MNNG诱发犬残胃粘膜癌前期病变组织中MG7—Ag表达的动态…

本实验在ＭＮＮＧ诱发犬胃粘膜癌前病变过程中，胃镜下定期粘膜活检。应用胃癌单克隆抗体ＭＧ７免疫经染色法及自动化图像分析仪，连续动态定量地监测犬残 癌前期病孪组织 ＭＧ７抗原物质（ＭＧ７－Ａｇ）的表达情况。实验结果表明，（１）慢性萎缩小胃炎、肠化生及异型增生的组织细胞内已具有胃癌的某些生物学特性。（２）胃癌前期病变的演变过程可能遵循由萎缩性胃炎肠化生异型增生的变化规律。（３）临床上，重度异型增生患者有     

中医药治疗胃癌前期病变的现状与展望

胃癌死亡率居于我国恶性肿瘤之首，有效地防治胃癌前期病变，阻断其向癌发展，是预防胃癌、减少其发病率的根本措施和手段，因此胃癌前期病变已成为学术界研究的重点。国外有文献报道‘”，浅表性胃炎中胃癌的危险性增加虽低于萎缩性胃炎，但显著高于正常胃粘膜，而且肠型和弥漫型胃癌的危险性均增高。比较而言，中、重度萎缩性胃炎肠型胃癌的危险性显著增高。萎缩性胃炎伴不完全型肠化生和（或）中、重度异型增生为真正的癌前病变已成为公认，胃粘膜发生癌变有一个演变过程即慢性胃炎～胃粘膜萎缩一肠化一异型增生一胃癌”’。目前西医对本…     

袁红霞教授用经方辨治慢性萎缩性胃炎癌前病变经验撷菁

正胃癌前病变是一个病理性概念,是指较易转变为胃癌组织的病理学变化,包括肠上皮化生(IM)和异型增生(Dys),是正常胃黏膜向胃癌转化过程中的一个重要阶段~[1]。慢性浅表性胃炎→慢性萎缩性胃炎→肠上皮化生→异型增生→胃癌的Correa级     

中医药辨证治疗胃癌前期病变临床观察

中医药辨证治疗胃癌前期病变临床观察张子理慢性萎缩性胃炎（ＣＡＧ）是常见而难治的消化道疾病。作者近年来采用中医药辨证施治结合活血化瘀、解毒抗癌、微观加药的方法治疗了ＣＡＧ合并中度以上异型增生（ＤＳ）或肠上皮化生（ＩＭ）的胃癌前期病变（ＰＣＬ）患者６８例...     

幽门螺杆菌感染、胃蛋白酶原和胃泌素-17与胃疾病的关系

幽门螺杆菌（ Helicobacter pylori, Hp ）感染与慢性胃炎、消化性溃疡以及低度恶性胃MALT淋巴瘤的发生密切相关．世界卫生组织已将其列为Ⅰ类致癌因子.根除Hp治疗能明显改善急性和慢性胃炎，降低消化性溃疡的复发，使低度恶性胃MALT淋巴瘤得到治愈，并可能终止胃癌的发生㈣。萎缩性胃炎是胃癌的主要癌前病变，在从慢性非萎缩性胃炎→萎缩性胃炎→肠化生→异型增生→肠型胃癌这一演变过程中，     

端粒酶在胃癌及癌前病变组织中的表达及其意义

目的：通过检测胃癌及癌前病变组织端粒酶的活性,探讨在这些病变演化中端粒酶活性表达的规律及其意义。方法：采用端粒酶TRAP－ELISA法定量检测33例胃癌、8例胃粘膜重度异型增生、5例轻度异型增生、 胃粘膜肠上皮化生、19例慢性浅表性胃炎组织端粒酶活性。结果：由慢性浅表性胃炎→胃粘膜肠上皮化生→轻度异型增生→重度异型增生→胃癌,端粒酶阳性率逐渐增高,分别为0％、42．9％、40．0％、75．0％、84．0％。端粒酶阳性率在胃癌及重度异型增生组明显高于其它各组（P＜0．005）。慢性浅表性胃炎与肠上皮化生及轻度异型增生组比较也有显著差异（P＜0．025）,而胃癌与重度异型增生组比较差异无显著性。结论：端粒酶在胃癌的发生中可能具有重要意义。追踪端粒酶阳性的胃癌前病变患者有利于早期发现胃癌。     

