儿茶素对溶血卵磷脂胆碱所致细胞损伤的保护作用

作者以体外培养的小牛主动脉内皮细胞为材料 ,研究了溶血卵磷脂胆碱 (LPC)和氧自由基(OFR)对血管内皮细胞 (VEC)的损伤 ,及儿茶素对VEC的保护。结果显示 :当VEC与LPC(5ug/ml)或黄嘌呤 /黄嘌呤氧化酶 (X/XO) (10umol/L + 2 0 0umol/L)共孵育 2 4小时时 ,表现为细胞内乳酸脱氢酶 (LDH)泄漏量增多 ,细胞内过氧化脂质丙二醛 (MDA)含量升高 ,细胞生长减缓 ,存活率下降 ;当加入不同浓度的儿茶素后则可明显抑制LDH的泄漏量 ,降低MDA含量 ,细胞生长正常 ,存活率提高。表明LPC与X/XO对VEC有损伤作用 ,而儿茶素则能通过抗氧化途径抵抗LPC与X/XO致VEC的损伤。

血管内皮细胞损伤和修复与2型糖尿病阿司匹林抵抗的相关性研究

目的:研究血管内皮细胞损伤和修复与2型糖尿病阿司匹林抵抗的相关性。方法:选择2013年—2014年收治的2型糖尿病患者310例,其中符合入选标准298例。根据TEG检测结果将患者分为阿司匹林抵抗组42例和阿司匹林敏感组256例。所有患者每天口服>100 mg的阿司匹林,1周后,抽取患者静脉血,置于枸橼酸和肝素试管中。检测血小板抑制率。以患者发病时间为起点进行为期12个月的随访,检测患者外周血中的血管内皮细胞的数量。结果:患者服用阿司匹林1周后,阿司匹林敏感组和阿司匹林抵抗组循环内内皮细胞的数量为(4.2±1.6)个和(3.3±1.1)个,随访1年后分别为(5.2±1.4)个和(2.2±0.7)个,两组患者在不同时间段循环内内皮细胞数量比较,差异有统计学意义,P<0.05。结论:血管内皮细胞损伤与阿司匹林抵抗具有明显的相关性,科学有效地降低阿司匹林抵抗率能够有效降低糖尿病患者并发心脑血管血栓性疾病的发生率,减少血管内皮细胞的损伤程度。

氟哌啶醇对N-甲基-D-门冬氨酸诱导的大鼠海马神经细胞损伤的保护作用

用原代培养大鼠海马神经细胞的方法 ,观察氟哌啶醇对 N-甲基 - D-门冬氨酸 (NMDA)诱导的大鼠海马神经细胞损伤的保护作用 .结果表明 ,氟哌啶醇能剂量依赖地抑制 NMDA诱导的大鼠海马神经细胞内乳酸脱氢酶 (L DH)的释放 ,并改善受损细胞形态 ,四唑盐比色法 (MTT)显示存活率增高 .提示氟哌啶醇对

益气活血中药防治大鼠血管内皮细胞损伤的实验研究

目的 :建立大鼠VEC损伤模型 ,观察益气活血中药是否具有防治大鼠VEC损伤的作用。方法 :SD大鼠 30只 ,随机分为正常对照组、模型组、益气活血组各 10只。建立大鼠VEC损伤模型 ,检测并比较CEC计数、t PA、PAI活性、6 Keto PGF1α含量及PAgTmax等指标变化。结果 :益气活血组与模型组比较 :CEC计数明显减少 ,t PA活性明显增强 ,PAI活性降低 ,活性型t PA升高 ,6 Keto PGF1α 含量升高 ,PAgTmax(P <0 .0 1～ 0 .0 5 )。结论 :益气活血中药具有良好的VEC保护作用 ,能改善和调节VEC的内分泌功能 ,增强其抗凝及纤溶活性。这为益气活血中药有效防治心脑血管疾病的作用机制提供了新的实验依据。

角膜转位移植的效果 自体和异体内皮细胞损失的比较

背景：异体角膜移植植片的慢性内皮损失特点尚不清楚。可能的原因是细胞移行到植床和慢性亚临床免疫反应。目的：比较自体角膜转位移植术和同种异体角膜移植术后内皮细胞损失的情况，并观察角膜转位移植术后的临床效果。

组织工程化许旺细胞培养及纯化的实验研究

目的获得组织工程化的乳鼠许旺细胞.方法采用出生1 d乳鼠的脊髓后根冲经节,以复合酶消化法进行乳鼠许旺细胞培养.通过Sigma-cote处理滴管和加入神经生长因子减少细胞损失、加速细胞分裂、增加细胞总量;通过低浓度胰酶快速消化、差速贴壁法的有机结合对许旺细胞进行纯化;继用抗S-100蛋白单抗通过(即用型)ABC免疫组化检测试剂盒,SABC-CY3试剂盒进行细胞鉴定.结果细胞纯度＞90%,细胞量＞2×10 7/ml.结论本实验方法具有高度重复性,可获得高纯度,大量的许旺细胞.

