血清胰岛素RIA在高血压病研究中的应用

文献报道在相当一部分高血压患者中存在高胰岛素血症和糖代谢异常,并指出这种胰岛素抵抗状态可能是这种病人血压升高的作用机制之一,为了解高血压患者血清胰岛素变化并探讨血清胰岛素放射免疫测定对高血压病的研究价值,本文对104例高血压病患者及80例正常对照组空腹胰岛素水平及胰岛素释放试验结果进行比较,现报道如下。     

胰岛素在某些心血管病中的作用

组织细胞对胰岛素的反应缺陷一胰岛素抵抗，促使胰岛代偿世分泌增多，导致高胰岛素血症，随之引起代谢紊乱和某些心血管疾病。治疗时如不考虑胰岛素的敏感性，则有可能加重代谢紊乱、高血压和动脉粥样硬化等。     

生长抑素在学习记忆中的作用

生长抑素广泛存在于中枢和外周神经系统， 参与了机体多种生理机能的活动和调节，在中枢神经系统中具有神经递质或神经调质的作用。生长抑素可增强海马的ＬＴＰ，促进学习与记忆； 临床一些痴呆症的认知和智力障碍与脑内生长抑素含量减少有关， 生长抑素能神经系统改变是Ａｌｚｈｅｉｍｅｒ’ｓ病的特异性致病机理之一。     

高血压病人血浆胰岛素RIA观察

近年来,高血压病人高胰岛素血症已引起重视,本文对35例高血压病人进行了胰岛素、C肽定量测定,现报告如下。 对象和方法 一、对象: (一)高血压病人35例(男25,女10),年龄38～71岁,平均51.4岁。诊断符合WHO高血压病诊断标准,病程1～30年。 (二)健康对照组:43例(男26,女17),年龄24～75岁,平均47.5岁。两组间年龄体重均无显著性差异,均无长期酗酒史,无糖尿病史。 二、方法:入选者禁食12小时以上,晨空腹抽血,常规测血生化、肝功、血糖等排除有明显肝肾功能损害。胰岛素、C肽试剂盒由中国原子能科学研究院提供。批量测定。操作按说明书。参考值:胰岛素4.0～16.8mIu/L,C肽0.6～3.8ng/ml。所得结果用t检验进行统计学处理。     

生长抑素在类固醇糖尿病大鼠胰腺中的表达

目的:探讨不同剂量地塞米松(DEX)对大鼠胰岛细胞激素表达的影响。方法:雄性成年SD大鼠140只随机平均分成4组,应用放射免疫及原位杂交等技术观察不同剂量DEX作用下胰岛激素合成、储存及释放改变。结果:在一定范围内空腹血糖(FBG)、血清胰岛素(Ins)与DEX给药呈剂量及时间依赖性。胰腺中生长抑素(SS)的mRNA和蛋白表达以及血清中Ins水平的改变均早于FBG的升高。结论:DEX改变胰岛细胞Ins和SS的表达,这在类固醇糖尿病(SDM)发生过程中可能发挥重要作用。     

老年高血压病和胰岛素抵抗综合征

在高血压病患者中,常同时存在胰岛素抵抗综合征的其它改变,老年人高血压的患病率高,且合并胰岛素抵抗综合征这一系列改变更加明显,因此,老年高血压病患者的心血管危险因素较中青年患者明显增加。     

生长抑素的免疫调节作用

生长抑素是一种抑制性神经肽，同时又具有免疫调节功能，是神经内分泌免疫网络中重要的信号传导分子。它降低淋巴细胞活性，影响细胞因子分泌，调节T细胞分化和功能及具有抗炎、抗增殖作用。     

生长抑素的免疫调节作用

生长抑素是一种抑制性神经肽 ,同时又具有免疫调节功能 ,是神经内分泌免疫网络中重要的信号传导分子。它降低淋巴细胞活性 ,影响细胞因子分泌 ,调节T细胞分化和功能及具有抗炎、抗增殖作用。     

高血压病患者胰岛素抵抗与血液流变学关系

高血压病患者胰岛素抵抗与血液流变学关系湖北医科大学附属第一医院心内科（武汉４３００６０）胡成林黎明江唐燕红李自成胰岛素抵抗是引起葡萄糖耐量降低、高胰岛素血症、高脂血症及高血压的中心环节。胰岛素抵抗是否也是引起血液流变学异常的重要原因，目前尚未见报道...     

