超声乳化白内障摘除治疗晶状体溶解性青光眼的临床效果

目的:探讨超声乳化白内障摘除治疗晶状体溶解性青光眼的效果。方法:对25例晶状体溶解性青光眼患者控制眼压后行白内障摘除联合人工晶状体囊袋内植入术,观察术中、术后并发症,术后视力及眼压。结果:所有患者手术顺利,后囊完整,术后视力恢复好,眼压得到控制。所有患者无明显术中、术后并发症的发生。结论:超声乳化白内障摘除治疗晶状体溶解性青光眼安全有效。     

高度近视眼LASEK治疗并发症53例

目的:探讨准分子激光上皮瓣下角膜磨镶术(laserepithelialkeratomileusis,LASEK)手术并发症的类型、产生原因及处理方法。方法:应用LASEK治疗等效球镜为-7.25～14.50D的高度近视眼53例(106眼),对术中和术后产生的并发症进行相关原因分析。结果:LASEK术中并发症主要有上皮瓣剥离困难、破碎、游离、皱褶、局限性缺损等,术后并发症主要有角膜上皮下雾状混浊(Haze)、最佳矫正视力下降、屈光度回退、眩光、上皮瓣溶解等。结论:严格掌握LASEK的手术适应证,熟练掌握手术技巧和正确处理角膜上皮瓣的各种并发症是保证LASEK成功的关键。     

姜黄素对培养的人胚胎视网膜色素上皮细胞增殖活性的影响

目的:研究姜黄素(curcumin,CUR)对培养人胚胎视网膜色素上皮(human fetal retinal pigmentepithelium,hfRPE)细胞增殖的影响。方法:用不同浓度CUR(2.5,5,10,20μg／ml)处理传代培养的hfRPE细胞24~48 h,采用MTT法和流式细胞术观察药物对hfRPE细胞增殖和细胞周期的影响。结果:CUR可明显抑制hfRPE细胞增殖,24、48 h的半数抑制浓度(IC50)分别为14.27μg／ml和12.7μg／ml;流式细胞仪分析表明姜黄素将hfRPE细胞阻滞在G2／M期。结论:在一定浓度范围内,姜黄素通过改变hfRPE细胞的周期分布来抑制其增殖。     

视网膜微血管周细胞内明胶酶的表达及影响

目的　检测糖基化终产物 (AGE)对培养的牛视网膜微血管周细胞 (BRPs)分泌明胶酶的作用 ,以探讨糖尿病视网膜病变 (DRP)的发病机制。方法　不同质量浓度AGE( 0、8、3 2、12 5、5 0 0、2 0 0 0 μg/mL)与BRPs作用 4d后 ,明胶酶谱分析细胞所分泌的明胶酶。结果　正常BRPs有明胶酶 A的分泌 ,相对分子质量分别为 72 0 0 0的原酶及 62 0 0 0的活性酶 ;扫描单位分别为 13 3 73± 6 66及 160 18± 15 2 9,另有少量 92 0 0 0的明胶酶 B分泌 ,扫描单位 93 0 1± 5 89。AGE能以剂量依赖的方式抑制BRPs内明胶酶 A的分泌 (原酶和活性酶与AGE相关系数分别为r =-0 798及r =-0 73 4,P <0 0 1)。结论　周细胞分泌明胶酶 A的下降可能是DRP中基底膜增厚的重要原因之一     

正常角膜基质细胞密度和角膜厚度的研究

目的观察Confoscan 2.0共焦显微镜下正常活体角膜影像表现,测量基质细胞密度与各层厚度.方法检查34例(48眼)正常人.记录图像,并计算基质细胞密度和各层厚度.结果基质细胞密度从前到后逐渐降低,前基质比后基质细胞密度明显增高(t=-9.016,P=0.000),Bowman膜下密度最高,为(1113.2±227)个/mm2.全基质细胞密度为(806.5±57)个/mm2.角膜中央厚度为(568.3±53.8)μm,基质层为(465.5±60.2)μm,上皮层为(58.5±20.4)μm.各层厚度均与全基质细胞密度无显著相关性(P＞0.05).结论Confoscan 2.0共焦显微镜能检测角膜基质细胞密度和各层厚度.     

口岸人员体重指数与心血管病危险因素聚集性关系探讨

目的探讨口岸人员体重指数(Body Mass Index-BMI)与心血管病危险因素聚集性的关系,为口岸工作人员预防和减少心血管病提供科学指导.方法对264名口岸工作人员的体检资料以体重指数为单因数作统计学的分析.结果在偏瘦、正常和肥胖体型间,男性甘油三脂(TG)、胆固醇(TC)和女性甘油三脂的水平有显著性差异(F值各为8.9、5.9、12.9,P＜0.01),血糖(GLU)男、女性组中均无显著性差异(F值各为0.9、0.3,P＞0.01).在血脂血糖异常检出率中,男性甘油三脂、胆固醇和女性甘油三脂的异常检出数在各组体重指数人数中有显著性差异(x2各为25.9、15.6、12.1,P＜0.01),血糖在男、女性组中无显著性差异(P值各为0.13、2.6,P＞0.01).高血压发生率在偏瘦、正常与肥胖体型者中差异较为明显(正常型为1.98%,肥胖型为5.17%).结论甘油三脂、胆固醇的水平与异常检出数和高血压的发生率均是随着体重指数升高而升高的.在多种心血管危险因素个体聚集性的比较中,男性肥胖者心血管危险因素发生的科学指导,有助于控制和减少心血管病的发生.     

