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| 1 | Intestinal acariasis in Anhui Province显示文摘INTRODUCTIONThe mites found in stored food and house comprise a largegroup of subclass Acari,belonging to the suborderAcardida of the order Acariformes.They can be found indust and vacuum samples from floors,furniture,mattresses,Chinese herbal medicine,dry fruit,grain, | Li CP Wang J | 2000 | World Journal of Gastroenterology2000，6，4： | 27 |
| 2 | 奥曲肽抑制人胃癌细胞株MKN45的生长显示文摘目的:研究奥曲肽(octreotide,OCT)对人胃癌细胞株MKN45生长的调控作用,并探讨其作用机制。 方法:采用MTT比色分析法测定OCT10^(-2),10^(-3),10^(-4),10^(-5),10^(-6)g·L^(-1)对MKN45细胞生长的调控作用;采用流式细胞术分析OCT10^(-3)g·L^(-1))对MKN45细胞的周期分布的影响。 结果;OCT 10^(-2),10^(-3),10^(-4)g·L^(-1)对MKN45细胞的生长均有抑制作用,以lO^(-3)g·L^(-1)浓度的抑制作用最显著,为10.4%;10^(-3)g·L^(-l)这一浓度可诱导MKN45出现G0/G1阻滞,于加入OCT后6h开始,为(64±4)%,24h最显著,达(75±3)%,36h已消失;与对照组(7±1)%相比,24h G2/M期细胞比例亦减少,为(2±2)%,但OCT未改变亚二倍体细胞的比例。 结论:OCT可抑制人胃癌细胞株MKN45的生长,其作用机制之一是诱导细胞出现GO/G1阻滞。 | 王消冰 王绪 张南征 | 2002 | 世界华人消化杂志2002，10，1： | 19 |
| 3 | 胃溃疡大鼠胃泌素、生长抑素和GD细胞的变化显示文摘目的:研究胃溃疡对大鼠G细胞分泌胃泌素(D细胞分泌生长抑素)和对G(D)细胞变化的影响.方法:建立冰乙酸性大鼠胃溃疡模型,采用大体、光镜、透射电镜观察胃窦黏膜组织学表现和胃窦黏膜细胞超微结构表现,采用放射免疫法检测血清和胃窦组织中的胃泌素、生长抑素含量,采用免疫组化法及定量分析检测G(D)细胞形态、数目、面积、和G/D细胞数目、面积比值,采用免疫电镜及定量分析观察与检测G(D)细胞及G(D)细胞中的胃泌素(生长抑素)分泌颗粒.结果:免疫电镜观察到了G(D)细胞和IG(D)细胞中的胃泌素(生长抑素)分泌颗粒.大鼠胃溃疡后,G细胞内胃泌素分泌量增加,D细胞内生长抑素分泌量减少,G细胞数目增加、面积减少,D细胞数目减少、面积减少,G/D细胞数目比值和G/D细胞面积比值增加,并且血清、胃窦组织中胃泌素含量增加,生长抑素含量减少.结论:大鼠胃溃疡可引起G、D细胞的变化,引起G、D细胞分泌胃泌素、生长抑素的变化,和引起胃泌素、生长抑素含量的变化. | 孙凤蓬 宋于刚 覃汉荣 | 2004 | 世界华人消化杂志2004，12，2： | 16 |
| 4 | Effects of tumor necrosis factor,endothelin and nitric oxide on hyperdynamic circulation of rats with acute and chronic portal hypertension显示文摘AIM:To evaluate the effect of tumor necrosis factor (TNF),endothelin (ET) and nitric oxide (NO) on hyperdynamic circulation (HC) of rats with acute and chronic portal hypertension (PHT).METHODS: Chronic portal hypertension was induced in Wistar rats by injection of carbon tetrachloride. After two weeks of cirrhosis formation, L-NMMA (25mg/kg) was injected into one group of cirrhotic rats via femoral vein and the experiment was begun immediately. Another group of cirrhotic rats was injected with anti-rat TNFα (300mg/kg) via abdominal cavity twice within 48h and the experiment was performed 24h after the second injection. The blood concentrations