TGF—β1对膀胱移行细胞癌细胞粘附性的调节

为了解ＴＧＦβ１对肿瘤粘附性的调节，采用Ｎｏｒｔｈｅｒｎ杂交分析测定了两个膀胱癌细胞系ＴＧＦβ１及ＦＮｍＲＮＡ的表达，并用体外测定方法检测了ＴＧＦβ１对两细胞系粘附性质的调节。结果表明：ＴＧＦβ１仅可使低表达ＦＮ的２５３Ｊ细胞的粘附性增强，而这种增强与ＦＮ表达的增加成正比；同样浓度的ＴＧＦβ１对高表达ＦＮ的６４７Ｖ细胞的粘附性无明显影响。提示肿瘤细胞粘附能力的可变性是其具有转移能力的原因之一。     

真皮下血管网岛状皮瓣抗菌力的实验研究

为研究真皮下血管网薄皮瓣用于感染创面的可行性，在家猪臀部两侧分别形成以旋髂深血管主干分支为蒂的传统岛状皮瓣和远侧５０％修薄的真皮下血管网岛状皮瓣。用细菌计数、吖啶橙荧光染色测定白细胞吞噬指数和白细胞内杀菌率，应用激光多普勒、墨汁灌注、透明标本等方法，对两种皮瓣的抗菌力作自身对照研究。结果表明，真皮下血管网岛状皮瓣的抗菌力明显降低，可能与皮瓣修薄后血供减少，白细胞功能相应降低有关。     

Perioperative specific management of blood volume loss in craniosynostosis surgery

Accurate assessment and replacement of blood loss and fluid–electrolyte deficit during craniosynostosis repair is difficult owing to patient size and the diversity of surgical technique. Forty-three patients undergoing primary craniosynostosis repair over a 10-year period were studied retrospectively to determine blood loss and fluid deficit and to assess blood transfusion practices during both intraoperative and postoperative periods. Blood loss was calculated on the basis of estimated red cell mass (ERCM) and fluid-electrolyte imbalance was investigated with blood samplings. Blood transfusion was considered appropriate if the postoperative or posttransfusion ERCM was within 12% of the preoperative value. Estimated fluid requirement (EFR) was used in 4 ml kg^–1 h^–1 except for neonates. Intraoperatively, 80% of all patients were appropriately managed with respect to blood transfusion and EFR. Postoperatively only 20% of the patients receiving transfusions were transfused appropriately. In 23.3% of these patients (10/43) unexpected respiratory distress developed immediately after their recovery from the anesthesia. With the measurement of estimated blood volume and allowable blood loss, appropriate transfusion could be achieved for the successful treatment of the primary craniosynostosis. Received: 16 February 1998     

P16、Cyclin D1蛋白表达与胰腺癌生物学行为

目的 探讨P16、CyclinD1蛋白表达水平与胰腺癌发生、发展及预后的关系。方法 应用免疫组织化学SP法结合微波抗原修复法对53例原发性胰腺癌和42例胰腺良性病变及正常组织中P16蛋白及CyclinD1蛋白进行检测。结果 胰腺癌组织、胰腺良性病变和正常组织中P16蛋白的阳性率分别为66．04％和87．71％（P＜0．05）；CyclinD1表达的阳性率分别为52．83％和23．81％（P＜0．05），P16及CyclinD1蛋白表达与胰腺癌的组织分化、病理分期及术后生存期密切相关。结论 P16及CyclinD1蛋白在胰腺癌中的表达可判断胰腺癌的预后。     

化学中毒与急性缺氧的双因素联合效应的实验研究

目的 研究化学中毒与急性缺氧两因素的联合效应。方法 建立常压常氧、常压缺氧和低压缺氧3种模型，以梭曼(Soman)、氰化钠(NaCN)和4-DMAP(4-dimethylaminophenol)为代表，测定大鼠、小鼠、家猫、PC12细胞、兔血红细胞等在3种模型条件下对毒物药物的行为、生化和生理指标变化。结果梭曼单独作用可导致动物协调运动下降、脑等组织含水率增加、脑组织AChE活性降低、MR下调、NE和cAMP含量增加。急性缺氧单独作用也可引起动物协调运动及自主活动的降低、脑等组织含水率的增加、外周血和脑组织AChE活性升高、MR受体上调、NE和cAMP含量增加、4-DMAP药效升高。化学中毒与急性缺氧同时作用，上述变化更加复杂。结论 化学中毒与急性缺氧两种因素同时作用于机体，对机体产生广泛而复杂的损伤作用。此种作用为两因素的联合效应。缺氧引起的机体功能下降对联合效应的增加部分贡献较大。急性缺氧既可使重要的组织成分发生质或量的变化，也会影响某些抗毒剂的作用强度。     

地塞米松在大鼠缺血随意皮瓣中的作用

目的：研究局部使用地塞米松对大鼠缺血随意皮瓣的作用。方法：建立大鼠背部缺血随意皮瓣的动物模型，随机分为2组，实验组术后皮瓣下一次给予地塞米松5mg(用生理盐水稀释至3ml)，对照组术后皮瓣下一次给予0．9％生理盐水3ml。均于术后7d取材，测定皮瓣坏死率和组织中丙二醛含量，观察大体及病理切片。结果：实验组皮瓣坏死率和丙二醛含量较对照组显著降低(P＜0．01)。光镜下，实验组的炎性反应较对照组明显减轻。结论：地塞米松能提高缺血随意皮瓣的成活率，大剂量一次性给药的方法是可行的。     

口腔固定修复学临床前期实习中的问题与对策

本文总结了北京大学口腔医学院3届八年制口腔医学专业学生口腔固定修复学临床前期实习教学的经验,针对实习中出现的典型问题进行了分析,采取了相应的对策和方法,取得了良好的效果.     

