Proteasome Inhibitors Sensitize Hepatocellular Carcinoma Cells to TRAIL

A poptosis, an evolutionarily conserved form of cell suicide, oc- curs in two physiological stages: commitment and execution.[1] It has been found that several Bcl-2 family proteins are located in the outer mitochondrial membrane, where they control relea…     

基底动脉缝隙连接蛋白的分布

目的：探讨正常脑血管缝隙连接蛋白的分布。方法：采用RT—PCR、免疫组化方法测定多种缝隙连接蛋白在大白兔基底动脉的表达。结果：(1)RT—PCR发现大白兔基底动脉血管组织中至少存在Xx45、Cx43、Cx40和Cx37四种缝隙连接蛋白mRNA表达；(2)免疫组化证实Cx45和Cx43主要分布于血管内皮，平滑肌细胞间末见Cx45和Cx43的染色。结论：大白兔基底动脉血管组织存在丰富的缝隙连接蛋白的表达，与体内其它弹力血管相比，缝隙连接蛋白的分布模式有其特殊性。     

The role of endotoxin in the pathogenesis of experimental multiple system organ failure: a preliminary report.

In this study, an animal model of multiple system organ failure (MSOF) in rabbits, engendered by feeding E. coli prior to severe hemorrhagic shock, was used for the purpose of investigating 1) the relationship between lipopolysaccharide (LPS) and MSOF, and 2) the effectiveness of Re-LPS antiserum in preventing MSOF. The results showed that endotoxemia occurred very early, and its degree correlated well with that of organ dysfunction. Re-LPS antiserum administration abated the toxic effects and lowered the incidence of MSOF. These results suggest that sequential analysis of circulating LPS levels may be useful for the early diagnosis of MSOF, and that gut-derived endotoxin might play an important role in the pathogenesis of experimental MSOF.     

Role of intestinal bifidobacteria in the pathogenesis of gut-derived bacteria/endotoxin translocation and the effect of bifidobacterial supplement on gut barrier function following burns

Early multiple organ dysfunction syndrome appears to be facilitated with bacterial translocation in severely burn injury, yet the mechanisms of bacterial translocation remains in dispute. The aim of this study was to investigate the potential role of intestinal bifidobacteria in the pathogenesis of gut-derived bacteria/endotoxin translocation following burns and the effects of bifidobacterial supplement on gut barrier. Methods: Wistar rats were randomly divided into burn group (Burn, n=60),sham burn group (SB, n=10) in experiment Ⅰ , and burn + saline group (BS, n=30), burn + bifidobacteria group (BB, n=30), and sham-burn + saline group (SS, n= 10) in experiment Ⅱ. Animals in BB group were fed bifidobacterial preparation (5 × 109 CFU/ml) after burns, 1.5ml,twice daily. Animals in BS and SS were fed saline. Samples were taken on days 1, 3, and 5 in burn groups, and on day 3 in sham-burn groups. The incidence of bacteria/endotoxin translocation and counts of Bifidobacterium, Fungi and Escherichia coli in gut mucosa were determined with standard methods. The levels of sIgA in mucus of small intestine were measured by RIA. The positive sIgA expression in lamina propria and ileum mucosal injury was evaluated light microscopically by blinded examiners. Results: Our results showed that the incidence of bacterial translocation was increased after burns, which was accompanied by significant decrease in number of bifidobacteria but significant increase in E. coli and fungi in gut mucosa, and elevation of levels of plasma endotoxin and IL-6 (P<0. 001).The incidence of bacterial translocation was markedly reduced after 3- and 5-day supplementation of bifidobacteria compared with control group (P<0.05). The counts of mucosal bifidobacteria were increased by 4- to 40-fold,while E. coli and fungi were decreased by 2- to 30-fold and 10- to 150-fold, respectively, after bifidobacterial supplementation in contrast to control group. The damage of mucosa tended to be less pronounced after 3-day bifidobacteria-supplemented formula compared with control group [grade 2(0-6) vs. grade 4(3-6), P<0.05]. Moreover, the expression and release of sIgA was markedly augmented after 3-day bifidobacteria-supplementation formula and it returned to normal range on day 5. Conclusion: The decrease in counts and proportion of bifidobacteria in mucous membrane flora may play an important role in the development of bacteria/endotoxin translocation following thermal injury. The supplement of exogenous bifidobacteria could per se improve gut barriers, and attenuate bacteria/endotoxin translocation secondary to major burns.     

腕关节融合钢板内固定术的临床疗效

目的评价腕关节融合钢板内固定术的临床疗效。方法2000年7月-2004年12月，采用腕关节融合钢板内固定术治疗创伤性腕关节炎21例。随访内容包括腕关节疼痛程度、手指关节活动度、握力和x线片。根据Buck—Gramcko／Lohrnanrm评分表评价腕关节总体功能，DASH调查表评价腕关节融合术对患者日常活动及生活质量的影响。结果术后21例获得随访，平均随访时间为20个月。术后患侧腕部疼痛值平均为1．5（术前4．5），12例掌指关节和lO例拇指指间关节出现轻微背伸功能障碍，腕部握力为30kg（健侧为38kg）。x线片示腕关节全部骨性融合。Buck—Gramcko／Lohmanrm评分值为8．7，其中优5例、良10例，中6例。DASH值为32，DASH调查表结果表明腕关节融合术后部分日常活动受限。结论腕关节融合钢板内固定成功率高，腕关节疼痛明显减轻，但术后腕关节部分功能丧失。     

