Review article: urease, gastric ammonium/ammonia, and Helicobacter pylori — the past, the present, and recommendations for future research

The presence of ammonium in gastric contents was described in 1852; urease activity in the stomach was identified 70 years later. The discovery of gastric urease resulted in intense research activity to discover its origin, function, and relation to the gastric levels of ammonium and urea. Interest in urease waned in the 1960s as most pertinent questions appeared to have been addressed and there was strong evidence that gastric urease was not a property of the stomach but was of microbial origin. Identification of Helicobacter pylori as the source of urease in the stomach in the last decade has resulted in a rebirth of interest in gastric urease and its products.^1–15 There is little actual evidence to support a role for toxicity of ammonia in relation to H. pylori and the bulk of the evidence suggests that the products of urease activity are not toxic and may even be beneficial. The purpose of this review is to examine the older literature and to examine- new findings in the perspective of what is already known and to suggest areas remaining to be examined. We ask, ‘What is old, what is new, and what needs to be done?’     

改良第二掌背动脉皮瓣修复示中指中末节套脱伤

Objective To investigate the operative procedure and the clinical results of the modified reversed island flap based on the second dorsal metacarpal artery (SDMA) for repairing index or long finger degloving defects.Methods From May 2004 to January 2010, circumferential soft tissue defect in the middle and distal phalanx of the index or long fingers in 17 patients were repaired by the modified reversed island flaps based on SDMA.The dorsal digital nerve in the flap was coapted to the severed proper digital nerve.The area of the flaps ranged from 2.5 cm × 5.6 cm to 5.0 cm × 6.5 cm.The donor sites were closed by skin graft.Results Postoperatively blister and necrosis of the distal flap occurred in 2 cases which was cured by dressing change.All the other flaps survived uneventfully.Primary healing of the flaps and donor sites was achieved.All 17 patients were follow-up for 4 to 27 months with an average of 15.3 months.The flaps were pliable, full but not bulky.Two-point discrimination was 7 to 11 mm (mean 8.6 mm).Hand function as judged by the total active range of motion of the fingers was excellent in 8 fingers, good in 7 fingers and fair in 2 fingers.The satisfactory rate was 88.2%.Conclusion Modified SDMA reversed island flap transfer with dorsal digital nerve coaptation is an ideal procedure to repair index or long finger degloving injuries.The area of the harvested flap is large enough to cover the circumferential soft tissue defect in the middle and distal phalanx.The surgery is safe due to the reliable flap circulation.     

How does Helicobacter pylori cause duodenal ulcer disease: The bug, the host, or both?

Abstract Helicobacter pylori infection is the most common cause of duodenal ulcer disease, yet duodenal ulcer is an uncommon outcome of H. pylori infection. We reviewed the possible explanations such as differences in the host or in the strain of H. pylori. Host factors reviewed included genetic susceptibility to H. pylori infection and excess gastric acid secretion. The role of potential H. pylori virulence factors not present in all strains such as the cagA gene and the results of other molecular methods to identify disease-specific differences among isolates was also reviewed. Although cure of H. pylori infection resolves gastrin releasing peptide stimulated acid secretion there was no change in parietal cell mass. Twin studies have shown genetic differences in H. pylori susceptibility. There was no difference in the prevalence of the cagA gene between H. pylori infected asymptomatic volunteers and duodenal ulcer patients ( P = 1.0). DNA-DNA hybridization of whole genomic DNA in solution and cluster analysis of rep-PCR genomic DNA fingerprints suggest that isolates from patients with duodenal ulcer disease are different from those obtained from individuals with asymptomatic gastritis. Cluster analysis of the rep-PCR DNA fingerprints revealed two major groups of the strains; one set consisted of strains from patients with duodenal ulcer disease and the second cluster consisted largely of strains from individuals with asymptomatic gastritis. Recent molecular studies suggest that disease-specific cell lineages or strains may exist among H. pylori isolates leading to the various outcomes observed in patients with H. pylori infection.     

