Helicobacter pylori and gastric mucin expression: A systematic review and meta-analysis

AIM: To investigate the relationship between Helicobacter pylori(H. pylori) and mucin expression in gastric mucosa.METHODS: English Medical literature searches were conducted for gastric mucin expression in H. pylori infected people vs uninfected people. Searches wereperformed up to December 31 th 2014,using MEDLINE,Pub Med,EMBASE,Scopus,and CENTRAL. Studies comparing mucin expression in the gastric mucosa in patients positive and negative for H. pylori infection,were included. Meta-analysis was performed by using Comprehensive meta-analysis software(Version 3,Biostat Inc.,Englewood,NJ,United States). Pooled odds ratios(ORs) and 95% confidence intervals(CIs) were calculated compared mucin expression in individual studies by using the random effects model. Heterogeneity between studies was evaluated using the Cochran Q-test,and it was considered to be present if the Q-test P value was less than 0.10. I2 statistic was used to measure the proportion of inconsistency in individual studies,with I2 > 50% representing substantial heterogeneity. We also calculated a potential publication bias.RESULTS: Eleven studies,which represent 53 substudies of 15 different kinds of mucin expression,were selected according to the inclusion criteria. Every kind of mucin has been considered as one study. When a specific mucin has been studied in more than one paper,we combined the results in a nested metaanalysis of this particular mucin: MUC2,MUC6,STn,Paradoxical con A,Tn,T,Type 1 chain mucin,Le A,SLe A,Le B,AB-PAS,MUC1,and MUC5 AC. The odds ratio of mucin expression in random analysis was 2.33,95%CI: 1.230-4.411,P = 0.009,higher expression in H. pylori infected patients. Odds ratio for mucin expression in H. pylori positive patients was higher for MUC6(9.244,95%CI: 1.567-54.515,P = 0.014),and significantly lower for MUC5AC(0.447,95%CI: 0.211-0.949,P = 0.036). Thus,H. pylori infection may increase MUC6 expression and decrease MUC5 AC expression by 924% and 52%,respectively.CONCLUSION: H. pylori inhibits MUC5 AC expression in the gastric epithelium,and facilitates colonization. In contrast,increased MUC6 expression may help inhibiting colonization,using MUC6 antibiotics properties.

Alterations in gastric mucin synthesis by Helicobacter pylori

INTRODUCTIONHelicobacter pylori is recognized as a cause of chronicactive gastritis,gastric and duodenal ulcers,and gastriccancer,though the mechanisms of pathogenesis for H.pylori-associated diseases are not yet well understood.The ecological niche to which H.pylori is well-adapted

Cytosolic phospholipase A2 S-nitrosylation in ghrelin protection against detrimental effect of ethanol cytotoxicity on gastric mucin synthesis ——Ghrelin in gastric mucosal protection

Ghrelin, a peptide hormone produced mainly in the stomach, has emerged recently as an important regulator of nitric oxide synthase (NOS) and cyclooxygenase (COX) enzyme systems, the products of which play direct cytoprotective function in the maintenance of gastric mucosal integrity. In this study, using gastric mucosal cells, we report on the role of ghrelin in countering the cytotoxic effect of ethanol on mucin synthesis. We show that the countering effect of ghrelin on mucin synthesis was associated with the increase in NO and PGE2 production, and characterized by a marked up-regulation in cytosolic phospholipase A2 (cPLA2) activity. The ghrelin-induced up-regulation in mucin synthesis, like that of cPLA2 activity, was subject to suppression by Src inhibitor, PP2 and ERK inhibitor, PD98059, as well as ascorbate. Moreover, the loss in countering effect of ghrelin on the ethanol cytotoxicity and mucin synthesis was attained with cNOS inhibitor, L-NAME as well as COX-1 inhibitor SC-560. The effect of L-NAME was reflected in the inhibition of ghrelin-induced mucosal cell capacity for NO production, cPLA2 S-nitrosylation and PGE2 generation, whereas COX-1 inhibitor caused only the inhibition in PGE2 generation. Our findings suggest that the activation of gastric mucosal cPLA2 through cNOS-induced S-nitrosylation plays an essential role in the countering effect of ghrelin on the disturbances in gastric mucin synthesis caused by ethanol cytotoxicity.

