红外光谱法研究改性Y型分子筛表面酸性与活性的关系

用红外光谱法研究了改性Y型分子筛的表面酸性,并考察了烷基化反应活性与酸性质的关系。结果表明:经过离子交换之后的Y型分子筛催化剂活性和寿命没有明显提高,但是加La2O3后,总B、L酸量减少,催化剂的活性和寿命都得到了提高。     

国人24h食管pH监测正常参考值初探

目的 :为研究胃食管反流病 (GERD) ,提供国人 2 4h食管pH监测有关指标的正常参考值。方法 :结合我院及国内外资料的有关正常人、GERD患者 2 4h食管pH监测结果分析研究。结果 :生理性反流立位较卧位多见 ;GERD时 ,卧位pH <4百分时间大于立位 ,提示夜间酸反流造成食管粘膜酸暴露时间明显延长 ,促发炎性损伤。结论 :综合 2 3 3例国人正常参考值 (及 95 %可信区间上限 ) ,pH <4总百分时间 ( % ) 1.14± 0 .95 ( 2 .70 ) ,其立位值大于卧位 1.3 6± 1.17( 3 .2 8)、0 .69± 0 .97( 2 .2 9) ;pH <4反流次数 (次 ) 17.85± 11.5 1( 3 6.78) ;反流持续≥ 5min次数 (次 )0 .3 2± 0 .3 5 ( 0 .90 ) ;最长反流持续时间 (min) 4 .4 2± 4 .0 7( 11.12 ) ;总积分 6.0 8± 3 .5 4 ( 11.90 )。 85例GERD患者上述各项指标均明显增高     

Control of Nocturnal Gastric Acidity: A Role for Low Dose Bedtime Ranitidine to Supplement Daily Omeprazole

In some patients, proton pump inhibitors do not abolish nocturnal gastric acidity and additional evening antisecretory medication may be required. In 16 subjects with chronic heartburn, 24-hr gastric and esophageal pH were measured at baseline and again after six days of 20 mg omeprazole alone at 08:00 hr followed by placebo, 75 mg ranitidine, or 20 mg omeprazole at 22:00 hr. Integrated acidity was calculated from the cumulative, time-weighted mean acid concentrations (derived from pH values for each second). Baseline integrated gastric acidity increased progressively over 24 hr, whereas integrated esophageal acidity increased only until 22:00 hr. Morning omeprazole nearly abolished 24-hr esophageal acidity and significantly decreased overall gastric acidity but did not abolish nocturnal gastric acidity. Adding evening ranitidine or omeprazole nearly eliminated the nocturnal increase in gastric acidity. Integrated acidity was more sensitive than time pH < 4 in assessing gastric and esophageal acidity as well as their inhibition by omeprazole and ranitidine. In conclusion, integrated acidity provides novel information regarding the synergy of omeprazole plus ranitidine. Adding low-dose ranitidine helps control nocturnal gastric acidity that can occur with conventional omeprazole administration. Although the heartburn patients in the present study had nocturnal gastric acidity without accompanying nocturnal esophageal acid reflux, other patients who do have nocturnal esophageal reflux might profit from addition of bedtime ranitidine or another gastric antisecretory agent.     

Cigarette smoking,gastric acidity and peptic ulceration

The influence of cigarette smoking on intragastric acidity was assessed in duodenal ulcer patients in symptomatic remission and in healthy volunteers in a retrospective study. Continuous 24-hr pH recordings in 150 nonsmokers and 174 smokers receiving placebo treatment were compared. Daytime intragastric acidity was higher in smokers with a median pH (interquartile range) of 1.56 (1.34–1.80) than in nonsmokers, who had a median pH of 1.70 (1.45–1.97) (P<0.001). There was no difference in 24-hr and nighttime median pH between the two groups. The small difference in daytime intragastric acidity in smokers and nonsmokers is unlikely to account for the increased prevalence of peptic ulcer disease in smokers. The analysis of smoking status in duodenal ulcer patients and healthy controls and males and females supports the general trend towards higher daytime acidity in smokers. Again, no differences in pH during the 24-hr or night period were found between the groups. The epidemiological and clinical correlation between smoking and duodenal ulcer disease is not adequately explained by increased intragastric acidity.     