袁红霞教授运用经方治疗慢性萎缩性胃炎并癌前病变临证举隅

正慢性萎缩性胃炎(chronic atrophic gastritis,CAG)是消化系统常见的疾病,表现为胃黏膜上皮及腺体萎缩、黏膜变薄、黏膜肌层增厚,常伴有肠化生及异型增生,而"慢性胃炎→胃黏膜萎缩→肠化生→异型增生→胃癌"这一模式[1]已被广泛接受,2010年《WHO消化系统肿瘤病理学和遗传学》第4版[2]新分类中,将肠化生和异性增生视为胃癌的癌前病变(precancerous lesion of gastric cancer,PLGC)。     

死亡相关蛋白激酶基因高甲基化在胃癌形成过程中作用的初步研究

背景：DNA启动子区甲基化可导致肿瘤抑制基因表达沉默，在胃癌的发生、发展中发挥重要作用。目的：观察正常胃黏膜、慢性萎缩性胃炎伴肠化生、异型增生和早期胃癌组织中死亡相关蛋白激酶（DAPK）基因启动子区甲基化状态，探讨其与胃癌发生、发展的关系。方法：以甲基化特异性聚合酶链反应（MSP）检测20例正常胃黏膜、14例慢性萎缩性胃炎伴肠化生、27例异型增生和16例早期胃癌组织中DAPK基因启动子区甲基化状态．并分析其与患者临床病理特征的关系。结果：早期胃癌组织中DAPK基因启动子区甲基化率显著高于正常胃黏膜、慢性萎缩性胃炎伴肠化生和异型增生组织（43.8％对0％、7．1％和11．1％，P〈0．05），而后三者之间DAPK基因启动子区甲基化率无明显差异。DAPK基因启动子区甲基化与患者性别、年龄和病变部位均无关，与幽门螺杆菌（H.pylori）感染和血清癌胚抗原（CEA）水平显著相关（P〈0．05）。结论：DAPK基因启动子区高甲基化是胃癌发生的早期分子事件，在由慢性萎缩性胃炎伴肠化生和异型增生进展至早期胃癌的过程中起重要作用。     

胃粘膜肠化和异型增生作为胃癌前兆的意义

目的：探讨胃粘膜肠化和异型曾生与胃癌发生的关系及其意义。方法；对７２例胃癌５７例胃粘膜异型增生２５６例肠化生病例进行粘液组织化学，菜豆凝集素（ＰＨＡ）亲合组织化学及抗人胃癌单抗ＭＧⅡ免疫组织化学（ＡＢＣ法）研究，１５例正常胃粘膜作为对照，结果：Ⅲ型肠化在癌旁肠化及异型增生伴肠化的检出率均显著高萎缩性胃炎伴肠化（Ｐ均〈０．０１），ＰＨＡ受体及ＭＧⅡ抗原在正常胃粘膜无表达，而在胃癌高度表达。ＰＨＡ受体     

8种肿瘤相关抗原在活检胃粘膜病变组织中的表达

应用免疫组织化学方法观察了８种肿瘤相关抗原（ＭＧ７、ＭＧｄ１、ＭＣ３、ＣＥＡ、涎酸化糖蛋白、ＣＡ１９─９、ＰＳ─４和ＴＡＧ─７２）在１１０例胃癌、３２例异型增生，１７３例萎缩性胃炎和２０例大致正常胃粘膜活检组织中的表达，发现胃癌组８种肿瘤相关抗原染色的阳性率显著高于良性病变和正常对照组（Ｐ＜０．０１～０．００１）。异型增生组和萎缩性胃炎组８种肿瘤相关抗原阳性率均显著高于正常对照组（Ｐ＜０．０５～０．０１）。除ＭＣ３外，各抗原在胎儿胃或肠粘膜均有部分阳性。以上结果说明，检测胃粘膜组织中的上述８种抗原，对胃癌的诊断和高危人群的筛选可能有重要意义。     

胃溃疡大鼠胃粘膜血流量与泌酸变化的研究

用手术将十二指肠内容物持续胃内反流制成大鼠胃溃疡及经转流后的溃疡愈合模型进行研究。结果表明,溃疡组于胃窦小弯侧可见8.84±3.08(m~2)~(-3)的慢性溃疡形成,并显示胃粘膜血流量降低,G细胞密度、壁细胞数增加。溃疡愈合组经转流后大部分溃疡已愈合,G细胞密度、壁细胞数降低,粘膜血流量增加。本实验提示,泌酸细胞增多,泌酸量增加和胃粘膜缺血可能是溃疡形成的重要因素,增加胃粘膜的血液供应,降低胃酸分泌可促进溃疡愈合。     

