瘦素与冠心病

瘦素是肥胖基因编码的一种蛋白质产物,主要由白色脂肪组织分泌,通过与其受体结合发挥抑制食欲、减少能量摄入、增加能量消耗的生物学作用。大量临床研究表明冠心病患者常存在高瘦素血症,表现为瘦素抵抗。本文就瘦素在冠心病发病中的作用机制作一综述。     

Mitochondrial dysfunction and delayed hepatotoxicity: another lesson from troglitazone

Aims/hypothesis  Troglitazone was approved for treatment of type 2 diabetes mellitus, but by 2000 it had been removed from all world markets due to severe drug-induced liver injury. Even today, we still do not know how many patients sustained a long-term liver injury. No system is in place to acquire that knowledge. Regarding toxicity mechanisms, controversy persists as to which ones are class effects of thiazolidinediones (TZDs) and which are unique to troglitazone. This study aims to provide long-term outcome data and new insights on mechanisms of troglitazone-induced liver injury. Methods  This case series reports the liver injuries sustained by eleven type 2 diabetic patients treated with troglitazone between 1997 and 2000. Exhaustive review of medical records was performed for all patients. Long-term outcomes were available for all the non-fatal cases. A comprehensive literature review was also performed. Results  Long-term liver injury progressing to cirrhosis was identified in seven patients. All eleven cases had liver injury patterns consistent with troglitazone toxicity. Analysis of these cases and of the experimental troglitazone toxicity data points to mitochondrial toxicity as a central factor. The general clinical patterns of mitochondrial hepatotoxic events are reviewed, as are the implications for other members of the TZD family. Conclusions/interpretation  This analysis enables the liver injury induced by troglitazone to be better understood. In future cases of delayed drug-induced liver injury that progresses after discontinuation, the possibility of mitochondrial toxicity should be considered. When appropriate, this can then be evaluated experimentally. Such proactive investigation may anticipate clinical risk before a large-scale therapeutic misadventure occurs. Drug-induced liver injury due to mitochondrial hepatotoxins may be less unpredictable than has previously been surmised. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorised users.     

肺癌转移机制的研究进展

肺癌患者总生存率较低的主要原因是肿瘤细胞的转移.目前认为肺癌细胞的转移是一个非常复杂的过程,主要包括肺癌细胞离开原发灶、进入淋巴系统和血液系统、远处生长等方面.本文就肺癌转移的各个参与因素以及相关的新靶向药物的临床研究作一综述.     

The Pathophysiological Mechanisms of GERD in the Obese Patient

Obesity has increased dramatically in the last 30 years, affecting 33% of the adult population in the United States. Increase in body mass index has been shown to be associated with the increase in the prevalence of gastroesophageal reflux disease (GERD) symptoms, esophageal mucosal injury, and GERD complications. The putative mechanisms responsible for the close relationship between GERD and increased body mass index include increased intragastric pressure, increased gastroesophageal pressure gradient, esophageal motor and sensory abnormalities, increase in prevalence of hiatal hernia, increase in serum female hormonal levels, diet, and increase in comorbidities. Whilst the current efforts are to focus on one major underlying mechanism, it is highly likely that multiple factors contribute to the increased prevalence of GERD in the obese patient.     

胃旁路术治疗2型糖尿病的研究进展

随着国内外相关减重手术治疗2型糖尿病（T2DM）病例报道的增多,并显现出了良好的短期及长期的临床效果,该方法更加引人关注。然而手术治疗2型糖尿病的机制如何尚无明确结论,认为可能的治疗机制是十二指肠和近端空肠被旷置,从而引发胃肠道激素分泌的变化,使T2DM得到控制。本文分别对手术的类别、治疗效果及治疗机制进行综述。     

中药治疗原发性骨质疏松症效应机制研究进展

随着全球社会老龄化,原发性骨质疏松症的发病率呈逐年上升趋势,其危害性大,早期不易诊断,起病隐匿,易造成骨折,是中老年人的“隐形杀手”。近年来随着科学技术的进步,有关中医药治疗原发性骨质疏松症的现代化研究发展迅速,国内外学者开展了大量的临床和基础研究,从对原发性骨质疏松症传统病因病机的现代化认识,到宏观骨生物力学深入至微观信号通路的研究都取得了重大进展,中药成为一条有效治疗原发性骨质疏松症的新途径。     

基于心血管获益浅谈SGLT-2抑制药在2型糖尿病管理中的价值

摘 要心血管疾病的风险管控是糖尿病管理过程中非常重要的环节。国内外权威机构和指南对降糖药物对心血管结局的要求非常严格。多项心血管结局研究显示,钠 葡萄糖协同转运蛋白2(SGLT-2)抑制药能显著降低心血管事件风险,降低心血管死亡率。SGLT-2抑制药心血管获益的机制不仅来自于对血糖、体质量等因素的改善,可能还源于对多重心血管风险因素的控制。在目前糖尿病管理追求个体化、以患者为中心的策略下,随着心血管结局研究的不断发布,SGLT-2抑制药在指南中的地位越来越高,在糖尿病的管理中的价值越来越大。本文通过SGLT-2抑制药心血管获益的研究及指南推荐的变迁,阐述SGLT-2抑制药在糖尿病管理中的价值,并简要分析SGLT-2抑制药带来心血管获益的可能机制。     

膳食纤维调节肠道菌群的作用机制研究进展

肠道菌群失调与多种系统疾病的发生发展密切相关,研究证明膳食纤维在肠道菌群结构和功能方面具有重要调节作用,有利于维持肠道菌群动态平衡。膳食纤维为肠道菌群提供生长代谢底物,且优化了菌群代谢,肠道菌群通过酵解在小肠中不能被消化吸收的膳食纤维,产生的代谢产物参与机体多种信号调节机制,从而影响宿主生理病理改变。本文将对近段时间关于膳食纤维调节肠道菌群的作用机制进行综述,以期为更有效利用膳食纤维,优化肠道菌群代谢,防治疾病提供更多的参考依据。     

伏立康唑致视觉障碍的研究进展

伏立康唑致视觉障碍常见,发生率约30%。 本文从伏立康唑致视觉障碍的危险因素、发生机制、防范措施等方面综述了近年来国内外有关伏立康唑致视觉障碍的研究状况,指出药物体内浓度、基因多态性、高龄、肝功能状态、药物相互作用、给药方式是伏立康唑致视觉障碍的危险因素;发生机制可能是选择性诱导视网膜的视锥和视杆双极细胞而引起可逆性功能障碍;医护人员要密切关注伏立康唑致视觉障碍的危险因素,根据血药浓度优化给药方案,减少不良反应发生。     

氙的神经保护机制

背景 氙的昂贵限制了其在医疗中的使用.近来的研究证明了氙吸入麻醉的安全性和有效性,使得其使用前景受人关注.目的 总结氙的神经保护机制.内容 氙对神经系统的保护可能与N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)受体、钙依赖性调节机制、钾离子通道等有关.趋向 氙的神经保护作用提示其在特定的临床领域将有很高的应用价值,例如在心肺转流术和新生儿窒息等.