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  #1  
Old 08-20-2012
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Default Some Q's check out...

TNF is the primary mediator of host responses initiated by LPS & leading to septic shock. LPS-mediated activation of transcription most likely depends on which of the following transcription factors?

a) C-ras
b) Nuclear factor-kappa B
c) P53
d) Rb protein
e) VP-16 (etoposide)

A 20 year old woman develops severe pain & erythema over sun-exposed skin & large bullae over her shoulders while vacationing in Florida. Skin testing results in major positive reactions to methylparaben, which is often used as a preservative in medicines. A sunscreen containing which of the following is CONTRAINDICATED in this patient?

a) Avobenzone
b) Benzophenones
c) Cinnamates
d) P-aminobenzoic acid esters
e) Salicylates

Q12) A 55 year old man with diabetes mellitus has burning dysesthesias over the lateral aspect of his left lower leg. Capsaicin-containing cream is effective in alleviating the symptoms. The substance most likely to have caused the dysesthesias is

a) ADH
b) Angiotensin II
c) Dopamine
d) Inositol
e) Neurpeptide Y
f) Nitric oxide
g) Norepinephrine
h) Substance P

In a student lab session, male medical student finds erythrocytes in his urine. This finding is confirmed by the hospital lab. He denies any history of renal problems or recent illness. Vital signs are within normal limits. Antistreptolysin O titer is less than 1:100. Microscopic examination of urine is unremarkable except for rare red cell casts. There is no proteinuria. The most likely diagnosis is

a) Diabetic glomerulosclerosis
b) IgA nephropathy
c) Lupus nephritis
d) Membranous glomerulonephritis
e) Poststrept glomerulonephritis
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  #2  
Old 08-20-2012
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Default my answers

1 - B Nuclear factor-kappa B
2 - D P-aminobenzoic acid esters???
3 - H Substance P
4 - B IgA nephropathy

Where are those questions from?
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i agree!

1b, 2d, 3h, 4b.
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Originally Posted by Casandra View Post
1 - B Nuclear factor-kappa B
2 - D P-aminobenzoic acid esters???
3 - H Substance P
4 - B IgA nephropathy

Where are those questions from?
NBME 2....Do you mind explaining no 1&2??
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Old 08-20-2012
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Originally Posted by obinocle View Post
NBME 2....Do you mind explaining no 1&2??
oh you've got to be kidding me!!!!! it's against this forum policy to copy-paste nbmes qs!!! plus it's really really really unfair to all of us who haven't taken any of the nbmes yet. it's an evaluation tool for us!!!!! so we shouldn't be exposed to those qs prior doing nbmes!!!!!!
it's been discussed sooo many times here that I can't even count.
when people want to discuss nbme qs they put it in the title of the thread to warn everyone else!!!!!!
not fair, not cool!!!!! dude...
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  #6  
Old 08-20-2012
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Default Plz mention NBME in question. Everytime you post.

1 - B Nuclear factor-kappa B (by exclusion)
2 - F ;-) NO IDEA
3 - H Substance P (As substance P is only element here for Pain perception. So thats my answer)
4 - B IgA nephropathy (Only answer i am confident about )
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Old 08-21-2012
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I don't know why some people are acting fussy?nbme 2 is outdated and yeah it's good to tag nbme questions but no one is using those outdated nbmes as accesment tool anymore.they are now for practice purpose and I am sure we all have seen these questions and answers
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Originally Posted by chux View Post
I don't know why some people are acting fussy?nbme 2 is outdated and yeah it's good to tag nbme questions but no one is using those outdated nbmes as accesment tool anymore.they are now for practice purpose and I am sure we all have seen these questions and answers
@obinocle
Check the discussion here
http://www.usmleforum.com/files/forum/2010/1/485259.php
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5.D
Methylparaben is an anti-fungal agent often used in hair gels. The compound is often found in carpules of local anaesthetic, acting as a bacteriostatic agent and preservative.

Methylparaben (also called Nipigin M, Tegosept, and Mycocten) is commonly used as a fungicide in Drosophila food media. Usage of methylparaben is known to slow Drosophila growth rate in the larval and pupal stages.