Effect of gastric dysrhythmias on postcibal motor activity of the stomach

The effect of electrical dysrhythmias on the mechanical activity of the fed stomach was investigated in 5 conscious dogs implanted with Ag-AgCl electrodes and strain gauge force transducers. Each dog was fed 1 can of ALPO^® and electromechanical activities of the stomach were recorded for the next 120 min. The results show that intraarterial boluses of met-enkephalin (75 g/kg), PGE₂ (36 g/kg), and epinephrine (36 g/kg) induced episodes of antral dysrhythmias whereas saline (1 cc) did not. The postcibal antrat motility index for the test period was not altered following saline injection, but it was reduced by 61%, 70%, and 81% following the administration of met-enkephalin, epinephrine, and PGE₂, respectively (p<0.01 vs. baseline period). During periods of normal electrical rhythm, PGE₂ and epinephrine significantly reduced the antral motility index (2.07±0.93 and 3.24±0.79, respectively) vs. saline (7.92±0.44) (p<0.05 for both drugs) whereas met-enkephalin (4.98±0.56) did not. In contrast, during episodes of dysrhythmia, met-enkephalin significantly depressed antral motility (1.70±0.74) (p<0.05 vs. periods with normal electrical rhythm) whereas neither epinephrine nor PGE₂ caused a further reduction in antral motility from what was seen during periods of normal electrical rhythm (1.84±0.72 and 1.34±0.37, respectively). We thus conclude that intraarterial administration of met-enkephalin, PGE₂, or epinephrine induce gastric dysrhythmias postcibally and depress antral contractile activity. The relaxatory effect of met-enkephalin on antral contractions is primarily due to its dysrhythmic effect whereas PGE₂ and epinephrine inhibit antral motility even when the electrical rhythm is undisturbed.This work was supported in part by the USPHS, NIH grants AM26428, AM07198, and AM34988 and the Mayo Foundation.     

Gastric Ulcer and Risk of Cancer

Abstract In 1976, 121 patients with benign gastric ulcer and 13 with gastric carcinoma were diagnosed in our department by endoscopy, cytology and directed biopsies. At a 5-year follow-up, 78 of these patients were re-examined with endoscopy and biopsies. None had developed gastric cancer during the observation time. Of the 78 patients who underwent endoscopy, 16 had gastric ulcer, 2 duodenal ulcer and 27 atrophic gastritis, including 3 with moderate dysplasia of the gastric mucosa. The patients with ulcer had remarkably few symptoms. Only few data are available concerning the postulated link between gastric ulcer disease and gastric malignancy. The cancer-ex-ulcere hypothesis seems to be a medical dogma. However, well planned prospective studies with endoscopic follow-up of gastric ulcers are needed to elucidate the question properly     

Abnormal gastric myoelectrical activity and delayed gastric emptying in patients with symptoms suggestive of gastroparesis

Gastric myoelectrical activity modulates gastric motor activity. Abnormalities in gastric myoelectrical activity may be associated with gastric motility disorders. The aim of this study was to investigate the correlation of gastric myoelectrical activity with gastric emptying in symptomatic patients with and without gastroparesis. Ninety-seven patients with symptoms suggestive of gastroparesis participated in the study. Gastric myoelectrical activity was recorded using surface electrogastrography. The electrogastrogram (EGG) was recorded for 30 min in the fasting state and for 120 min after a solid test meal. Gastric emptying of the solid meal was simultaneously monitored for 120 min. Patients with delayed gastric emptying showed a significantly lower percentage of normal gastric slow waves (P<0.03) and a significantly reduced increase of the dominant power in the postprandial EGG (P<0.02). Postprandial EGG parameters were found to be able to predict delayed emptying of the stomach. Postprandial gastric dysrhythmia predicts delayed gastric emptying with an accuracy of 78%, while the abnormality in postprandial EGG power predicts delayed gastric emptying with an accuracy of 75%. All patients with abnormalities in both the rhythmicity and the power had delayed gastric emptying. Patients with delayed gastric emptying have a lower percentage of normal gastric slow waves in the EGG and a lower postprandial increase in the dominant power. Abnormalities in the postprandial EGG seem to be able to predict delayed emptying of the stomach. However, a normal EGG does not seem to guarantee normal emptying of the stomach.     

Is There a One-to-One Correlation Between Gastric Emptying of Liquids and Gastric Myoelectrical or Motor Activity in Dogs?

