Effect of dexamethasone on nitric oxide synthase and Caspase-3 gene expressions in endotoxemia in neonate rat brain

INTRODUCTION Fifty percent to seventy percent of the patientsare complicated with brain damage at various degreesduring endotoxemia, which is characterized bydamage to the neurons, microvascular injury,increased endothelial permeability, and neutrophilinfiltration and accumulation in the brain. It has beenrecognized that bacterial endotoxin (lipopolysaccharideLPS) plays important roles in this pathophysiologicalprocess, but the mechanism and approach toprevention of brain damage during en…     

脑活素改善血管性痴呆患者智能状况的临床研究

目的:探索脑活素对血管性痴呆患者智能状况的改善效果。方法:将29例符合血管性痴呆标准的患者分为对照组和治疗组。对照组用血塞通0.4g,治疗组在对照组的基础上加用脑活素20mL,10d为1个疗程,3年共6个疗程,其后分别采用中文版简易智能状态检查(MMSE)量表进行积分,用中国人修订韦氏成人量表(WAIS-RC)进行智力测验比较。结果:根据WAIS-RC测验结果,两组3年后知识(11.32±1.76比9.23±1.78)、领悟(13.19±1.85比11.24±2.12)、算术(10.18±1.32比8.63±1.25)、相似(9.46±0.68比7.56±0.98)、数字广度(10.12±0.69比8.68±0.97)、词汇(31.25±0.78比27.32±1.02)、数字符号(31.35±1.20比25.35±0.78)、填图(9.78±0.98比7.45±0.65)、图片排列(19.16±0.74比15.23±1.52)等项目比较,治疗组积分明显高于对照组(t=1.96～5.21,P<0.05或0.01)。治疗组治疗前后上述项目自身对照积分亦有显著提高(t=1.96～5.21,P<0.05或0.01)。结论:脑活素能有效抑制神经细胞的凋亡,减少脑功能的受累,治疗血管性痴呆,对老年群体的康复有一定的治疗作用。     

High persistence rate of hepatitis B virus in a hydrodynamic injection-based transfection model in C3H/He N mice

AIM: To optimize the viral persistence rate in a hydrodynamic injection(HI) based hepatitis B virus(HBV) transfection mouse model.METHODS:(1) 5-6-wk-old male C3H/He N and C57BL/6 mice were hydrodynamically injected with 10 μg endotoxin-free p AAV/HBV1.2 plasmid DNA via the tail vein. Hepatitis B surface antigen(HBs Ag), hepatitis B e antigen(HBe Ag) and HBV DNA, both in the serum and liver, were detected at different time points post HI by ELISA, immunohistochemical staining or quantitative polymerase chain reaction(PCR);(2) male C3H/He N and C57BL/6 mice, either hydrodynamically injected mice at 10 wk post HI or na?ve mice, were all immunized subcutaneously with 5 μg HBs Ag formulated in complete Freund’s adjuvant three times at a 2-wk interval. Two weeks after the final immunization, splenocytes were isolated for T cell function analysis by ELISPOT assay; and(3) five weeks post HI, C3H/He N mice were intragastrically administered 0.1 mg/kg entecavir once a day for 14 d, or were intraperitoneally injected with 1 mg/kg interferon(IFN)-α twice a week for 2 wk, or were treated with PBS as controls. The sera were collected and assayed for HBV DNA on days 0, 7 and 14 after drug treatment. RESULTS:(1) Approximately 90%(22/25) of the injected C3H/He N mice were still HBs Ag-positive at 46 wk post HI, whereas HBs Ag in C57BL/6 mice were completely cleared at 24 wk. Serum levels of HBe Ag in C3H/He N mice were higher than those in C57BL/6 mice from 4 wk to 46 wk. HBV DNA levels in the hydrodynamically injected C3H/He N mice were higher than those in the C57BL/6 mice, both in the serum(from 4 wk to 46 wk) and in the liver(detected at 8 wk and 46 wk post HI). Histology showed that hepatitis B core antigen and HBs Ag were expressed longer in the liver of C3H/He N mice than in C57BL/6;(2) HBs Ag specific T cell responses after HBs Ag vaccination in hydrodynamically injected C3H/He N and C57BL/6 mice, or naive control mice were detected by ELISPOT assay. After stimulation with HBs Ag, the frequencies of IFN-γ producing splenocytes in the hydrodynamically injected C3H/He N mice were significantly lower than those in hydrodynamically injected C57BL/6 mice, control C3H/He N and control C57BL/6 mice, which were 0, 17 ± 7, 18 ± 10, and 41 ± 10 SFCs/106 splenocytes, respectively, and the mean spot sizes showed the same pattern. Even just stimulated with PMA and ionomysin, T-cell responses elicited in the vaccinated control C3H/He N were much higher than those in hydrodynamically injected C3H/He N mice; and(3) For drug treatment experiments on the hydrodynamically injected C3H/He N mice, serum HBV DNA levels in the entecavir treatment group declined(131.2 folds, P < 0.01) on day 7 after treatment and kept going down. In the group of IFN-α treatment, serum HBV DNA levels declined to a lowest point(6.42 folds, P < 0.05) on 7 d after treatment and then rebounded.CONCLUSION: We have developed a novel HI-based HBV transfection model using C3H/He N mice, which had a higher HBV persistence rate than the classic C57BL/6 mouse model.     