Clinicopathological and prognostic differences between mucinous gastric carcinoma and signet-ring cell carcinoma

Objective： To analyze the differences in clinicopathologic characteristics and prognosis between mucinous gastric carcinoma （MGC） and signet-ring cell carcinoma （SRCC）. Methods： Clinicopathologic and prognostic data of 1,637 patients with histologically confirmed MGC or SRCC who received surgical operations in the Department of Gastroenterological Surgery, Beijing Cancer Hospital between December 2004 and December 2009 were retrospectively collected and analyzed. The clinicopathological features were analyzed statistically using Z2 test. Survival was analyzed using the Kaplan- Meier method and multivariate analysis of Cox proportional hazards regression model （backward, stepwise）. Results： A total of 181 patients with gastric cancer （74 MGC, 107 SRCC） were included. MGC, when compared with SRCC, was featured by senile patients, stage III and I~, upper third stomach, large tumor size, positive lymph node metastasis, and positive lymphatic vascular invasion （P〈0.05）. The overall 5-year survival rate showed no difference between the two groups （48.8% vs. 44.8%, P〉0.05）. However, the survival rate for MGC patients was significant lower than that for SRCC patients when compared among the age 〈60 years, negative distant metastasis, and tumor localized at upper third stomach （P〈0.05）. Multivariate Cox proportional hazards models revealed that distant metastasis was a significant independent prognostic indicator in MGC group, and lymph node metastasis and distant metastasis was significant independent prognostic indicators in SRCC group. Conclusions： While compared with SRCC, MGC is associated with a more aggressive tumor biologic behavior. There is no statistically significant difference in distant metastasis, an independent prognostic indicator for both MGC and SRCC, which might be the reason for no significant difference of the overall survival rate between the patients with MGC and SRCC.

Combination of endoscopic submucosal dissection and laparoscopic sentinel lymph node dissection in early mucinous gastric cancer:Role of lymph node metastasis

BACKGROUND Recent evidence showed that combining endoscopic submucosal dissection(ESD)and laparoscopic sentinel lymph node dissection may avoid unnecessary gastrectomy in treating early mucinous gastric cancer(EMGC)patients with risks of positive lymph node metastasis(pLNM).AIM To explore the predictive factors for pLNM in EMGC,and to optimize the clinical application of combing ESD and sentinel lymph node dissection in a proper subgroup of patients with EMGC.METHODS Thirty-one patients with EMGC who had undergone gastrectomy with lymph node dissection were consecutively enrolled from January 1988 to December 2016.Univariate and multivariate logistic regression analyses were used to estimate the association between the rates of pLNM and clinicopathological factors,providing odds ratio(OR)with 95%confidence interval.And the association between the number of predictors and the pLNM rate was also investigated.RESULTS Depth of invasion(OR=7.342,1.127-33.256,P=0.039),tumor diameter(OR=9.158,1.348-29.133,P=0.044),and lymphatic vessel involvement(OR=27.749,1.821-33.143,P=0.019)turned out to be significant and might be the independent risk factors for predicating pLNM in the multivariate analysis.For patients with 1,2,and 3 risk factors,the pLNM rates were 9.1%,33.3%,and 75.0%,respectively.pLNM was not detected in seven patients without any of these risk factors.CONCLUSION ESD might serve as a safe and sufficient treatment for intramucosal EMGC if tumor size≤2 cm,and when lymphatic vessel involvement is absent by postoperative histological examination.Combining ESD and sentinel lymph node dissection could be recommended as a safe and effective treatment for EMGC patients with a potential risk of pLNM.

Mucin phenotype of gastric cancer and clinicopathology of gastric-type differentiated adenocarcinoma

Differentiated adenocarcinoma of the stomach is classified into gastric or intestinal phenotypes based on mucus expression. Recent advances in mucin histochemistry and immunohistochemistry have highlighted the importance of such a distinction, and it is important clinically to distinguish between gastricand intestinal-type differentiated adenocarcinoma. However, a clinical and pathological diagnosis of this type is often difficult in early gastric cancer because of histological similarities between a hyperplastic epithelium and lowgrade atypia. Furthermore, determining tumor margins is often difficult, even with extensive preoperative examination. It is therefore critical to consider these diagnostic difficulties and different biological behaviors with high malignant potential when treating patients with gastric-type differentiated adenocarcinoma.

