肿瘤坏死因子基因多态性与慢性萎缩慢胃炎和胃腺癌的相关性

研究发现 ,肿瘤坏死因子 (ＴＮＦ)基因多态性与ＴＮＦ的分泌有关[1] ,甚至可调节其转录水平[2 ] 。ＴＮＦ基因多态性是否与人类某些肿瘤、自身免疫性疾病、感染性疾病相关 ,国外学者的研究尚无定论。迄今为止 ,国内外有关ＴＮＦ基因多态性与慢性萎缩性胃炎和胃癌关系的报道极少。因此 ,我们对湖北地区汉族人群ＴＮＦ α和ＴＮＦ β基因多态性分布与慢性萎缩性胃炎和胃腺癌的相关性进行了分析 ,以阐明ＴＮＦ基因多态性在慢性萎缩性胃炎和胃腺癌中的作用。一、对象随机选取健康体检者 16 4例 ,其中男 113例 ,女 5 1例 ,平均年龄 (5 2 3± 11 …     

肿瘤坏死因子基因多态性与胃癌易感性的研究

肿瘤坏死因子是体内具有多种生物活性的重要致炎细胞因子,其基因多态性影响着转录和表达调控。与包括胃癌在内的多种疾病的发生发展有关。研究肿瘤坏死因子基因多态性有助于筛选发生胃癌的高危人群,在基因水平上为胃癌的早期防治提供理论基础。     

慢性萎缩性胃炎癌前病变治疗体会

慢性萎缩性胃炎（ChronicAtrophicGastritis,CAG）是消化系统常见病。多发病。因其与胃癌的发生有一定关系．1978年WHO将其列为胃癌的癌前疾病或癌前状态，而在CAG基础上伴发的肠上皮化生和异型增生，则是胃癌的癌前病变[1]．癌变的可能性大，成为目前研究的重点。一般认为．胃     

慢性酒精性胰腺炎患者体外肿瘤坏死因子和肿瘤坏死因子受体的诱导

肿瘤坏死因子(TNFa)是急性胰腺炎导致全身多器官损害的一种重要介质。本文研究的目的是了解慢性酒精性胰腺炎TNFa和可溶性肿瘤坏死因子受体p55、p75(sTNFRp55、sTNFRp75)是否升高,及其升高是否是内毒素或酒精的作用。我们对12例慢性酒精性胰腺炎患者和8例健康者用内毒素脂多糖(LPS)和乙醇(Ethanol)刺激后的周围血单核细胞上清液用ELISA方法进行了TNFa、sTNFRp55、p75的检测。LPS刺激后的单核细胞上清液中TNFa、sTNFp55、p75浓度不论是患者还是健康组均较自然表达明显增加,其中sTNFRp55、p75浓度在胰腺炎组较正常组明显增加,P值分别<0.05、<0.001。Ethanol刺激后 TNFa和sTNFRp55的表达在胰腺炎组与正常组之间无差异.但sTNFRp75较正常组增加。我们的结果提示慢性酒精性胰腺炎前炎性介质TNFa和sTNFRp55、p75的诱导与内毒素活化的单核细胞表达有关,而酒精对单核细胞活化不起直接作用。     

慢性酒精性胰腺炎患者体肿瘤坏死因子和肿瘤坏死因子受体的诱导

肿瘤坏死因子（ＴＮＦα）是急性胰腺炎导致全身器官损害的一种重要介质。本文研究了目的是了解慢性酒精性为ＴＮＦα和可溶性肿瘤坏死因子受体Ｐ５５、Ｐ７５（ｓＴＮＦＲｐ５５、ｓＴＮＦＲｐ７５）是否升高，及其升高是是内毒素或酒精的作用。我们对１２例慢性酒清胰腺炎患者和８例健康者用内毒素脂多糖（ＬＰＳ）和乙醇刺激后的周围血单核细胞上清液用ＥＬＩＳＡ方法进行了ＴＮＦα、ｓＴＮＦＲｐ５５、ｐ７５的检测。ＬＰＳ刺激     

