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Popular diabetes drugs associated with fractures in type 2 diabetic patients - Eureka! Science News
Camagüey Improves Assistance to Diabetic Children - Radio Cadena Agramonet
National magazine names Christiana Care among the best hospitals in nation - Cape Gazette
Lack Of Vitamin D May Lead To Artery Damage In African American Teens - BETTER Health Research
Thiazolidinediones May Up Fracture Risk in Older Women Concurrent ... - ModernMedicine
Amgen Ahead of Earnings - TradersHuddle.com
Cheers! Red wine can suppress inflammation in humans - Sify
Novel approach to treat diabetes - Sify
Dr. Selna Kaplan dies - pioneer UCSF researcher - San Francisco Chronicle
Rosiglitazone Video: Certain Diabetes Drugs Linked to Fracture Risk, Sleep ... - Insidermedicine
The role of leptin in the development of the cerebral cortex in mouse embryos. Posted by stemcellmarketing to PC:00331 PC:05704 PC:05703 "Area of Interest:Neuroscience" "Popular cell type:Neural stem & progenitor cells" PC:05702 PC:05701 PC:05700 "Popular product line:NeuroCult" on Wed Feb 03 2010
Gonadotropin secretion in cryptorchid and castrate rams and the acute effects of exogenous steroid treatment. Posted by mabin15 to 00000 N on Thu Feb 04 2010
Minireview: the AMP-activated protein kinase cascade: the key sensor of cellular energy status "All cells must maintain a high ratio of cellular ATP:ADP to survive. Because of the adenylate kinase reaction (2ADP ATP + AMP), AMP rises whenever the ATP:ADP ratio falls, and a high cellular ratio of AMP:ATP is a signal that the energy status of the cell is compromised. The AMP-activated protein kinase (AMPK) is the downstream component of a protein kinase cascade that is switched on by a rise in the AMP:ATP ratio, via a complex mechanism that results in an exquisitely sensitive system. AMPK is switched on by cellular stresses that either interfere with ATP production (e.g. hypoxia, glucose deprivation, or ischemia) or by stresses that increase ATP consumption (e.g. muscle contraction). It is also activated by hormones that act via Gq-coupled receptors, and by leptin and adiponectin, via mechanisms that remain unclear. Once activated, the system switches on catabolic pathways that generate ATP, while switching off ATP-consuming processes that are not essential for short-term cell survival, such as the synthesis of lipids, carbohydrates, and proteins. The AMPK cascade is the probable target for the antidiabetic drug metformin, and current indications are that it is responsible for many of the beneficial effects of exercise in the treatment and prevention of type 2 diabetes and the metabolic syndrome." Posted by sarah999 to file-import-10-03-14 on Thu Mar 25 2010
Regulation of Progesterone Receptor Expression by Estradiol Is Dependent on Age, Sex and Region in the Rat Brain Posted by lfrench to "estrogen receptor" estrogen rat on Tue Mar 30 2010
Orphanin FQ/nociceptin is a physiological regulator of prolactin secretion in female rats Posted by miamiunivsci to emurphree 2006 statistics on Fri Apr 23 2010
Uncoupling by cooling of secretion and adenosine 3',5'-monophosphate accumulation in stimulated dog thyroid slices. Posted by Martin1982 to 00000 N on Wed May 19 2010
Minireview: Primary Aldosteronism--Changing Concepts in Diagnosis and Treatment Posted by gidza to HTA HAp on Mon Jun 21 2010
Impaired Glucose-Stimulated Insulin Secretion, Enhanced Intraperitoneal Insulin Tolerance, and Increased {beta}-Cell Mass in Mice Lacking the p110{gamma} Isoform of Phosphoinositide 3-Kinase Posted by cananda to IR on Tue Jun 22 2010
Regulation of (pro)renin receptor expression by glucose-induced mitogen-activated protein kinase, nuclear factor-kappaB, and activator protein-1 signaling pathways. "Renal (pro)renin receptor (PRR) expression is increased in diabetes. The exact mechanisms involved in this process are not well established. We hypothesized that high glucose up-regulates PRR through protein kinase C (PKC)-Raf-ERK and PKC-c-Jun N-terminal kinase (JNK)-c-Jun signaling pathways. Rat mesangial cells exposed to 30 mm d-glucose demonstrated significant increase in PRR mRNA and protein expression, intracellular phosphorylation of Raf-1 (Y340/341), ERK, JNK, nuclear factor-kappaB (NF-kappaB) p65 (S536) and c-Jun (S63). By chromatin immunoprecipitation assay and EMSA, high glucose induced more functional NF-kappaB and activator protein (AP)-1 dimers bound to corresponding cis-regulatory elements in the predicted PRR promoter to up-regulate PRR transcription. Conventional and novel PKC inhibitors Chelerythrine and Rottlerin, Raf-1 inhibitor GW5074, MEK1/2 inhibitor U0126, JNK inhibitor SP600125, NF-kappaB inhibitor Quinazoline, and AP-1 inhibitor Curcumin, respectively, attenuated glucose-induced PRR up-regulation. Chelerythrine and Rottlerin also inhibited glucose-induced phosphorylation of Raf-1 (Y340/341), ERK1/2, JNK, NF-kappaB p65 (S536), and c-Jun (S63). GW5074 and U0126 inhibited the phosphorylation of ERK1/2 and NF-kappaB p65 (S536). SP600125 inhibited phosphorylation of NF-kappaB p65 (S536) and c-Jun (S63). We conclude that high glucose up-regulates the expression of PRR through mechanisms dependent on both PKC-Raf-ERK and PKC-JNK-c-Jun signaling pathways. NF-kappaB and AP-1 are involved in high-glucose-induced PRR up-regulation in rat mesangial cells." Posted by Samarat to Pro-Renin diabetes on Tue Jul 06 2010
Characteristics and Functions of {alpha}-Amino-3-Hydroxy-5-Methyl-4-Isoxazolepropionate Receptors Expressed in Mouse Pancreatic {alpha}-Cells Posted by chiaofenglin to "alpha cell" on Mon Jul 26 2010
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