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22 Nov 2018

Nutrition

An athlete is assessed for riboflavin status using erthyrocyte glutathionine reductase activity coefficient. The cut-off is 1.2, and this athlete's result was 1.3. What does this result indicate for the athletes riboflavin status (i.e. deficient, normal, toxic)? How does the enzyme coefficent measure riboflaviin status?

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Nestor RutherfordLv2

22 Nov 2018

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The people of Malaysia belong to three communities: the local people called Malays, immigrants from South India called Tamils, and immigrants from China. During the early 20th century, the Malays lived mainly in coastal villages, the Tamils worked on rubber estates, and the Chinese worked in tin mines. In general, the people were very poor and they consumed a limited variety of foods.[1] Rice was the staple diet of all three communities and therefore the key source of caloric and nutrient content. Malays typically grew their own rice and dehulled it before consuming it; dehulling partially removes the aleurone layer of the rice seed. Following their South Indian food habits, the Tamils ate parboiled rice, and the Chinese ate polished white rice imported from Thailand. It was found that among the three Malaysian communities, the Chinese community was much more prone to suffer from some degree of sub-optimal thiamin intake. Out of every 1,000 Chinese inhabitants, about 120 had mild thiamin deficiency, about 80 had severe thiamin deficiency, and about 16 people had died of it. Suboptimal intake of thiamin was rare in Malays and was not reported at all in Tamils.[1] Thiamin, also called Vitamin B1, is required for all tissues, and its deficiency causes the disease Beriberi. Less severe deficiency results in non-specific symptoms such as weight loss, malaise, irritability, and confusion. Although the origin of the word Beri-beri is disputed, it is believed to be a Philippine word meaning âI canât, I canâtâ and was probably coined to refer to the lack of neuromotor coordination in people afflicted with this disease.[2] Thiamin is water-soluble and is stable in the acidic medium. It is unstable to heat, oxygen, and UV light in neutral and alkaline medium. The active form of thiamin is thiamin pyrophosphate (TPP). This active form is a cofactor for pyruvate dehydrogenase and transketolase enzymes that are involved in the metabolism of carbohydrates. These enzymes play an important role in the biosynthesis of a number of cell constituents such as neurotransmitters, pentoses, and reduced equivalents, used in oxidant stress. The human body cannot store thiamin and therefore requires a continuous supply of the vitamin. The thiamin in an individual on a thiamin-free diet typically depletes in fewer than two weeks. Thiamin absorption is affected by compounds, called thiamin antagonists or anti-thiamin factors, that alter the structure of thiamin. These compounds include alcohols, polyphenols, flavonoids, and thiaminase, a heat labile enzyme found in certain foods.[2] In affluent countries, where the diet is rich in thiamin, the most common cause of thiamin deficiency is excessive alcohol consumption. Alcohol intake affects thiamin status in two ways. First, alcoholics get a significant percentage of their daily energy intake from alcoholic beverages, which are nutrient deficient. In other words, alcoholics replace their consumption of nutrient dense foods that are part of their normal diet with the consumption of nutrient deficient alcohol. Second, alcohol inhibits the intestinal ATPase involved in the absorption of thiamin.[4] Sub-clinical thiamin insufficiency associated with excessive alcohol consumption produces an encephalopathy called Wernicke-Korsafoff syndrome. Patients with this syndrome have a higher than normal incidence of abnormal transketolase, which has a very low binding affinity to TPP. This problem can be overcome by putting patients on high-dose thiamin therapy. Some patients, however, might have a form of abnormal transketolase that does not bind at all with TPP. Such people do not respond to high-dose thiamin therapy.[4] Thiamin deficiency is observed in individuals who have low thiamin intake and a diet rich in polished rice, especially if their diet also consists of anti-thiamin factors such as tea, coffee, raw fermented fish, and betel nuts. The minimum amount of thiamin needed by the body can increase because of increased physiological or metabolic demands arising from pregnancy and lactation, heavy physical exertion, illnesses like cancer, liver diseases, hyperthyroidism, and surgery. Since TPP is required for carbohydrate metabolism, the recommended dietary allowances for thiamin are based on the assumption that its intake is related to total energy intake. The recommended dietary allowance in the United States is 0.5 mg/1000 Kcal.

Questions
1. Thiamin deficiency was observed only in the Chinese community even though all three
communities had the same staple (rice) diet. Explain.
2. On packages of enriched rice sold in supermarkets, the rice preparation directions state that the
rice should not be washed before cooking. Explain.
3. Severe metabolic acidosis caused by high levels of lactate is often associated with thiamin
deficiency. Explain.
4. Provide two plausible explanations for what might cause above normal levels of pyruvate in blood
and urine. How can one determine which of the two explanations is correct?
5. Why does thiamin utilization increase among cancer patients?
6. A negative correlation exists between the need for thiamin and the amount of fat in the diet.
Explain.

