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.     

Dipeptidyl peptidase IV is down-regulated in rat hepatoma cells at the mRNA level

Dipeptidyl peptidase IV (DPP-IV) is a cell surface ectopeptidase that has been implicated in cell-extracellular matrix interactions, lymphocyte growth and the regulation of biological peptides. Previous studies have shown that immunostaining for DPP-IV and DPP-IV enzyme levels is decreased in hepatoma cells and levels have been correlated with the ability of such cells to adhere in vitro. The aim of this paper was to measure DPP-IV enzyme levels in rat hepatoma cells and to examine whether changes were associated with alterations at the mRNA level. The results indicate a greater than 90% reduction in DPP-IV enzyme levels in two rat hepatoma cell lines, HTC and H35, compared with rat hepatocytes. Enzyme levels of the control enzyme leucine aminopeptidase (LAP) were not decreased. mRNA studies indicated that these changes were associated with similar reductions in rat DPP-IV mRNA. It is concluded that DPP-IV is markedly reduced at the protein, enzyme and mRNA levels in rat hepatoma cells. The significance of these changes is unclear but may lead to decreased extracellular matrix interactions by such cells.     

大鼠肝细胞Ⅰ，Ⅲ型前胶原基因表达及PDGF的影响

目的观察大鼠肝细胞Ⅰ，Ⅲ型前胶原基因的表达及ＰＤＧＦ对其表达的影响．方法应用原位杂交技术检测分离培养的ＳＤ大鼠肝细胞（ｎ＝３０）内Ⅰ，Ⅲ型前胶原基因的表达．同时观察１０μｇ／Ｌ（ｎ＝３０）和３０μｇ／Ｌ（ｎ＝３０）ＰＤＧＦ促进前胶原基因表达的作用．测定基因表达颗粒总面积占细胞总面积的百分比，并作比较分析．结果无论正常肝细胞或是在两种浓度的ＰＤＧＦ存在时，肝细胞内均可见到Ⅰ，Ⅲ型前胶原基因的表达．正常肝细胞Ⅰ，Ⅲ型前胶原基因表达面积的百分比（％）为７７±１９和７５±２１；加１０μｇ／ＬＰＤＧＦ后为１１５±１９和１１２±１０，而加３０μｇ／Ｌ后为１５２±３４及１８１±２８，且在后者中表达明显增强（Ｐ＜００５及Ｐ＜００１）．结论ＰＤＧＦ在转录水平上促进肝细胞胶原的合成．     

原发性小肠肿瘤41例分析

本文报道我院1981年8月～1986年10月间收治的41例原发性小肠肿瘤,所有病例均经手术切除并经病理检查证实。本组男性24例,女性17例;年龄最小9个月,最大68岁。其中良性肿瘤5例,恶性肿瘤36例。肿瘤位于十二指肠者7例,空肠10例,回肠24例。 原发性小肠肿瘤的临床表现无一定规律,早期多无明显症状,且目前尚缺乏简便可靠的诊断措施,往往导致诊断延误。本文就本病的发生率,临床表现与诊断,误诊原因及辅助诊断等进行了讨论。     

地高辛标记核酸探针技术在家兔视网膜C－sis原癌基因检测中的应用

用ＡＧＰＣ法抽提幼年家兔视网膜总ＲＮＡ，并应用了地高辛标记核酸探针的方法。经斑点杂交显示幼年家兔视网膜出现Ｃ—ｓｉｓ原癌基因表达。对实验方法以及Ｃ－ｓｉｓ原癌基因表达的意义进行了探讨。认为此方法快速、灵敏，检测Ｃ－ｓｉｓ原癌基因表达对深入研究视网膜生长发育及肿瘤等病变有一定意义。     

二甲亚砜对人表皮的核酸和蛋白质合成的影响

用体外培养的人的伪表皮作为模型，进行药物毒理学作用的研究，观察了二甲亚砜（ＤＭＳＯ）在不同浓度和不同接触时间条件下，对人的伪表皮细胞脱氧核糖核酸（ＤＮＡ）、核糖核酸（ＲＮＡ）和蛋白质合成的影响：随着接触时间的延长，ＤＮＡ、ＲＮＡ和蛋白质合成均受抑制。低浓度条件下（１％），ＤＮＡ、ＲＮＡ和蛋白质合成增加；在１５～５０％浓度下，ＤＮＡ和蛋白质合成抑制，而ＲＮＡ合成仍增加；在高浓度条件下（７０％～１００％），ＤＮＡ、ＲＮＡ和蛋白质合成均明显抑制。     

参附注射液对大鼠缺血再灌注小肠细胞Bax、Bcl-2及c-myc蛋白表达的影响

目的　探讨参附注射液对大鼠缺血再灌注小肠细胞Bax、Bcl 2及c myc蛋白表达的影响及它们与肠细胞凋亡的内在联系。方法　健康SD大鼠 36只随机分为 3组 ,空白对照组 (S组 )、缺血再灌注 +生理盐水组 (IR +NS组 )、缺血再灌注 +参附注射液组 (IR +SF组 ) ,每组 12只。采用钳闭肠系膜前动脉制备小肠缺血再灌注模型。免疫组化检测Bax、Bcl 2及c myc蛋白的表达 ,每组选 2 4个视野分别测量光密度值 (OD值 )。TUNEL法检测凋亡的小肠细胞并计算凋亡指数。结果　IR +NS组BaxOD值明显高于S组 (P <0 .0 1) ,IR +SF组BaxOD值明显低于IR +NS组 (P <0 .0 1) ,且低于S组 (P <0 .0 5 )。IR +NS组Bcl 2OD值高于S组 (P <0 .0 5 ) ,且IR +SF组Bcl 2OD值高于S组 (P <0 .0 1) ,但IR +NS组与IR +SF组比较无显著差异。IR +NS组c mycOD值明显高于S组 (P<0 .0 1) ,且明显高于IR +SF组 (P <0 .0 1)。IR +NS组细胞凋亡指数明显高于S组和IR +SF组 (P <0 .0 1) ,而IR +SF组高于S组 (P <0 .0 5 )。结论　参附注射液增加小肠组织Bcl 2蛋白的表达 ,降低Bax及c myc蛋白的表达 ,抑制小肠细胞凋亡 ,保护缺血再灌注小肠。