Grains questions

1) How many types of Resistant Starch are there?

2) What are other carbohydrates we eat that we must ferment, and why must we ferment them?

3)What is the major problem with storing wholegrain foods?

4) What type of compounds lead to rancid aromas? What is the chemical source of these compounds?

Explain the entire process of contraction in a skeletal muscle, starting with how the signal enters the muscle cell at the neuromuscular junction. Include all relevant ions, molecules, structures, and processes in your explanation. How does the muscle carry out a sustained contraction? How does a muscle relax? How does skeletal muscle differ from the other two muscle types?

<sup>12) The toxin produced by the bacterium Clostridium botulinum is a potent neurotoxin. When
used in high doses, the toxin causes death through paralysis. When used in high doses,
the toxin causes death through paralysis. However at low doses the toxin can be used for
cosmetic purposes or to treat overactive muscles. Botulinum toxin (BTX) prevents
neurons from being able to activate muscle contractions. BTX accomplishes this through
proteolytic activity (by degrading specific proteins). (6 points)
- One explanation is that BTX prevents the budding of neurotransmitter containing
vesicles from the Golgi apparatus. If this explanation is correct, what class of proteins
would BTX most likely target for degradation? Briefly explain.
- Another explanation is that BTX prevents the fusion of neurotransmitter containing
vesicles with the plasma membrane. If this explanation is correct, what class of proteins
would BTX most likely target for degradation. Briefly explain.
- In the presence of BTX, the membrane protein is found in intracellular vesicles,
however none is seen on the plasma membrane. Which explanation, a or b, does this
data support?</sup>

Grains Question

1) Pulses are considered under the category of grains. How do pulse grains differ botanically from cereal grains?

2) What is nutritious about the proteins and carbohydrates in pulses

3) Comparing white bread and baked beans, what is the major nutritional difference?

Dihybrid crosses of (virtual) fruit flies (Drosophila melanogaster) were carried out at the computer lab at this course. The mutant alleles studied were “vestigial wing” (vg) and “ebony body” (eb). The mutant P‐generation flies were homozygous recessive at both studied loci. The wild type alleles were homozygous dominant at both loci. The loci for vestigial wing and ebony body are located at separate chromosomes. Show the Punnett crosses from the P‐generation to the F1‐generation of mutant and wild type flies, and the Punnett cross when two individuals from the F1‐generation were crossed.

1. What are discrepancies between calf intestinal mucosa alkaline phosphatase and human alkaline phosphatase?

2. A solution was made up with p-Nitrophenyl phosphate (pNPP), 0.1 M borate buffer at pH 9.5 and and alkaline phosphatase. This solution has good enzyme activity. Why does changing the pH to 9 decrease the apparent activity of alkaline phosphatase?

3. solution was made up with p-Nitrophenyl phosphate (pNPP), 0.1 M borate buffer at pH 9.5 and and alkaline phosphatase. 50 uM of phosphate was added into the solution. Does the addition of phosphate to the assay mix cause competitive or non-competitive inhibition? Is this expected?

What change occurs in the bone to make conformational abnormalities permanent? ( regarding foals)

Which of the following statements is correct for primates in general?

Select one:

a. Species that are pair-bonded have the minimum degree of sexual dimorphism in body size.

b. Multimale, multifemale groups tend to have a higher degree of sexual dimorphism in body size than one-male, multifemale groups.

c. Multimale, multifemale groups with polygynandry are not sexually dimorphic in body size.

d. One-male, multifemale polygynous groups have less sexual dimorphism in body size relative to pair-bonded species.

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’