NADPH氧化酶家族在心血管疾病中作用的研究进展

烟酰胺腺嘌呤二核苷酸磷酸氧化酶是心血管系统中活性氧(reactive oxygen species,ROS)的主要来源,它包 括7种亚型并分别表达在不同的心血管细胞及其细胞器中,参与调节细胞增殖、迁移、分化、凋亡、衰老和炎症反应 等多种活动,其衍生的ROS参与高血压、动脉粥样硬化、糖尿病血管病变、心肌梗死后心室重构等多种心血管疾病 的病理过程。     

肾移植病人配组淋巴细胞毒抗体的检测

目的：通过对肾移植病人的配组淋巴细胞毒抗体（ｐａｎｅｌ ｒｅａｃｔｉｖｅ ａｎｔｉｂｏｄｙ ＰＲＡ）的检测,了解与分析肾移植病人配组淋巴细胞毒抗体的差异。方法：以３６名健康成人外周血淋巴细胞作为群体淋巴细胞来源,采用补体依赖微量淋巴细胞毒方法,检测病人血清中的配组淋巴细胞毒抗体。结果：５５例病人进行血清淋巴细胞毒交叉配合实验检测,只有１例阳性１．８２％。而ＰＲＡ检测８例病人血清为阳性（６女２男）占     

玉屏风散对强的松反应及NSI型病程的影响——附58例分析

探讨中药玉屏风散加味对强的松不良反应的拮抗作用及对肾病综合征Ⅰ型的病程的影响 ,将病人随机分为玉屏风散加味治疗组(37例 ) 和对照组(2 1例 ) ,观察用药后 2、4、6周自汗、心悸症状及心率变化情况及治疗后 1年内各种感染次数 ,治疗 1年后强的松服药量及 2 4小时尿蛋白定量情况。结果 :治疗第 4、6周自汗、心悸症状发生率及心率治疗组均低于对照组 ,感染次数治疗组低于对照组 ,1年未服强的松量及其 2 4小时尿蛋白量均低于对照组 ,两组数据经统计学处理有显著性差异。结论 :玉屏风散加味能明显减轻强的松引起的自汗、心悸等不良反应 ,减少感染次数 ,缩短NSI型的病程。     

Hematogenous metastases of the human brain – Characteristics of peritumoral brain changes: A review

The brain is an important site of hematogenous metastases from malignanttumors in other organs. The effects on the brain is a combination of tissuedestruction induced by invading tumor cells and reactive alterationsoccurring around the metastases. This review focuses on neuropathologicalchanges around hematogenous metastases of the human brain. The peritumoralbrain parenchyma shows structural and functional changes of theintracerebral microvessels and edema. The endothelial cells of peritumoralmicrovessels express glucose transporter protein (GLUT 1) in the same way asthe normal brain. Reduction in immunostaining to GLUT 1 may occur in themicrovessels located within the metastases. This would indicateabnormalities of the blood-brain barrier in tumor vessels but normal barrierfunction in the peritumoral region. Reactive astrocytes and activatedmicroglial cells are both involved in the process of peritumoral gliosis.Activated glial cells produce numerous biological active compounds includingendothelin-1 which after release from such cells can influence the structureand function of the peritumoral brain tissue. Lesions of oligodendrocytesand edema may be implicated in myelin degeneration. Finally, metastases willinduce axonal and neuronal injuries as indicated by a recent study onexpression of -amyloid precursor protein (APP) in reactive axonalswellings.     

进行期银屑病患者活性氧代谢变化探讨

目的：探讨进行期银屑病患者活性氧代谢变化。方法：采用细胞化学发光分析技术测定患者及健康对照组外周血淋巴细胞化学发光强度（ Ｌｙｃｌ）及多形核白细胞化学发光强度（ Ｐ Ｍ Ｎｃｌ）,同时测定血浆超氧化物歧化酶（ Ｓ Ｏ Ｄ）、全血谷胱甘肽过氧化物酶（ Ｇ Ｓ Ｈ Ｐｘ）以及血浆丙二醛（ Ｍ Ｄ Ａ）含量。结果：银屑病患者 Ｌｙｃｌ及 Ｐ Ｍ Ｎｃｌ较对照组显著增强（ Ｐ＜ ０．０５）,血浆 Ｓ Ｏ Ｄ活力明显增强（ Ｐ＜ ０．０５）, Ｍ Ｄ Ａ 浓度较对照组明显增高（ Ｐ＜ ００５）。全血 Ｇ Ｓ Ｈ Ｐｘ 活力较对照组显著下降（ Ｐ＜ ０．０５）。结论：进行期银屑病患者细胞功能改变,机体活性氧代谢增强,抗氧化功能下降,组织细胞损伤加快。活性氧损伤可能是该病患者皮损炎症的重要原因。     

