My some review points and images before exam. - medicalspirit

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http://www.egydocs.com/forum/t4673/

[ArchivalUser]

hypohypoestrogen condition=( turner's , ovary removal, postmenapausal , Prolactionoma)
* Low estrogen = low bone mass
* hypohypoestrogen condition = over expression of RANK receptors cause increase bone resorption due to increased osteoclastic activity.

[ArchivalUser]

http://www.medscape.com/viewarticle/408911_4


Estrogen:
Estrogen withdrawal after ovariectomy or menopause leads to an increase in growth factors, such as M-CSF, and inflammatory cytokines, such as IL-1, IL-6, and TNF, with concomitant increased recruitment of myeloid progenitors, osteoclast formation, and bone resorption. Estrogen deficiency also increases activation and reduces apoptosis of mature osteoclasts.

Reciprocally, estrogen replacement reverses these effects and has a bone-protective effect; estrogen stimulates production of OPG in osteoblastic cells; as mentioned earlier, OPG treatment of oophorectomized rats completely prevents bone loss.[19] Together, these results suggest that enhancement of OPG may play a major role in the antiresorptive action of estrogen on bone. In a study presented at a recent meeting of the ASBMR, estrogen was found to be an inhibitor of RANKL and RANKL-stimulated osteoclastogenesis.[45] In another paper presented at the ASBMR meeting, estrogen was found to decrease the responsiveness of osteoclast precursors to RANKL by downregulating RANKL-induced JNK activity.[46] All of these data are consistent with multiple roles of estrogen: to regulate resorption-stimulating cytokine expression and OPG production by osteoblasts/stromal cells and to act directly on osteoclast progenitors to inhibit RANKL-induced and M-CSF-induced osteoclast differentiation.

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Glucocorticoids. Systemic glucocorticoid administration results in increased (or sustained) bone resorption and a decrease in bone formation, leading to osteoporosis.
glucocorticoids reduce OPG expression in human osteoblastic cells in vitro. As important, the decrease in OPG is more marked than the glucocorticoid-induced increase in RANKL, which leads to an increased RANKL/OPG ratio; this change in RANKL/OPG ratio may mediate the proresorptive effect of glucocorticoids. Serum OPG concentrations are reduced significantly in patients undergoing systemic glucocorticoid therapy

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TRAP positive mononuclear and multinucleated cells located in the synovium at the cartilage-synovial interface produce MMP-2 and MMP-9, and may have an important role in articular cartilage destruction in patients with RA.

* hairy cell leukemia
* Paget disease of bone
* RA.

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* Transformation : S. pneumoniae got resistant to penicillin by the process of transformation
also H. influezae and Neisseria sp have the same properties of transformation.
http://highered.mcgraw-hill.com/sites/00...uiz_1.html

* F+ to F- Conjugation: transfer of drug resistance; a property of Gram -ve bacteria which is plasmid encoded
http://highered.mcgraw-hill.com/sites/00...uiz_4.html

* Transduction: Generalized transduction is an accident during life cycle of lytic phage and Staph aureus beleived to get methicillin resistance and Pseudomonas getting imipenem resistance by these process.
http://highered.mcgraw-hill.com/sites/00...uiz_2.html

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Mitral valve stenosis
Aortic valve stenosis

http://www.cvphysiology.com/Heart%20Disease/HD004.htm

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*BOTH ANP & BNP activate guanulate cyclase which induces an increase of intracellular cyclic GMP.
* natriuresis cause vasodilation therefore decrease in blood pressure.

http://cgmp.blauplanet.com/adv/scheme.html

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* Endothelins are proteins that constrict blood vessels and raise blood pressure. They are normally kept in balance by other mechanisms, but when they are over-expressed, they contribute to high blood pressure (hypertension) and heart disease.

* ET-1 has been implicated in the development and progression of vascular disorders such as atherosclerosis and hypertension. Endothelial cells upregulate ET-1 in response to hypoxia, oxidized LDL, pro-inflammatory cytokines, and bacterial toxins. Initial studies on the ET-1 promoter provided some of the earliest mechanistic insight into endothelial-specific gene regulation. Numerous studies have since provided valuable insight into ET-1 promoter regulation under basal and activated cellular states.
The ET-1 mRNA is labile with a half-life of less than an hour. Together, the combined actions of ET-1 transcription and rapid mRNA turnover allow for stringent control over its expression. It has previously been shown that ET-1 mRNA is selectively stabilized in response to cellular activation by Escherichia coli O157:H7-derived verotoxins, suggesting ET-1 is regulated by post-transcriptional mechanisms. Regulatory elements modulating mRNA half-life are often found within 3'-untranslated regions (3'-UTR).

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http://highered.mcgraw-hill.com/sites/00...ction.html