原发性十二指肠梭形细胞鳞癌的组织形态学及蛋白表达的研究

目的：探讨十二指肠梭形细胞鳞癌的组织形态学及蛋白表达的特点,明确其组织学来源,以提高对该疾病的认识和诊断水平。方法运用HE染色法了解十二指肠梭形细胞鳞癌的组织形态学特点;通过免疫组织化学染色法进一步了解其蛋白表达特点。结果 HE染色显示黏膜层、黏膜下层及肌层见大小不等异型性明显的梭形肿瘤细胞,并见部分不典型细胞间桥和角化珠形成。免疫组织化学染色结果显示梭形肿瘤细胞区域：⑴胞浆着色：CK5/6（＋＋＋）、CEA（＋＋＋）、CK8/18（＋＋）、Syn（＋）、NSE（＋）、CgA（＋）及S-100蛋白（＋）;⑵胞核着色：Ki-67（＋＋＋）;⑶CD34和CD117显示阴性。结论十二指肠鳞状细胞癌起源于十二指肠黏膜基底层多潜能干细胞。     

Cyclops and cyclopoid formation after anterior cruciate ligament reconstruction: clinical and histomorphological differences

Prospectively, 119 patients were pursued clinically and by follow-up-arthroscopy for the occurrence of a “cyclops syndrome” after ACL reconstruction with a patellar tendon autograft, augmented by LAD. Twenty-one patients showed nodular formations. Ten of these (group 1) developed early clinical evidence of a “cyclops syndrome” with a mean extension deficit of 19° before follow-up-arthroscopy, on average 5.9 months after the index operation. The nodular formations found and excised during débridement had a hard consistency. Histomorphological undecalcified microtome section evaluation of six specimens revealed fibrocartilagineous tissue with active bone formation in the center. The other 11 patients showed no clinical symptoms (group 2). A similar but soft nodulous scar formation was detected at follow-up-arthroscopy, on average 9.5 months after the index operation. Histomorphologically these so-called “cyclopoid” formations were only built-up fibrocartilagineous islands surrounded by granulation tissue. Neither remnants of tendon graft fibers nor old bone particles were found in specimens of either group. It can be concluded that both the hard cyclops and the soft “cyclopoid” are de novo scar formations. Received: 4 November 1998 Accepted: 5 May 1999     

动静力失衡性大鼠颈椎间盘组织形态学及超微结构

[目的]动态观察大鼠颈部动、静力失去平衡后颈椎间盘组织形态学及超微结构的改变。[方法]SD大鼠60只，随机分为3、5、7个月模型组和对照假手术组，每组10只，通过破坏大鼠颈部肌肉、韧带诱导颈椎间盘退变，按月取材。各组椎间盘HE、Toluidine blue染色，在光镜下观察用体视学分析软件、Dissector自动计数法分析软骨终板内血管芽的数量、面积和软骨终板的厚度，Miyamoto分级法综合评判颈椎间盘退变的程度；透射电镜观察椎间盘细胞凋亡的超微结构。[结果]与对照假手术组比较，3个月造模组动物颈椎间盘已开始退行性变化，纤维环板层结构紊乱，关节软骨钙化层增厚，软骨下血管明显减少；5个月模型组髓核完全纤维化，纤维环板层状结构消失，血管芽稀少，血管壁充血曲张；7个月模型组椎间盘内部结构与5个月模型组相似，部分椎体边缘骨赘形成。在电镜下，3个月造模组椎间盘细胞，细胞表面突起减少，细胞器稀少，胞质内有脂滴，可见到凋亡细胞形成的凋亡小体。5个月和7个月模型组椎间盘组织中细胞较少，基质中胶原纤维断裂，可见到许多坏死空化的细胞。[结论]模型组大鼠颈椎间盘都出现典型的退变形态学变化，随着造模月份的延长退变程度越严重；早期和中期退变椎间盘中可观察到凋亡细胞，在退变的晚期可观察到坏死细胞。     

人类外周神经在化学萃取前后的组织形态变化研究

目的研究人类外周神经在化学萃取前后的组织形态变化，探讨化学萃取法制备人类长段粗大去细胞神经的可行性。方法用TritonX-100和脱氧胆酸钠对人体长段胫神经作不同次数的萃取处理，经常规HE染色、砂罗铬花青、网状纤维组织化学染色和S-100免疫组织化学染色后，在光镜下观察神经萃取前后的组织形态变化，并比较不同萃取次数对神经结构的影响。结果人体长段胫神经经2次萃取后，其轴突、髓鞘、许旺细胞及其他结缔组织中的细胞均已消失，仅见网格纤维，而神经基底膜管、神经柬膜等纤维性支架保存完整，与未经萃取的神经相仿。萃取1次者仍残留少量细胞碎屑，而萃取3次者，细胞清除更彻底，但纤维性支架结构明显破坏。结论人类长段粗大神经干经化学萃取后不含细胞，而保留有完整的纤维性支架结构。化学萃取法制备人类长段粗大去细胞神经可行。     

十八味中药组方对雄性大鼠不育模型生殖系统的影响

目的探讨十八味中药组方缓解不育大鼠模型生殖系统损害状况的作用。方法建立雷公藤多甙生殖系统损害动物大鼠模型,检测用药前后大鼠睾丸、附睾,精囊腺、前列腺质量,计算脏器系数,组织病理切片,观察中药组方对大鼠生殖系统的影响。结果十八味中药组方显著提高大鼠脏器系数及附睾腺管壁厚度,促进组织病理修复,促进腺体分泌。结论十八味中药组方有改善病理生殖系统损害的作用。     

A pilot histomorphology and hemodynamic of vasculogenic mimicry in gallbladder carcinomas in vivo and in vitro

Background

Vasculogenic mimicry (VM), as a new blood supply for tumor growth and hematogenous metastases, has been recently described in highly aggressive human melanoma cells, etc. We previously reported VM in human gallbladder carcinomas and its clinical significance. In this study, we further studied histomorphology and hemodynamic of VM in gallbladder carcinomas in vivo and in vitro.