小儿高热惊厥的护理对策

小儿高热惊厥如不及时处理，可使脑细胞损坏，严重者可引起不同程度的癫痫和智力低下等并发症，现将多年来在儿科工作积累的经验总结如下。

Effect of Platelet Activation and Endothelial Cell Injury on Malignant Cancer

Objective: To study the effects of platelet activation and endothelial cell injury on the patients with malignant tumor and their prognoses.Methods: Radioimmunity and ELISA methods were employed to detect the TXB2, GMP-140, vWF, cGMP and FN in 78 cases of malignant tumor and 40 healthy control persons.Results: The levels of TXB2, MP-140 and cGMP were increased in intestinal cancer group, lung cancer group and hepatic cancer group, while FN decreased in intestinal cancer and lung cancer group. cGMP was positively related to TXB2, GMP-140, vWF in malignant tumor group. FN was decreased in the group complicated with infection and the group with metastasis, while the other indexes increased. GMP-140, vWF and cGMP was decreased after operation except for the increasing of FN.Conclusion: Activations of platelet and injury of endothelial cells developed in patients with malignant tumor, and both of them affected the metastasis and prognosis of malignant tumor. Key words platelet activation - epithelium injury - malignant tumor - metastasis This work was supported by grants from Guangdong Medical Science foundation (A2000633).

Ex vivo non-viral vector-mediated neurotrophin-3 gene transfer to olfactory ensheathing glia: effects on axonal regeneration and functional recovery after implantation in rats with spinal cord injury

Objective Combine olfactory ensheathing glia （OEG） implantation with ex vivo non-viral vector-based neurotrophin- 3 （NT-3） gene therapy in attempting to enhance regeneration after thoracic spinal cord injury （SCI）. Methods Primary OEG were transfected with cationic liposome-mediated recombinant plasmid pcDNA3.1 （＋）-NT3 and subsequently implanted into adult Wistar rats directly after the thoracic spinal cord （T9） contusion by the New York University impactor. The animals in 3 different groups received 4x 1050EG transfected with pcDNA3.1 （＋）-NT3 or pcDNA3.1 （＋） plasmids, or the OEGs without any plasmid transfection, respectively; the fourth group was untreated group, in which no OEG was implanted. Results NT-3 production was seen increased both ex vivo and in vivo in pcDNA3.1 （＋）-NT3 transfected OEGs. Three months after implantation of NT-3-transfected OEGs, behavioral analysis revealed that the hindlimb function of SCI rats was improved. All spinal cords were filled with regenerated neurofilament-positive axons. Retrograde tracing revealed enhanced regenerative axonal sprouting. Conclusion Non-viral vector-mediated genetic engineering of OEG was safe and more effective in producing NT- 3 and promoting axonal outgrowth followed by enhancing SCI recovery in rats.

Influence of Copper Stress on Ultra-structure of Wheat Seedlings

Transmission Electron Microscope (TEM) Technology was used to investigate the effect of 25,100 and 200 mg/kg copper on ultra-structure of root tip and leaf blade of wheat. Result showed that serious damage was found with Copper of 25,100 and 200 mg/kg. Plasmolysis,concentrated cytoplasm,chloroplast inflation,lamellar structure disturbance,capsule disappearance and disintegration,mitochondria structures ambiguity and vacuolization were all symptoms under Cu stress. There were positive correlation between concentration of coper stress and the degree of injury,and the degree of injury of copper were different in different organelles. Mitochondria were the most sensitive organelles,and there was patient difference in the same organelles of different parts.

The Superiority of Like-rocket Immunoelectrophoresis Using in Single Cell Gel Electrophoresis Assay

[Objective] The like-rocket immunoelectrophoresis was used to explore a new feasible electrophoresis method for single cell gel electrophoresis assay （comet assay）.[Method] The like-rocket immunoelectrophoresis was used for single cell gel electrophoresis assay to detect DNA damage at single cell level,then it was compared with traditional electrophoresis method to analyze its advantage and disadvantages.[Result] Under cell DNA undamaged state,the results of two electrophoresis methods were consistent.When cell DNA was damaged,the comet tail divergence of some cells under traditional electrophoresis method were drifted,however,the comet tail image of like-rocket immunoelectrophoresis was concentrated and not shifted.[Conclusion] The like-rocket immunoelectrophoresis had some advantages.