和胃合剂治疗慢性萎缩性胃炎作用机制探讨

目的探讨和胃合剂治疗萎缩性胃炎的疗效及作用机制。方法将45只雄性BALB／c小鼠随机分为正常组、胃炎组以及干预组,后两组采用水杨酸钠法复制慢性萎缩性胃炎模型。造模后干预组予和胃合剂灌胃21周,另两组等量生理盐水灌胃。免疫组化法检测各组胃黏膜腺体中TFF1和H^＋／K^＋-ATP酶表达情况;半定量实时荧光PCR法检测胃黏膜TFF-1 mRNA的表达,琼脂糖凝胶电泳检测表达产物的特异性。结果胃炎组胃黏膜细胞中TFF1蛋白、mRNA表达水平及H^＋/K^＋-ATP酶阳性细胞数量显著低于正常组（P〈0．05）,干预组TFF1蛋白和mRNA的表达水平及H^＋/K^＋-ATP酶阳性细胞数量显著高于胃炎组,P〈0．05。结论和胃合剂治疗慢性萎缩性胃炎效果确切;主要作用机制为上调TFF1表达。     

Diagnosing chronic atrophic gastritis by gastroscopy using artificial intelligence

BackgroundThe sensitivity of endoscopy in diagnosing chronic atrophic gastritis is only 42%, and multipoint biopsy, despite being more accurate, is not always available.AimsThis study aimed to construct a convolutional neural network to improve the diagnostic rate of chronic atrophic gastritis.MethodsWe collected 5470 images of the gastric antrums of 1699 patients and labeled them with their pathological findings. Of these, 3042 images depicted atrophic gastritis and 2428 did not. We designed and trained a convolutional neural network-chronic atrophic gastritis model to diagnose atrophic gastritis accurately, verified by five-fold cross-validation. Moreover, the diagnoses of the deep learning model were compared with those of three experts.ResultsThe diagnostic accuracy, sensitivity, and specificity of the convolutional neural network-chronic atrophic gastritis model in diagnosing atrophic gastritis were 0.942, 0.945, and 0.940, respectively, which were higher than those of the experts. The detection rates of mild, moderate, and severe atrophic gastritis were 93%, 95%, and 99%, respectively.ConclusionChronic atrophic gastritis could be diagnosed by gastroscopic images using the convolutional neural network-chronic atrophic gastritis model. This may greatly reduce the burden on endoscopy physicians, simplify diagnostic routines, and reduce costs for doctors and patients.     

胃癌患者肿瘤坏死因子基因型与其血清水平的关系

目的 研究胃癌患者肿瘤坏死因子(TNF)-α308和TNF-β252基因型与血清TNF-α、β水平的关系.方法 收集病理诊断证实的57例胃癌患者,49例来白武汉大学中南医院,8例来自湖北省肿瘤医院.同时选取年龄与性别相匹配的18名健康体检者作为对照.采用限制性片段长度多态性聚合酶链反应(PCR-RFLP)方法检测患者外周静脉血.采用ELISA方法检测57例胃癌患者及18名对照者的血清TNF-α、β水平,比较胃癌患者各TNF基因型之间血清TNF水平的差异及其与对照者血清TNF水平的差异.分析胃癌患者TNF水平与临床病理特征的关系.结果 胃癌患者总体血清TNF-α水平较对照组明显增高(中位数445×10-3 μg/L比5×10-3 μg/L,P＜0.05),而且TNF-α308和TNF-β252各基因型(TNF α308 GA基因型6例、GG基因型51例,TNF-β252 GG基因型17例,GA和AA基因型各20例)的血清TNF-α水平较对照组也明显增高(P＜0.05),但血清总体TNF-β水平与对照组比较差异无统计学意义(P＞0.05).此外,TNF α308G/TNF-β252G和TNF-α308G/TNF-β252A单倍型胃癌患者血清TNF-α水平较对照组也明显增高(P＜0.05),其增高与血清总体TNF-α水平一样,与患者年龄、淋巴结转移显著相关(P＜0.05).TNF-α308A和TNF-β252G的高危等位基因携带者的TNF β水平与吸烟史显著相关(P＜0.05).结论 胃癌患者血清TNF-α水平增高与TNF-α308和TNF-β252基因型无显著相关性.TNF- α308G/TNF-β252G和TNF-d308G/TNF- β252A单倍型胃癌患者的血清TNF-α水平增高与年龄、淋巴结转移显著相关,提示TNF基因单倍型对胃癌TNF的表达及临床类型可能具有一定的影响.     

吸烟、肿瘤坏死因子及其受体与慢性阻塞性肺疾病

慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)发病率高.发病机制不清.外界环境的刺激导致气道和血管损伤与修复的失平衡可能与COPD的发生相关.其中吸烟致细胞因子、炎症细胞及炎症介质增多,气道和肺实质慢性炎症,导致气道损伤和重构.最终导致气流受限,在肺气肿的形成中起主要作用.肿瘤坏死因子a是重要的炎症因子,通过其主要受体肿瘤坏死因子受体1参与COPD的形成,在COPD的发生、发展中起重要作用.     