The pathogenesis and modulation of the post-treatment reactive encephalopathy in a mouse model of Human African Trypanosomiasis

Drug treatment of late-stage human African Trypanosomiasis (HAT) in which the central nervous system (CNS) is involved may be complicated by a severe post-treatment reactive encephalopathy (PTRE) which can be fatal in up to 10% of cases. In order to understand the immunopathogenesis of this complication, an experimental mouse model has been developed that mirrors many of the pathological features of the PTRE in humans, and which allows various anti-inflammatory therapeutic regimes to be evaluated. Following the development of the PTRE in this model a number of cytokines are increased within the CNS including tumour necrosis factor (TNF) alpha, interleukins 1, 4 and 6, and macrophage inflammatory protein (MIP)-1. These cytokines appear at the same time as astrocyte activation which is an early event occurring before the development of the marked meningoencephalitic inflammatory response. The immunosuppressant drug azathioprine prevents but does not reduce the severity of an established PTRE and has a minimal effect on astrocyte activation. The ornithine decarboxylase inhibitor eflornithine prevents the induction, and ameliorates the severity, of the PTRE, and also reduces the degree of astrocyte activation. The Substance P antagonist RP-67,580 ameliorates the severity of an established PTRE, and also reduces astrocyte activation, indicating an important role of SP in the generation of the inflammatory response. Continued use of this mouse model should lead to further enhancement of our understanding of the pathogenesis of the PTRE and to improved drug regimes to prevent and/or treat it.     

Reactive oxidant species in piriform cortex extracellular fluid during seizures induced by systemic kainic acid in rats

Kainic acid (KA) administered systemically to rats produces seizures and brain damage. We measured an increase in reactive oxidant species (ROS) during KA-induced seizures in the extracellular fluid (ECF) of the piriform cortex, a brain region known to be subsequently damaged. Intracerebral microdialysis samples were collected and assayed for isoluminol-dependent chemiluminescence before and after injection of KA (16 mg/kg, ip). Hydrogen peroxide (H₂O₂) concentrations were calculated from catalase-sensitive chemiluminescence, the difference between total and catalase-resistant chemiluminescence. During generalized tonic-clonic seizures, both total and catalase-resistant chemiluminescence increased significantly in samples from brain ECF. Catalase-resistant chemiluminescence, most likely produced by ascorbic acid, increased for a full hour during sustained seizure activity. H₂O₂ concentrations showed a trend towards elevation during seizures. Increased ROS suggest that oxidative stress occurs in brain ECF during sustained seizure activity.     

骨立拮抗维甲酸所致大鼠骨质疏松的实验研究

目的　观察骨立对维甲酸所致骨质疏松大鼠的股骨骨密度、骨矿含量的影响。方法　采用ig维甲酸造成大鼠骨质疏松模型 ,使用骨立高、中、低 3种剂量分别进行治疗 ,观察其结果并与空白对照组和阳性对照药物组进行比较。结果　骨立 3个剂量治疗的骨质疏松大鼠的股骨骨密度和骨钙、骨磷含量均明显高于骨质疏松模型组大鼠 (P <0 .0 1或 0 .0 5 ) ,骨立高、中剂量组大鼠的尿钙排泄量明显低于骨质疏松模型组大鼠 (P <0 .0 1) ,其中以高剂量组疗效最佳。结论　骨立可明显提高骨质疏松大鼠的骨密度并升高其骨钙、骨磷的含量 ,降低尿钙排泄量 ,从而拮抗维甲酸所致的大鼠骨质疏松症。     

紫石英和寒水石超微饮片粉末粒径的研究

目的：为矿物类药材超微粉末粒径提供试验数据。方法：采用电镜扫描，X射线定性，原子发射光谱定量。结果：选择粒度为K4的微粉制备超微饮片，Ca^2 成分溶出度较高。结论：使用超微紫石英和寒水石，会减少服用量。