of TNFα, ET-1 and NO in portal vein and the nitric oxide synthase (NOS) activity in hepatic tissue were determined pre-and post-injection of anti-rat TNFα or LNMMA. Stroke volume (SV), cardiac output (CO), portal pressure (PP), superior mesenteric artery blood flow (SMA flow) and lilac artery blood flow (IAflow) were measured simultaneously. Acute portal hypertension was established in Wistar rats by partial portal-vein ligation (PVL). The parameters mentioned above were determined at 0.5h,24h, 48h, 72h and 120h after PVL. After the formation of stable PHT, the PVL rats were injected with anti-rat TNFα or L-NMMA according to different groups, the parameters mentioned above were also determined.RESULTS:In cirrhotic rats, the blood levels of TNFα, NO in portal vein and the liver NOS activity were significantly increased (P<0.05) while the blood level of ET-1 was not statistically different (P>0.05) from the control animals(477.67±83.81pg/mL vs 48.87±32.79pg/mL, 278.41±20.11μmol/L vs 113.28±14.51μmol/L, 1.81±0.06μ/mg.prot vs 0.87±0.03μ/mg.prot and 14.33±4.42pg/mL vs8.72±0.79pg/mL, respectively). After injection of anti-rat TNFα,the blood level of TNFα was lower than that in controls (15.17±18.79pg/mL vs 48.87±32.79pg/mL). The blood level of NO and the liver NOS activity were significantly decreased, but still higher than those of the controls. The blood level of ET-1 was not significantly changed. PP,SV,CO, SMAflow and IAflow were ameliorated. After injection of L-NMMA, the blood level of NO and the liver NOS activity were recovered to those of the controls. PP and CO were also recovered to those of the controls. SV, SMAflow and IAflow were ameliorated. In PVL rats, the blood levels of TNFα NO in portal vein and the liver NOS activity were gradually increased and reached the highest levels at 48h after PVL. The blood level of ET-1 among different staged animals was not significantly different from the control animals. PP among different staged animals (2.4±0.18kPa at 0.5h, 1.56±0.08kPa at 24h, 1.74±0.1kPa at 48h,2.38±0.05 kPa at 72h, 2.39±0.16 kPa at 120h) was significantly higher than that in controls (0.9±0.16kPa). After injection of anti-rat TNFα in 72h PVL rats, the blood level of TNFα was lower than that in controls (14±14pg/mL