SCD5‐induced oleic acid production reduces melanoma malignancy by intracellular retention of SPARC and cathepsin B

A proper balance between saturated and unsaturated fatty acids (FAs) is required for maintaining cell homeostasis. The increased demand of FAs to assemble the plasma membranes of continuously dividing cancer cells might unbalance this ratio and critically affect tumour outgrowth. We unveiled the role of the stearoyl‐CoA desaturase SCD5 in converting saturated FAs into mono‐unsaturated FAs during melanoma progression. SCD5 is down‐regulated in advanced melanoma and its restored expression significantly reduced melanoma malignancy, both in vitro and in vivo, through a mechanism governing the secretion of extracellular matrix proteins, such as secreted protein acidic and rich in cysteine (SPARC) and collagen IV and of their proteases, such as cathepsin B. Enforced expression of SCD5 or supplementation of its enzymatic product, oleic acid, reduced the intracellular pH (pHe > pHi) and, in turn, vesicular trafficking across plasma membranes as well as melanoma dissemination. This intracellular acidification appears also to depend on SCD5‐induced reduction of the C2 subunit of the vacuolar H⁺‐ATPase, a proton pump whose inhibition changes the secretion profile of cancer cells. Our data support a role for SCD5 and its enzymatic product, oleic acid, in protection against malignancy, offering an explanation for the beneficial Mediterranean diet. Furthermore, SCD5 appears to functionally connect tumour cells and the surrounding stroma toward modification of the tumour microenvironment, with consequences on tumour spread and resistance to treatment. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

Effects of omeprazole or anti-reflux surgery on lower oesophageal sphincter characteristics and oesophageal acid exposure over 10 years

Objective: To compare the effect of anti-reflux surgery (ARS) versus proton pump inhibitor therapy on lower oesophageal sphincter (LOS) function and oesophageal acid exposure in patients with chronic gastro-oesophageal reflux disease (GORD) over a decade of follow-up.

Material and methods: In this randomised, prospective, multicentre study we compared LOS pressure profiles, as well as oesophageal exposure to acid, at baseline and at 1 and 10 years after randomisation to either open ARS (n?=?137) or long-term treatment with omeprazole (OME) 20–60?mg daily (n?=?108).

Results: Median LOS resting pressure and abdominal length increased significantly and remained elevated in patients operated on with ARS, as opposed to those on OME. The proportion of total time (%) with oesophageal pH <4.0 decreased significantly in both the surgical and medical groups, and was significantly lower after 1 year in patients treated with ARS versus OME. After 10 years, oesophageal acid exposure was normalised in both groups, with no significant differences, and bilirubin exposure was within normal limits. After 10 years, patients with or without Barrett’s oesophagus did not differ in acid reflux control between the two treatment options.

Conclusions: Open ARS and OME were both effective in normalising acid reflux into the oesophagus even when studied over a period of 10 years. Anatomically and functionally the LOS was repaired durably by surgery, with increased resting pressure and abdominal length.     

胃食管反流病患者餐后近端胃酸分布及其与酸反流的关系

目的探讨胃食管反流病(GERD)患者餐后近端胃内酸分布及其与食管酸暴露的关系。方法应用三通道锑电极在下食管括约肌(LES)上缘近侧5cm、远侧5cm和远侧10cm处(LES-5cm,LES 5cm,LES 10cm),对受试者行空腹1h和餐后4h食管和胃内pH监测。计算食管酸暴露和胃内整合酸度(IA)。健康志愿者(HS)组和GERD组各10例。结果(1)HS组餐后LES 5cm处总IA有低于LES 10cm处的趋势,但GERD组未发现酸缓冲作用的部位差异。(2)餐后2h,HS组LES 5cm和LES 10cm处IA回升未超过基线;GERD组近端胃IA回升高于基线水平:LES 5cm:5.4(1.8~6.8)比较1.8(0.3~3.1)mmol/L.h(P<0.05);LES 10cm:5.6(2.4~7.6)比较2.3(0.8~3.1)mmol/L·h(P=0.05)。(3)两组食管酸暴露均主要发生在餐后2h,但GERD组显著高于HS组。食管酸暴露和胃内酸度无显著性相关关系。结论餐后近端胃酸分布异常以及胃酸分泌增高,可能部分地解释餐后GERD患者食管过度酸暴露。