Relationship between clinicopathological features and mucin phenotypes of advanced gastric adenocarcinoma

AIM: To investigate a relationship between the clinicopathological features and mucin phenotypes in advanced gastric adenocarcinoma (AGA). METHODS: Immunohistochemical staining was performed to determine the mucin phenotypes in 38 patients with differentiated adenocarcinomas (DACs), 9 with signet-ring cell carcinomas (SIGs), and 48 with other diffuse-type adenocarcinomas (non-SIGs) of AGA. The mucin phenotypes were classified into 4 types: gastric (G), gastrointestinal (GI), intestinal, and unclassified. RESULTS: The G-related mucin phenotypes were highly expressed in all the histological subtypes of AGA. The expression of the GI phenotype in SIG patients was lower than that in DAC patients (P = 0.02), and this phenotype was observed in 56% of the non-SIG patients in the intramucosal layer. Among non-SIG cases, the expression of the GI phenotype was significantly higherin patients with extended adenocarcinomas and those with positive rates of lymph node metastasis. There was no difference between the expressions of the G and other GI phenotypes factors. Among DAC and non-SIG patients, there were no differences between the survival rates of the corresponding patient groups. CONCLUSION: The GI phenotype might possess more invasive characteristics than the G phenotype in nonSIG. Neither of the phenotypes indicated a poor prognosis of DAC and non-SIG.

Oxyntic gland adenoma endoscopically mimicking a gastric neuroendocrine tumor: A case report

Gastric adenocarcinoma is one of the most common malignancies worldwide.Histochemical and immunohistologic analyses classify the phenotypes of gastric adenocarcinoma into several groups based on the variable clinical and pathologic features.A new and rare variant of gastric adenocarcinoma with chief cell differentiation(GA-CCD)has recently been recognized.Studies reporting the distinct clinicopathologic characteristics proposed the term oxyntic gland polyp/adenoma because of the benign nature of the GACCD.Typically,GA-CCD is a solitary mucosal lesion that develops either in the gastric cardia or fundus.Histologically,this lesion is characterized by tightly clustered glands and anastomosing cords of chief cells.Immunohistochemically,GA-CCD is diffusely positive for mucin(MUC)6 and negative for MUC2and MUC5AC.However,other gastric tumors such as a gastric neuroendocrine tumor or fundic gland polyp have been difficult to exclude.Because GA-CCD tends to be endoscopically misdiagnosed as a neuroendocrine tumor or fundic gland polyp,comprehensive assessment and observation by an endoscopist are strongly recommended.Herein,we report a rare case of oxyntic gland adenoma endoscopically mimicking a gastric neuroendocrine tumor that was successfully removed by endoscopic mucosal resection.

Phagocytosis(cannibalism) of apoptotic neutrophils by tumor cells in gastric micropapillary carcinomas

AIM:To identify those with a micropapillary pattern,ascertain relative frequency and document clinicopathological characteristics by reviewing gastric carcinomas.METHODS:One hundred and fifty-one patients diagnosed with gastric cancer who underwent gastrectomy were retrospectively studied and the presence of a regional invasive micropapillary component was evaluated by light microscopy.All available hematoxylin-eosin(HE)-stained slides were histologically reviewed and 5 tumors were selected as putative micropapillary carcinoma when cancer cell clusters without a vascular core within empty lymphatic-like space comprised at least5%of the tumor.Tumor tissues from these 5 invasive gastric carcinomas were immunostained using an antimucin 1(MUC1)antibody(clone MA695)to detect the characteristic inside-out pattern and with D2-40antibody to determine the presence of intratumoral lymph vessels.Detection of intraepithelial neutrophil apoptosis was evaluated in consecutive histological tissue sections by three independent methods,namely light microscopy with HE staining,the conventional terminal deoxynucleotidyl transferase-mediated d UTP-biotin nick end-labeling(TUNEL)method and immunohistochemistry for activated caspase-3(clone C92-605).RESULTS:Among 151 gastric cancers resected for cure,5(3.3%)were adenocarcinomas with a micropapillary component.Four of the patients died of disease from 6 to 23 mo and one patient was alive with metastases at 9 mo.All patients had advanced-stage cancer(≥p T2)and lymph node metastasis.Positive MUC1 immunostaining on the stroma-facing surface(inside-out pattern)of the carcinomatous cluster cells,together with negative immunostaining for D2-40 in the cells limiting lymphatic-like spaces,confirmed the true micropapillary pattern in these gastric neoplasms.In all five cases,several micropapillae were infiltrated by neutrophils.HE staining,TUNEL assay and immunostaining for caspase-3 demonstrated apoptoticneutrophils within cytoplasmic vacuoles of tumor cells.These data suggest phagocytosis(cannibalism)of apoptotic neutrophils by micropapillary tumor cells.Tumor cell cannibalism is usually found in aggressive tumors with anaplastic morphology.Our data extend these observations to gastric micropapillary carcinoma:a tumor histotype analogously characterized by aggressive behavior and poor prognosis.The results are of interest because they raise the intriguing possibility that neutrophil cannibalism by tumor cells may be one of the mechanisms favoring tumor growth in gastric micropapillary carcinomas.CONCLUSION:This is the first study showing phagocytosis(cannibalism)of apoptotic neutrophils by tumor cells in gastric micropapillary carcinomas.

