Therapeutic Effect of Berberine on 60 Patients with Non－Insulin Dependent Diabetes Mellitus and Experimental Research

ＴｈｅｒａｐｅｕｔｉｃＥｆｆｅｃｔｏｆＢｅｒｂｅｒｉｎｅｏｎ６０ＰａｔｉｅｎｔｓｗｉｔｈＮｏｎ－ＩｎｓｕｌｉｎＤｅｐｅｎｄｅｎｔＤｉａｂｅｔｅｓＭｅｌｌｉｔｕｓａｎｄＥｘｐｅｒｉｍｅｎｔａｌＲｅｓｅａｒｃｈＮｉＹａｎ－ｘｉａ（倪艳霞）；ＬｉｕＡｎ－ｑ...     

严重急性呼吸综合征的流行和防治

严重急性呼吸综合征 (SARS) ,目前认为是由SARS冠状病毒 (SARSCo V)引起的急性呼吸系统传染病。迄今为止 ,尚无有效的治疗方法。据世界卫生组织 (WHO)估计 ,SARS全球病死率约为 15 % ,因感染年龄而异 :2 4岁以下病死率低于 1% ,2 5～ 4 4岁 6 % ,4 5～ 6 4岁 15 % ,6 4岁以上者超过 5 0 % [1] 。一、流行概况(一 )当地传播　 2 0 0 2年 12月 ,中国广东省发现高传染性非典型肺炎。医务人员和患者家属是高危人群 ,疾病的高病死率以及病情恶化快引起了公众的关注。(二 )全球蔓延　SARS全球蔓延开始于 2 0 0 3年 2月的香港 ,一个广东…     

全国创伤骨科新技术研讨会纪要

由中国残疾人康复协会肢体残疾康复专业委员会、《中国矫形外科杂志》《人民军医杂志》《解放军医学杂志》主办，解放军第89医院全军创伤骨科研究所承办的“全国创伤骨科新技术研讨会暨学习班”于2006年6月4—8日在美丽的国际风筝之都潍坊举行。参加大会的特邀嘉宾有：中国残疾人康复协会副理事长、《中国矫形外科杂志》主编宁志杰教授，《人民军医杂志》编辑部王敏主任，解放军第89医院全军创伤骨科研究所所长王成琪教授，山东省骨科学会主任委员、山东省人民医院骨科周东生教授，上海蒌葑医院院长张成中教授，大连大学中山医院院长赵德伟教授等。     

普通人及医学专家的医疗保健规则

普通人的八条保健规刚1.找到一位受过良好教育的,可以信赖的保健专家.2.具备健康知识,有能力处置健康风险,确定你自己的生命质量标准.3.广泛利用预测医学和预防医学.4.虽期望通过医疗得到康复或缓解,但也意识到医疗本身的局限和风险.5.要从医生和其他保健专家那里得到信息和咨询,在治疗中做他们的负责的和可靠的同伴.     

盐酸曲马多硬膜外注药用作术后镇痛54例报告

<正>我院自1993年6月至9月选择持硬麻醉的手术病人54例,用曲马多作硬膜外注射,观察术后止痛效果、持续时间及副作用等,现报告如下。 临床资料 男性18例,女性36例,年龄最小18岁,最大76岁,体重45～77kg,择期手术48例,急诊手术6例,病情按ASA分级:Ⅰ～Ⅱ级45例,Ⅲ级8例,Ⅳ级1例。     

E1 Tor Vibio Cholerae Strain SM_6 and Jiangsu 1d Strain

Ｅ１ＴｏｒＶｉｂｉｏＣｈｏｌｅｒａｅＳｔｒａｉｎＳＭ_６ａｎｄＪｉａｎｇｓｕ１ｄＳｔｒａｉｎ￥ＪｉａｎｇＸｉａｏｗａｎ，ｅｔａｌ．ＡＣＴＡＡＣＡＤＥＭＩＡＥＭＥＤＩＣＩＮＡＥＮＡＮＪＩＮＧ，１９９４，１４（２）：１６３－１６４ＡｂｓｔｒａｃｔＥ１Ｔｏ?..     

Morphine Preconditions Purkinje Cells against Cell Death under In Vitro Simulated Ischemia-Reperfusion Conditions

Background: Morphine pretreatment via activation of [delta]1-opioid receptors induces cardioprotection. In this study, the authors determined whether morphine preconditioning induces ischemic tolerance in neurons.

Methods: Cerebellar brain slices from adult Sprague-Dawley rats were incubated with morphine at 0.1-10 [mu]m in the presence or absence of various antagonists for 30 min. They were then kept in morphine- and antagonist-free buffer for 30 min before they were subjected to simulated ischemia (oxygen-glucose deprivation) for 20 min. After being recovered in oxygenated artificial cerebrospinal fluid for 5 h, they were fixed for morphologic examination to determine the percentage of undamaged Purkinje cells.

Results: The survival rate of Purkinje cells was significantly higher in slices preconditioned with morphine (>= 0.3 [mu]m) before the oxygen-glucose deprivation (57 +/- 4% at 0.3 [mu]m morphine) than that of the oxygen-glucose deprivation alone (39 +/- 3%, P < 0.05). This morphine preconditioning-induced neuroprotection was abolished by naloxone, a non-type-selective opioid receptor antagonist, by naltrindole, a selective [delta]-opioid receptor antagonist, or by 7-benzylidenenaltrexone, a selective [delta]1-opioid receptor antagonist. However, the effects were not blocked by the [mu]-, [kappa]-, or [delta]2-opioid receptor antagonists, [beta]-funaltrexamine, nor-binaltorphimine, or naltriben, respectively. Morphine preconditioning-induced neuroprotection was partially blocked by the selective mitochondrial adenosine triphosphate-sensitive potassium channel antagonist, 5-hydroxydecanoate, or the mitochondrial electron transport inhibitor, myxothiazol. None of the inhibitors used in this study alone affected the simulated ischemia-induced neuronal death.     

Mild Hypercapnia Induces Vasodilation via Adenosine Triphosphate-sensitive K+ Channels in Parenchymal Microvessels of the Rat Cerebral Cortex

Background: Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex.

Methods: Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 [mu]m) was monitored using computerized videomicroscopy.

Results: During contraction to prostaglandin F2[alpha] (5 x 10-7 m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10-6 m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10-7 m) as well as the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (10-4 m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10-8 to 3 x 10-7 m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide.