Trematodes (flukes)- What is the difference between the definitive and the intermediate hosts, what organism is needed in the lifecycle of all of these flukes, and where are these organisms found?

1. Describe enzyme regulation: Direct vs Indirect, and each subtype. Describe what the regulatory molecules are, different names to describe each type of regulation (i.e. feedback regulation, allosteric regulation, etc.), and what types of reactions each are (catabolic or anabolic).

1) What is the definition of a wholegrain? Two Examples?

2)In terms of resistant starch or dietary fibre,what is the nutritional problem with the definition of wholegrain?

3) Why do we want resistant starch and dietary fibre to ferment in our large intestine?

1. Your 5-month-old son wakes up this morning with a high fever and hoarse cry, with what looks like a highly inflamed throat.  You decide to take him in for an examination.  The doctor believes he has a bacterial infection, likely Streptococcus.
   1. What three considerations should the doctor take before prescribing an antimicrobial drug?
   2. Describe the five sites of drug action.  Give an example of a drug that affects each site and explain the mode of action for each.
   3. When the doctor asks if you or your son have been exposed to the same disease recently, you recall that you’d seen something very similar at the healthcare clinic you work at just a few days prior.  Alarmingly, you also remember that some of the patients in your clinic were testing positive for MRSA.  
      1. What are the mechanisms of drug resistance and how are each acquired?
      2. How can the doctor determine the resistance of your son’s pathogen (Kirby Bauer)?

Genetic Mapping of Innate Immune Defects.

Septic shock is a very dangerous medical condition that is described in your textbook on page 135. It is essentially an acute hyper-activation of the macrophage innate immune response, resulting in systemic (instead of localized) production of cytokines, with deleterious effects. Normally, local cytokine production at an infection causes “leakiness” in blood vessels, so that leukocytes can exit and migrate to the infection site (erythrocytes also leak out in the process, leading to the “redness” characteristic of inflammation). However, when cytokines are released throughout the body (“systemically”), then all the blood vessels become leaky (“vascular permeability”), leading to precipitous drops in blood pressure, and frequently organ failure and death. Septic shock has a 50% mortality rate, and is the leading cause of death in intensive care units (ICU’s) in hospitals.

One of the most common triggers of septic shock is LPS. In normal Gram-negative infections, this outer-membrane molecule is only present at the site of infection; however, if the bacteria reach the blood-stream, then LPS can quickly disseminate and trigger massive cytokine release throughout the body. This dangerous property of LPS led to its original name, “endotoxin”. (“endo” was meant to distinguish it from secreted “exo” bacterial toxins; unlike exotoxin virulence factors like cholera toxin, LPS/endotoxin is not a virulence factor evolved to exploit host cells).

Mice were often used to study septic shock, and a mouse strain that was resistant to septic shock was discovered in the 1960s. Normally, mice injected with LPS would succumb quickly to septic shock and death, but these mutant mice (C3H/HeJ strain) showed no effect upon LPS injection. On the other hand, when infected with live Gram-negative bacteria, the C3H/HeJ mice were unusually susceptible to infection and death.

In some ways, the C3H/HeJ mice were analogous to the boys diagnosed with CGD (chronic granulomatous disease) in the 1960s, in that both had heritable conditions that impaired immunity. A heritable defect implies the existence of a mutated gene that normally contributes to the affected process.

2a. The typical process for identifying an unknown gene that has a “phenotype” of interest is to “map” it to a particular chromosome, and then narrow its location to a smaller and smaller portion of this chromosome. Using animal models, this involves many generations, and tests of each generation to see which regions of which chromosome are always inherited in the individuals that exhibit the trait. This implies that chromosomes are not inherited intact from generation to generation: if chromosomes are strands of nucleotides covalently linked to each other, how is it that they are not inherited intact from parent to child?

2b. When mapping a trait in humans, instead of following inheritance through multiple generations (even if the disease status of ancestors is recorded, mapping is not feasible within family trees since DNA samples of ancestors were not preserved), researchers instead work with multiple independent families that seem to exhibit the same genetic disorder. For CGD genetic mapping, it was fortuitous that in the 1960s the disorder was identified in multiple unrelated patients. What feature of the CGD disease made identifying the affected gene a little easier by allowing the researchers to narrow their focus to a single chromosome?

2c. Is CGD a recessive or dominant genetic disorder?

2d. What traits or defects were observed in patients with CGD?

2e. Identifying the gene affected in CGD patients led to the discovery of an enzyme complex important in innate immunity. What is the name of this enzyme complex, and what does it do?

2f. The C3H/HeJ mice had a genetic syndrome with both beneficial and detrimental traits. In your own words, describe the beneficial vs detrimental aspects.

Duchenne’s muscular dystrophy is a recessive X-linked disease (Xd). A cross takes place between a heterozygote normal female and a male with the disorder. A) Determine the genotypes of the parents. B) What would be the phenotypic and genotypic ratios of males and females of the F1 generation?

For each of the following single strands of DNA, write the correct DNA counterstrand using the rules of Watson-Crick DNA structure. To get the correct answer, your final structure must have:

i) Antiparallel strands

ii) Watson-Crick base pairs at each position

1. 5’-GCTGCATCCGTTAA

2. 3’-ATGGCTACTACGTA

3. TCGAATCCAGCTAGGC-5’

1. What is the relationship between dose, clearance, bioavailability and Steady State plasma concentration?

i need it in 160 words please

  How do people become infected with Fasciola hepatica and what type of patient sample would be needed to diagnose this infection?

A dog breeder has a female black Labrador Retriever that was one of a litter of puppies from a mating of a yellow lab with a brown lab. If he breeds this dog with a black stud that is also from a mating between a yellow lab and a brown lab, what phenotypes and ratio which you expect among the puppies. (The answer is 9 black, 3 brown and 4 yellow. I just don't know how to get these answers). Thanks!

Starch structure questions

1) Which feature of amylose leads to increased intensity of the blue colour of the amylose iodine complex?

2) What part of the DSC endotherm gives the value of Gelatinisation Temperature?

3) When starch is cooled, what are the two processes that occur?

Describe how the Ames test can be used as a test for screening potential carcinogenic compounds. Include in your answer what an auxotroph is, why you need an auxotrophic mutant, limits of the test. Why is meant by spontaneous reversion?

A: 56, B: 11, AB: 8, O: 25 . Draw Punnett Square:

Assume the population is in Hardy-Weinberg equilibrium

Calculate the allele frequencies:   p =      

q =       

r =

Algebraic equation    Numerical freq.

Expected freq of   A:

B:

AB:

O: