Ultrasonographic findings in gastric cancer: in vitro and in vivo studies

Ultrasonography was performed in 45 cases of gastric cancer. Specimens from all 45 cases of gastric cancer were subjects to ultrasonographic study by the water immersion method for comparison with histology. In 32 of these 45 cases in vivo ultrasonographic evaluation was performed prospectively. The overall accuracy rates for the diagnosis of the depth of cancerous invasion were almost 80% in both in vitro and in vivo studies. In vivo ultrasonographic findings agreed well with those from the specimen studies. Ultrasonography was considered to be useful in the diagnosis of gastric malignancies.     

荷瘤鼠乳腺癌组织的飞秒双光子荧光诊断

目的：检测荷瘤鼠乳腺癌组织的双光子荧光光谱。方法：乳腺癌荷瘤鼠腹腔注射血卟啉（HpD)。以飞秒激光照射小鼠的癌组织部位及周围正常组织部位。观察HpD双光子荧光光谱。结果：小鼠的癌组织部位可观察到外源性HpD双光子荧光光谱，而正常组织部位未观察到明显的双光子荧光光谱。结论：结论：飞秒激光外源性血卟啉双光子荧光诊断可作为癌症诊断的新方法。     

Leukemia clusters around nuclear facilities in Britain

He bas been retained for the defense by British Nuclear Fuelsplc in two suits in which leukemia and non-Hodgkin's lymphoma have been alleged to result from radiation exposures due to the operation of the nuclear reprocessing plant at Sellafield. This paper has been sent to the senior authors of the papers reporting clusters of leukemia or other malignancy in the vicinity of nuclear facilities in Britain and their comments invited. Subject to considerations of space and CCC style, these comments will be published as submited.     

痛力克对癌症疼痛镇痛效果的临床观察

应用印度ＬＵＰＩＮ公司提供的痛力克（酮酷酸氨丁三醇 ）对中重度癌症疼痛３０例进行镇痛效果的临床观察，有效率９３％，平均显效时间９ｍｉｎ，均数缓解时间５．１ｈ，并用哌替啶做了同期交叉自身镇痛对比研究，结果表明：两药的镇痛效果相似（Ｐ＞０．０５），但痛力克的不良反应发生率明显低于哌替啶。     

Characterization of cell death events induced by anti-neoplastic drugs cisplatin, paclitaxel and 5-fluorouracil on human hepatoma cell lines: Possible mechanisms of cell resistance.

Two different hepatoma cell lines were incubated for 48h with chemotherapeutic drugs cisplatin, paclitaxel and 5-FU to determine their ability to induce cytotoxicity and DNA fragmentation as well as to modify the expression of some cell death-related genes that could be involved in the resistance to therapy. We observed that cisplatin and paclitaxel induced cytotoxicity, but significant differences between both cell lines, were found only in the case of paclitaxel. At 48h, apoptosis was clearly present in Hep3B cells treated with cisplatin and HepG2 cells treated with paclitaxel. 5-FU induced cytotoxicity in both cell lines but only at higher concentrations than the other two drugs, triggering apoptosis and necrosis in HepG2 cells and only necrosis in Hep3B. When a time course was performed for the first 8h of treatment to elucidate the initial mechanism of cell death responsible for DNA fragmentation, we observed that 5-FU in Hep3B, and cisplatin in both cell lines, induces primary necrosis, whereas at the concentration tested here, paclitaxel clearly triggers apoptosis in both cell lines. HepG2 cells were weakly sensitive to 5-FU in the first 8h of treatment, so the primary mechanism of cell death was not clear, but results seem to indicate that it could be apoptosis. At 48h, Bax was not up-regulated with any of the treatments, whereas cisplatin was able to induce Bcl-xL down-regulation in both cell lines. Treatment with 5-FU also down-regulated Bcl-xL in HepG2 cells. We also measured variations in the expression of survivin, an inhibitor of apoptosis that has also been involved in mitototic catastrophe. Hep3B cells seem to show an increase in protein levels with all treatments. Exposure to paclitaxel resulted in the highest effect. In the case of HepG2 cells, there was a decrease in survivin expression when cells were treated with 5FU and paclitaxel, both treatments showing complete loss of the protein. Using an antibody that recognizes unprocessed caspase-3, we observed that the enzyme was assumingly activated in HepG2 cells treated with 5FU and paclitaxel, but only weakly after treatment with cisplatin. Hep3B cells did not show activation since the levels of the pro-enzyme remained the same as that in the control. In conclusion, the three drugs tested in this study could induce cell death, with paclitaxel being more effective inducing apoptosis. 5FU was only effective at high doses and its mechanism seems to be primarily related to necrosis in Hep3B and probably apoptosis in HepG2. Cisplatin mechanism of cell death is probably mediated by the decrease in anti-apoptotic protein Bcl-xL whereas paclitaxel and 5FU are decreasing the apoptosis inhibitor survivin. According to pro-enzyme levels, caspase-3 was only activated in HepG2 cells, whereas in the case of Hep3B cells the mechanisms of toxicity appear to be caspase-3-independent at the time and concentrations tested in this study. The resistance of Hep3B cells to death induced by chemotherapy could be related to an increase in the expression of IAP survivin, which can decrease cell response to the treatment or even switch the type of death from apoptosis to another kind, making therapy less efficient.     

14年间住院病人主要病因和死因变化趋势

目的　探讨 1990～ 2 0 0 3年住院病人的主要病因和死因及变化趋势的方向、强度。方法　分析我院 1990～ 2 0 0 3年录入广东省卫生厅“广东省医院统计病案管理系统”的统计资料 ,计算住院病人主要疾病、死亡病因 1990～ 1999年、2 0 0 0～ 2 0 0 3年两个阶段的年均构成比 ,观察顺位变化 ,用回归分析的方法计算变化趋势。结果　 1) 1990～ 1999年主要住院病因顺位是消化系统疾病 (15 .6 2 % )、损伤和中毒 (13.16 % )、循环系统疾病 (11.2 4 % )、呼吸系统疾病 (10 .4 7% )、恶性肿瘤 (10 .4 3% ) ;2 0 0 0～ 2 0 0 3年顺位是循环系统疾病 (16 .4 1% ) (其中缺血性心脏病占 2 2 .98% ,脑血管病占 39.6 8% ) ,损伤和中毒(12 .80 % )、消化系统疾病 (11.76 % )、呼吸系统疾病 (9.5 3% )、恶性肿瘤 (8.73% ) ,循环系统疾病呈显著上升趋势 (B =4 .2 6 ,P <0 .0 5 ) ,消化系统疾病呈显著下降趋势 (B =- 3.17,P <0 .0 5 ) ;2 ) 1990～ 2 0 0 3年住院死因顺位为恶性肿瘤 (2 9.2 9% )、循环系统疾病 (2 5 .91% )、损伤和中毒 (12 .6 3% )、呼吸系统疾病(6 .18% ) ,消化系统疾病 (5 .77% ) ;2 0 0 0～ 2 0 0 3年恶性肿瘤呈显著下降趋势 (B =- 3.88,P <0 .0 5 ) ,循环系统疾病呈上升趋势但无显著性 (B =0 .84 ,P >0     

电子计算机监护慢性肝病程序的验证

用参与建立数学模型的521例资料和307例没参与建立数学模型的病例资料验证电子计算机监护慢性肝病的程序。以病理学检查、或以3个月至3年的临床观察结果作为诊断的金标准。254例临床诊断作为对照。验证结果表明（1）计算机监护优于临床诊断，（2）本程序敏感度高。