艾灸“足三里”对慢性萎缩性胃炎模型大鼠胃动力及胃黏膜黏蛋白表达的影响

目的:观察艾灸“足三里”对CAG模型大鼠胃动力相关指标胃窦运动指数、胃排空率及胃黏膜MUC1、MUC5AC和MUC6表达的影响。方法:健康SD大鼠随机分为空白组10只、造模组120只。以复合病因法复制CAG大鼠模型,造模成功后造模组随机分为模型组、药物组和艾灸组,又按治疗时间分为1、2、3和4周4个时相,每组10只。空白组和模型组不予治疗,艾灸组予温和灸“足三里”,每次30 min, 1次/d,药物组予替普瑞酮溶液13.5 mg/kg灌服,1次/d,共1个月。胃动力检测:按时相用彩色多普勒超声诊断仪测量大鼠胃窦舒张时面积、胃窦收缩时面积及3 min内胃窦收缩的总次数以计算胃窦运动指数,然后灌胃30 min后处死检测胃排空率。胃黏膜黏蛋白检测:大鼠按时相处死取材,分别用免疫组化法和免疫印迹法检测MUC1、MUC5AC及MUC6表达范围和相对表达量。结果:胃动力结果显示:与空白组比较,模型组大鼠胃窦运动指数及胃排空率均明显下调,差异具有统计学意义(P<0.01或P<0.05);与同时相模型组比较,药物组和艾灸组的胃窦运动指数上调在2周、3周和4周3个时相差异具有统计学意义(P<0.05);与同时相药物组比较,艾灸组的胃窦运动指数上调在2周、3周和4周3个时相差异有统计学意义(P<0.05);免疫组化结果显示:与空白组比较,模型组大鼠MUC1、MUC5AC及MUC6表达均下调,差异具有统计学意义(P<0.05);与同时相模型组比较,各时相艾灸组和药物组MUC1表达均上调,差异具有统计学意义(P<0.05);与同时相药物组比较,艾灸组3周、4周2个时相的MUC1表达上调,差异具有统计学意义(P<0.05)。免疫印迹结果示:与空白组比较,模型组大鼠MUC1、MUC5AC和MUC6的相对表达量均下调,差异具有统计学意义(P<0.05);与同时相模型组比较,艾灸组、药物组各时相MUC1表达均上调,差异具有统计学意义(P<0.05);与同时相药物组比较,艾灸组4周时相MUC1相对表达量上调,差异具有统计学意义(P<0.05)。结论:替普瑞酮作为一种胃黏膜保护剂,具有促进大鼠胃黏膜修复的作用,但对胃动力基本没有影响;艾灸足三里既能促进大鼠胃黏膜修复也能促进胃动力,但艾灸起效较晚,至少需要持续艾灸2周左右才能逐渐起效,且艾灸时间越长疗效越好。