FK506和RS-61443对大鼠异体肢体移植的联合免疫抑制作用

目的　通过大鼠异体肢体移植模型 ,旨在分析 FK5 0 6和 RS- 6 14 4 3对大鼠异体肢体移植中急性排斥反应的免疫抑制作用。　方法　选择雄性 Wistar和 SD大鼠为供、受体 ,以 FK5 0 6和 RS- 6 14 4 3为免疫抑制剂 ,对照组为术后不用药组 ,实验组根据用药剂量和药物不同分为 6组 ,各组用药时间均为 5周 (每日 1次共 2周 ,然后每周 2次共 3周 ) ,进行了 10 1例异体肢体移植动物实验。观察大鼠一般情况、移植肢体排斥反应及存活时间。　结果　对照组肢体平均存活时间为 (7.0 0± 0 .78)天 ;实验组 1～ 6组移植肢体平均存活时间分别为 (17.0 8± 4 .5 0、2 3.2 0± 5 .0 5、11.19±2 .2 8、16 .33± 1.83、13.33± 3.2 2和 5 8.76± 6 .81)天。　结论　 FK5 0 6和 RS- 6 14 4 3能抑制大鼠同种异体肢体移植术后急性移植排斥反应的发生 ,并能延长移植肢体的存活时间。     

经皮椎板关节突螺钉固定的应用解剖及影像学研究

[目的]为经皮椎板关节突螺钉的器械设计及临床应用提供解剖学依据。[方法]利用30例干燥腰椎标本，用游标卡尺及量角器测量腰椎椎板上缘及下缘的厚度，椎板关节突螺钉的长度。通过影像学测量椎板的内倾角和下倾角。[结果]椎板的上缘薄而下缘厚。从L1～5椎板的厚度、螺钉的长度及从内倾角逐渐增加，而下倾角逐渐减小。[结论]上缘的厚度太薄不适合螺钉的放置。从L1～5使用4．5mm的皮质骨螺钉固定是安全的，但应该在椎板的下缘置人。注意下倾角和内倾角的变化。设计的瞄准器应该具有调节角度的装置。     

腰椎间盘突出症治疗方法与肌电图变化的相关性研究

腰椎间盘突出症(lumbar disc herniation，LDH)是导致腰腿痛的主要病因，本研究对具有典型临床症状、相应体征及MR或CT等影像学资料确诊的LDH，采用规范化非手术治疗，经规范化保守治疗无效者选用手术治疗，治疗前后均行肌电图(elec-tromyograptly，EMG)检查，旨在探讨肌电图变化与治     

颅内出血性椎动脉夹层的治疗

目的探讨颅内出血性椎动脉夹层的治疗方法。方法回顾分析了2000-2005年40例出血性颅内段椎动脉夹层的治疗。其中支架辅助的弹簧圈栓塞33例,夹层段动脉闭塞6例,夹层近端主干动脉闭塞1例。结果手术无死亡病例。术后随访1-46个月,平均16.3个月。发现夹层动脉通畅,无夹层再出血,无新发后循环梗死。1例支架辅助弹簧圈栓塞患者夹层复发,行补充填塞弹簧圈。结论血管内夹层近端闭塞以及夹层段动脉闭塞是治疗颅内出血性椎动脉夹层的经典术式。支架辅助的弹簧圈栓塞治疗保留了载瘤动脉,避免了术后对侧椎动脉血流负荷量的增加;减少了后循环缺血的危险,扩大了血管内治疗出血性椎动脉夹层的手术适应证。本组结果显示支架辅助弹簧圈栓塞术并未增加夹层再通以及穿支动脉闭塞。本组经验初步表明支架辅助的弹簧圈栓塞是治疗出血性颅内椎动脉夹层的合理选择之一。     

人钠/二羧酸协同转运蛋白3基因调控肾小管上皮细胞线粒体膜电位的研究

目的 观察人钠／二羧酸协同转运蛋白3(hNaDC3，)对人肾脏近曲小管上皮细胞(HKC)线粒体膜电位的变化及其对细胞能量代谢的影响。方法 应用亚克隆技术构建正义pcDNA3-hNaDC3和反义pcDNA3-AhNaDC3两个真核表达载体，通过脂质体LipofectAMINE将pcDNA3-hNaDC3及pcDNA3-AhNaDC3转染至HKC细胞。克隆筛选后，用RT—PCR、Northern印迹及Western印迹鉴定外源基因的整合和表达。荧光探针JC-1观察各细胞系线粒体膜电位的变化。结果 外源hNaDC3基因稳定整合到HKC细胞基因组中，并获得高、低表达。转染正义hNaDC3cDNA的HKC细胞线粒体膜电位降低，JC-1在线粒体内形成单体，发出绿色荧光；而转染反义hNaDC3cDNA的HKC细胞线粒体膜电位略微升高，JC-1形成聚合体，发出红色荧光。结论 hNaDC3过表达引起线粒体膜电位降低，反义hNaDC3则使线粒体膜电位略微升高。提示NaDC3可能通过使线粒体膜电位下降，参与了细胞能量代谢。