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Neuropeptide Y Attenuates Stress‐Induced Bone Loss Through Suppression of Noradrenaline Circuits
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![点击此处可从《Journal of bone and mineral research》网站下载免费的PDF全文](/ch/ext_images/free.gif)
PA Baldock S Lin L Zhang T Karl Y Shi F Driessler A Zengin B Hörmer NJ Lee IPL Wong EJD Lin RF Enriquez B Stehrer MJ During E Yulyaningsih S Zolotukhin ST Ruohonen E Savontaus A Sainsbury H Herzog 《Journal of bone and mineral research》2014,29(10):2238-2249
Chronic stress and depression have adverse consequences on many organ systems, including the skeleton, but the mechanisms underlying stress‐induced bone loss remain unclear. Here we demonstrate that neuropeptide Y (NPY), centrally and peripherally, plays a critical role in protecting against stress‐induced bone loss. Mice lacking the anxiolytic factor NPY exhibit more anxious behavior and elevated corticosterone levels. Additionally, following a 6‐week restraint, or cold‐stress protocol, Npy‐null mice exhibit three‐fold greater bone loss compared to wild‐type mice, owing to suppression of osteoblast activity. This stress‐protective NPY pathway acts specifically through Y2 receptors. Centrally, Y2 receptors suppress corticotropin‐releasing factor expression and inhibit activation of noradrenergic neurons in the paraventricular nucleus. In the periphery, they act to control noradrenaline release from sympathetic neurons. Specific deletion of arcuate Y2 receptors recapitulates the Npy‐null stress response, coincident with elevated serum noradrenaline. Importantly, specific reintroduction of NPY solely in noradrenergic neurons of otherwise Npy‐null mice blocks the increase in circulating noradrenaline and the stress‐induced bone loss. Thus, NPY protects against excessive stress‐induced bone loss, through Y2 receptor‐mediated modulation of central and peripheral noradrenergic neurons. © 2014 American Society for Bone and Mineral Research. 相似文献
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Inhibition of platelet aggregation by a monoclonal antibody against human fibronectin. 总被引:9,自引:1,他引:9
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V M Dixit D M Haverstick K O''Rourke S W Hennessy T J Broekelmann J A McDonald G A Grant S A Santoro W A Frazier 《Proceedings of the National Academy of Sciences of the United States of America》1985,82(11):3844-3848
A monoclonal antibody (A3.3) has been generated against human platelet fibronectin (FN). A3.3 reacts with human plasma FN but with no other plasma proteins. A3.3 was found to inhibit thrombin- or ionophore A23187-stimulated aggregation of gel-filtered platelets in a concentration-dependent manner in both an aggregometer assay and a sensitive well plate aggregation assay. The antibody does not block secretion of serotonin. Four other anti-FN monoclonal antibodies that recognize different epitopes on FN than A3.3 does have no effect on platelet aggregation. A3.3 does not block the adhesion of CHO cells to FN-coated surfaces, indicating that it does not bind to the identified cell-binding domain of FN. A3.3 reacts with a 160/140-kDa doublet, known to contain the cell-binding domain, that is produced by digestion of FN with elastase or thermolysin. However, the antibody does not react with lower molecular weight species that also contain the cell-binding domain or with any of the other identified domains of FN. The A3.3 epitope is extremely protease sensitive and the smallest fragment found in any digest that retains reactivity with A3.3 is a 70-kDa peptide produced in low yield by mild thermolytic cleavage of FN. These data suggest that A3.3 defines a functional site present on both the platelet and plasma FN molecule that has a direct role in platelet aggregation. 相似文献
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Placebo controls play a critical role in the evaluation of any pharmacotherapy. This review surveys the placebo arm in 12 randomized controlled trials (RCTs) investigating burning mouth syndrome (BMS) and documents a positive placebo response in 6 of them. On average, treatment with placebos produced a response that was 72% as large as the response to active drugs. The lack of homogeneity in the use of placebos adds to the difficulty in comparing results and aggregating data. Future RCTs investigating BMS would benefit from larger sample sizes, adequate follow‐up periods, and use of a standard placebo. 相似文献
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艾滋病合并隐球菌脑膜炎18例临床分析 总被引:6,自引:1,他引:6
目的 提高对艾滋病 (AIDS)合并隐球菌脑膜炎的认识。方法 对赤道几内亚巴塔地区医院 18例AIDS合并隐球菌脑膜炎患者进行临床综合分析。结果 18例AIDS合并隐球菌脑膜炎患者的临床主要表现为 :发热、剧烈头痛、极度乏力、肢体痛、脑膜刺激征及消瘦与脱水等。脑脊液 (CSF)培养均为新型隐球菌生长 ;涂片及隐球菌多糖荚膜抗原 (ELISA法 )检测的阳性率分别为 77 8% (14/ 18) ,94 4% (17/ 18)。结论 隐球菌脑膜炎为AIDS常见机会性感染及主要致死病因之一。 相似文献
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PHILIPPE MAURY M.D. EMILIE THOMSON M.D. ANNE ROLLIN M.D. MATHIEU BERRY M.D. THOMAS COGNET M.D. ALEXANDRE DUPARC M.D. PIERRE MONDOLY M.D. MATHIEU GAUTIER M.D. OLIVIER LAIREZ M.D. SIMON MÉJEAN M.D. PIERRE MASSABUAU M.D. CHRISTELLE CARDIN M.D. STÉPHANE COMBES M.D. JEAN‐PAUL ALBENQUE M.D. NICOLAS COMBES M.D. 《Pacing and clinical electrophysiology : PACE》2015,38(5):617-624
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