor showed competitive inhibition, and a family of lines of 1/v vs. 1/[substrate] at changing-fixed concentrations of this inhibitor were as below: Slope (apparent Km/Vmax) (sec): 17,241 21,072 24,904 28,735 32,567 [Inhibitor] (M): 0 10 20 30 40 The Ki value for this inhibitor is _________________Utilizing Bentham's "Felicific Calculus" step-by-step, give a justification in practicing proper use of facemasks outdoors as a health protocol during this time of COVID-19.Penicillin was first used in the 1940s to treat gonorrhea infections produced by the bacterium Neisseria gonorrhoeae. In 1984, according to the CDC, fewer than 1% of gonorrhea infections were caused by penicillin-resistant N. gonorrhoeae. By 1990, more than 10% of cases were penicillin resistant and a few years later the level of resistance was 95%. Explain the various ways this resistance could be spread among the cells. Could this resistance pass to other infectious bacteria from N. gonorrhoeae?
- Hookworms, parasitic nematodes transmitted through contact between bare feet and soil,infect nearly a half billion people. In the small SE Asian nation of Timor-Leste, infection rates insome regions approach 70%, and the resulting anemia from these infections has a serious impacton quality of life. Health officials are concerned by a recent rise in Ivermectin-resistant cases inthe isolated enclave of Oecussi, and are worried about these drug resistance genes spreading tothe capital Dili, 165 km away. You genotype diploid female hookworms, Ancylostoma ceylanicum,from 100 patients in each location for a neutral locus with two alleles A1 & A2.You find the following genotypic count data: A1/A1 A1/A2 A2/A2 Oecussi 36 48 16 Dili 9 42 3a. Use these data to calculate FST between these two populations. 3b. Assuming that these two populations are in drift/migration equilibrium, what is the effectivenumber of migrants moving between them each generationScientists used a Rat6-Raf transformed cell line for the anchorage-independent growth control experiment. This cell line is transformed with an activated form of Raf. The CP788 drug had no effect on anchorage-dependent growth iwith this cell-line. Explain why this cell line was used as a control in this experiment and why no inhibition of cell growth was observed with CP788refer to this paper: Cytosolic Malic Enzyme 1 (ME1) Mediates High Fat Diet-Induced Adiposity, Endocrine Profile, and Gastrointestinal Tract Proliferation-Associated Biomarkers in Male Mice What is the question that this research aims to answer? Figure 2. Look at each of these graphs and indicate the differences or similarities between each group of mice (WT CAS-HF, WT SPI-HF, MOD-1 CAS-HF, MOD-1 SPI-HF). Figure 3.A. What causes insulin release? Why is insulin being looked at (look in the discussion section) Where is leptin produced? What does it do? What is adiponectin? What does it do? What does a high leptin/adiponectin ratio mean? (Hint: Look at the introduction section). Figure 4. What is mTOR (look at the discussion section)? What enzymes/proteins were significantly different between the WT and MOD-1 mice? What enzymes/proteins were significantly different between the CAS-HF diet and the SPI-HF diet? Answer the same two questions above. Is there any…