GATA结合蛋白3和粘蛋白1在近端和远端胃癌组织中的表达及临床意义

目的探究GATA结合蛋白3(GATA3)和粘蛋白1(MUC1)在近端胃癌(PGC)和远端胃癌(DGC)组织中的表达及临床意义。方法收集孝感市中心医院2014年2月至2016年3月收治的121例胃癌患者经手术切除的胃癌组织及癌旁组织标本,根据肿瘤发生位置将患者分为PGC组(n=62)和DGC组(n=59),采用实时荧光定量PCR检测两组胃癌组织及癌旁组织中GATA3和MUC1的表达水平;免疫组织化学法检测GATA3和MUC1在各样本中的阳性表达情况,分析GATA3、MUCI与PGC和DGC临床病理特征的关系;Pearson法分析PGC和DGC胃癌组织中GATA3和MUC1表达相关性;Kaplan-Meier曲线分析GATA3和MUC1表达与两组患者5年生存率的关系。结果两组胃癌组织中GATA3和MUC1的表达水平及阳性表达率均高于两组癌旁组织(P<0.05),且PGC组胃癌组织中GATA3、MUCI的表达水平及阳性表达率均明显高于DGC组胃癌组织(P<0.05);两组胃癌组织中GATA3和MUC1的表达呈显著正相关(P<0.05);两组胃癌组织中GATA3和MUC1阳性表达水平与肿瘤TNM分期、淋巴结转移、分化程度以及浸润程度有关(P<0.05);而与患者年龄、性别及肿瘤大小无关(P>0.05),两组GATA3和MUC1阳性表达者的5年生存率低于阴性表达者(P<0.05)。结论GATA3和MUC1在PGC和DGC患者胃癌组织中的表达水平显著增加,且二者的表达与患者临床病理特征及预后有关。

MEX3A、CDX2、MUC2与MUC5AC判断可癌变胃肠化生的应用价值

目的 探讨MEX3A与胃癌和肠上皮化生(以下简称肠化生)分化特性的相关性及其联合尾型同源盒转录因子2(caudal-related homeobox transcription factor 2,CDX2)、黏蛋白2(mucin 2,MUC2)和黏蛋白5AC(mucin 5AC,MUC5AC)判断可癌变肠化生的作用。方法 选取2010年1月至2014年12月沈阳医学院附属中心医院、沈阳医学院附属第二医院外科手术切除的胃癌及癌旁石蜡包埋组织样本410例,根据病理诊断将其分为对照组(轻度浅表性胃炎,79例)、肠化生组(149例)和胃癌组(182例)。免疫组织化学检测各组MEX3A、CDX2、MUC2和MUC5AC的表达。结果 MEX3A高表达于胃癌组及肠化生组,特别是弥漫型胃癌、低分化胃癌和Ⅲ型肠化生(P<0.05);CDX2和MUC2高表达于胃癌组和肠化生组,特别是肠型胃癌、高中分化胃癌、Ⅰ型和Ⅱ型肠化生(P<0.05);MUC5AC高表达于对照组,低表达于胃癌组和肠化生组,特别是肠型胃癌、Ⅰ型和Ⅲ型肠化生(P<0.05)。胃癌和肠化生分化程度与MEX3A和MUC5AC表达均呈负相关,与CDX2和MUC2表达呈正相关(P<0.05)。胃癌组织中MEX3A与CDX2、MUC2表达呈负相关,与MUC5AC表达呈正相关(P<0.05);肠化生组织中MEX3A与CDX2、MUC2表达呈负相关(P<0.05),CDX2与MUC2表达呈正相关(P<0.05)。结论 MEX3A与胃癌和肠化生分化程度呈负相关,胃癌具有MEX3A高表达、CDX2和MUC2低表达的特点。

猪胃黏蛋白偶联磁珠和聚乙二醇富集检测青葱和葡萄中诺如病毒的比较研究

目的:以青葱与葡萄为材料,建立以猪胃黏蛋白偶联磁珠(PGM-MB)和聚乙二醇8000(PEG8000)富集检测水果、蔬菜中诺如病毒的方法。方法:确定病毒原液中的相对病毒量,梯度稀释病毒原液并进行实时荧光-聚合酶链式反应检测,以每个反应管内的荧光信号达到设定的域值时所经历的循环数值与病毒量(实时荧光-聚合酶链式反应单位数)的常用对数值绘制标准曲线和线性方程;人工接种诺如病毒于青葱与葡萄表面,洗脱后,分别用PEG8000和PGM-MB富集诺如病毒,实时荧光-聚合酶链式反应扩增,用标准曲线对回收的病毒进行相对定量。结果:基质为青葱时,高接种量条件下,两种富集方法的病毒回收效果相当,低接种量下,PGM-MB法的富集回收率高于PEG8000法,且PGM-MB的检测下限更低;基质为葡萄时,PGM-MB法的富集回收率均高于PEG8000法,且检测下限更低。结论:PGM-MB富集效果良好,快速方便,适合应用于水果和蔬菜中的诺如病毒的富集检测。