vs 48.87±32.79pg/mL). The blood level of NO and the liver NOS activity were significantly decreased, but still higher than those of the controls. The blood level of ET-1 was not significantly changed. PP was decreased from 2.38±0.05kPa to 1.68±0.12kPa, but significantly higher than that in controls. SV, CO, SMAflow and IAflow were ameliorated.After injection of L-NMMA in 72h PVL rats, the blood level of NO and the liver NOS activity were recovered to those of the controls. PP, SV, CO, SMAflow and IAflow were also recovered to those of the controls.CONCLUSION:NO plays a critical role in the development and maintenance of HC in acute PHT and is a key factor for maintenance of HC in chronic PHT. TNFα may not participate in the hemodynamic changes of HC directly, while play an indirect role by inducing the production of NO through activating NOS. No evidence that circulating ET-1 plays a role in both models of portal hypertension has been found. | Ji-JianWang Gen-WuGao Ren-ZhongGao Chang-AnLiu XiongDing Zhen-XiangYao | 2004 | World Journal of Gastroenterology2004，10，5： | 14 |
| 5 | 门奇静脉断流术对门脉高压症一氧化氮及氧自由基的影响显示文摘目的:探讨NO系统、OFR系统对门脉高压症(PHT)的影响及门奇静脉断流术的作用。 方法:门脉高压症患者19例,肝功能A级9例,B级10例;正常对照组15例。术前、术后d3晨空腹抽静脉血应用硝酸盐还原酶法测定NO,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD),比色法测定一氧化氮和酶(NOS),硫代巴比妥酸(TBA)法测定丙二醛(MDA)。 结果:肝硬化PHT患者术前血清NO(μmol·L^(-1))含量、NOS活性(kU·L^(-1))A级分别为63.8±10.7,26.3±7.9,B级分别为79.2±14.8,36.7±9.0,较正常对照组32.7±6.2,12.5±4.1显著升高(p<0.01);术前肝功能B级NO、NOS较A级显著升高(p<0.01);门奇静脉断流术后3dNO、NOSA级分别为40.2±9.4,16.9±5.3,B级分别为58.7±12,26.6±6.5与术前比均有显著降低(p<0.05,p<0.01),但仍高于正常对照组(p<0.05,p<0.01);且门奇静脉断流术后肝功能A级的NO、NOS的下降幅度分别为37.0%,35.8%较B级的25.8%,26.3%明显。肝硬化PHT患者术前血清SOD活性(kNU·L^(-1))A、 B级分别为70.5±16.7,53.3±11.1均较正常对照组119.1±20.1显著降低(p<0.01);而PHT患者术前血情MDA含量(μmol·L^(-1))A、B级分别为21.4±4.8,32.6±6.3则显著高于对照组6.7±2.0(p<0.01);术前肝功能B级SOD、MDA与A级比也有显著性差异(p<0.01,p<0. | 姚常柏 吴硕东 夏振龙 | 2002 | 世界华人消化杂志2002，10，1： | 4 |
| 6 | 实验性胃溃疡大鼠前脑生长抑素神经元的变化显示文摘目的观察大鼠实验性胃溃疡期间前脑生长抑素免疫反应(somatostatin,SS)和 SSmRNA 神经元的变化.方法用成年♂Wistar 大鼠38只,分为实验性胃溃疡组(EUG)、盐水对照组(SCG)和正常对照组(NCG).于术后1,4,10 d 和23 d 分批取脑,石蜡切片,用 Stemberger 免疫组化 PAP法显示弓状核后段水平前脑 SS 神经元;用地高辛标记反义SScRNA 探针和碱性磷酸酶标记抗地高辛抗体检测系统,显示SSmRNA 神经元.