胃癌中p53基因失活及其蛋白产物的免疫组化分析

应用ＰＣＲ－ＳＳＣＰ银染，Ｓｏｕｔｈｅｒｎ杂我及免疫组化等方法同步研究２５例胃癌标本的ｐ５３基因突变，杂合性丢失及蛋白持表达，在２２例胃癌中同时获得有关ｐ５３基因突变和杂合性丢失的检测结果，被检出ｐ５３基因突变的５例胃癌中，２例伴有杂合性丢失，３例仅有ｐ５３基因突变。     

二齿差活齿传动齿形综合反解研究

给出了中心轮常用齿形曲线及对应的等效机构;应用等效机构法,推导出齿形综合反解的激波凸轮原始轮廓方程及其等距方程;齿形综合反解实例验证了方法的实用性。     

胃多参数信号的提取及EGG后处理方法

介绍自行研制的胃多参数监测诊断仪中多参数信号的提取方法,重点讨论了采用自适应滤波的方法消去胃电信号中的呼吸干扰的原理.给出了实验结果,实验结果表明这种方法是有效的.     

The trefoil protein TFF1 is bound to MUC5AC in humangastric mucosa

The trefoil protein TFF1 is expressed principally in the superficial cells of the gastric mucosa. It is a small protein and forms homo- and hetero-dimers via a disulphide bond through Cys58 which is located three amino acids from the C terminus. TFF1 is co-expressed with the secreted mucin MUC5AC in superficial cells of the gastric mucosa suggesting that it could be involved in the packaging or function of gastric mucus. We have previously shown that TFF1 co-sediments with mucin glycoproteins on caesium chloride gradients. To extend this observation we have now used gel filtration under physiological conditions, immunoprecipitation and Western transfer analysis to characterise the interaction of TFF1 with gastric mucin glycoproteins. We show that TFF1 co-elutes with MUC5AC but not MUC6 on gel filtration and that immunoprecipitation and Western transfer analysis confirms that TFF1 interacts with MUC5AC. We also demonstrate that the TFF1 dimer is the predominant molecular form bound to MUC5AC. Salt and chelators of divalent cations such as EDTA and EGTA disrupted the TFF1- MUC5AC interaction and increased the degradation of MUC5AC, whereas calcium increased the amount of TFF1 bound to MUC5AC. These data support the contention that TFF1 is pivotal in the packaging and function of human gastric mucusa.Received 24 March 2004; received after revision 14 May 2004; accepted 7 June 2004     

江西省胃癌与地形地貌类型

利用４５０２个地形地貌数据资料,１０２９５例胃癌死亡调查资料,研究了胃癌死亡率与人群生存区的地形地貌（山区、丘陵、岗地、平原）的相关性。在此基础上,综合评价了地形地貌类型对胃癌的产生和发展的影响。     

钴铬合金网加强基托在义齿镶复中的临床应用

目的：为评研铸造钴铬合金网加强基托在全口义齿镶复中的临床效果。方法：作者应用铸造钴铬合金网加强基托镶复全口义齿54例．并与应用传统塑料基托镶复全口义齿264例临床效果进行对比。结果：铸造钴铬合金网加强基托在抗折率、薄度及不变形等均优于传统塑料基托（P＜0．01）。结论：铸造钴铬合金网加强基托能增强塑料基托强度,延缓塑料基托疲劳及老化,抗折力明显提高,价格低廉,故值得基层医院临床广泛应用。     

渐开线小齿数齿轮传动的最小螺旋角

对小齿数齿轮传动的特点和计算要点进行分析，为在设计中避免小齿轮发生根切和齿顶变尖，合理选择基本参数提供了依据，并提出了小齿数齿轮传动中最小螺旋角的概念。     

脑室注射GABA对小鼠实验性胃溃疡及其粘液屏障的影响

报道小白鼠脑室注射ＧＡＢＡ（４ｍｌ）对无水乙醇（０．ｌｍｌ灌胃）、盐酸（０．２Ｎ，０．２ｍｌ灌胃）、消炎痛（３２ｍｇ·ｋｇ－１肌肉注射）和冷束缚应激（１℃）四种不同实验性胃溃疡及其粘液屏障的影响。实验结果表明：乙醇、盐酸和冷束缚诱导胃溃疡时，胃壁粘液量都显著减少，而消炎痛则无变化。脑室注射ＧＡＢＡ能加剧乙醇诱导型、消炎痛诱导型这两种胃溃疡，但对胃壁粘液量无明显影响。而脑室注射ＧＡＢＡ能抑制盐酸诱导型、冷束缚应激型胃溃疡，并使固壁粘液明显升高。本文对中枢ＧＡＢＡ能机制参与胃溃疡及胃粘液调节作了进一步探讨。     

胃粘膜HCO_3~－分泌的细胞机制和调节

正常的胃粘膜上皮细胞依赖新陈代谢的过程分泌ＧＣＯ－３。它依赖于跨膜Ｎａ＋梯度和Ｎａ＋－Ｋ＋－ＡＴＰ酶的活性；也可伴随ＮａＨＣＯ３协同转运。粘膜损伤时，紧密连结被损害或上皮脱落，可增加粘膜渗透性，使ＨＣＯ－３被动转运进入胃腔。酸可刺激依赖新陈代谢的ＨＣＯ－３分泌，也可造成其被动转运．中枢神经系统参与调节胃ＨＣＯ－３分泌，迷走神经促进其分泌，而交感神经抑制其分泌。ＨＣＯ－３参与组成一个胃粘液－ＨＣＯ－３屏障，保护胃粘膜免受损伤，促进粘膜自身修复和再生。     

糜烂性胃炎合并消化性溃疡289例分析

本文报告糜烂性胃炎合并消化性溃疡２８９例，占同期糜烂性胃炎８８４例的３２．７％．其中合并十二指肠球部溃疡２１１例（２３．９％）．幽门螺杆菌检出率为９０％．提示胃酸过高又幽门螺杆菌感染可能是糜烂性胃炎及消化性溃疡共同的发病因素．内镜检查是诊断本病的最重要手段．采用抗酸、抗幽门螺杆菌感染、粘膜保护剂以及微波凝固等综合疗法是有效的治疗措施．