小肠浆肌膜腔内自体脾组织移植动物模型的建立与意义

目的探讨增加自体脾组织移植量的方法,提高自体移植脾组织的功能。方法贵州小型香猪3头,经肌注麻醉后剖腹切除脾脏,取脾脏的1/2约150g,切成1mm×1mm×1mm小块备用。在距Treitz韧带50cm处,切取保留肠系膜血管的空肠30cm旷置,再吻合肠管恢复肠腔通道,缝闭肠系膜裂口。旷置空肠等分2段,去除肠粘膜,缝闭一端,将约50g脾组织块分别植于2段肠浆肌膜腔内,缝闭另一端口,妥善固定于肠系膜上。大网膜内移植30g脾组织作为对照观察。结果4个月饲养期间内无肠梗阻发。3段肠浆肌膜腔内脾组织再生良好,组织结构与大网膜内移植脾组织无明显差别,2段再生较差,1段形成脓肿。结论肠浆肌膜腔内移植脾组织的量较大,可作为自体脾组织的移植术式。     

膀胱小细胞癌诊治体会(附六例报告)

目的　提高对膀胱小细胞癌的认识。　方法　回顾性分析 6例膀胱小细胞癌患者的病理及临床资料。男 4例 ,女 2例 ,平均年龄 5 1岁。其中 2例膀胱小细胞癌含有移行细胞癌和 (或 )腺癌成分。行膀胱部分切除术 2例 ,行膀胱全切术 4例。 5例患者接受 2～ 6疗程化疗。　结果　 6例患者随访 12～ 6 0个月 ,均因肿瘤复发死亡。平均生存时间 2 8个月。　结论　膀胱小细胞癌占原发膀胱恶性肿瘤的 0 .4 4 % ,恶性程度高 ,易发生淋巴结、肝、骨等转移 ,预后差 ,根治性膀胱全切加联合化疗可获得较好疗效。     

survivin、P53蛋白在非小细胞肺癌的表达及其相关性研究

目的 :研究survivin、P5 3蛋白在非小细胞肺癌 (NSCLC)组织的表达及其生物学意义 ,并探讨其相关性。　方法 :用免疫组化 (S P法 )染色技术对 95例NSCLC组织石蜡标本进行survivin、P5 3蛋白表达的检测和分析。　结果 :survivin、P5 3在肺癌细胞中阳性表达率 (6 2 .1 %、5 5 .8% )明显高于癌旁的正常肺组织 (1 4 %、7% ) (P <0 .0 1 )。survivin的表达与肿瘤病理分级、组织学分型、淋巴结转移、TNM分期无明显相关 (P >0 .0 5 ) ;P5 3表达与淋巴结转移相关 (P <0 .0 5 ) ,而与肿瘤病理分级、组织学分型、TNM分期无明显相关 (P >0 .0 5 ) ;此外 ,survivin与P5 3蛋白的表达呈显著正相关 (r =0 .5 72 ,P <0 .0 1 )。　结论 :凋亡抑制蛋白survivin与突变型P5 3蛋白在NSCLC的发生发展中可能起协同作用 ,也提示抑癌基因p5 3(野生型 )可能对survivin的表达起负反馈调节作用。survivin和P5 3蛋白可作为靶点用于NSCLC靶向治疗的研究     

宜昌市20年结肠镜检查大肠癌患病率回顾性分析

目的探讨该市大肠癌流行病学和临床特点。方法以所有结肠镜受检对象为研究群体,对大肠癌患病率、大肠癌患者性别、年龄、肿瘤部位进行统计分析;比较大肠癌临床症状与大肠癌患者年龄、肿瘤发生部位的关系。结果自1980年以来,大肠癌年度患病率呈非线性缓慢上升,男性大肠癌患病率7.1%;女性大肠癌患病率5.5%;在3个年限段(80年代、90年代和21世纪5年)大肠癌中位患病年龄分别为男53.5、56.7和59.0岁;女51.9、53.7和55.2岁。986例大肠癌中直肠癌691例,乙状结肠癌82例,降结肠癌18例,脾曲癌4例,横结肠癌37例,肝曲癌30例,升结肠、回盲部癌79例,大肠多发性癌45例。临床症状以便血为主,其次为腹痛、腹部包块和肠梗阻发生率较低,半数以上患者有不同程度贫血。结论该市大肠癌患病率和中位发病年龄呈缓慢上升,低于国内大肠癌高发区。大肠癌肿瘤发生部位有近移和多发趋势。便血是直肠癌主要症状,中老年患者便血发生率高于青年患者,但腹痛发生率低于青年患者。     

4例活体部分小肠移植术后早期并发症的防治经验

目的总结4例活体部分小肠移植术后早期并发症（1月内）的防治办法，为进一步开展活体小肠移植提供经验。方法4例活体部分小肠移植术后1月内，早期并发症重点在于防治吻合血管血栓、出血、感染、排斥反应、移植肠功能障碍等。结果3例移植受体术后1月内分别发生出血倾向、急性排斥反应、感染、移植肠功能障碍等并发症，但经及时准确的诊断与治疗得以好转，移植肠存活及功能均良好。结论注重活体部分小肠移植术后对于早期并发症的预防及治疗，对于患者预后有重要意义。     

The interactive role of mucosal T lymphocytes in intestinal growth, development and enteropathy