Leptin在大鼠肝缺血/再灌注介导的肠道损伤中的作用

目的:研究瘦素(leptin)在肝缺血/再灌注(H-I/R)后肠道内的表达变化,并探讨 leptin在H-I/R介导的肠道损伤中的作用.方法:建立大鼠70%H-I/R模型,大鼠随机分成5组,每组9只,依次为假手术(Sham)组、肝缺血60 min/再灌注60 min(I60'R60')组、I60'R150'组、I60'R240'组和I60'R360'组.采用酶比色法检测损伤后血清二胺氧化酶活性,采用HE染色和免疫组织化学法分别检测损伤后十二指肠的病理改变和leptin蛋白表达,并采用逆转录-PCR法观察损伤后十二指肠leptin mRNA达的变化.结果:与损伤后Sham组比较,四个再灌注组血清二胺氧化酶活性无显著差异,但I60'R60'组显著高于I60'R360'组(P=0.0077).病理学观察提示H-I/R早期的十二指肠损伤较重而后期逐步减轻.与损伤后sham组十二指肠leptin蛋白表达相比,I60'R240'、I60'R360'组显著升高(0.126503±0.005873,0.129458±0.003755VS 0.079269±0.001995,均P＜0.01),再灌注组之间按I60'R360'、I60'R240'、I60'R60'、I60'R150'组的顺序依次递减.与损伤后Sham组十二指肠leptin mRNA表达相比,I60'R150'组显著降低(0.944±0.033 VS 1.022±0.011,P=0.049).结论:Leptin在H-I/R后肠道内发生的表达变化与肠道损伤密切相关,提示 leptin可能作为一种保护因子对抗H-I/R介导的肠道损伤.     

Gradual upregulation of OCI-5 expression during occurrence and progression of rat hepatocellular carcinoma

BACKGROUND: OCI-5, the rat homologene of human glypican 3 ( GPC3), is confirmed upregulated in hepatocellular carcinoma (HCC). The present study was undertaken to detect gene expression change of OCI-5 during occurrence and progression of rat HCC. METHODS: Male Sprague-Dawley rats were given diethyl-nitrosamine ( DENA) to induce HCC. Three DENA-induced rats and one control rat were sacrificed every week for 18 weeks during the development of HCC. Tissues specimens were snap-frozen in liquid nitrogen and total RNA was isolated. Sk-Hepl cells were treated with DENA at different concentrations. The gene expression levels of OCI-5 and GPC3 were detected with the RT-PCR method. RESULTS: OCI-5 was not expressed in normal rat liver tissues. When HCC occurred and aggravated, OCI-5 expression was gradually elevated to a very high level. GPC3 was not expressed in the DENA-treated Sk-Hepl cells. CONCLUSIONS: OCI-5 was not expressed in normal rat liver tissues but in rat HCC tissues. High-expression of OCI-5 in DENA-induced rat HCC model was the gene expression change of HCC not the DENA-induced gene expression. The expression level of OCI-5 was not only elevated in rat HCC but also gradually along the occurrence and progression of HCC, indicating that GPC3 might serve as a sensitive marker of early stage HCC.     

