人脐静脉内皮细胞清除补体攻膜复合物的机制

目的：探讨内皮细胞清除补体攻膜复合物（MAC）的途径及其清除动力学，方法：原代培养的人脐静脉内皮细胞以RH414荧光标记质膜双层，0℃组装亚溶剂量的MAC，37℃复苏后，LSCM实时监MAC沉积诱导的质膜囊泡化形成和胞吞，胞吐情况,流式细胞仪定量检测内皮细胞表面MAC抗原的清除情况，结果：MAC沉积后，内皮细胞有的质膜囊泡化形成，囊泡以胞吞和胞吐2种方式离开细胞，并以前者占优，37度条件下，内皮细胞清除表面MAC的半衰期约为5min。结论：内皮细胞可通过胞吞和胞吐2种机制清除细胞表面沉积的MAC，并以胞吞方式为主。     

平板运动试验不同阶段出现的室性心律失常分析

目的：通过进行平板运动试验鉴别室性早搏的性质。方法：从所有做平板运动试验的2383例室性心律失常病例中，选出在不同阶段出现室行早搏的217例患者进行分析。结果：经冠状动脉造影证实确定为冠心病的174例，高血压性心脏病合并冠心病12例，X综合症4例，心律失常15例，植物神经功能紊乱12例。174例冠心病患者7例为左主干病变，58例为双支病变，109例为单支病变。结论：平板运动试验对室性心律失常的定性分析具有较高的临床价值。     

Inhibitory effect of ketamine on phosphorylation of the extracellular signal-regulated kinase1/2 following brain ischemia and reperfusion in rats with hyperglycemia

To determine if the inhibitory effects of ketamine on the extracellular signal-regulated kinase (ERK) 1/2 are involved in reduction of the hyperglycemia-exaggerated cerebral ischemic lesion, rats with normoglycemia, hyperglycemia, or hyperglycemia supplemented with ketamine were subjected to 15 min of forebrain ischemia, and then, reperfusion for 0.5, 1, and 3h. Phosphorylation of ERK1/2 in the brain tissues was assessed by immunohistochemistry and Western blot analysis. In rats with normoglycemia, we demonstrated a moderate increase of the ERK1/2 phosphorylation in the cingulum cortex and hippocampus CA3 following an ischemic intervention. It quickly dropped to control levels after reperfusion for 0.5h. In rats with hyperglycemia, however, the increase of the ERK1/2 phosphorylation in these areas was significantly higher in all animals reperfused. The neuronal death, detected by the TdT-mediated-dUTP nick end labeling assays, was found in the cingulum cortex (5.23+/-2.34, per high power feild) and hippocampus CA3 areas (6.29+/-3.68, per 1mm(2)) in hyperglycemic group after reperfusion for 3h. With ketamine treatment, the ERK1/2 phosphorylation in cingulum cortex and hippocampus CA1 and CA3 areas was found to be the same as that in normoglycemia rats. Our results suggest that hyperglycemia may increase the ischemic insult through modulation of the signal transduction pathways involving ERK1/2. The inhibitory effects of ketamine on the hyperglycemia-activated ERK1/2 phosphorylation are probably through inhibition of the N-methyl d-aspartate-mediated calcium influx, which subsequently reduce the hyperglycemia-exaggerated cerebral damage.     

Translocation of Enterococcus faecalis strains across a monolayer of polarized human enterocyte-like T84 cells

We used a two-chamber system to study transcytosis of Enterococcus faecalis across monolayers of human colon carcinoma-derived T84 cells, which show structural resemblance to the native intestine. Among 16 E. faecalis isolates from different sources, the well-characterized strain OG1RF and 8 other isolates (2 endocarditis isolates, 1 urine isolate, and all 5 fecal isolates) showed translocation in this assay, while 6 clinical isolates (3 endocarditis and 3 urine isolates), the recipient strain JH2-2, and the control, Escherichia coli DH5alpha, had no detectable translocation. Of two OG1RF mutants involving the previously studied epa (enterococcal polysaccharide antigen) gene cluster, known to be needed for virulence and resistance to killing by polymorphonuclear leukocytes, one epa mutant (TX5179) was unable to translocate, while TX5180, with an epa disruption farther downstream, showed a moderate decrease in translocation relative to that of the wild-type strain OG1RF (P < 0.01), indicating that the epa gene cluster is important for translocation across a T84 monolayer. This observation was confirmed by complementation of the epa mutant (TX5179) with epa genes and restoration of its translocation ability. In conclusion, we have demonstrated translocation of at least some strains of E. faecalis across T84 monolayers, although strains differ considerably in this ability, and we have demonstrated that epa mutations can cause marked changes in successful translocation. These results suggest that this model may be a useful in vitro system for studying the process of translocation from the intestinal tract.     