Abstract Over the past 15–20 years, research has progressively focused on the mucosal T cell as the central factor in the initiation of physiological or pathological changes, first in the growth and maturation of the early (postnatal) intestine, and second in adult-type enteropathies resulting from sensitivity to either food or pathogen-derived antigens. T cell-mediated events may be measured, for example, in terms of specific immunopathologic patterns of change and injury, such as type 1 (lymphocyte infiltration), type 2 (crypt hyperplasia) and type 3 (flat-destructive), which can be recognized and quantitated microscopically; by determination of lymphocyte reactivity through secretion of interleukin-2 receptors (IL-2R) into plasma or expression by mucosal lymphocytes; by quantitation of lymphocyte subsets emigrating into inflamed tissues by immunoperoxidase-labelled monoclonal antibodies; or by the determination of T cell receptor polymorphisms. Alterations in intestinal growth, structure and function at weaning are likely to be T cell-mediated as they are analogous to the same type 1/2 lesions that reflect modulation of adult mucosal architecture in food and parasite-induced hypersensitivity reactions. Enteropathies associated with HIV infection and T cell deficiency display a milder degree of villous flattening and impaired crypt hyperplasia than that typical of gluten-sensitivity, suggesting a reversion to lesser degrees of mucosal pathology (type 1/2). Clearly more information will accrue; meanwhile the remarks in this brief survey should provide a firm basis whereby clinician and scientist can meet, and together recognize and further dissect the modulatory effect of T lymphocytes on mucosal structure and function.     

小横切口手术治疗小儿腹股斜疝

目的：探讨小儿腹股沟斜疝手术方法。方法：经外环小横切口行疝囊高位结扎加修补术。结果：全组126例，平均手术时间12min，无一例出现并发症。结论：此方法有切口小、时间短、创伤轻、恢复快、费用低、疤痕不明显等优点，值得推广。     

Ultrastructural and immunohistochemical study of Ewing's sarcoma and related tumors: Morphological neural markers suggesting neural histogenesis in 32 small round-cell sarcomas

The purpose of this study was to validate the hypothesis of neural histogenesis of Ewing's sarcoma of bone and related tumors by light microscopic, electron microscopic, and immunohistochemical analysis. We studied 32 round-cell sarcomas (19 cases of Ewing's sarcoma of bone, 3 extraskeletal Ewing's sarcomas, 5 peripheral primitive neuroectodermal tumors (PNET) and 5 cases of unclassified small round-cell type of neurogenic sarcoma (NS). Immunoreactivity for MIC2 was observed in all cases of Ewing's sarcoma and PNET, and in 1 cases of NS. Positive immunoreactivity for neural markers (NSE, synaptophysin, S-100) was found frequently in some tumors. Ultrastructurally, some specific features of neural differentiation, such as a fragmented basal lamina and neurosecretory granule-like particles, were found even in typical cases of Ewing's sarcoma of bone, which presented without a rosette arrangement and were almost negative for neural immuno-markers, but positive for MIC2. These ultrastructural neural features were observed less frequently in Ewing's sarcoma of bone than in PNET and NS. However, no significant correlation was demonstrated between the immunoreactivity for neural markers and the ultrastructural and histological neural features. These results support the hypothesis of a neural origin of Ewing's sarcoma and related neoplasms, and suggest that some overlapping entity could persist in PNET and Ewing's sarcoma and that this entity could be seen in histological and immunohistochemical studies of both tumors.     

Ascorbic acid prevents ischemia-reperfusion injury in the rat small intestine

Ischemia-reperfusion injury by free radicals and lipid peroxides is observed in various organs. Ascorbic acid (AsA) or glutathione (GSH) in various doses (AsA:2, 0.5, 0.1 mmol/kg, GSH:2 mmol/kg) was intraperitoneally administered to male Wistar rats. The entire small intestines were resected just before ischemia, after ischemia, and after 20 min of reperfusion (n = 7–10 at each time point). At each time point, the specimens were subjected to assays of lipid peroxides, GSH, and glutaminase activity of the tissues; they were also examined histologically. In the AsA group, the production of lipid peroxides after reperfusion was significantly suppressed in a dose-dependent manner, and the ratio of oxidized GSH to total GSH was also significantly low. Tissue glutaminase activity decreased to a lesser extent, and the degree of injury was apparently less marked in the AsA group. This study indicates that AsA acts as an antioxidant against peroxidative tissue injury, possibly by scavenging radicals, preserving reduced GSH, and reducing the peroxidative reaction. Received: 21 June 1996 Received after revision: 8 October 1996 Accepted: 12 November 1996     

Characterization of apoptosis in intestinal ischaemia-reperfusion injury — a light and electron microscopic study.

Intestinal ischaemia-reperfusion (IR) injury has largely been attributed to cellular necrosis. Apoptosis, a distinct form of cell death has been observed following IR to the brain, heart, adrenals and the kidneys. In order to characterize the role of apoptosis in intestinal IR, small bowel grafts were stored in saline ( n  = 6) or modified University of Wisconsin solution ( n  = 6) at 4 °C for 12 h and reperfused for 6 h in syngeneic rats. Samples of normal, stored and reperfused intestines at 1, 3 and 6 h were analysed by light and electron microscopy. Following reperfusion, there was crypt and villous epithelial apoptosis, loss of crypt and villous structures, and an increase in mucosal inflammatory cell infiltration. Ongoing apoptosis was maximum at 1 h, its degree decreasing with increasing reperfusion intervals. Large numbers of apoptotic bodies dominated the picture from 3 h of reperfusion. This study has demonstrated the induction of apoptosis by intestinal IR injury, which begins within an hour of reperfusion and is probably responsible for the observed crypt and villous loss. This has potential therapeutic implications as, opposed to necrosis, apoptosis is an active process with genetic regulators and biochemical effectors, which can be specifically targeted to prevent or alleviate IR injury.