Safety
Methylparaben is readily absorbed from the gastrointestinal tract or through the skin.[1] It is hydrolyzed to p-hydroxybenzoic acid and rapidly excreted without accumulation in the body.[1] Acute toxicity studies have shown that methylparaben is practically non-toxic by both oral and parenteral administration.[1] In a population with normal skin, methylparaben is practically non-irritating and non-sensitizing; however, allergic reactions to ingested parabens have been reported.[1] Methylparaben can be found in many of the leading skin/face products.

However, some concerns involving products containing parabens (including Methylparaben) are discussed in the toxicology section of the paraben article. This includes a section on allergic reactions, breast cancer, estrogenic activity, as well as paraben controversy.


No 1 explanation
1. B
this question confused me too... i have searched in wikepedia...

a) Ras is a family of genes encoding small GTPases that are involved in cellular signal transduction. Activation of Ras signalling causes cell growth, differentiation and survival. Ras is the prototypical member of the Ras superfamily of proteins which are all related in structure and regulate diverse cell behaviours.
Since Ras communicates signals from outside the cell to the nucleus, mutations in ras genes can permanently activate it and cause inappropriate transmission inside the cell even in the absence of extracellular signals. Because these signals result in cell growth and division, dysregulated Ras signaling can ultimately lead to oncogenesis and cancer.[1] Activating mutations in Ras are found in 20-25% of all human tumors and up to 90% in specific tumor types.[2]
Ras proteins function as binary molecular switches that control intracellular signaling networks. Ras-regulated signal pathways control such processes as actin cytoskeletal integrity, proliferation, differentiation, cell adhesion, apoptosis, and cell migration. Ras and ras-related proteins are often deregulated in cancers, leading to increased invasion and metastasis, and decreased apoptosis.
Ras activates several pathways, of which the mitogen-activated protein (MAP) kinase cascade has been well-studied. This cascade transmits signals downstream and results in the transcription of genes involved in cell growth and division.[13] There is a separate AKT pathway that inhibits apoptosis.

... although c-ras is transcriptin factor it is not involved in TNF production...

b) NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls the transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens.[1][2][3][4][5] NF-κB plays a key role in regulating the immune response to infection. Conversely, incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes of synaptic plasticity and memory.[6]

c) p53 (also known as protein 53 or tumor protein 53), is a tumor suppressor protein that in humans is encoded by the TP53 gene.[1][2][3] p53 is important in multicellular organisms, where it regulates the cell cycle and thus functions as a tumor suppressor that is involved in preventing cancer. As such, p53 has been described as "the guardian of the genome," "the guardian angel gene," and the "master watchman," referring to its role in conserving stability by preventing genome mutation.[4]
The name p53 is in reference to its apparent molecular mass: it runs as a 53 kilodalton (kDa) protein on SDS-PAGE. But based on calculations from its amino acid residues, p53's mass is actually only 43.7kDa. This difference is due to the high number of proline residues in the protein which slow its migration on SDS-PAGE, thus making it appear heavier than it actually is.[5] This effect is observed with p53 from a variety of species, including humans, rodents, frogs, and fish.
In its anti-cancer role, p53 works through several mechanisms:
It can activate DNA repair proteins when DNA has sustained damage.
It can induce growth arrest by holding the cell cycle at the G1/S regulation point on DNA damage recognition (if it holds the cell here for long enough, the DNA repair proteins will have time to fix the damage and the cell will be allowed to continue the cell cycle.)
It can initiate apoptosis, the programmed cell death, if the DNA damage proves to be irreparable.
p53 pathway: In a normal cell p53 is inactivated by its negative regulator, mdm2. Upon DNA damage or other stress, various pathways will lead to the dissociation of the p53 and mdm2 complex. Once activated, p53 will either induce a cell cycle arrest to allow repair and survival of the cell or apoptosis to discard the damage cell. How p53 makes this choice is currently unknown.Activated p53 binds DNA and activates expression of several genes including WAF1/CIP1 encoding for p21. p21(WAF1) binds to the G1-S/CDK (CDK2) and S/CDK complexes (molecules important for the G1/S transition in the cell cycle) inhibiting their activity. p53 has many anticancer mechanisms, and plays a role in apoptosis, genetic stability, and inhibition of angiogenesis.
When p21(WAF1) is complexed with cdk2 the cell cannot pass through to the next stage of cell division. Mutant p53 can no longer bind DNA in an effective way, and as a consequence the p21 protein is not made available to act as the 'stop signal' for cell division. Thus cells divide uncontrollably, and form tumors.[13]
Recent research has also linked the p53 and RB1 pathways, via p14ARF, raising the possibility that the pathways may regulate each other.[14]
p53 by regulating LIV has been shown to facilitate implantation in the mouse model and possibly in humans.[15]
When p53 expression is stimulated by sunlight, it begins the chain of events leading to tanning.[16][17]