The aim of this study was to investigate the correlation of gastric emptying with gastric myoelectrical activity recorded from internal serosal electrodes and with gastric motility measured from strain gauges. The study was performed in eight healthy dogs chronically implanted with four pairs of electrodes and two strain gauges on the gastric serosa and equipped with a duodenal fistula for the assessment of gastric emptying. Each dog was fed four liquid test meals on four separate days with identical calories (320 kcal) and volume (473 ml). A correlation was found between gastric emptying and the energy of contraction in the frequency band of 3.75–7.50 cycles/min during the first 30 min after the meal (r = 0.46, P < 0.05). While none of the parameters of gastric myoelectrical activity was correlated with gastric emptying, two major parameters, percentage of regular gastric slow waves and percentage of slow-wave coupling, were found to be associated with delayed gastric emptying. A significant correlation was found between the frequency of gastric slow waves and that of the contractions in both fasting (r = 0.83, P < 0.001) and fed state (r = 0.70, P < 0.001 at 30 min, r = 0.86, P < 0.001 at 60 min). It was concluded that gastric emptying is correlated with the strength of gastric contractions in a frequency range identical to that of the gastric slow waves, and there is no one-to-one correlation between gastric emptying of liquids and any parameters of gastric myoelectrical activity. However, major parameters of gastric myoelectrical activity are associated with gastric emptying.     

Effects of intragastric and intravenous glucose on restraint model of stress ulceration

Intragastric glucose prevents acute stress-induced gastric mucosal injury in the restrained rat. Because increased gastric contractions contribute to mucosal injury in this model and because parenteral glucose infusions have been shown to suppress gastric contractility, we hypothesized that centrally mediated responses to hyperglycemia might contribute to the cytoprotective effect of intragastric glucose. We compared intragastric and intravenous 25% glucose with saline infusions during cold restraint and measured their impact on gastric contractility), acidity, and mucin concentration. We found that both intravenous and intragastric glucose infusions increased serum glucose to over 500 mg/dl after 4 hr of stress. Intragastric glucose increased residual volume and gastric pH, as well as decreased gastric mucosal injury, but intravenous glucose had no effects on gastric function. We found that none of the potentially protective effects of intragastric glucose are mediated by central responses to hyperglycemia, and likewise that intravenous glucose has no effect on gastric mucosal injury.Presented in poster format at the 91st Meeting of the American Gastroenterological Association, May 12, 1990, San Antonio, Texas. Supported by Veterans Affairs Medical Research funds and by Dr. Kleiman-Wexler's BSG NIH.     

Gastric lesions secondary to long-distance running

Gastrointestinal disorders have been reported during long- distance running. The purpose of this study was to evaluate the effects of prolonged exercise on the upper digestive tract. Seven subjects were submitted to a standard endoscopic examination of the upper digestive tract before and after long- distance running (range 18– 50 km). Mucosal biopsy specimens were taken during all endoscopies. After running, all runners had histologically pathological features in the stomach. Vascular lesions were present in the chorion in six subjects after running, with the intensity of the lesions ranging from congestion to hemorrhage. Postexercise histological examination also showed a decrease in mucosal secretion. These lesions secondary to prolonged exercise indicate the presence of hemodynamic perturbations in the upper digestive tract.     

Gastric Electrical Stimulation Does Not Significantly Affect Canine Gastric Acid Secretion and 24-Hour Gastric pH

Gastric electrical stimulation (GES) was shown to improve symptoms in patients with gastroparesis. However, the underlying mechanisms remain unclear. This study assessed the influence of various patterns of GES on fasting and postprandial gastric acid secretion and 24-hr gastric pH. Eight healthy dogs were studied and we found that in the fasting state, low-frequency, long-pulse (6/12-cpm, 375-msec, 4-mA) GES at the proximal stomach significantly inhibited the secretion of gastric juice (P < 0.05). No such effect was observed during GES (6/12 cpm) at the distal stomach. In the postprandial period, low-frequency, long-pulse GES at both proximal and distal sites and at both frequencies did not significantly affect gastric acid secretion. High-frequency, short-pulse GES, investigated for obesity (21 Hz, 8 mA, and 250 microsec, with 2 secs on, 3 sec off), at the proximal and distal stomach did not significantly affect the 24-hr gastric pH profile. In conclusion, GES with various stimulation parameters, and at various sites, has little effect on gastric acid secretion. The clinical effects induced by GES at these parameters may not be related to their effect on gastric acid homeostasis.