胃癌高发区IL-1基因多态性、H.pylori感染和胃黏膜萎缩关系的研究

目的:分析胃癌高发区普通人群的IL-1B-511基因多态性、H.pylori感染率及胃粘膜萎缩的血清学指标(血清胃蛋白酶原I(pepsinogenI,PGI)、胃蛋白酶原I/胃蛋白酶原II的比值(PGI/PGII)和胃泌素(gastrin)浓度,探讨IL-1B-511基因多态性对幽门螺旋杆菌(Helicobacterpylori,Hp)感染后胃黏膜萎缩的影响。以期进一步明确IL-1B基因多态性与胃黏膜萎缩关系,IL-1B基因多态性增加胃癌发病危险性的可能机理。方法:采用PCR-限制性长度片段多态性(RFLP)分析法检测胃癌高发区陕西省普通人群169例的基因型。采用酶联免疫吸附法(ELISA)检测上述人群的Hp感染率、PGI、PGII和Gastrin的浓度。结果:在胃癌高发区,Hp阳性者PGI/PGII显著低于Hp阴性者(P<0.01),但1L-1B-511T/T基因型人群PGI/PGII与1L-1B-511C/T和C/C基因型者无显著差异(P值均>0.05)。血清胃泌素浓度与IL-1B-511的基因型没有明确的关系(P>0.05)。结论:在胃癌高发区,Hp感染可能在20~23岁年龄段已是胃黏膜萎缩的危险因素,1L-1B-511T/T基因型者可能增加Hp后胃黏膜萎缩形成的危险性;胃黏膜萎缩的发生、发展除与Hp感染和遗传有关外,环境因素可能起相当重要的作用。     

脑氧与葡萄糖摄取量变化对重型颅脑损伤患者预后影响的研究

目的探讨重型颅脑损伤患者脑氧摄取量(CEO2)及脑葡萄糖摄取量(CEG)的变化规律及对预后的影响。方法选择同期存活超过7天的重型颅脑损伤患者62例,在入院或手术后12h内、第3天、第7天分别同步在颈内静脉球部及股动脉抽取血样进行血气分析及血糖检查,计算出CEO2及CEG,对存活病人及死亡病人进行对比分析。结果存活47例,死亡15例。在伤后12h内存活组及死亡组的CEO2、CEG差异无显著性(P均>0.05),第3天起出现进行性下降;第7天死亡组病人的CEO2和CEG均显著低于存活组(P均<0.01)。结论对重型颅脑损伤患者实施动态监测CEO2及CEG,对正确掌握病情、估计预后和指导抢救治疗具有重要意义。     

胃癌的腹腔镜治疗

胃癌是常见的消化道恶性肿瘤之一,在我国早期胃癌所占比例很小,约90%的病例确诊时已为进展期胃癌,但随着胃镜、超声、超声内镜等诊疗技术的发展,早期胃癌的检出率逐渐增多[1].近年来有关胃癌,尤其是早期胃癌的微创治疗进展很快.腹腔镜技术用于胃癌手术始于20世纪90年代,Ohgami等于1994年首先报道了腹腔镜的局部胃切除治疗早期胃癌.     

群体性铅中毒事故一起

2006年6月,我省某铅厂一批工人相继出现腹痛、乏力、食欲缺乏、关节痛等症状.我们对该厂进行了职业卫生学调查,现报告如下.     

葡糖胺聚糖对糖尿病肾病血浆内皮素及血清一氧化氮的作用

目的探讨葡糖胺聚糖（GAGs）对糖尿病肾病（DN）血浆内皮素（ET）及血清一氧化氮（NO）的作用。方法60例24h尿白蛋白排泄率（UAER）30～300mgDN患者，随机分为对照组和GAGs组。所检测指标包括UAER、ET、NO等。采用放射免疫分析法测定ET；采用酶法高密度测定（ELASAI）NO。结果对照组UAER治疗前后变化不明显（P〉0．05）；GAGs组治疗前后UAER比较，差异有统计学意义（P〈0．01）。治疗3个月后UAER下降26、31％。对照组ET和NO治疗前后变化不明显（P〉0．05）；GAGs组治疗后较治疗前ET下降5．91％，NO升高6．46％，差异有统计学意义（P〈0．01）。UAER与ET呈正相关（r=0．8391，P〈0．01）；与NO呈负相关（r=-0．8725，P〈0．01）。结论GAGs能够减少微量白蛋白尿期2型DN患者的UAER，升高血清NO，降低ET。     

兰索拉唑口服治疗消化性溃疡急性大出血

目的：观察兰索拉唑口服治疗消化性溃疡急性大出血的疗效。方法：３０例消化性溃疡急性大出血病人（男性２４例，女性６例，年龄４８±ｓ１６ａ）予兰索拉唑３０ｍｇ，ｐｏ，ｑｄ×（１０～１４ｄ），并酌情输液、输血。结果：兰索拉唑３０例（１００％）止血成功，住院天数为１４．１±２．１ｄ；输血量为０。未见药物不良反应。结论：兰索拉唑口服对消化性溃疡急性大出血有良好疗效。     