taupehound665

Question #05: CV Integration and the Respiratory System The question for this week is as follows: Select a position on the question âhow good an athlete is the horseâ. Do you think the respiratory limitations of this specie (e.g. pulmonary hypertension, exercise induced pulmonary hemorrhage or EIPH) are expression of physiological compensation for a fit athlete, or are they manifestation of a system being ârun down to the ground in a very stressed athleteâ? Your answer must follow the outline shown in the introduction (sub-questions a, b, c, d, see above). Please notice that in this question both the structure and the function you are asked to select must be related to the EIPH syndrome. Hint: think on âthe circleâ.
a) Name the structure and the function on which your overall answer will be based? Be as specific as you can in delimiting the boundaries of your example (the most important part of your answer, since the following b, c, & d sub-questions are based on your answer to this first sub-question, a). Please notice that only 1 item is required (in your answer it should be labeled as âaâ). This answer should look like: âa.- My structure (S) is â¦. and its function (F) is â¦â. In same cases a second sentence might be needed. b) Why do you think that your structure and your function are related? Support your contention based on 3 lines of evidence based on the chemistry, physics, anatomy, or physiology involved in your example. Please notice that 3 items are required (answers should be labeled as âb1, b2, and b3â). One of this answers might look like: âb1.- If I do this experiment and measure this variable using this technique, this result will suggest that my S/F is correctâ. Please notice that MY question does not ask you to tell me what happens since this can be copy from any source, but it asked how do you know that your S/F relationship is true. c) Which are the levels of organization involved in your example (c1)? Cite events occurring at its main level of organization (c2) and indicate how they relate to the whole body level (c3). Please notice that 3 items are required (thus, answers should be labeled as âc1, c2, and c3â). These answers should look as follows: âc1.- molecularâ or any level of organization involved in your âaâ answer (S/F); âc2.- the first event is; the next even is; the middle event is; the next event is; the last event isâ. Five events distributed equidistant from each other is a good summary for the story line of the your S/F named in your âaâ answer. Finally, âc3.- at a whole individual level my S/F described in âaâ plays this roleâ. d) Which are the main feedback mechanisms involved in your example (cite at least two) (d1)? Expand on one of them (d2) and name 2 absolute requirement for that feedback to work (d3). Please notice that 3 items are required (answers should be labeled as âd1, d2, and d3â). These answers should look as follows: âd1.- an increase in this negative feedback ligand must decrease this variable under controlâ. This is how you NAME a negative feedback. For d1 you need to name two negative feedbacks; âd2.- the first event is; the next even is; the middle event is; the next event is; the last event isâ. Five events distributed equidistant from each other is a good summary for the most important negative feedback story line involved as a control of the your S/F named in your âaâ answer, that you named in d1; âd3.- this two components are absolutely necessary for the negative feedback described in d2 to be operational.

cerisegoat49

1)What are the inputs of photosynthesis?

2)What are the outputs of photosynthesis?

3)Light-Dependent Reactions

Where does the first stage of photosynthesis, the light-dependent reactions, occur within a chloroplast?

Where does the energy come from that drives these reactions?

What molecule donates an electron to the reaction center of photosystem II?

How is the energy of an electron changed as it moves along the ETC?

How does the electrical charge of the thylakoid membrane affect protons (H+) within the chloroplast?

Where does the electron that is donated to photosystem I come from?

What are the final products of this series of reactions?

What happens to each of the final products from this series of reactions?

4)Light-Independent Reactions (Calvin Cycle)

a.Where does the second stage of photosynthesis, the Calvin Cycle, occur within a chloroplast?

b.What are the direct inputs for these reactions?

c.What are the three steps to the Calvin cycle?

d.What are the final products of this reaction?

e.What role does rubisco play in the Calvin Cycle?

1)What experiment was performed that allowed for scientists to finally agree that DNA is the genetic material within living organisms?

a.Understand the materials and scientific techniques used to come to this result.

2)What group of experiments led to the discovery of the mechanism used in DNA replication?

a.Understand the materials and scientific techniques used to come to this result.

i.What is a cesium chloride gradient?

ii.Where do 14N and 15N respectively fall along this gradient?

b.The results revealed that DNA replicates using which of the three proposed models?

i. Describe the mechanism of each model.

3)What is the role of the following proteins in DNA replication?

a.Helicase

b.Single strand binding proteins

c.Topoisomerase

d.DNA polymerase III

e.DNA polymerase I

f.Primase

g.Ligase

4)What extra steps are taken to be sure the lagging strand does not shorten each time DNA is replicated?

a.What is the role of telomerase in these âstepsâ?

5)In DNA repair, which enzyme has âproof-readingâ capabilities?

1)Which type of cells within our bodies use mitosis to reproduce?

2)Does mitosis create a cell that is different or the same as the parent cell undergoing division?

3)Describe the DNA found in sister chromatids.

4)Describe the DNA found in homologous chromosomes.

5)What occurs during the following stages of the cell cycle?

a.G₁ Phase

b.S Phase

c.G₂ Phase

d.M Phase

What are the phases of mitosis? What events occur in each phase?

1)Does mitosis separate homologous chromosomes, sister chromatids, or both?

2)What is cytokinesis?

a.Which fibers of the cytoskeleton contract to pinch parent and daughter cells apart from one another in animals?

b.How do microtubules move chromosomes to the two poles of a dividing cell?

3)How are centrioles involved in this process?

a.How do plants form two complete cells during cytokinesis?

4)How do bacterial cells reproduce?

5)The cell cycle is controlled at âcheckpointsâ. What occurs at each of the following checkpoints?

a.G₁ Checkpoint

b.G₂ Checkpoint

c.M Checkpoint

6)How do cyclin and cdk act to control the G2 checkpoint?

7)If presented with the schematic of the M checkpoint, you should be able to explain perturbations to the system as well as if the cell will divide or stall at metaphase.

8)Cancerous cells form when the cell cycle checkpoints do not function correctly and continues to divide even though it is damaged in some way. How does the protein p53 function to keep these cells from dividing?

9)Normal cells follow certain rules of growth that cancerous cells do not follow. What are these rules (provide a short definition for each as well)?

10)What is the difference between a benign tumor and a malignant tumor?