糖尿病酮症酸中毒28例诊治体会

糖尿病酮症酸中毒（DKA）是糖尿病常见的急性并发症。是糖尿病患者的主要死因，及时诊断治疗可使病死率显著降低，我院近5年来共抢救的28例DKA患者，报告如下。     

FGFR1在增生性瘢痕和正常皮肤中的表达

目 的研究FGFR1在增生性瘢痕和正常皮肤中表达的差异。方法 用免疫组织化学、WesteRN—blot、流式细胞仪分析等方法检测FGFR1在增生性瘢痕和正常皮肤组织及相关细胞中的表达差异以及在成纤维细胞中的亚细胞分布状况。结果 FGFR1阳性细胞主要存在于角质形成细胞、汗腺、皮脂腺、血管内皮细胞及成纤维细胞等．细胞爬片观察到阳性颗粒主要位于细胞核，细胞浆中不如细胞核中明显。FGFR1在单个细胞中的表达量无明显差异。结论 FGFR1在增生性瘢痕和正常皮肤中表达无差异。     

血清睾酮与妊高征发病相关性研究

目的:测定妊高征患者血清睾酮水平并探讨其临床意义。方法:采用放射免疫分析法测定妊高征患者30例、正常孕妇20例血清及其新生儿脐血睾酮水平。结果:妊高征患者血清睾酮水平(0.153±0.078nmol/L)明显高于正常孕妇组(0.023±0.015nmol/L),有显著性差异(P<0.001)。妊高征组脐血睾酮水平(0.052±0.041nmol/L)低于正常孕妇组(0.119±0.059nmol/L),有显著性差异(P<0.05),两组睾酮水平与新生儿性别无关(P>0.05)。结论:孕妇血清睾酮在妊高征的病理生理中起调节或加强作用。     

Effect of water restrictions on the physiological parameters,psychological behavior and brain c-Fos expression in rat

1 Introduction Exposure to hostile stressors causes a series of coor- dinated responses in the body, such as alterations of neu- roendocrine secretion, immune reaction and behavioral manifestation to maintain homeostasis stability and sur-vival of the organisms. Stressors are divided into two main categories: physical, or systemic, and psychological, or emotional / processive. Each stressor might activate a spe- cific central pathway to induce a special neuroendocrine response, even cause stre…     

小剂量倍他乐克对难治性心力衰竭的疗效观察

小剂量倍他乐克对难治性心力衰竭的疗效观察丁秀华，商月茹（滨州地区人民医院，２５６６１０）关键词β受体阻滞剂；倍他乐克；心力衰竭；难治性心力衰竭近年来，应用β－受体阻滞剂治疗充血性心力衰竭（ＣＨＦ）已受到临床广泛关注。在ＣＨＦ其他治疗的基础上加用β－受...     

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.     

Isoflurane Preconditions Hippocampal Neurons against Oxygen-Glucose Deprivation: Role of Intracellular Ca2+ and Mitogen-activated Protein Kinase Signaling

Background: Isoflurane preconditions neurons to improve tolerance of subsequent ischemia in both intact animal models and in in vitro preparations. The mechanisms for this protection remain largely undefined. Because isoflurane increases intracellular Ca2+ concentrations and Ca2+ is involved in many processes related to preconditioning, the authors hypothesized that isoflurane preconditions neurons via Ca2+-dependent processes involving the Ca2+- binding protein calmodulin and the mitogen-activated protein kinase-ERK pathway.

Methods: The authors used a preconditioning model in which organotypic cultures of rat hippocampus were exposed to 0.5-1.5% isoflurane for a 2-h period 24 h before an ischemia-like injury of oxygen-glucose deprivation. Survival of CA1, CA3, and dentate neurons was assessed 48 later, along with interval measurements of intracellular Ca2+ concentration (fura-2 fluorescence microscopy in CA1 neurons), mitogen-activated protein kinase p42/44, and the survival associated proteins Akt and GSK-3[beta] (in situ immunostaining and Western blots).

Results: Preconditioning with 0.5-1.5% isoflurane decreased neuron death in CA1 and CA3 regions of hippocampal slice cultures after oxygen-glucose deprivation. The preconditioning period was associated with an increase in basal intracellular Ca2+ concentration of 7-15%, which involved Ca2+ release from inositol triphosphate-sensitive stores in the endoplasmic reticulum, and transient phosphorylation of mitogen-activated protein kinase p42/44 and the survival-associated proteins Akt and GSK-3[beta]. Preconditioning protection was eliminated by the mitogen-activated extracellular kinase inhibitor U0126, which prevented phosphorylation of p44 during preconditioning, and by calmidazolium, which antagonizes the effects of Ca2+-bound calmodulin.