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NBME 6 block 3 q1 to 50 - maryam2009
#21
@ rawalian

the colonies will grow from the" SAMPLE "..."ONLY on the Streaking Lines" , so any colony is off the streaking line can not be from the sample hence it must be the contaminant and that is "D"
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#22
21.DD

1.first exposure to allergen
2.Th2 release of IL4,13 stimulate B cell to produce IgE....class switching occurs
3.B cell produces IgE in attaches to Fc receptor on mast cell
4.secound exposure to allergen
5.Allergen cross-links several IgEmolecules on mast cell and cell degranulates,releasig powerful chemicals

22.BB

q^2=1/2500....q=1/50
2pq=2/50=1/25

23.CC

24.BB

Vit C deficiency....neccessery for hydroxylation of proline and lysine in collagene synthesis
it also necessery for dopamine beta hydroxylase ....converts dopamine to NE
and facilates iron absorption by keeping iron in Fe2+ reduced state...more absorbable

25.AA

OTC affects the body's ability to get rid of ammonia, a toxic breakdown product of the body's use of protein.
Another symptom of OTC is a buildup of orotic acid in the blood. This is due to an anapleurosis that occurs with carbamoyl phosphate entering the pyrimidine synthesis pathway.

Ornithine transcarbamylase deficiency often becomes evident in the first few days of life, however it can present at middle age. An infant with ornithine transcarbamylase deficiency may be lacking in energy (lethargic) or unwilling to eat, and have poorly-controlled breathing rate or body temperature. Some babies with this disorder may experience seizures or unusual body movements, or go into a coma.
Ornithine transcarbamylase deficiency is an X-linked recessive disorder .

Treatment includes strategies to decrease the intake of nitrogen (low-protein diet), prevention of excessive body protein breakdown during acute illnesses (hydration and nutrition) and administration of medications scavenging nitrogen (sodium benzoate and sodium phenylbutyrate). Some patients may need to have supplemental amino acids (arginine, citrulline, valine, leucine, isoleucine).




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#23
26.EE

The capsule is considered a virulence factor because it enhances the ability of bacteria to cause disease (i.e. prevents phagocytosis). The capsule is slippery and fragile, so when a phagocyte tries to phagocytose the bacteria, it can slip away. A capsule-specific antibody may be required for phagocytosis to occur. Capsules also contain water which protects bacteria against desiccation. They also exclude bacterial viruses and most hydrophobic toxic materials such as detergents.
Immunity to one capsule type does not result in immunity to the other types. Capsules also help cells adhere to surfaces.

27.CC

Histamine is produced in the skin and especially in the burn wound by the increased number of mast cells present.

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#24
28.AA

waiting for explanation

29.AA

1-protein syntheis starts on the free ribosomes in the cytoplasm and continues in the ER

2-Almost all proteins that are transported to the endoplasmic reticulum have a sequence consisting of 5-10 hydrophobic amino acids on the N-terminus

3-The protein is guided to the ER by a signal-recognition particle (SRP), which moves between the ER and the cytoplasm

4- The N-terminus (one end) of a polypeptide chain (i.e., a protein) contains a few amino acids that work as an address tag, which are removed when the polypeptide reaches its destination

the N terminus corresponds to the 5' end.....as the carboxy terminus is for the 3' end

posted by yeabiruh
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#25
30 D

Multiple polymorphismSad aka Genetic Variation or Genetic polymorphism)

-SNPs (Single Nucleotide Polymorphism) is the most common


Hypervariable DNA----- region within the DNA where there are Base pairs of "Nucleotide Repeats" and most of the time they are located in the Non-coding region(spacer DNA).They are used as "MARKERS".Variablity of these Repeats help us in RFLP, paternity testing, Forensic and linkage analysis.

posted by Sarim

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#26
28.AA +explanation

1.Lack of oxygen causes the neuron's normal process for making ATP for energy to fail.
2.The cell switches to anaerobic metabolism, producing lactic acid.
3.ATP-reliant ion transport pumps fail, causing the cell to become depolarized, allowing ions, including calcium (Ca++), to flow into the cell.
4.The ion pumps can no longer transport calcium out of the cell, and intracellular calcium levels get too high.
5.The presence of calcium triggers the release of the excitatory amino acid neurotransmitter glutamate.
6.Glutamate stimulates AMPA receptors and Ca++-permeable NMDA receptors, which open to allow more calcium into cells.
7.Excess calcium entry overexcites cells and causes the generation of harmful chemicals like free radicals, reactive oxygen species and calcium-dependent enzymes such as calpain, endonucleases, ATPases, and phospholipases in a process called excitotoxicity.
] Calcium can also cause the release of more glutamate.
8.As the cell's membrane is broken down by phospholipases, it becomes more permeable, and more ions and harmful chemicals flow into the cell.
9.Mitochondria break down, releasing toxins and apoptotic factors into the cell.
10.The caspase-dependent apoptosis cascade is initiated, causing cells to "commit suicide."
11.If the cell dies through necrosis, it releases glutamate and toxic chemicals into the environment around it. Toxins poison nearby neurons, and glutamate can overexcite them.
12.If and when the brain is reperfused, a number of factors lead to reperfusion injury.
13.An inflammatory response is mounted, and phagocytic cells engulf damaged but still viable tissue.
14.Harmful chemicals damage the blood brain barrier.
15.Cerebral edema (swelling of the brain) occurs due to leakage of large molecules like albumins from blood vessels through the damaged blood brain barrier. These large molecules pull water into the brain tissue after them by osmosis. This "vasogenic edema" causes compression of and damag.
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#27
....AMPA
The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (also known as AMPA receptor) is a non-NMDA-type ionotropic transmembrane receptor for glutamate that mediates fast synaptic transmission in the central nervous system (CNS).

.....NMDA (N-methyl D-aspartate)
The NMDAR is a specific type of ionotropic glutamate receptor.
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#28
31.EE
Graph shows..... no relationship btw two components,so mutation causes... no affinity of repressor for operator

A repressor is a DNA-binding protein that regulates the expression of one or more genes by binding to the operator and blocking the attachment of RNA polymerase to the promoter, thus preventing transcription of the genes. This blocking of expression is called repression.

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#29
32.DD

33.CC

http://www.google.com/imgres?imgurl=http...29,r:0,s:0
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#30
34.CC

CD4+ T lymphocytes play an important part in the pathogenesis of scleroderma (systemic sclerosis, SSc) and predominate in perivascular SSc skin lesions.

Epitopes and subtypesAnti Scl-70 antibodies (also called anti-topoisomerase I after the type I topoisomerase target,it is a type of anti-nuclear autoantibody seen mainly in diffuse systemic scleroderma, but is also seen the more limited form of systemic scleroderma called CREST syndrome.

35.AA

Aplastic anemia.....pancytopenia with normal cell morphology ,hypocellular bone marrow with FATTY infiltration

Treatment....withdrawal of offending agent
immunosuppresive regimens.....antithymocyte globulin,cyclosporin
allogenic BM transplantation
RBC and platelet transfusion
G-CSF or GM-CSF
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