Methods

The invasive potential of human gallbladder carcinoma cell lines GBC-SD and SGC-996 were identified by Transwell membrane. The vasculogenic-like network structures and the signal intensities i.e. hemodynamic in gallbladder carcinomas stimulated via the three-dimensional matrix of GBC-SD or SGC-996 cells in vitro, the nude mouse xenografts of GBC-SD or SGC-996 cells in vivo were observed by immunohistochemistry (H&E staining and CD₃₁-PAS double staining), electron microscopy and micro-MRA with HAS-Gd-DTPA, respectively.

Results

Highly aggressive GBC-SD or poorly aggressive SGC-996 cells preconditioned by highly aggressive GBC-SD cells could form patterned networks containing hollow matrix channels. 85.7% (6/7) of GBC-SD nude mouse xenografts existed the evidence of VM, 5.7% (17/300) channels contained red blood cells among these tumor cell-lined vasculatures. GBC-SD xenografts showed multiple high-intensity spots similar with the intensity observed at tumor marginal, a result consistent with pathological VM.

Conclusions

VM existed in gallbladder carcinomas by both three-dimensional matrix of highly aggressive GBC-SD or poorly aggressive SGC-996 cells preconditioned by highly aggressive GBC-SD cells in vitro and GBC-SD nude mouse xenografts in vivo.     

摄食因素对SD大鼠肝脏相对重量及组织形态学影响

目的探讨摄食因素对SD大鼠肝脏相对重量及组织形态学影响。方法称量禁食/摄食条件下,不同性别无特定病原体(Specific pathogen Free,SPF)级SD大鼠体重及肝脏重量,计算相对重量。制作肝脏切片,进行HE和过碘酸雪夫染色法(Periodic Acid-Schiffstain,PAS)染色,观察其组织形态学改变。结果摄食使SD大鼠肝脏相对重量显著增大;摄食SD大鼠肝细胞肿胀,胞浆透亮,肝细胞内可见大量糖原;而禁食SD大鼠肝细胞呈多边形,胞浆红染,肝细胞内未见糖原。结论摄食因素对SD大鼠肝脏相对重量及其组织形态具有显著影响,建议在毒性试验中,动物剖检前隔夜禁食。     

胎儿宫内发育迟缓胎盘大体和组织形态学观测

本文对胎儿宫内发育迟缓(IUGR)A、B两组55例胎盘进行了大体及组织形态学观测。结果表明:IUGR—A、B两组胎盘的重量减少、胎盘系数升高、梗死及绒毛周围纤维蛋白沉积比率增加,以IUGR—B组明显,合体结节增多及血管合体膜减少亦以IUGR—B组表现突出,IUGR两组都有细胞滋养细胞增多、基底膜增厚及纤维蛋白坏死绒毛比率增高,绒毛发育迟缓胎盘出现率亦增高。认为IUGR的发病与胎盘缺血缺氧及绒毛发育迟缓有关。     

自体移植脾组织的血流量及形态学的变化

对自体移植脾的组织量和血流量以及形态学进行动态观察，实验用大鼠分别于术后３、５、７、１２月通过生物微球法对和人动物保留１／４原位脾和地脾进行检测。结果得出，自体移植各时相点的单位重量血流量、血容积和吞噬指数与原位保留的相差不显著。原位保留的残脾重量代偿性增加，但移植脾组织量明显减轻，因而移植脾的绝对血流量也相应减少，揭示移植脾组织应尽量增多。镜检移植脾组织随着时间推移显示正常结构。     

Comparison of the course of infection of virulent Yersinia enterocolitica serotype O:8 with an isogenic sodA mutant in the peroral rabbit model

Peroral infections of rabbits with a virulent Yersinia enterocolitica serotype O:8 wild-type strain (WA-314) and its isogenic Mn-cofactored superoxide dismutase (sodA) mutant were analyzed with respect to the following parameters: clinical findings, bacterial ability to colonize and persist in different tissues, bacterial resistance to the killing effect of leukocytes and blood sera, IgG antibody response, pathomorphological and immunomorphological changes. In comparison to WA-314, the sodA mutant was markedly impaired in its ability to disseminate into the brain and viscera, and to cause hyperthermia, leukocytosis with monocytosis, granulocytosis and initial lymphopenia. The sodA mutant strain was more susceptible to bactericidal activity of leukocytes and blood sera than the parent strain WA-314. Moreover, in comparison to WA-314, the sodA mutant was attenuated for mice after oral, intravenous, and intraperitoneal inoculation and totally avirulent for rats. Strikingly, the sodA mutation led not only to attenuation of virulence but also enhanced immunogenicity (as reflected by the specific antibody response). These features are consistent with the mild immunomorphological changes observed after infection with the sodA mutant as compared to the severe tissue lesions caused by the virulent strain WA-314. In conclusion, this study demonstrates that the sodA mutation in Y. enterocolitica leads to loss of virulence and gain of immunogenicity in rabbits. These are promising features for a live oral vaccine carrier strain.