结果正常大鼠 SS 神经元广泛分布于前脑各核区,溃疡组术后1 d,大脑皮质纹状皮质区 SS 神经元减少,但可见大量 SS 强阳性纤维,SS 神经元数与盐水组相比无差异;在杏仁复合体和下丘脑各核区,溃疡组 SS 神经元数增多,与盐水组、正常组相比有差异[杏仁中央核(ce):EUG 57.1±3.0 vs SCG 41.7±1.2,杏仁外侧核(1a):EUG 56.3±1.2 vs SCG 49.3±2.7,杏仁皮质后核(pco):EUG 66.7±6.7 vs SCG 44.9±3.8,杏仁基外侧核(blp):EUG 65.0±8.3 vs SCG 34.2±3.0,下丘脑弓状核(ar):EUG 92.7±8.0 vs SCG 60.9±1.5,下丘脑腹内侧核(vmh):EUG 78.7±7.3 vs SCG 47.5±1.5,P<0.01;杏仁内侧核(me):EUG 77.3±6.0 vs NCG 41.7±2.2 andEUG vsSCG 49.8±2.1,下丘脑背外侧核(dmh):EUG 93.7±4.3 vsNCG 44.7±2.0 and EUG vs SCG 61.3±0.9,ce:EUG vsNCG 35.7±4.3,1a:EUG vs NCG 11.7±4.3,pco:EUG vsNCG 35.7±1.7,blp:EUG vs NCG 29.7±0.5,ar:EUG vsNCG 30.3±1.0,vmh:EUG vs NCG 30.7±4.3,P<0.001].术后4 d,溃疡组大脑皮质纹状皮质区、杏仁复合体和下丘脑各核区 SS 神经元密集,并在下丘脑弓状核及其周围可见较多'点样'阳性结构和串珠状 SS 阳性纤维;SS 神经元数明显增多,与盐水组、正常组相比均有差异(纹状皮质Ⅱ~Ⅲ:EUG 88.0±5.9 vs SCG 79.3±2.3.me:EUG 106.4±14.7 vs SCG 77.3±8.0 P<0.05;纹状皮质Ⅳ:EUG 83.5±3.8 vs SCG 50.7±2.0,纹状皮质Ⅴ~Ⅵ:EUG 79.5±4.4 vs SCG 70.0±1.3,ce:EUG 106.9±14.7 vs SCG 62.0±11.0,1a:EUG 83.5±6.6 vs SCG 60.0±5.3.pco:EUG 112.8±11.4 vs SCG 85.7±4.5,blp:EUG 90.1±8.4 vs SCG 60.0±3.3,ar:EUG152.5±16.1 vs SCG 95.3±5.7,wnh:EUG 130.1±10.8 vsSCG 84.7±18.0,P<0.01;dmh:EUG 145.3±8.0 vs SCG114.0±4.7,纹状皮质Ⅱ~Ⅲ:EUG 88.0±5.9 vs NCG 40.7±1.3,,纹状皮质Ⅳ:EUG vs NCG20.4±1.3,纹状皮质Ⅴ~Ⅵ:EUG vs NCG 32.3±1.7,me:EUG vs NCG,ce:EUG vsNCG,la:EUG vs NCG,pco:EUG vs NCG,blp:EUG vsNOD,ar:EUG vs NCG,vmh:EUG vs NCG,dmh:EUG vsNCG,P<0.001).术后10 d 和23 d,各核区 SS 神经元数仍多于盐水组和正常组,术后4 d,SSmRNA 神经元数量于溃疡组大脑皮质(EUG 239±7,SCG 122±6)、杏仁复合体(EUG 637±53,SCG 256±16)和下丘脑弓状核(EUG 96±18,SCG 51±5)明显多于盐水组(P<0.001).结论实验性胃溃疡大鼠前脑 SS-ir 和 SSmRNA 神经元可能参与了胃溃疡自愈过程的调节. | 王建伟 周济远 郑慧娥 杨天祝 | 2000 | 世界华人消化杂志2000，8，9： | 2 |
| 7 | 超声图预测肝硬化患者食管静脉曲张程度显示文摘目的:筛选有意义的超声检查指标,结合Child-Pugh分级对中度以上食管静脉曲张的肝硬化患者进行预测,探讨超声检查预测肝硬化患者食管静脉曲张程度的价值. 方法:将所有病例按Child-Pugh评分分级,进行超声及胃镜检查,用Spearman等级相关分析筛选出与食管静脉曲张程度相关并且对其判断贡献较大的指标,建立Logistic 回归方程. 结果:食管静脉曲张程度与Child-Pugh分级呈正相关(r=0.39, P<0.01),Child-Pugh C级患者中度以上食管静脉曲张占93.3%.对Child-Pugh A级患者,判断食管静脉曲张程度贡献较大的指标是PUV,Logistic回归方程:P(A)=1/[1+e-(- 0.405+1.686PUV],其判断准确率为68.0%,敏感性为60.0%, 特异性为78.3%.对Child-Pugh B级患者判断食管静脉曲张程度贡献较大的指标有PVD,PUV,GBBL和AS,Logistic 回归方程:P(B)=1/[1+e-(-19.554+9.295AS-2.757PUV-4.278GBBL+1.288PVD)], 其判断准确率为92.7%,敏感性为96.8%,特异性为80.0%. 结论:Child-Pugh c级肝硬化患者绝大部分有中度以上的食管静脉曲张;以超声检查指标建立的回归方程对Child- Pugh A,B级患者中度以上的食管静脉曲张判断符合率较高,可以用于肝硬化患者食管静脉曲张程度的预测. | 张晓红 张宇锋 宁方芹 杨绍基 | 2004 | 世界华人消化杂志2004，12，4： | 0 |
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