3H-1,2-二氢-1-吡里酮衍生物的合成

发现3 H-1,2-二氢-1-吡咯里嗪酮具有明显的抗炎镇痛作用。用Friedel-Crafts酰化和Dieckmann缩合等反应制备了该酮的一些衍生物,其中五个未见于文献报道。药理实验证明,这些化合物均有不同程度的抗炎镇痛作用。     

Twist、E-cadherin和β-catenin在肝细胞肝癌中的表达及其与预后的关系*

目的:探讨Twist、E-cadherin 和β-catenin 在肝细胞肝癌复发与转移中的作用及与预后的相关性。方法:以石蜡包埋组织切片,免疫组化SP法染色分别检测97例肝细胞肝癌,其中复发与转移组49例,非复发与转移组48例Twist、E-cadherin 和β-catenin 的表达情况。结果:复发、转移与性别、年龄无关（P=0.424,P=0.738）,与临床分期密切相关（P=0.000）。 复发与转移组Twist、β-catenin 表达高于无复发与转移组（P=0.000;P=0.000）,复发与转移组E-cadherin 表达低于无复发与转移组（P=0.027）。Twist,β-catenin 阳性组平均生存时间分别为（28.880 ± 3.285）、（ 31.477 ± 3.359）个月,中位生存时间分别为26、28个月,阴性组平均生存时间分别为（44.603 ± 3.521）、（ 42.009 ± 3.720）个月,中位生存时间分别49、45个月,Twist、β-catenin 阳性组生存期较阴性组缩短差别具有统计学意义（P=0.002,P=0.029）。 E-cadherin 阳性组平均生存时间为（44.514 ± 3.447）个月,中位生存时间为49个月,阴性组为（29.110 ± 3.581）个月,中位生存时间为25个月,E-cadherin 阳性组生存时间较阴性组延长有统计学意义（P=0.002）。 结论:Twist、β–catenin 过度表达,E-cadherin 表达缺失可能与HCC 复发转移、不良生存预后存在相关性。      

美国国家骨髓库20年回顾:成人无关供者造血干细胞移植

自1987年起,美国国家骨髓库(NMDP)提供了>30 000份URD-HCT,其中70%以上的受者是患有恶性血液病或获得性血液疾病的成人.在此期间发生很大变化,包括无偿捐献队伍的扩大、PBSCs采集、脐血库(UCB)的加入、HLA分型技术的进步、新药物的使用、低强度预处理(RIC)以及移植后免疫调节等.本文就过去20年NMDP成人受者HCT的数据及分析作一介绍.     

来比林镇痛复合液用于神经阻滞的临床研究

目的：探讨来比林（Aspegic)镇痛复合液用于神经阻滞的作用。方法：120例腰椎间盘突出症和颈椎病的患者随机分为四组。I组：对照组（30例）;Ⅱ组：来比林组（30例）;Ⅲ组：地塞米松组（30例）;Ⅳ组：来比林静滴组（30例）。Ⅰ－Ⅲ组患者均采用神经根或外周神经阻滞治疗,间隔3－4天治疗一次,一疗程4次。Ⅳ组患者用来比林静滴治疗,每天一次,7天为一疗程。各组治疗前后疼痛情况用VAS评估,并进行统计学处理。结果：（1）来比林组神经阻滞治疗后的镇痛效果明显优于对照组和来比林静滴组。（2）来比林组和地塞米松组神经阻滞治疗后镇痛效果无统计学差异。结论：来比林镇痛复合液用于神经阻滞治疗,镇痛效果优于单纯全身用药和常规局麻药镇痛复合液。来比林和地塞米松镇痛复合液比较,镇痛作用相似。     

Abnormalities of iron metabolism and erythropoiesis in vitamin E- deficient rabbits

Rabbits fed a vitamin E-deficient diet developed severe muscular dystrophy in 3-4 wk, but they did not become anemic. Nevertheless, reticulocyte counts increased in deficient rabbits (3.2%) compared to control rabbits (0.9%), and erythroid hyperplasia was evident in the bone marrow. Comparing deficient rabbits to controls, the plasma iron concentration was lower (134.4 versus 206.6 microgram/dl); the TIBC was higher (335.9 versus 228.3 microgram/dl); the whole blood protoporphyrin concentration was higher (131.6 versus 81.7 microgram/dl); and the total iron content was lower in spleen (71 versus 153 microgram), higher in skeletal muscle (4956 versus 3054 microgram), and unchanged in bone marrow, liver, and heart. Studies of iron absorption and excretion using 59Fe showed no abnormalities in deficient rabbits. There were abnormalities of ferrokinetics, however. The half-time of disappearance of 59Fe was shorter (100.6 versus 169.4 min), the plasma iron turnover was greater (1.25 versus 0.95 mg/dl blood/day), and the reappearance of 59Fe in circulating erythrocytes at day 9 was greater (77.2% versus 57.2%) in deficient rabbits. Anemia induced by phlebotomy accentuated the abnormal iron metabolism of deficient rabbits, and the animals were unable to correct the anemia. These findings show that vitamin E deficiency in rabbits causes abnormal erythropoiesis associated with abnormal iron metabolism and sequestration of iron in skeletal muscle.