要设计了可检测十二指肠胃返流的光纤传感器，该传感器由470nm的信号光、595nm参考光和光纤束构成，主要检测十二指肠返流物中的胆红素在470nm与595nm的吸光度，本文还对影响传感器检测的因素诸如波长、pH、胃液中悬浮颗粒造成的散射作用以及其他的因素，做了详细评价。传感器可以达到10mg/dl优良的动态响应范围，离体实验结果表明，该传感器可以作为临床动态检测手段。

目的 探讨自发性夜间胃碱化的形成是否与十二指肠胃反流（DGR）及迷走神经功能有关。方法 20例功能性消化不良（FD）患者采用胃内pH和胆红素同步监测法，比较夜间自发性碱化与胆汁反流的关系；另外20倒无心血管疾病的FD患者采用胃内pH和心电Holter同步监测，进行心率变异性（HRV）时域分析，以SDNN、rMSSD、PNN50为指标，观察夜间自发性碱化与迷走神经功能的关系。结果 20例FD患者中出现夜问自发性碱化者12例，其中8例（占66.7%）同时有胆红素吸光值升高；20例无心血管疾病的FD患者中13例有夜间自发性碱化，7例无自发性碱化，二者比较SDNN、rMSSD均在正常范围，差异无显著性（P>0.05）；24h胃pH与PNN50对照观察表明，夜间时段与白天相比PNN50明显升高，有自发性碱波组与无自发性碱化组二者相比，PNN50无显著差别。结论 自发性夜间胃碱化的形成与DGR有关，并不是迷走神经张力降低导致胃酸分泌减少所致。

AIM: To explore the effect of six bile salts, including glycocholate (GC), glycochenodeoxycholate (GCDC), glycodeoxycholate (GDC), taurocholate (TC), taurochenodeoxycholate (TCDC), taurodeoxycholate (TDC), and two bile acids including cholic acid (CA) and deoxycholic acid (DCA) on esophageal cancer Eca109 cell line. METHODS: Eca109 cells were exposed to six bile salts, two bile acids and the mixed bile salts at different concentrations for 24-72h. 3-[4, 5-Dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay was used to detect the cell proliferation. Apoptotic morphology was observed by phase-contrast video microscopy and deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Sub-G1 DNA fragmentations and early apoptosis cells were assayed by flow cytometry (FCM) with propidium iodide (PI) staining and annexin V-FITC conjugated with PI staining. Apoptosis DNA ladders on agarose were observed. Activation of caspase-3 was assayed by FCM with FITC-conjugated monoclonal rabbit anti-active caspase-3 antibody and expressions of Bcl-2 and Bax proteins were examined immunocytochemically in 500μmol/L-TCinduced apoptosis cells. RESULTS: Five bile salts except for GC, and two bile acids and the mixed bile salts could initiate growth inhibition of Eca109 cells in a dose-and time-dependent manner. TUNEL, FCM, and DNA ladder assays all demonstrated apoptosis induced by bile salts and bile acids at 500μmol/L, except for GC. Early apoptosis cell percentages in Eca109 cells treated with GCDC, GDC, TC, TCDC, TDC, CA at 500μmol/L for 12h, DCA at 500μmol/L for 6 h, and mixed bile salts at 1000μmol/L for 12h were 7.5%, 8.7%, 14.8%, 8.9%, 7.8%, 9.3%, 22.6% and 12.5%, respectively, all were significantly higher than that in control (1.9%). About 22% of the cell population treated with TC at 500μmol/L for 24h had detectable active caspase-3, and were higher than that in the control (1%). Immunocytochemical assay suggested that TC down-regulated Bcl-2 protein level and up-regulated Bax protein level. CONCLUSION: GCDC, GDC, TC, TCDC, TDC, CA and DCA, except for GC, can inhibit growth and induce apoptosis of esophageal cancer Eca109 cells. Activation of caspase-3, decreased Bcl-2 protein and increased Bax protein are involved in TC-induced apoptosis of Eca109 cells.