... so p53 is not involved in TNF synthesis....

d) The retinoblastoma protein (abbreviated pRb or Rb) is a tumor suppressor protein that is dysfunctional in many types of cancer.[1] One highly studied function of pRb is to prevent excessive cell growth by inhibiting cell cycle progression until a cell is ready to divide.It is also a recruiter of several chromatin remodelling enzymes such as methylases and acetylases.
pRb belongs to the pocket protein family, whose members have a pocket for the functional binding of other proteins.[2][3] Should an oncogenic protein, such as those produced by cells infected by high-risk types of human papillomaviruses, bind and inactivate pRb, this can lead to cancer.
pRb prevents the cell from replicating damaged DNA by preventing its progression along the cell cycle through G1 (first gap phase) into S (synthesis phase).[7] pRb binds and inhibits transcription factors of the E2F family, which are composed of dimers of an E2F protein and a DP protein.[8] The transcription activating complexes of E2 promoter-binding–protein-dimerization partners (E2F-DP) can push a cell into S phase.[9][10][11][12][13] As long as E2F-DP is inactivated, the cell remains stalled in the G1 phase. When pRb is bound to E2F, the complex acts as a growth suppressor and prevents progression through the cell cycle.[3] The pRb-E2F/DP complex also attracts a histone deacetylase (HDAC) protein to the chromatin, reducing transcription of S phase promoting factors, further suppressing DNA synthesis.

... so Rb protein is not involved in TNF synthesis...

e) Etoposide phosphate (brand names: Eposin, Etopophos, Vepesid, VP-16) is an inhibitor of the enzyme topoisomerase II. It is used as a form of chemotherapy for malignancies such as Ewing's sarcoma, lung cancer, testicular cancer, lymphoma, non-lymphocytic leukemia, and glioblastoma multiforme. It is often given in combination with other drugs. It is also sometimes used in a conditioning regimen prior to a bone marrow or blood stem cell transplant.
Its chemical make-up derives from podophyllotoxin, a toxin found in the American Mayapple.

...so VP-16 is also not involved in TNF synthesis...


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  #10  
Old 08-21-2012
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Originally Posted by chux View Post
I don't know why some people are acting fussy?nbme 2 is outdated and yeah it's good to tag nbme questions but no one is using those outdated nbmes as accesment tool anymore.they are now for practice purpose and I am sure we all have seen these questions and answers
It's not being fussy or something. Some people don't like to come across NBME questions in middle of there prep. So mentioning NBME can solve the purpose.



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It's not being fussy or something. Some people don't like to come across NBME questions in middle of there prep. So mentioning NBME can solve the purpose.



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Those nbmes are outdated.they are nolonger online so you can't even use them for assessment anymore.form 1-6 are strictly for practice ..
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Originally Posted by koolkiller88 View Post
1 - B Nuclear factor-kappa B (by exclusion)
2 - F ;-) NO IDEA
3 - H Substance P (As substance P is only element here for Pain perception. So thats my answer)
4 - B IgA nephropathy (Only answer i am confident about )
@kolllkiller
Why IgA nephropathy?I thought IgA nephropathy is sequel of URTI/GI but in question stem pxt has not been sick?
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@kolllkiller
Why IgA nephropathy?I thought IgA nephropathy is sequel of URTI/GI but in question stem pxt has not been sick?
Nephrology is always my week part but young age, RBC in urine, ASO negative ( so not PSGN)
So seems very much IgA nephropathy to me. Came across lot of patients like this during my clinical rotation.
And other options seems less probable then this option.

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Those nbmes are outdated.they are nolonger online so you can't even use them for assessment anymore.form 1-6 are strictly for practice ..
Ya I read about this and I totally understand u but remember this is public forum so it's better to avoid misunderstanding. That's also with minor rectification.



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Old 08-21-2012
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Default Hi

Ok Guyz thanks for the Explanations and getting me informed about the need for warning in posting NBME Q's. I Honestly didn't know about it, so next time i'll stick a warning.
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