Effect of Intravascular Irradiation on Intimal Smooth Muscle Cells Proliferation and Apoptosis in Balloon Injuried Arteries

Objective: To investigate the effect of intravascular in radiation on thearterial wall smooth muscle cells (SMCs) proliferation and apoptosis after iliac artery bollominjury in figs. Methods: Twenty-seven miniature figs were divided into three groups. All pigsunderwent iliac artery balloon over-stretch. An^(192) Ir source through afterloader was positionedat the injuried segments to give 10 Gy in 9 pigs and 20 Gy in the other 9 pigs, and the rest 9 pigswere, used as control group. The pigs were killed on the 3rd, 10th and 28th days respectively forobservation. The injured segments were processed to examine SMCs proliferation by proliferation cellnuclear antigen (PCNA) and apopto-sis by terminal deoxynucleotidyl transferase-mediated dUTPnick-end labeling (TUNEL). Results: PC-NA index analysis has some that SMCs proliferation inneointima was significantly inhibited in irradiation group on the 10th and 28th days. The value forintimal SMCs apoptosis in control vs 10 Gy and 20 Gy irradiation groups were: (1. 185+-0. 49)% vs(2. 27+-0. 49)%(P>0. 05) and (1. 85+-0. 49)% vs (2. 53+-0. 45)%(P<0. 05), at the 10th day; (1.61+-0. 35)% vs (3. 11+-0. 51)%(P<0. 05), and (1.61+-0. 35)% vs (7. 05+-1. 82)% (P<0. 05), on the28th day. In irradiated arteries, the maximal incidence of intimal SMCs apoptosis was (7. 05+--1.82)% in 20 Gy group vs (3. 11+-0. 51)% in 10 Gy group (P<0. 05), on the 28th day. In the same doseirradiation group, the incidence of intimal SMCs apoptosis was higher on the 28th day than that onthe 10th day. Conclusion: Intra-arterial gamma irradiation can inhibit intimal SMCs proliferationand stimulate SMCs apoptosis in balloon-in jured arteries. These may be contributive to preventionof restenosis of arteries after balloon injury.

EFFECTS OF ELECTROACUPUNCTURE ON EXPRESSION OF INTERCELLULAR ADHESION MOLECULE-1 IN THE RAT OF LOCAL CEREBRAL ISCHEMIA-REPERFUSION

Objective To investigate effects of electroacupuncture （EA） on expression of intercellular adhesion molecule-1 （ICAM-1） in the rat of local cerebral ischemia-reperfusion. Methods Eighty SD rats were randomly divided into a normal control group, a sham operation group, a model group and an EA treatment group, 20 rats in each group. The thread-obstruction method was used for preparation of ischemia-reperfusion model. Zea-Longa rating criteria were used for evaluation of nervous function disorder; Immunohistochemical SABC method was used for detection of ICAM-1 expression in the microvascular endothelial cell of the ischemic brain region, and ELISA method for the soluble ICAM-1 （slCAM-1） content in peripheral blood. Re. suits After cerebral ischemia-reperfusion, both ICAM-1 expression level in the microvascular endethelium cell of the ischemic brain region and slCAM-1 content in the peripheral blood significantly increased in the model group as compared with the normal group and the sham operation group （P〈0.01）; After EA treatment, the ICAM-1 expression level in the microvascular endothelial cell of the ischemic brain region and slCAM-1 content in the peripheral blood were significantly down-regulated in the EA treatment group as com- pared with the model group （P〈 0.05）. Conclusion After cerebral ischemia-reperfusion, the microvascular endothelial cell of the ischemic brain region releases ICAM-1, which induces inflammatory injury of cerebral tissues; EA treatment can decease the expression of ICAM-1, so as to prevent the brain from the injury.

补充铜(Cu)元素的食疗方法

若缺铜,人早衰,细胞损,骨质败,既愚蠢,又笨傻,男变疯,女变呆,多贫血,多畸形,冠心病,又多患,易病危,易得癌,常见病,白癜风,胆固醇,速高升,应早治,不徘徊,食疗法,喜开怀.

补充铜(Cu)元素的食疗方法

若缺铜,人早衰,细胞损,骨质败,既愚蠢,又笨傻,男变疯,女变呆,多贫血,多畸形,冠心病,又多患,易病危,易得癌,常见病,白癜风,胆固醇,速高升,应早治,不徘徊,食疗法,喜开怀.其-法：取胆矾,用-克,经炮制,研为末,用布包,加在豆,煮米粥,去包药,日-剂,吃数日,病自愈.