Characterization of signal transduction and glucose transport in skeletal muscle from type 2 diabetic patients

We characterized metabolic and mitogenic signaling pathways in isolated skeletal muscle from well-matched type 2 diabetic and control subjects. Time course studies of the insulin receptor, insulin receptor substrate (IRS)-1/2, and phosphatidylinositol (PI) 3-kinase revealed that signal transduction through this pathway was engaged between 4 and 40 min. Insulin-stimulated (0.6-60 nmol/l) tyrosine phosphorylation of the insulin receptor beta-subunit, mitogen-activated protein (MAP) kinase phosphorylation, and glycogen synthase activity were not altered in type 2 diabetic subjects. In contrast, insulin-stimulated tyrosine phosphorylation of IRS-1 and anti-phosphotyrosine-associated PI 3-kinase activity were reduced 40-55% in type 2 diabetic subjects at high insulin concentrations (2.4 and 60 nmol/l, respectively). Impaired glucose transport activity was noted at all insulin concentrations (0.6-60 nmol/l). Aberrant protein expression cannot account for these insulin-signaling defects because expression of insulin receptor, IRS-1, IRS-2, MAP kinase, or glycogen synthase was similar between type 2 diabetic and control subjects. In skeletal muscle from type 2 diabetic subjects, IRS-1 phosphorylation, PI 3-kinase activity, and glucose transport activity were impaired, whereas insulin receptor tyrosine phosphorylation, MAP kinase phosphorylation, and glycogen synthase activity were normal. Impaired insulin signal transduction in skeletal muscle from type 2 diabetic patients may partly account for reduced insulin-stimulated glucose transport; however, additional defects are likely to play a role.     

Cell-cell adhesion molecules and signaling intermediates and their role in the invasive potential of prostate cancer cells

PURPOSE: The highly variable natural history of prostate carcinoma may be reflected in heterogeneity of invasive potential between tumors. MATERIALS AND METHODS: We have examined two prostate cancer cell lines of low invasive potential (CAHPV10 and PZHPV7) and three cell lines of high invasive potential (DU-145, PC-3, LNCapFGC), to determine whether specific adhesion molecule profiles correlated with their invasive behavior. RESULTS: Using an in vitro invasion assay, we demonstrated that DU-145, LNCapFGC and PC-3 cells were highly invasive compared with CA-HPV-10 and PZ-HPV-7 cells. LNCapFGC cells expressed high levels of E-cadherin, alpha-, beta- and gamma-catenin, desmoglein, desmoplakin and GSK3beta using immunoblotting. This was, in general, comparable to immunohistochemical staining. PC-3 cells had no E-cadherin or alpha-catenin, but expressed a high level of the HGF/SF receptor c-Met. In contrast, DU-145 cells were found to express E-cadherin and low levels for all other protein molecules, except c-Met. The DU-145 cell line also lacked alpha-catenin expression. In CA-HPV-10 and PZ-HPV-7 cells, there was no detection of APC, PECAM-1, P-cadherin or Wnt-1. DU-145, LNCapFGC and PC-3 cells formed cell-cell aggregates, which were reduced by inclusion of anti-E-cadherin antibody and the motogen HGF/SF. CONCLUSION: These results show that prostate cancer cells exhibit a diverse expression of cell-cell adhesion molecules and their signaling intermediates. The expression of these adhesion molecules bears an important relationship with the invasive phenotype of these cells.     

灯盏细辛注射液治疗脑梗死的疗效观察

目的 :观察灯盏细辛注射液治疗脑梗死的临床疗效与安全性。方法 :对46例脑梗死患者 ,随机单盲分为治疗组 (灯盏细辛注射液 )30例 ,对照组 (复方丹参注射液 )16例。结果 :治疗组、对照组治疗脑梗死的总有效率分别为90 0%和68 8%。疗效差异有显著性 (P<0 05)。结论 :灯盏细辛注射液治疗脑梗死比复方丹参注射液效果更好 ,且安全性较好 ,副作用少     

人巨细胞病毒感染对脐血巨核系祖细胞体外增殖的影响

目的　探讨人巨细胞病毒 (HCMV)对脐血巨核系祖细胞 (CFU Mk)体外增殖的影响及其机制。方法　采用造血祖细胞体外培养技术 ,观察、计数HCMV AD169感染的CFU Mk集落产率、抑制率、集落峰值及维持时间 ;并采用聚合酶链反应 (PCR)技术检测集落细胞内HCMV AD169DNA。结果　 1.HCMV AD169感染组集落产率较对照组明显减少 ,HCMV对CFU Mk集落的抑制程度与病毒滴度有关 ,集落产率随病毒感染滴度增高而减少 ,抑制率随病毒感染滴度增高而渐增加 ;各组集落峰值出现时间无明显差异 (P均 >0 .0 5 ) ,但各感染组集落维持时间明显短于对照组 (P <0 .0 1) ;2 .用PCR在集落细胞内检测到HCMV AD169DNA。结论　CFU Mk是HCMV的宿主细胞之一 ,HCMV能直接感染CFU Mk ;在体外HCMV AD169对CFU Mk的增殖和集落形成有明显抑制作用 ,此作用可能与临床HCMV感染后患者血小板减少有关