不同危险分层的原发性高血压患者球结膜微循环的改变

目的 研究高血压病不同危险分层对原发性高血压患者球结膜微循环形态及功能的影响。方法 根据血压水平（1、2、3级）、其他心血管危险因素（年龄、吸烟、血胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、早发心血管家族史、体质量指数、高敏C反应蛋白等）、靶器官损害及并发症的情况,对118例高血压病患者进行分层,研究不同危险分层的高血压病患者和同期20例健康志愿者球结膜微循环的变化。结果 与健康对照组比较,低危组高血压病患者球结膜微循环改变主要表现为稀疏网格结构、微血管数目减少及细静脉管径变细,两者差异有统计学意义（P＜0.05）。中危以上（含中危）组高血压病患者球结膜微循环出现形态、流态和袢周状态的明显改变。其形态改变主要为视野清晰度下降、微血管数减少、细动脉及细静脉管径变细、微血管粗细不均增多,并出现网格结构、微血管瘤、囊状扩张及缺血区。其流态改变主要为微血管内血流速度减慢、红细胞聚集。其管周渗出增加、含铁血黄素沉着增多。随着高血压危险分层的增加,球结膜微血管密网格结构比例逐渐增多、微血管数逐渐减少、微血管内血流速度逐渐减慢、红细胞聚集程度逐渐加重,差异有统计学意义（P＜0.05）。结论 高血压病患者出现与危险分层相关的球结膜微循环改变。     

阿苯达唑对华支睾吸虫体壁和肠管超微结构的影响

阿苯达唑对实验大鼠体内华支睾吸虫体壁和肠管影响的超微结构观察结果表明,该药对虫体皮层和肠绒毛,在给药1h即出现皮层突起肿胀、粘连和肠绒毛肿胀,其内的点线模糊不清。给药24h损害已相当严重,皮层突起出现坏死、崩溃,部分肠绒毛溶解、坏死。而且皮层和肠管损害的发生发展过程是同步的。可以认为阿苯达唑是通过对皮层和肠管的双重损害,进而影响其生理机能,使虫体死亡的。     

特发性血小板减少性紫癜患者B细胞活化因子的表达及其基因多态性

目的 检测特发性血小板减少性紫癜(ITP)患者血浆B细胞活化因子(BAFF)水平及其基因多态性,并探讨二者在ITP中的作用.方法 采用AS-PCR及琼脂糖凝胶电泳法检测133例ITP患者及117名健康对照者的BAFF启动子-871 C/T基因多态性,采用ELISA法测定其血浆BAFF抗原表达水平(BAFF∶Ag).结果 ITP组BAFF基因启动子C/C、C/T、T/T三种基因型分布分别为33.1%、42.1%和24.8%,对照组分别为55.6%、33.3%及11.1%.ITP组T等位基因频率为45.9%,对照组为27.4%,两组比较差异均有统计学意义(P值均＜0.05).初发ITP组、治疗组和对照组BAFF∶Ag分别为875.86、502.59和736.88 pg/ml,两组比较差异均有统计学意义(P值均＜0.05).ITP组和对照组T/T基因型BAFF∶Ag中较C/C、C/T基因型高,但差异无统计学意义(P＞0.05).结论 BAFF过表达可能是ITP发病的危险因素.BAFF启动子-871 C/T基因多态性在ITP发病中具有一定作用,但与BAFF基因表达无关.