Analytical model for power dissipation in cell membranes in suspensions exposed to electric fields

Due to interaction among cells, it is too complex to build an exactanalytical model for the power dissipation within the cell membrane in suspensions exposed toexternal fields. An approximate equivalence method is proposed to resolve this problem. Based on theeffective medium theory, the transmembrane voltage on cells in suspensions was investigated by theequivalence principle. Then the electric field in the cell membrane was determined. Finally,analytical solutions for the power dissipation within the cell membrane in suspensions exposed toexternal fields were derived according to the Joule principle. The equations show that theconductive power dissipation is predominant within the cell membrane in suspensions exposed todirect current or lower frequencies, and dielectric power dissipation prevails at high frequenciesexceeding the relaxation frequency of the exposed membrane.

Bile-acid-induced cell injury and protection

Several studies have characterized the cellular and molecular mechanisms of hepatocyte injury caused by the retention of hydrophobic bile acids （BAs） in cholestatic diseases. BAs may disrupt cell membranes through their detergent action on lipid components and can promote the generation of reactive oxygen species that, in turn, oxidatively modify lipids, proteins, and nucleic acids, and eventually cause hepatocyte necrosis and apoptosis. Several pathways are involved in triggering hepatocyte apoptosis. Toxic BAs can activate hepatocyte death receptors directly and induce oxidative damage, thereby causing mitochondrial dysfunction, and induce endoplasmic reticulum stress. When these compounds are taken up and accumulate inside biliary cells, they can also cause apoptosis. Regarding extrahepatic tissues, the accumulation of BAs in the systemic circulation may contribute to endothelial injury in the kidney and lungs. In gastrointestinal cells, BAs may behave as cancer promoters through an indirect mechanism involving oxidative stress and DNA damage, as well as acting as selection agents for apoptosis-resistant cells. The accumulation of BAs may have also deleterious effects on placental and fetal cells. However, other BAs, such as ursodeoxycholic acid, have been shown to modulate BA-induced injury in hepatocytes. The major beneficial effects of treatment with ursodeoxycholic acid are protection against cytotoxicity due to more toxic BAs; the stimulation of hepatobiliary secretion; antioxidant activity, due in part to an enhancement in glutathione levels; and the inhibition of liver cell apoptosis. Other natural BAs or their derivatives, such as cholyI-N- methylglycine or pharmacological properties. cholylsarcosine, interest owing have also aroused to their protective

Biochemical mechanisms in drug-induced liver injury:Certainties and doubts

Drug-induced liver injury is a significant and still unresolved clinical problem. Limitations to knowledge about the mechanisms of toxicity render incomplete the detection of hepatotoxic potential during preclinical development. Several xenobiotics are lipophilic substances and their transformation into hydrophilic compounds by the cytochrome P-450 system results in production of toxic metabolites. Aging, preexisting liver disease, enzyme induction or inhibition, genetic variances, local 02 supply and, above all, the intrinsic molecular properties of the drug may affect this process. Necrotic death follows antioxidant consumption and oxidation of intracellular proteins, which determine increased permeability of mitochondrial membranes, loss of potential, decreased ATP synthesis, inhibition of Ca^2＋-dependent ATPase, reduced capability to sequester Ca^2＋ within mitochondria, and membrane bleb formation. Conversely, activation of nucleases and energetic participation of mitochondria are the main intracellular mechanisms that lead to apoptosis. Non-parenchymal hepatic cells are inducers of hepatocellular injury and targets for damage. Activation of the immune system promotes idiosyncratic reactions that result in hepatic necrosis or cholestasis, in which different HLA genotypes might play a major role. This review focuses on current knowledge of the mechanisms of drug-induced liver injury and recent advances on newly discovered mechanisms of liver damage. Future perspectives including new frontiers for research are discussed.

Novel insight into mechanisms of cholestatic liver injury

Cholestasis results in a buildup of bile acids in serum and in hepatocytes.Early studies into the mechanisms of cholestatic liver injury strongly implicated bile acidinduced apoptosis as the major cause of hepatocellular injury.Recent work has focused both on the role of bile acids in cell signaling as well as the role of sterile inflammation in the pathophysiology.Advances in modern analytical methodology have allowed for more accurate measuring of bile acid concentrations in serum,liver,and bile to very low levels of detection.Interestingly,toxic bile acid levels are seemingly far lower than previously hypothesized.The initial hypothesis has been based largely upon the exposure of μmol/L concentrations of toxic bile acids and bile salts to primary hepatocytes in cell culture,the possibility that in vivo bile acid concentrations may be far lower than the observed in vitro toxicity has far reaching implications in the mechanism of injury.This review will focus on both how different bile acids and different bile acid concentrations can affect hepatocytes during cholestasis,and additionally provide insight into how these data support recent hypotheses that cholestatic liver injury may not occur through direct bile acid-induced apoptosis,but may involve largely inflammatory cell-mediated liver cell necrosis.