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排序方式: 共有1668条查询结果,搜索用时 31 毫秒
31.
Avneesh Chhabra Vibhor Wadhwa Rashmi S Thakkar John A Carrino A Lee Dellon 《CANADIAN JOURNAL OF PLASTIC SURGERY》2013,21(3):186-189
The authors describe the correlation between 3-Tesla magnetic resonance neurography (MRN) and surgical findings in two patients who underwent multiple previous failed ulnar nerve surgeries. MRN correctly localized the site of the abnormality. Prospectively observed MRN findings of perineural fibrosis, ulnar nerve re-entrapment abnormalities, medial antebrachial cutaneous neuroma and additional median nerve entrapment were confirmed surgically. 相似文献
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Rashmi Chandra Yu Wang Rafiq A. Shahid Steven R. Vigna Neil J. Freedman Rodger A. Liddle 《The Journal of clinical investigation》2013,123(8):3343-3352
Cholecystokinin (CCK) is a satiety hormone produced by discrete enteroendocrine cells scattered among absorptive cells of the small intestine. CCK is released into blood following a meal; however, the mechanisms inducing hormone secretion are largely unknown. Ingested fat is the major stimulant of CCK secretion. We recently identified a novel member of the lipoprotein remnant receptor family known as immunoglobulin-like domain containing receptor 1 (ILDR1) in intestinal CCK cells and postulated that this receptor conveyed the signal for fat-stimulated CCK secretion. In the intestine, ILDR1 is expressed exclusively in CCK cells. Orogastric administration of fatty acids elevated blood levels of CCK in wild-type mice but not Ildr1-deficient mice, although the CCK secretory response to trypsin inhibitor was retained. The uptake of fluorescently labeled lipoproteins in ILDR1-transfected CHO cells and release of CCK from isolated intestinal cells required a unique combination of fatty acid plus HDL. CCK secretion secondary to ILDR1 activation was associated with increased [Ca2+]i, consistent with regulated hormone release. These findings demonstrate that ILDR1 regulates CCK release through a mechanism dependent on fatty acids and lipoproteins and that absorbed fatty acids regulate gastrointestinal hormone secretion. 相似文献
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Roongta Rashmi Mondal Sumantro Haldar Subhankar Kumar Mavidi Sunil Ghosh Alakendu 《Clinical rheumatology》2022,41(5):1591-1596
Clinical Rheumatology - We report the case of an 18-year-old male with Still’s disease for the last 3 years, in remission, who developed two flares of his disease after receiving two... 相似文献
38.
Parihar Rashmi Shukla Ruchi Baishya Bikash Kalita Jayantee Haldar Rudrashish Misra Usha Kant 《Metabolic brain disease》2022,37(3):773-785
Metabolic Brain Disease - We report the potential role of 1H Nuclear Magnetic Resonance (NMR) based metabolomics in tuberculous meningitis (TBM). We also correlate the significant metabolites with... 相似文献
39.
Rashmi Jain Udaya Kabadi M. Kabadi 《International journal of diabetes in developing countries.》2008,28(1):1-5
BACKGROUND:
In the UK Prospective Diabetes Study (UKPDS), many subjects maintained glycemic goal (HbA1c < 7.0%) at 9 years, showing that β-cell function was preserved and that the initial decline in β-cell function recovered with sulphonylureas. Moreover, obese subjects using high daily doses of insulin for several years rarely require insulin or oral hypoglycemic agents to maintain their glycemic goal following weight loss achieved by gastric bypass surgery. Thus, declining β-cell function during the course of type 2 diabetes mellitus (T2DM) is neither universal nor permanent.OBJECTIVE:
To assess β-cell function in morbidly obese subjects before insulin withdrawal and on attaining the glycemic goal with weight loss and oral agents.MATERIALS AND METHODS:
Serum C-peptide (CPEP) and glucose (G) concentrations were determined up to 180 min during an oral glucose tolerance test (OGTT) with 75 glucose in 10 obese men with T2DM, before insulin withdrawal, and on achieving the glycemic goal with metformin, glimepiride, and weight loss. Ten age-matched healthy men participated as controls. Cumulative responses (CR) of CPEP and G were calculated by adding differences between the level at each time-period during OGTT and fasting (F) concentration. β-Cell function was expressed as the FCPEP as well as the insulinogenic index (CRCPEP/CRG). Insulin sensitivity was determined as FCEP × FG.RESULTS:
FCPEP was decreased, though still present, prior to insulin withdrawal. Moreover, on attaining the glycemic goal over 6-9 months, FCPEP, CRPEP/CRG, and FCPEP × FG improved markedly (P < 0.001).CONCLUSION:
Decline in β-cell function in morbidly obese T2DM may not be progressive and is reversible on improving insulin sensitivity and on eliminating the inhibition by exogenous insulin. 相似文献40.