生长抑素在乳腺癌中的研究进展

目的：分析生长抑素与乳腺癌的发生发展之间关系的最新研究进展。方法：通过对国内外一些最新研究报道及文献资料的整理,总结生长抑素与乳腺癌的发生发展之间存在的关系。结果：生长抑素与乳腺癌的发生发展之间存在着一定的关系,生长抑素受体的不同亚型在乳腺癌中的表达程度不同。生长抑素在乳腺癌中的表达具有明显差异性,同时生长抑素受体显像（SRS）使表面表达SSTR的细胞显影。结论：生长抑素及其类似物（SSTA）对于乳腺癌的发生发展的诊断具有重要意义,在乳腺癌的靶向化疗、基因治疗等方面将得到进一步的发展。     

The role of anger in hypertension

We report a study about the administration of two Dutch questionnaires (the State-Trait Anger Scale and the State-Trait Anxiety Inventory) to a sample of patients with essential hypertension and to a matched control group. Analyses of the test results demonstrated that some significant differences could be observed in the levels of anxiety and anger. Special attention was paid to certain test-item answers, showing that hypertensives, although feeling irritated and angry, retreat to some extent from showing their anger.     

胰岛素抵抗大鼠血压升高的血管机制

目的：探讨胰岛素抵抗在高血压发病中的作用和血管机制。方法：复制胰岛素抵抗大鼠模型，采用血管功能实验方法观察其血管收缩及舒张功能的变化以及胰岛素对血管舒缩功能的影响。结果：（１）高糖喂养一个月能引起正常大鼠出现胰岛素抵抗和血压升高；（２）胰岛素抵抗大鼠血管对苯肾上腺素的收缩反应增强，自动舒张功能减弱；（３）胰岛素能抑制血管的收缩反应，促进血管的舒张和直接舒张血管，但这些作用在ＩＲＨ大鼠中均减弱或消失。结论：胰岛素抵抗是发生高血压病的因素之一，其血管机制为血管舒缩功能改变及胰岛素对血管舒缩功能调节作用的异常     

The role of biomaterials in insulin delivery systems

The control of blood glucose levels in diabetes involving devices are critically reviewed, and the role of blood-contacting biomaterial components analyzed. These include mechanical insulin-delivery systems of the closed-loop type that require an electronic glucose sensor and feedback, and open-loop systems that deliver insulin without a sensor and feedback. Whole pancreatic and islet transplantations, islet encapsulation, and the potential role of polymeric sustained drug delivery systems are discussed. The medical and social impacts of diabetes mellitus are of prime public health concern and of even greater magnitude than those of heart disease in the United States. While future advances in device design, miniaturization, and biomaterials technology will significantly add to the arsenal of therapeutic alternatives, devices capable of controlling blood glucose levels ought to be viewed as mere interim phases rather than as final goals of the problem.     

The role of intramuscular lipid in insulin resistance

There is interest in how altered lipid metabolism could contribute to muscle insulin resistance. Many animal and human states of insulin resistance have increased muscle triglyceride content, and there are now plausible mechanistic links between muscle lipid accumulation and insulin resistance, which go beyond the classic glucose-fatty acid cycle. We postulate that muscle cytosolic accumulation of the metabolically active long-chain fatty acyl CoAs (LCACoA) is involved, leading to insulin resistance and impaired insulin signalling or impaired enzyme activity (e.g. glycogen synthase or hexokinase) either directly or via chronic translocation/activation of mediators such as a protein kinase C (particularly PKC theta and epsilon ). Ceramides and diacylglycerols (DAGs) have also been implicated in forms of lipid-induced muscle insulin resistance. Dietary lipid-induced muscle insulin resistance in rodents is relatively easily reversed by manipulations that lessen cytosolic lipid accumulation (e.g. diet change, exercise or fasting). PPAR agonists (both gamma and alpha) also lower muscle LCACoA and enhance insulin sensitivity. Activation of AMP-activated protein kinase (AMPK) by AICAR leads to muscle enhancement (especially glycolytic muscle) of insulin sensitivity, but involvement of altered lipid metabolism is less clear cut. In rodents there are similarities in the pattern of muscle lipid accumulation/PKC translocation/altered insulin signalling/insulin resistance inducible by 3-5-h acute free fatty acid elevation, 1-4 days intravenous glucose infusion or several weeks of high-fat feeding. Recent studies extend findings and show relevance to humans. Muscle cytosolic lipids may accumulate either by increased fatty acid flux into muscle, or by reduced fatty acid oxidation. In some circumstances muscle insulin resistance may be an adaptation to optimize use of fatty acids when they are the predominant available energy fuel. The interactions described here are fundamental to optimizing therapy of insulin resistance based on alterations in muscle lipid metabolism.     

