大鼠颌下腺切除对CCl4所致肝损伤修复的影响

实验大鼠分为颌下切除＋ＣＣｌ４组，假手术＋ＣＣｌ４对照组及正常对照组，结果假手术＋ＣＣｌ４第２ｄ时Ⅲ带细胞轻度受损，第４ｄ、８ｄ时受损面积略大，第１２ｄ时大部分细胞恢复，而颌下腺切除＋ＣＣｌ４组则损伤明显，第８ｄ时胞质极度稀疏，１２ｄ时大部分细胞尚未恢复，与假手术组比较，该组Ｆｅｕｌｇｅｎ反应略弱，ＰＡＳ反应减弱，第４～８ｄ时较明显，Ｇ－６－Ｐ，ＳＤＨ活性均减弱。结果表明颌下腺切除导致内源性表皮生     

上海市外来人员肺结核病分布与临床特征

目的：了解上海市外来人口中肺结核病人的分布和临床特征。方法：对1996年1～12月全市外来人口活动性肺结核病报告登记资料进行分析。结果：外来人员肺结核病人总数达2279人，青壮年占总病例65％以上；男性病例为主；主要来源于江苏、浙江、安徽、四川、江西等省；登记病人来沪暂居地主要集中在市区及城乡地区，外来人口结核病管理重点在市区及城乡地区。病人分型以Ⅲ型为主。查痰率仅60．1％，但排菌率高达40％。外来人。的病例发现工作及治疗管理难度较大，目前登记病例规则化疗仅占10．4％。结论：有必要通过有关部门的共同协作，拟定切实可行的外来人口结核病管理办法。     

酸性染料比色法测定甲氧异腈冻干品含量

本文采用酸性洒料比色法测定甲氧异腈冻干品的含量。结果表明，使用溴甲酚紫１．５ｍｌ，ＰＨ值为６．０的磷酸盐缓冲液５ｍｌ，氯仿５ｍｌ提取，经振摇２ｍｉｎ，静置１５ｍｉｎ为较理想比色条件，显色液稳定，甲氧异腈浓度在４－２０μｇ／ｍｌ范围内与吸收度呈良好线性关系。     

上尿路结石致肾积水患者锂清除率的测定

采用原子吸收光谱法对４０例上尿路结石致肾积水患者进行了锂清除率测定。结果显示：梗阻所致肾积水患者的ＣＬｉ明显低于正常人（Ｐ〈０．００１），ＣＣｒ、ＣＮａ、Ｃｋ与正常对照组相比差异无显著意义（Ｐ〉０．０５）；并发现ＣＬｉ与肾积水程度呈负相关。认为可将ＣＬｉ作为发现梗阻性肾病早期肾功能损害的可靠指标，评价肾功能损害的程度和预后。     

日本血吸虫病患者幽门螺杆菌感染分析

目的：探讨日本血吸虫病患者中Hp的感染状况。方法：利用Hp全菌抗原ELISA定量检测不同类型日本血吸虫病患者血清抗HpIgG。结果：日本血吸虫病患者组血清抗HpIgG检出率（75％）明显高于对照组（46％），平均抗体水平（2.30±0.42）亦高于对照组（2.02±0.38），抗HpIgG的检出率和平均抗体水平随病程的发展而升高，血清抗HpIgG水平与血清抗AWA抗体水平高度相关（r＝0.92）。结论：日本血吸虫病患者的Hp感染率明显高于其他人，早期诊断并及时治疗Hp感染，对于控制晚期血吸虫病病变的发展和改善其预后具有重要意义。     

准分子激光心肌血管重建的实验研究

为研究心肌血管重建的机理,在15只鼠心、12只免心,用308nm的XeCl准分子激光在活体上照射左心室壁,形成边缘清楚而光滑的圆筒状心肌管道。在活体心室壁的激光管道周围,心肌细胞的损伤很轻微,无炭化焦痂层,未见碎片和凝固坏死层,只有薄层嗜伊红性变和肌浆凝聚两个断续的条形变化带。当心室壁由激光穿透时,血液从心腔进入激光管道,并与周围扩张的血管相通。实验结果提示,由于准分子激光不造成明显的热损伤,因而可能适合于心肌血管的重建。     

Interaction of 2-halogenated dATP analogs (F, Cl, and Br) with human DNA polymerases, DNA primase, and ribonucleotide reductase

