虫草菌丝对实验性肝硬化大鼠肝组织胰岛素酶活性的影响

目的 :探讨虫草菌丝对实验性肝硬化大鼠肝组织匀浆上清液胰岛素酶活性的动态影响及其可能机制。方法 :以CCl4诱导大鼠肝硬化模型 ,设立正常组、模型组和虫草组。正常组于实验开始时便处死大鼠 ,而后 2组则于造模 3 ,6,9wk分批处死 ,取血及肝组织标本。生化法测定血清丙氨酸转氨酶(ALT)、清蛋白 (ALB)含量 ,放射免疫法测定血清透明质酸 (HA)、血清胰岛素 (INS)含量及肝组织匀浆上清液的胰岛素酶活性。结果 :(1 ) 3 ,6wk虫草组大鼠血清ALT ,ALB及HA含量与对应模型组差异无显著意义 (P >0 .0 5 ) ,9wk虫草组大鼠血清ALT ,HA含量显著低于对应模型组 (P <0 .0 5 ) ,而其血清ALB含量则显著高于对应模型组 (P<0 .0 5 ) ;(2 ) 3wk虫草组及模型组大鼠血清INS水平及肝组织胰岛素酶活性与正常组大鼠差异无显著意义 (P >0 .0 5 ) ,6,9wk虫草组及模型组大鼠血清INS水平显著高于正常组 (P <0 .0 5 ) ,而对应的肝组织胰岛素酶活性则显著低于正常组 (P <0 .0 5 ,或P <0 .0 1 ) ;(3 ) 3 ,6,9wk虫草组大鼠血清INS水平及肝组织胰岛素酶活性与对应模型组差异无显著意义(P >0 .0 5 )。结论 :虫草菌丝可减轻CCl4对肝细胞的损伤 ,并可抑制肝纤维化 ;造模 6wk后实验性肝硬化大鼠肝组织胰岛素酶活性开始降低 ,血清INS含量开始升高     

纳洛酮治疗急性脑梗死的临床有效性分析

目的探讨纳洛酮治疗急性脑梗死的临床疗效.方法将122例急性脑梗死病人随机分为纳洛酮组(62例)和对照组(60例).纳洛酮组用5% GS 250 ml+纳络酮注射液 0.8 mg 静滴,每日2次;对照组用5% GS 250 ml+复方丹参 16 ml 静滴,每日1次.疗程均为 14 d,在1个疗程后进行疗效和起效时间比较.结果纳洛酮组总有效率为 93.5%,对照组为 76.7%,两组比较有显著性差异(P<0.05);纳洛酮组的起效时间明显快于对照组(P<0.05).结论纳洛酮治疗急性脑梗死临床疗效显著.     

急性非等容血液稀释对开颅病人颅内压及凝血功能影响

目的 探讨急性非等容血液稀释对开颅病人的颅内压和凝血功能的影响。方法 选择择期开颅肿瘤切除病人18例，麻醉诱导前行蛛网膜下腔穿刺，监测颅内压(ICP)，并由足背动脉放血400—600ml，开始诱导同时经外围静脉快速补充2—2．5倍于采血量的等效肢体和晶体。麻醉采用静吸复合全麻，术中连续监测有创血压、心率、氧饱和度，分别于血液稀释前后监测ICP，中心静脉压(CVP)、活化部分凝血活酶(APTT)、凝血酶原时间(PT)、凝血因子1(FIB)、血小板(PLT)、血球压积(HCT)。结果 与血液稀释前相比，血流动力学稳定；PT明显延长(P＜0．05)，PLT、HCT明显降低(P＜0．05)，但仍在正常范围内，APTT、FIB差异无显著意义(P＞0．05)；颅内压无明显增高。结论 急性非等容血液稀释对开颅手术病人的颅内压和凝血功能无明显影响，是一种安全有效的、简便的血液保护方法。     

In vitro tests for essential sperm functions using the phyto-oestrogen genistein as a test substance

Sperm motility, binding of spermatozoa to the zona pellucida and induction of the acrosome reaction are prerequisites for successful oocyte fertilization. Examination of the physiological and nonphysiological effects of particular compounds on sperm functions requires high-quality in vitro test systems. In this short methodological overview, a reliable combined in vitro test system with bovine gametes is described. The purpose of the study was to evaluate whether aliquots of pooled post-thaw spermatozoa are suitable for examination of environmental substances that affect essential sperm functions. The combined test system includes a number of known methods for the assessment of sperm vitality and motion parameters, acrosomal status, inducibility of acrosome reaction and sperm zona pellucida binding. First observations indicate that genistein inhibits the induction of acrosomal exocytosis and binding of spermatozoa to the zona pellucida. Motility parameters and the viability of bovine spermatozoa were not affected by this substance. It is concluded that genistein, a phyto-oestrogen which is abundant in several plants, can be used as a test substance for the evaluation of effects upon essential bovine sperm functions in vitro.     

Injury of Mouse Brain Mitochondria Induced by Cigarette Smoke Extract and Effect of Vitamin C on It in vitro

Objective To investigate the toxicity of cigarette smoke extract (CSE) and nicotine on mouse brain mitochondria as well as the protective effect of vitamin C in vitro. Method Mouse brain mitochondria in vitro was incubated with CSE or nicotine in the absence or presence of vitamin C for 60 minutes, and the changes of mitochondrial function and structure were measured. Results CSE inhibited mitochondrial ATPase and cytochrome C oxidase activities in a dose-dependent manner.However, no significant changes in the peroxidation indices were observed when mitochondrial respiratory enzymes activity was inhibited, and protection of mitochondria from CSE-induced injury by vitamin C was not displayed in vitro. The effect of CSE on mouse brain mitochondria swelling response to calcium stimulation was dependent on calcium concentrations. CSE inhibited swelling of mitochondria at 6.5 μmol/L Ca^2 , but promoted swelling response at 250μmol/L Ca^2 . Nicotine, the major component of cigarette smoke, showed no significant damage in mouse brain mitochondria in vitro. The CSE treatment induced mitochondrial inner membrane damage and vacuolization of the matrix, whereas the outer mitochondrial membrane appeared to be preserved. Conclusion The toxic effect of CSE on brain mitochondria may be due to its direct action on enzymatic activity rather than through oxygen free radical injury. Nicotine is not the responsible component for the toxicity of CSE to brain mitochondria.     