动脉粥样硬化斑块中内皮素生成及分布的免疫组织化学观察

应用免疫组化方法对人动脉粥样硬化（ＡＳ）斑块中内皮素（ＥＴ）进行分析，发现除内皮细胞外，增生的平滑肌细胞（ＳＭＣ）中也含有大量的内皮素；在内皮剥脱的大鼠胸主动脉，增生的内膜ＳＭＣ能产生丰富的内皮素。内皮素放射免疫测定证实ＳＭＣ增生的活跃程度与内皮素量呈正比。提示内皮素合成增多与ＡＳ斑块内ＳＭＣ增生关系密切。     

CD44+/CD24-细胞在乳腺癌组织及细胞系中的数量与分布

Objective To study the distribution and quantity of CD44VCD24- cells in breast cancer tissue and the cell lines,and as well as its correlation with the expression of various breast cancer markers and molecular subtyping of breast carcinoma.Methods The expression of CD44 / CD24,estrogen receptor,progesterone receptor,HER2,human estrogen-induced protein PS2,bcl-2 and nm23 in 60 cases of invasive ductal carcinoma of breast were studied by either single or double immunohistochemical staining.The co-expression of CD44 and CD24 in 3 breast cancer cell lines (MCF-7,MDA-MB-468,and MDA-MB- 231) was also examined.Results The quantity and distribution of CD44 + /CD24- cells varied greatly and no specific patterns were identified.The percentage of CD44 + /CD24- in breast cancer was 65%.The amount of CD44+/CD24- cells did not correlate with the age of patients,lymph node metastasis,tumor　 size,molecular subtypes and expression of various breast cancer markers in breast carcinoma.The proportion of CD44+/CD24- cells in MCF-7,MDA-MB-468,and MDA-MB-231 cell lines was < 1%,5% and > 80% ,respectively.Conclusions CD44+ /CD24- cells are demonstrated in certain breast cancer tissues and cell lines.However,there is no relationship obtained between the quantity or the distribution of these cells and the molecular subtyping or the clinicopathologic parameters in breast cancer.     

NF-κB哑铃形诱骗剂ODN对骨髓瘤细胞生长及IL-6表达的抑制作用

目的设计合成靶向NF-κB的哑铃形诱骗剂ODN,分析靶向NF-κB的哑铃形诱骗剂对NF-κB转录活性、多发性骨髓瘤细胞8266的生长及其分泌的IL-6的抑制效应。方法采用电泳迁移率变动分析(EMSA)体外检测诱骗剂ODN对NF-κB转录活性的抑制效应。将8266细胞随机分为传代培养的8266细胞组;诱骗剂ODN处理组及脂质体处理组。通过阳离子脂质体以2mg/L、4mg/L、8mg/L不同剂量诱骗剂ODN转染8266细胞。转染后8、12、18h,ELISA法检测8266细胞培养上清中IL-6的表达。用MTT比色检查诱骗剂ODN对IL-6刺激的8266细胞生长的影响。结果硫代磷酸的诱骗剂ODN在体外能有效地抑制NF-κB与其顺式元件的结合;2mg/L、4mg/L、8mg/L等不同浓度的脂质体-ODN复合物对8266细胞表达IL-6的抑制程度不同。脂质体-ODN复合物对8266细胞的生长及IL-6的活性均有抑制作用。结论靶向NF-κB的诱骗剂ODN在体外可抑制NF-κB的转录活性,从而抑制8266细胞的生长,降低瘤细胞中IL-6的表达。     

用于电刺激听神经方波刺激器的研制

本文主要介绍了用于电刺激听神经方波刺激器的基本设计原理 ,组成结构和三个主要性能指标 ,脉宽 相位 :2 5 μs phase、 5 0 μs phase、 10 0 μs phase ;电流强度 :5 0 μA～ 4 0 0 0 μA (每 5 0 μA一档上、下可调 ) ;频率 :30次 秒、 2 0 0次 秒、 4 0 0次 秒、 10 0 0次 秒、 12 0 0次 秒、 2 0 0 0次 秒 ,其特点有人机界面友好 ,性能稳定 ,安全性好 ,无需安装光电藕合器。为研究听神经兴奋性、优化电刺激听神经参数、以及评估电极的有效性和安全性提供实验仪器     

海藻酸钙/聚组氨酸微胶囊的毒性试验研究

为了考察海藻酸钙/聚组氨酸微胶囊的毒性特征,我们利用MTT比色法和小鼠尾静脉注射法,分别考察了该微胶囊的细胞毒性和急性全身毒性。结果表明：微胶囊浓度≤1.0mg/mL时,材料对L929细胞生长无明显抑制作用;微胶囊浸提液即使在高浸提比（10.0mg/mL）下,浸提产物也无细胞毒性作用。急性全身毒性试验结果显示：微胶囊浸提液不引起急性全身毒性反应,表明微胶囊浸提液无有毒的沥滤物和降解产物产生。说明海藻酸钙/聚组氨酸微胶囊无明显毒性。