Recently, 2-halogenated deoxyadenosine analogs (F, Cl, and Br) have been shown to have antitumor activity. These analogs are phosphorylated by cells and are believed to exert their cytotoxic action at the nucleoside triphosphate level. In this work the interaction of these nucleoside triphosphate analogs with potential targets, such as DNA polymerase alpha, beta, and gamma, DNA primase, and ribonucleotide reductase was examined in detail. All of these compounds competitively inhibited the incorporation of dAMP into DNA by DNA polymerase alpha, beta, or gamma. F-dATP was able to completely substitute for dATP using DNA polymerase alpha and gamma, but not with DNA polymerase beta. Cl-dATP and Br-dATP substituted poorly for dATP using DNA polymerase alpha and beta. Extension of a 32P-labeled primer by DNA polymerase alpha, beta, or gamma on a single-stranded M13 template showed that these compounds were incorporated into the 3' end of the growing DNA chain and that elongation beyond the incorporated analogs was significantly retarded for Cl-dATP and Br-dATP using either DNA polymerase alpha or beta. DNA primase using poly(dC) as template was inhibited by these compounds at a concentration 4 to 5 times greater than that required for 2-F-araATP. The 2-halogenated dATP analogs were potent inhibitors of ADP reduction by ribonucleotide reductase. In conclusion, the cytotoxic action of 2-Cl-deoxyadenosine and 2-Br-deoxyadenosine may partially be mediated through the mechanism of "self-potentiation," by depression of the deoxynucleoside triphosphate pools due to inhibition of ribonucleotide reductase, which would facilitate their incorporation into DNA and result in the inhibition of DNA synthesis.     

Activation of the cardiac ATP-sensitive K+ channel by ER-001533, a newly synthesized vasorelaxant.

Effects of ER-001533 (ER), a newly synthesized vasorelaxant, on the membrane currents were examined in single ventricular cells of guinea pigs. The patch-clamp technique was used in the "whole-cell" and "inside-out" patch configurations. In the whole-cell clamp condition, ER induced a time-independent K(+)-dominant current, which was inhibited by glibenclamide (1-3 microM), suggesting that ER activated the cardiac ATP-sensitive K+ channel (KATP). To elucidate the mechanism of ER-mediated KATP channel activation, the drug was applied to the inside-out patches before and after channel "run-down." Since nucleotide diphosphates could induce the channel openings after complete run-down, effects of the drug on the nucleotide diphosphate-induced channel openings were also examined. Before run-down, ER activated the KATP channel only in the presence of ATP. ER shifted the relation between [ATP]i and the channel activity to the right in a concentration-dependent fashion without a significant alteration of the slope. After channel run-down, ER did not affect the channel openings either in the absence or in the presence of UDP. However, ER could relieve the ATP-gamma-S inhibition of the UDP-induced channel openings. Thus, we conclude that ER antagonizes the inhibitory effect of ATP on the KATP channel in a competitive manner, thereby enhancing the channel openings.     

GALC transduction leads to morphological improvement of the twitcher oligodendrocytes in vivo

Globoid cell leukodystrophy (GLD, Krabbe disease) is a severe demyelinating disease caused by a genetic defect of beta-galactocerebrosidase (GALC). To date treatment to GLD is limited to hematopoietic stem cell transplantation. Experimental approaches by means of gene therapy in twitcher mouse, an authentic murine model of human GLD, showed significant but only marginal improvements of the disease. To clarify whether the introduction of GALC could provide beneficial effects on the oligodendrocytes in GLD, we transduced twitcher oligodendrocytes by stereotactically injecting recombinant retrovirus encoding GALC-myc-tag fusion gene into the forebrain subventricular zone of neonatal twitcher mouse. In vivo effects of exogenous GALC on twitcher oligodendrocytes were studied histologically by combined immunostaining for the myc-epitope and the oligodendroglial specific marker, pi form of glutathione-S-transferase, at around 40 days of age. We show here that GALC transduction led to dramatic morphological improvement of the twitcher oligodendrocytes comparing with those in untreated twitcher controls. This study provided direct in vivo evidence that GALC transduction could prevent or correct aberrant morphology of oligodendrocytes in GLD which may be closely related to the dysfunction and/or degeneration of oligodendrocytes and the demyelination in this disease.