乌司他汀对重症急性胰腺炎血浆内毒素水平的影响及其疗效观察

目的　观察乌司他汀治疗重症急性胰腺炎对血清内毒素水平的影响。方法　 4 0例重症急性胰腺炎患者随机分为乌司他汀治疗组和一般常规治疗组两组 ,两组患者住院后分别在第 1、4、7、10天抽血测定血清淀粉酶、血浆内毒素水平 ,结合APACHEⅡ评分系统分析观察乌司他汀的临床疗效。结果　重症急性胰腺炎入院后第 1天血浆内毒素水平明显高于正常健康对照组 ,分别为 (1.10± 0 .2 3)IU/L和 (0 .2 0± 0 .5 0 )IU/L(P <0 0 0 1) ,治疗组血清淀粉酶、血浆内毒素水平下降均较对照组明显 (P <0 0 1) ,住院第 7天APACHEⅡ评分值低于对照组 (P <0 0 5 )。结论　重症急性胰腺炎患者早期存在不同程度的内毒素血症 ,乌司他汀治疗重症急性胰腺炎疗效肯定 ,并能降低患者血浆内毒素水平和改善预后     

直肠癌盆腔放疗后肠受照射影响因素的研究

目的 评价体位、性别、手术、膀胱充盈状态对直肠癌放疗后肠受照射的影响。方法36例直肠癌患者被研究，盆腔放疗采用1后2侧野三维适形放射治疗（3DCRT）的方法，处方剂量为50Gy。利用每个计划的剂量．体积直方图（DVH）对盆腔内肠的受照剂量和体积进行分析。结果膀胱充盈差和好时肠受照射的平均剂量分别是23．8和18．3Gy（P=0．004），V45高剂量受照体积分别是15．7％和7．8％（P=O．004）；体位仅对肠V15，低剂量受照体积有显著影响；性别对肠受照射的最大剂量和V15，有显著影响；手术对肠受照射的平均剂量有显著影响，分别是术前19．0Gy和术后22．5Gy（P=0．015）；在仰卧或俯卧、术前或术后膀胱充盈好时均比差时肠受照射剂量要低或体积要小。膀胱充盈好和差时肠受到高剂量照射的体积V4，在俯卧位分别是15．3％和7．4％（P=0．023），术后分别是14．1％和7．2％（P=0．014），差异有统计学意义。结论 患者治疗体位、性别、手术对盆腔内肠受照射剂量和体积有一定的影响，膀胱充盈状态有显著影响。     

Establishment of a human hepatocellular carcinoma cell line highly expressing sodium iodide symporter for radionuclide gene therapy.

To evaluate the possibility of radionuclide gene therapy and imaging in hepatocellular carcinoma cancer, we investigated the iodine accumulation of a human hepatocellular carcinoma cell line, SK-Hep1, by transfer of human sodium iodide symporter (hNIS) gene. By targeting NIS expression in SK-Hep1, we could also investigate whether these cells concentrate 99mTc-pertechnetate and 188Re-perrhenate as well as 125I in vitro and in vivo. METHODS: The hNIS gene was transfected to human hepatocellular carcinoma SK-Hep1 cell lines using lipofectamine plus reagent. The uptake and efflux of 125I, 99mTc-pertechnetate, and 188Re-perrhenate were measured in the transfected and parental cells. Biodistribution was studied in nude mice bearing SK-Hep1 and SK-Hep1-NIS at 10 and 30 min and at 1, 2, 6, 16, and 23 h after injection of 125I, 99mTc- pertechnetate, or 188Re-perrhenate. In tumor imaging studies, the nude mice were intravenously injected with 188Re-perrhenate and imaged with a gamma-camera equipped with a pinhole collimator at 30 and 60 min after injection. The survival rate (%) was determined by the clonogenic assay after 37 MBq/10 mL (1 mCi/10 mL) 131I and 188Re-perrhenate treatment. RESULTS: SK-Hep1-NIS, stably expressing the NIS gene, accumulated 125I up 150 times higher than that of SK-Hep1. Iodine uptake of SK-Hep1-NIS is completely blocked by perchlorate. NIS gene transfection into SK-Hep1 also resulted in 112- and 87-fold increases of 99mTc-pertechnetate and 188Re-perrhenate uptake, respectively. Iodide efflux from SK-Hep1-NIS was relatively slow, with only 10% released during the initial 5 min, and 60% remained at 25 min. In the biodistribution study using SK-Hep1-NIS-xenographed mice, the tumor uptake of 125I, 188Re-perrhenate, and 99mTc-pertechnetate was 68.0 +/- 15.0, 46.2 +/- 9.1, and 59.6 +/- 16.2 %ID/g (percentage injected dose per gram) at 2 h after injection, respectively. After 188Re-perrhenate injection in SK-Hep1 and SK-Hep1-NIS-xenographed nude mice, whole-body images clearly visualized the SK-Hep1-NIS tumor, whereas the control tumor was not visualized. The survival rate (%) of SK-Hep1-NIS was markedly reduced to 46.3% +/- 10.1% and 28.9% +/- 5.2% after 37 MBq/mL (1 mCi/10 mL) 131I and 188Re-perrhenate treatment compared with the survival rates of the parental cells. These results demonstrated that SK-Hep1-NIS could be selectively killed by the induced 131I and 188Re-perrhenate accumulation through NIS gene expression. CONCLUSION: NIS-based gene therapy using beta-emitting radionuclides has the potential to be used in hepatocellular carcinoma management.