检测肾小球滤过功能的新方法——血清巯基蛋白酶抑制肽C

目的探讨测定血清巯基蛋白酶抑制肽C(CysC)的方法并评价其检测肾小球滤过功能的价值。方法对照组 2 1例、患者 10 7例 ,用全自动生化分析仪检测CysC、血清肌酐 (Scr)、尿肌酐 ,计算肌酐清除率 (Ccr)。根据Ccr将患者分成 4组。CysC用颗粒增强透射免疫比浊法 ,肌酐用肌氨酸氧化酶 PAP法测定。结果对照组CysC浓度为 1 2 5± 0 14mg/L ,患者组CysC随Ccr下降而升高 ,各组间差异显著 (P <0 0 0 1)。CysC与Ccr的相关性优于Scr与Ccr的相关性。CysC与性别、年龄无相关 ,而Scr男性显著高于女性 (P <0 0 0 1)。受试者工作特征 (ROC)曲线分析 ,CysC区别正常或异常肾功能的准确性较高 ,优于Scr。结论检测肾小球滤过功能CysC较Scr更好 ,不受年龄、性别的影响 ;本法可大批量、快速、准确测定 ,适于临床常规应用。     

老年人非酒精性脂肪性肝病与血脂血糖水平及体重指数的关系

目的探讨老年人非酒精性脂肪性肝病(NAFLD)与血脂血糖水平、体重指数等指标的关系。方法298例老年人按非酒精性脂肪性肝病诊断标准分为脂肪肝组(114例)和非脂肪肝组(184例),观察临床表现,检测血脂、血糖、体重指数、肝功能等指标并进行分析。结果脂肪肝组血脂、血糖水平、体重指数明显增高,和非脂肪肝组比较差异有显著性(P相似文献   

Tissue dosimetry expansion and cross-validation of rat and mouse physiologically based pharmacokinetic models for trichloroethylene.

Trichloroethylene (TCE), a volatile liquid used as a degreasing agent, is a common environmental pollutant. In 2001, the EPA published a draft risk assessment for TCE that incorporates dosimetry predictions of physiologically based pharmacokinetic (PBPK) models. The current modeling effort represents an expansion and extensive tissue dosimetry validation of rodent PBPK models for TCE. The pharmacokinetics of TCE in male Sprague-Dawley (S-D) rats were characterized (1) during and after inhalation exposure to 50 or 500 ppm TCE, (2) following administration of 8 mg/kg TCE PO, and (3) following intra-arterial injection of 8 mg/kg TCE. Blood and tissues (including liver, kidney, fat, skeletal muscle, heart, spleen, gastrointestinal tract, and brain) were collected at selected time-points from 5 min up to 24 h post initial exposure. The fat compartment was modified to be diffusion-limited to predict the observed slow release of TCE from the fat. The addition of a deep liver compartment was necessary to accurately predict the slower hepatic clearance of TCE for all three exposure routes. Simulations of liver concentrations following gavage of male B6C3F1 mice with 300-2000 mg/kg TCE were also improved with the addition of a deep liver compartment. Liver predictions were calibrated and validated using a cross-validation technique novel to PBPK modeling. Splitting of compartments did not significantly affect predictions of TCE concentrations in the liver, fat, or venous blood. This model expansion and validation increases both the utility and our confidence in the current use of rodent TCE PBPK models in human health risk assessment.     

Role of neutrophils in the synergistic liver injury from monocrotaline and bacterial lipopolysaccharide exposure.

Synergistic liver injury develops in Sprague-Dawley rats from administration of a small, noninjurious dose (7.4 x 10(6) EU/kg) of bacterial lipopolysaccharide (LPS) given 4 h after a nontoxic dose (100 mg/kg) of the pyrrolizidine alkaloid, monocrotaline (MCT). Previous studies demonstrated that liver injury is mediated through inflammatory factors, such as Kupffer cells and tumor necrosis factor alpha (TNF-alpha), rather than through simple interaction between MCT and LPS. In the present study, the hypothesis that neutrophils (polymorphonuclear leukocytes or PMNs) are causally involved in this injury model is tested, and the interdependence between PMNs and other inflammatory components is explored. Hepatic PMN accumulation and the appearance of cytokine-induced neutrophil chemoattractant-1 in plasma preceded the onset of liver injury, suggesting that PMNs contribute to toxicity. Hepatic PMN accumulation was partially dependent on TNF-alpha. Prior depletion of PMNs in MCT/LPS-cotreated animals resulted in attenuation of both hepatic parenchymal cell (HPC) and sinusoidal endothelial cell (SEC) injury at 18 h. PMN depletion did not, however, protect against early SEC injury that occurred before the onset of HPC injury at 6 h. This observation suggests that SEC injury is not entirely dependent on PMNs in this model. In vitro, MCT caused PMNs to degranulate in a concentration-dependent manner. These results provide evidence that PMNs are critical to the HPC injury caused by MCT/LPS cotreatment and contribute to the progression of SEC injury.