吻合血管的腓骨瓣移植一期重建双侧下颌骨

目的探讨下颌骨巨大肿瘤截骨切除后应用游离腓骨复合组织瓣一期重建双侧下颌骨方法和疗效。方法2000年7月至2002年10月,分别对波及双侧下颌骨的4例巨大成釉细胞瘤、2例牙龈癌施行截骨切除,手术造成跨中线的双侧下颌骨巨大缺损。根据下颌骨缺损的特点,以腓动静脉为血管蒂切取腓骨肌(皮)瓣,经截骨塑形后,用微形钛板将移植骨与双侧下颌骨残端坚固内固定,腓动、静脉与颈部小血管吻合,形成血管化腓骨复合组织瓣一期重建双侧下颌骨。结果6例移植腓骨复合组织瓣全部成活。随访6个月-2年,面下部外形恢复良好,移植腓骨与上颌骨相对位置正常,接受活动义齿修复后咬合关系和咀嚼功能均较满意。结论腓骨复合组织瓣节段性的骨膜供血和骨髓滋养动脉的双重供血特点十分适合塑造成下颌骨的弓状形态,是修复下颌骨巨大肿瘤导致的跨中线双侧下颌骨巨大缺损的理想材料。     

Thrombin induces expression of cytokine-induced SH2 protein (CIS) in rat brain astrocytes: involvement of phospholipase A2, cyclooxygenase, and lipoxygenase

Previously we have reported that thrombin induces inflammatory mediators in brain glial cells (Ryu et al. 2000. J Biol Chem 275:29955). In the present study, we found that thrombin induced a negative regulator of a cytokine signaling molecule, cytokine-induced SH2 protein (CIS), in rat brain astrocytes. In response to thrombin, CIS expression was increased at both the mRNA and protein levels. Although STAT5 is known to regulate CIS expression, thrombin did not activate STAT5, and inhibitors of JAK2 (AG490) and JAK3 (WHI-P97 and WHI-P154) had little effect on thrombin-induced CIS expression. In contrast, cytosolic phospholipase A(2) (cPLA(2)), cyclooxygenase (COX), and lipoxygenase (LO) play a role in CIS expression, since inhibitors of cPLA(2), cyclooxygenase (COX), and LO significantly reduced CIS expression. Reactive oxygen species (ROS) scavengers (N-acetyl-cysteine [NAC] and trolox) reduced thrombin-induced CIS expression, and inhibitors of COX and LO reduced ROS produced by thrombin. Furthermore, prostaglandin E(2) (PGE(2)) and leukotriene B(4) (LTB(4)), products of COX and LO, respectively, potentiated thrombin-induced CIS expression, indicating that ROS, and PGE(2) and LTB(4) generated by COX and LO, mediate CIS expression. Since interferon-gamma (IFN-gamma)-induced GAS-luciferase activity and tyrosine phosphorylation of STAT1 and STAT3 were lower in CIS-transfected cells compared to control vector-transfected cells, CIS could have anti-inflammatory activity. These data suggest that thrombin-stimulation of ROS and prostaglandin and leukotriene production via the cPLA(2), COX and LO pathways results in CIS expression. More importantly, CIS expression may be a negative feedback mechanism that prevents prolonged inflammatory responses.     

严重真菌性角膜炎患者就诊史调查分析

目的　分析真菌性角膜炎延误诊治的原因。方法　对 2 0 0 0年 1～ 12月山东地区 6 9例(6 9只眼 )因严重真菌性角膜炎行穿透性角膜移植术 (penetratingkeratoplasty ,PKP)或眼球摘除术患者的完整资料进行回顾性分析 ,调查内容包括发病原因、就诊时间、检查经过、诊断及治疗情况等 ,分析延误诊治的可能原因。结果　 6 3例行PKP ,6例行眼球摘除术。其中 5 2例角膜植片直径 >8 0mm。农民占就诊患者的 93%。患者就诊的基本程序为村卫生诊所、乡镇医院、县医院及市级以上医院。平均就诊时间为 2 2 9d。 5 4例 (78% )患者曾到县级医院就诊 ,确诊率为 2 4 % ;其中经角膜刮片检查 12例(2 2 % ) ,阳性率为 5 0 %。 30例在市级以上医院就诊 ,确诊率为 6 3% ;其中角膜刮片检查 2 2例 (73% ) ,阳性率为 73%。 35例 (46 % )术前应用抗真菌药物治疗 ,主要为氟康唑。结论　忽视基本诊断技术、缺乏有效眼科抗真菌药物和供体角膜材料、缺少角膜病专业医师是目前真菌性角膜炎延误诊治的主要原因。     

Changes in thyrotropin receptor antibody after subtotal thyroidectomy in Graves' disease: comparison with the degree of lymphocytic infiltration in the thyroid

To evaluate changes in TSH receptor antibody after surgery in Graves' disease and its relationship with the degree of lymphocytic infiltration, serial serum levels of TSH receptor antibody were measured before and after the subtotal thyroidectomy in 50 patients with Graves' disease. In 22 (44%) out of 50 patients, thyrotropin binding inhibitor immunoglobulin (TBII) levels gradually decreased and disappeared completely within 12 months after surgery (TBII disappearing group). Twenty-eight (56%) patients showed persistent TBII activity and their levels were not changed until 12 months after surgery (TBII persistent group). The changes of thyroid stimulating antibody (TSab) levels were very similar to those of TBII in both groups. The thyroidal lymphocytic infiltration was more prominent in the TBII disappearing group. The degree of the decrease of TBII levels after surgery correlated with the grade of thyroidal lymphocytic infiltration. There was no significant difference of TSH receptor antibody (both TBII and TSab) levels between the thyroid and peripheral venous blood. These data suggest that the persistence or disappearance of TSH receptor antibody after surgery may reflect the difference between patients in whom the thyroid is the major site of TSH receptor antibody and those in whom additional sites of TSH receptor antibody synthesis exist.