The role of omega 3 fatty acids on insulin secretion and insulin sensitivity

Carbohydrate intolerance is positively correlated with animal fat consumption and is more common in beef eating populations. In contrast, individuals consuming diets comprised of polyunsaturated fats have a lower incidence of diabetes mellitus. This is especially apparent in the Eskimos living in Alaska and Greenland whose diet is highly enriched with omega 3 fatty acids. It is hypothesized that dietary enrichment with omega 3 fatty acids increases the incorporation of these fatty acids into the beta cell phospholipid membrane thus enhancing insulin secretion. It is also proposed that similar changes occur in the phospholipid membrane composition of peripheral cells. These changes in the membrane phospholipids would then theoretically increase both insulin receptor binding affinity and sensitivity, thus enhancing glucose transport across their membranes. Augmented insulin secretion and increased insulin sensitivity induced by chronic omega 3 fatty acid ingestion would positively influence carbohydrate metabolism and improve glucose homeostasis.     

Endogenous hyperglycemia restores insulin release impaired by somatostatin analogue

These studies assessed the ability of des-Asn5-[D-Trp8-D-Ser13]-somatostatin (d-ATS-SS) to selectively inhibit insulin release and produce a hyperglycemia sufficient to compensate for the original impairment. d-ATS-SS at 0.017 micrograms/min inhibited basal insulin output (delta = -38 +/- 6%, P less than 0.005) and increased basal pancreatic glucagon output (delta - +21 +/- 6%, P less than 0.05, n = 5). d-ATS-SS at 0.17 micrograms/min markedly inhibited insulin output (delta = -84 +/- 4%, P less than 0.0005) and slightly inhibited glucagon output (delta = -14 +/- 6%, P less than 0.05, n = 5). d-ATS-SS at 0.055 micrograms/min decreased basal and stimulated insulin release but not basal nor stimulated glucagon release. By 3.5 of analogue infusion, plasma glucose had risen by 116 +/- 13 mg/dl, and base-line insulin levels and the insulin responses to both isoproterenol and arginine, but not glucose, increased toward control values. We conclude that d-ATS-SS produces selective insulinopenia resulting in hyperglycemia which in turn compensates for the original impairment. Thus, the hyperglycemia observed in other states of selective insulin deficiency (e.g., noninsulin-dependent diabetes mellitus) may compensate for defects in beta-cell function.     

5-羟色胺在野百合碱引起大鼠肺动脉高压发病中的作用

目的：探讨５－ＨＴ在ＭＣＴ性肺动脉高压中的作用。方法：用免疫组化方法和图象分析技术,测定肺组织中５－ＨＴ及其受体的变化;采用ＭＴＴ法和测微网及钙荧光指示剂Ｆｕｒａ２／Ａｍ测定培养的肺动脉平滑肌细胞生长情况和收缩功能以及细胞内游离Ｃａ２＋浓度。结果：发现ＭＣＴ引起大鼠肺动脉高压时肺组织中５－ＨＴ（１２７４９４±２０７３６／ｍｍ２）及其受体（１４６２４±３０１０／ｍｍ２）阳性细胞数目比对照组（３７２０±１０１８,３４３０±８２１／ｍｍ２）的均显著增加（Ｐ＜００１）。５－ＨＴ能使培养的肺动脉平滑肌细胞增生和收缩这种作用与其引起的Ｃａ２＋内流有关。结论：５－ＨＴ的收缩血管作用和促血管平滑肌细胞增殖作用在ＭＣＴ性肺动脉高压的发病机制中可能具有重要的意义     

The role of aquaporin-1 in idiopathic and drug-induced intracranial hypertension

Idiopathic intracranial hypertension is a common disorder affecting mainly healthy, young, overweight women. The pathogenesis of this condition is unknown, but it has been shown to follow treatment with several compounds including corticosteroids and vitamin A derivatives. This paper will offer a novel hypothesis and insight on the pathogenesis of drug induced intracranial hypertension following a review and analysis of the literature. Both corticosteroids and vitamin A derivatives have been shown to upregulate the expression of aquaporin 1, a water channel protein. Aquaporin 1 is widely distributed in the human brain and is associated with water secretion into the subarachnoid space. Aquaporin 1 was also shown to participate in the regulation of weight. Agents used for treating idiopathic intracranial hypertension reduce aquaporin 1 expression. Based on these observations, we propose that aquaporin 1 has a pathogenetic role in drug induced idiopathic intracranial hypertension. Over expression of this gene causes increased intracranial pressure, and downregulation reduces pressure and alleviates the symptomatology and complications of idiopathic intracranial hypertension.