健胃愈疡颗粒对复发胃溃疡大鼠胃黏膜黏蛋白5AC mRNA 的影响

目的:观察不同药物干预对胃溃疡大鼠胃黏膜组织中黏蛋白5AC(Mucin5AC,MUC5AC)mRNA 表达的影响及其抗溃疡复发作用的影响。方法:采用 Okabe 改良法制做大鼠胃溃疡模型,应用 Watanabe 法复制胃溃疡复发模型。采用逆转录聚合酶链反应(RT-PCR)技术,检测胃黏膜组织 MUC5AC mRNA 的表达。结果:(1)在灌胃后第10天健胃愈疡组、正常组、假手术组、雷尼替丁组、中西药结合组 MUC5AC mRNA 表达显著高于模型组(P<0.05或 P<0.01);(2)在第92天诱发溃疡复发,健胃愈疡组、正常组、假手术组、模型未复发组、雷尼替丁组、中西药结合组 MUC5AC mRNA 表达显著高于模型复发组(P<0.05或 P<0.01),健胃愈疡组、中西药结合组 MUC5AC mRNA 表达显著高于雷尼替丁组(P<0.01);(3)健胃愈疡组溃疡复发率、溃疡指数均显著低于模型复发组(P<0.01)。结论:健胃愈疡颗粒可显著提高胃溃疡大鼠胃黏膜组织中 MUC5ACmRNA 的表达水平,起到保护胃黏膜的作用,参与胃溃疡的修复及抗溃疡复发的病理生理过程。

多层螺旋CT术前初步评估胃癌分化类型的应用

目的探讨多层螺旋CT(MSCT)术前对胃癌病理分化类型进行初步评估的可行性。方法79例经胃镜诊断为胃癌并经手术证实的患者在术前进行MSCT平扫及双期增强(延迟时间为20s和70s)扫描。分析病灶生长方式、厚度及病变胃壁三期扫描CT值与病理分化类型间的关系。结果病变胃壁厚度及其生长方式均与病理分化类型相关。增强扫描时黏液癌强化较非黏液癌明显(P<0.01),而在非黏液癌中,低分化腺癌强化又较高分化腺癌明显(P<0.01)。结论利用MSCT可以在术前初步判断胃癌的病理分化类型。

幽门螺杆菌感染对患儿胃黏液蛋白表达的影响

目的探讨幽门螺杆菌（Hp）感染患儿胃黏液蛋白MUC5AC和MUC6的表达。方法2005年1月-2006年6月对有反复腹痛、恶心、呕吐、腹胀、嗳气、纳差等消化道表现,临床诊断为慢性胃炎、消化性溃疡等而行胃镜检查的66例患儿。男39例,女27例;年龄（8.8±3.0）岁。以快速尿素酶试验及Hp-PCR检测Hp感染,并根据Hp感染与否分为Hp感染组和非Hp感染组。HE染色对其进行病理学检测,用RT-PCR检测其胃黏液蛋白MUC5AC和MUC6 mRNA水平。用t及χ^2检验进行组间分析,P〈0.05为有统计学意义。结果Hp阳性39例,感染率为59.09%。其中男26例（66.67%）,女13例（48.15%）,男女比较无显著性差异（χ^2=2.26 P〉0.05）。Hp感染阳性1～6岁4例（33.33%）,〉6～9岁12例（52.17%）,〉9～14岁23例（74.19%）,各年龄段比较有显著差异（χ^2=6.67%P〈0.05）。Hp阳性患儿病理组织学检查表明,其炎性反应程度及炎性反应活动度均较无Hp感染患儿重。主要表现为上皮细胞变性,小凹上皮细胞增生,固有膜炎性反应细胞浸润。炎性反应细胞主要为淋巴细胞和浆细胞。Hp感染组MUC5AC mRNA水平明显低于非Hp感染组;Hp感染组MUC6 mRNA水平高于非Hp感染组。结论儿童Hp感染可使其胃黏膜MUC5AC水平下调及MUC6水平上调,使胃黏液蛋白保护作用减弱,导致胃黏膜炎性反应程度及炎性反应活动度加重。

