Symptom Presentation:

Glutamate: Increased production of the neurotransmitter Glutamate

Memory Loss: Recent demonstrated memory loss

Previously, you researched and considered three conditions through the process of differential diagnosis that would present with varying abnormalities in homeostasis, metabolism, triglycerides and DNA in week 1. Abnormalities in oxidation, plasma and tissue enzyme activity, inflammation and alopecia respectively in week 2. Increased cortisol and demonstrated bone loss in week 3 and fibromyalgia and muscle atrophy in week 4. Given the new symptom presentation above, written presentation: . If choosing a written presentation, create a 2-3 paragraphs per each of the questions listed below. Is there a connection between the previous increased cortisol symptoms and an increase production in the neurotransmitter glutamate? Explain or debunk this connection. Are increased cortisol and increased glutamate associated with memory loss and neuron degradation in the central nervous system (CNS)? Rationalize and explain your answer. Do you believe this recent memory loss to be purely psychologically associated, purely biochemically associated or a mixture of both? Rationalize and explain your answer.you can choose one symptom from week one to three and compare with the two new symptom provided.

• Know-how p53 is activated during the cell cycle and what two outcomes are possible – know the signaling pathways (you do not have to know how PUMA induces apoptosis, just that it does)

• Know the types of chemical modulators of receptors – agonist/antagonist

• Know the G-protein-linked signaling pathway – how it is activated and what happens downstream – be able to describe the signaling pathways that lead to PKA and PKC activation

• Know the tyrosine-kinase signaling pathway – how it is activated and what happens downstream

• Be able to explain a dominant-negative mutant and constitutive mutant receptor in signaling

• Know the types of cell junctions

• Difference between a benign and malignant tumor

• “Seed & soil” hypothesis of cancer metastasis

• Know & describe the 10 hallmarks of cancer

• Know the four most common causes of cancer

• Know the difference between an oncogene and a tumor suppressor

• Understand the immune surveillance theory

• Know the phases of the cell cycle and what occurs at each stage

• Know where the checkpoints (restriction points) occur in the cell cycle and what influences each checkpoint

• Understand the role of cyclins and CDKs – which one is regulatory and which one has the enzyme activity

1. Imagine you have a plasmid and you cut it with three different restriction enzymes (enzymes 1, 2, 3). You then run these fragments through a gel and get this separation.
   1. Label the positive and negative terminals on this gel with a (+) and (-) sign.

2. If you were working with a single plasmid, how many cut sites did restriction enzyme 1 have? Explain?

3. When creating a gel, we stain it with Ethidium Bromide or Gel Red. What is the purpose of this? Explain.

2- When separating plasmids from proteins and ribosomes, why do you add N Buffer and THEN centrifuge? Why not just centrifuge? What is the advantage of adding the N Buffer?

1. I give you 100mL of a 3 M aqueous glucose stock solution. I need you to dilute it to make 100mL of a solution that is 0.03M. To accomplish this task, you have 2 additional 100 mL graduated cylinders and however much distilled water you need. The graduated cylinders are not really accurate at measuring any volume less than 5mL. (10 pts)

1. How would you dilute 3M stock solution into 0.03 M solution? Explain strategy.

Show your calculations:  

answer the following regarding DNA repair mechanisms

What is "direct repair"? Give a couple of examples of the enzymes involved. Which one requires light and what kind of mutation does it repair? Which one repairs bases with alkyl groups attached? Which base is involved?

What is “nucleotide-excision repair”? What kinds of mutations can it repair? In prokaryotes, what four key proteins are involved and how did they get their names? What two enzymes are involved?

What is “mismatch repair”? What does it do? This system corrects mistakes that have been missed by the normal correction system that occurs during DNA replication. Which enzyme normally corrects these mistakes during replication?

What source of DNA is usually used in “homologous recombination repair” to fix the mutated strand of DNA? During which parts of the cell cycle can this type of repair occur? HRR can also occasionally occur at other times, but the homologous regions may not be identical. Why might that be the case?

What happens during “nonhomolgous end joining”? During which part of the process might some of the sequence be lost? When during the cell cycle can this type of repair occur?

Bobby, a 72-year-old retired male went to his doctor, complaining of leg pain that started in his lower back, ran across the side of his thigh and over the front of his knee. Next, he developed pain that radiated from his back to his front at the chest through the level of his nipples and also at the umbilicus.

A physical and laboratory tests showed hard nodule on his prostate and an elevation in several of the blood tests. His PSA (prostate specific antigen), an enzyme secreted by normal prostate tissue was very high. Alkaline phosphatase was also elevated, an indication of bone involvement.

A bone scan was ordered to visualize the bone involvement.

Usually prostate cancer's growth is initially influenced by the presence of testosterone. If testosterone is removed by castration, the cancer will often shrink for some period of time before the remaining fraction of testosterone-independent cancer cells grow.

Bobby was not interested in castration and asked if there was another form of treatment. He was treated was a single shot of a drug which is slowly released into the body over a three month time period. Within that time the patient noticed marked relief in his pain.

Why would the scan show bone abnormalities? What would cause it?

It has been determined that an agent of S.H.I.E.L.D. spends an average of 108 days per year identifying potential threats to human existence, with a standard deviation of 13.5 days. A random sample of 36 S.H.I.E.L.D. agents is taken.

a. What is the probability that the sample will have a mean of less than 105 days?

b. What is the probability that the sample will have a mean of more than 110 days?

c. What is the probability that the sample will have a mean between 109 and 114 days?

d. What is the probability that the sample will have a mean of no more than 104 days?

Thalassemia is a genetic disorder where affected individuals have red blood cells that produce too much iron. This disease is inherited as an autosomal recessive (tt). However, heterozygous individuals (carriers= Tt) may have some immunity to malaria (similar to sickle cell anaemia). Human blood samples are obtained from a Mediterranean population of 100 people where malaria is endemic. Of these, 50 people are found to be carriers (Tt), and additional 3 people have thalassemia (tt). Use these observed results to explain if heterozygous individuals have partial immunity to malaria?

1. The tolerance interval of 95.44 percent is ________ a 95.44 percent confidence interval.

the same width as

narrower than

wider than

2.

The U.S. Department of Health and Human Services collected sample data for 772 males between the ages of 18 and 24. That sample group has a mean height of 69.7 inches with a standard deviation of 2.8 inches. Find the 99 percent confidence interval for the mean height of all males between the ages of 18 and 24.

[63.19, 76.21]

[62.49, 76.91]

[69.65, 69.75]

[69.47, 69.93]

[69.44, 69.96]

A geneticist wants to identify genes that may be involved in resistance to COVID-19 infection. While you cannot perform mutational screens in humans, (you could - but it's highly unethical and illegal) you can perform these in human tissue culture. The experiment is designed to screen for cells that gain the ability to resist infection after being treated with a mutagen. This approach would be considered a: