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13 Feb 2019

9-A skeletal muscle develops from the fusion of large number of myoblasts (embryonic muscle forming stem cells). Growth and enlargement of muscles is called________________________ which results from the increase in number of muscle fibers/ activity myosatellite cells persisting in skeletal muscles.

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14 Feb 2019

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Related questions

3. a) The neurotransmitter that is responsible for “communication” at the neuromuscular junction between motor nerve cells and skeletal muscle fibers is acetylcholine (ACh). The ACh receptor protein is a channel that opens when ACh binds. Upon the opening of this channel, the membrane at the motor end plate region of the muscle cell becomes depolarized, resulting in the generation of an action potential in the muscle fiber membrane. The ACh receptor channel is equally permeable to both Na+ and K+ ions. Explain how opening a channel that allows both potassium and sodium to cross the membrane results in membrane depolarization. (2 points)

b) In normal individuals, a single end-plate potential (EPP) is always sufficient to elicit an action potential (and hence contraction) in a skeletal-muscle fiber. This is not the case in individuals suffering from myasthenia gravis (MG). MG is an autoimmune disorder in which antibodies are produced that attack the AChRs at skeletal-muscle endplates reducing their number. Patients suffering from the disease present with significant muscle weakness. Explain why patients with MG would exhibit muscle weakness. (2 points)

c) Treatment strategies for myasthenia gravis include thymectomy (removing the source of the antibody producing cells) or immunosuppressant drug therapy (inhibiting the synthesis and release of the antibodies). In addition, the drug neostigmine administered at carefully monitored doses is highly effective in treating myasthenia gravis. Investigate the actions of neostigmine, and discuss in detail why it may be an effective treatment. (2 points)

A well-studied autoimmune and neuromuscular disease affects the neuromuscular junction of afflicted individuals. It turns out that antibodies attack the ligand receptor found on the skeletal muscle cells and reduces the number of these receptors, leading to weakness in eye muscles, facial muscles and in severe cases affects respiratory muscles.

The name and location of the receptor this disease attacks.

What neurotransmitter binds the affected receptors?

In comparing the monosynaptic pathway for an individual without the disease and with the disease, if the sensory neuron in both individuals received the same stimulus (both in intensity and frequency), would the relative amount of neurotransmitter released at the neuromuscular junction differ? Why or why not (meaning explain using the physiology)? (

Would the end plate potential (EPP) differ in a person without the disease versus someone with this disease? How, explain.]

Given the scenario, what branch of the nervous system does this disease affect, central or peripheral? Somatic, parasympathetic, or sympathetic?

Propose a targeted drug treatment for an individual with this disease that would help to improve the effects of the disease. Said in a different way, what is the mechanism that is failing in this disease, and what could be changed to bring it back to “normal”.

16. Muscle glycogen cannot contribute directly to blood glucose levels because:

A. Muscle glycogen cannot be converted to glucose-6-phosphate

B. Muscle lacks glucose-6-phosphatase

C. Muscle contains no glycogen phosphoyrlase

D. Muscle lacks phophoglucoisomerase

_____17. Which of one of the following tissues requires insulin for glucose transport into the cell?

A. Brain

B. Liver

C. Skeletal muscle

D. Red blood cells

_____18. The mobilization of triaclyglycerol-bound fatty acids from adipose tissue and their subsequent oxidation by muscle mitochondria require all of the following compounds except:

A. Serum albumin

B. Carnitine

C. Acetyl CoA carboxylase

D. Hormone sensitive lipase

_____19. Which one of the following reactions is unique to gluconeogenesis?

A. Lactate ® pyruvate

B. Phosphoenolpyruvate® pyruvate

C. Oxalacetate® Phosphoenolpyruvate

D. 1,3bisphosphoglycerate ® 3-phosphoglycerate

_______20. A newborn vomits after each feeding of milk-based formula and doesn’t gain weight. Biochemical testing reveals a sever deficiency of galactose-1-phosphate uridyltransferase. If this condition goes untreated, which of the following is the likely outcome for this patient?

A. Benign disease except for cataract formation

B. Chronic emphysema appearing in early adulthood

C. Chronic renal failure appearing in adolescence

D. Death in infancy

E. Gastrointestinal symptoms that remit with puberty

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