阿帕替尼联合替吉奥二线治疗晚期胃黏液腺癌观察

目的:观察靶向药物阿帕替尼联合替吉奥二线治疗晚期胃黏液腺癌的疗效和安全性。方法:二线治疗晚期胃黏液腺癌患者48例随机分为观察组和对照组各24例。对照组单用替吉奥方案化疗,观察组在对照组基础上加用甲磺酸阿帕替尼治疗。观察其不良反应及客观疗效。结果:观察组客观有效率(ORR)为54.1%,疾病控制率(DCR)为83.3%;对照组ORR和DCR分别为33.3%和54.2%,两组比较差异有统计学意义(P<0.05)。两组药品不良反应均较轻,差异无统计学意义(P>0.05)。结论:阿帕替尼联合替吉奥二线治疗晚期胃黏液腺癌近期疗效好,不良反应可耐受。

三种粘蛋白在胃癌组织中表达及其临床意义

目的研究粘蛋白(MUC1,MUC2,MUC5AC)在胃癌组织中表达及它们与临床病理学行为之间的关系。方法应用免疫组化S—P法检测94例原发性的胃癌组织标本中MUC1,MUC2,MUC5AC在胃癌组织中的表达。结果 1.MUC1的阳性表达率为82％,不同组织学之间的表达有明显差异(P<0.05),在中高分化管状腺癌中表达最强,表达程度与病人年龄、淋巴结有无转移及肿瘤大小密切相关(P<0.05);2.MUC2表达的阳性率为84％,不同组织学类型肿瘤组织中的表达有显著性差异(P<0.05),在粘液腺癌中表达最强100％(7/7);3.MUC5的阳性率为40％(38/94),除性别之间存在差异外,与其它的临床资料无关。4.相关分析发现MUCl的表达与MUC2的表达呈正相关。结论 1、MUC1在不同的组织学类型的胃癌中表达不同,在中高分化腺癌中最高,并与淋巴结转移、肿瘤大小有关;2.MUC2在不同的组织学类型的胃癌中表达不同,粘液腺癌中表达最强,可作为研究粘液腺癌的较好指标;3.MUC5AC在胃癌组织中的表达下降,可作为研究胃癌发生、进展的较好指标。4.MUCl和MUC2之间可能有协同作用。

猪胃黏膜中胃膜素提取工艺的优化

以猪胃黏膜为原料,优化胃膜素的提取工艺。以盐酸溶液为提取液,选取液料比、盐酸体积分数、提取温度、提取时间4个因素,对胃膜素得率进行评价,在单因素试验基础上,采用二次回归正交旋转组合设计优化胃膜素提取的工艺条件。结果表明:最佳提取工艺条件为液料比0.61:1(mL/g)、盐酸体积分数5.4%、提取温度44.9℃、提取时间2.0h;在此条件下,胃膜素得率为3.74%,所得产品中总氮质量分数为8.7%,还原性物质质量分数为26.3%,符合《化药部颁标准》规定的质量标准,说明该优化方法可行。

不同程度脾虚胃脘痛患者胃粘膜防御功能变化

为探讨不同程度脾虚胃粘膜防御功能变化规律，本研究参考孙弼纲等的“脾虚证分度诊断标准”将脾虚证胃脘痛住院患者分为脾虚Ⅰ、Ⅱ、Ⅲ度，分别测定其胃粘膜血流量（ｇａｓｔｒｉｃｍｕｃｏｓａｂｌｏｄｆｌｏｗ，ＧＭＢＦ）、胃液氨基已糖、胃粘膜前列腺素（ＰＧＥ２、６－Ｋ－ＰＧＦ１α）、木糖吸收率含量变化。结果：脾虚程度越重，ＧＭＢＦ、ＰＧＥ２、６－Ｋ－ＰＧＦ１α、木糖吸收率越降低，而胃液氨基已糖则相反。表明：随着脾虚程度加重，胃粘膜局部防御功能逐渐降低；