肿瘤坏死因子α基因多态性与慢性乙型肝炎病毒感染的相关性

乙型肝炎病毒（HBV）感染后临床表现的多样性，除与病毒因素有关，还与宿主的遗传因素密切相关。细胞因子在宿主清除病毒的免疫应答中发挥着重要作用，其基因多态性可影响细胞因子的整个转录，翻译和分泌过程，导致不同人群中细胞因子水平的差异，从而影响HBV感染后的转归。肿瘤坏死因子（TNF）α基因启动子区存在有多个多态性位点，分别为-1031（T／C）、-863（C／A）、-857（C／T）、-376（G／A）、-308（G／A）、-238（G／A）和-163（G／A）。     

Association of tumor necrosis factor genetic polymorphism with chronic atrophic gastritis and gastric adenocarcinoma in Chinese Han population

AIM:To investigate the association of TNF polymorphisms with chronic atrophic gastritis (CAG) and gastric adenocarcin-oma in Chinese Han patients.METHODS:The TNFa-e 5 microsatellites and 3 RFLP sites were typed using PCR technique,followed by high-voltage denaturing PAGE with silver staining and restriction enzyme digestion respectively in specimens from 53 patients with CAG and 56 patients with agstric daenocarcinoma and 164 healthy controls.The PCR products were cloned and sequenced.RESULTS:The frequency of TNF-β Ncol*1/2 genotype was higher in patients with chronic atrophic gastritis than in healthy controls,but no significant difference was observed(60.38% vs 46.34%,p=0.076).The frequency of TNa10 allele was significantly higher in patients with chronic atrophic gastritis than in healthy controls(19.81% vs 11.89%,p=0.04).However,it did not relate to age,gender,atrophic degree or intestinal metaplasin in patients with chronic atrophic gastritis,The frequency of TNF-β Ncol*1/2 and d2/d6 genotypes were significantly higher in patients with gastric adenocarcinoma than in healthy indiveduals(p&gt;0.05).However,TNF-β Ncol*1/2 and d2/d6 genotypes did not relate to age,gender,grade of differentiation and clinicopathologic state in patients with gastric adenocarcinoma.The frequency of TNFa6b5c1 hapolotype homoaygote was significantly lower in patients with gastric adenocarcinoma than in healthy controls (1.79% vs 15.85%,p=0.006).CONCLUSION:TNFa10 allele may be a risk factor for chronic atrophic gastritis ,TNF-β Ncol*1/2 and d2/d6 genotypes are associated with the suscepotibility to gastric adenocarcinoma,whereas TNFa6b5c1 haplotype homozygote may contribute to the resistance against gastric adenocarcinoma.     

血清胃蛋白酶原检测在慢性萎缩性胃炎筛查中的价值

目的探讨血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅰ/胃蛋白酶原Ⅱ(PGⅠ/PGⅡ)比值(PGR)与慢性萎缩性胃炎的关系,确定其在萎缩性胃炎中的变化规律。方法选择在我院消化科行胃镜检查符合入选研究标准的200例患者,根据组织病理学诊断结果分为慢性非萎缩性胃炎组(135例)和慢性萎缩性胃炎组(65例)。采用化学发光方法定量测定空腹血清PGⅠ、PGⅡ,并计算PGⅠ/PGⅡ比值(PGR)。结果慢性萎缩性胃炎组与非萎缩性胃炎组血清PGⅠ分别为(78.55±15.42)μg/L和(130.51±55.23)μg/L,有显著差异(P<0.05)。PGR分别为4.09±2.15和8.95±5.18,显著差异(P<0.05);以PGⅠ≤70μg/L且PGR≤3.0为界值来计算诊断慢性萎缩性胃炎的敏感性和特异性分别为72.3%和93.3%。结论检测血清PG及PGR可用于慢性萎缩性胃炎的筛查,如有异常,应进一步行胃镜检查以确诊并指导治疗。     

肿瘤坏死因子α基因多态性与吸烟所致慢性阻塞性肺疾病相关性的研究进展

研究表明，COPD的发生存在一定的遗传易感性，目前已发现十余种候选基因与之有关，肿瘤坏死因子α基因是其中之一。本文综述了肿瘤坏死因子α基因多态性与吸烟所致COPD关系的研究进展，并对可能的机制作了分析。     

Effects of He-Ne laser irradiation on chronic atrophic gastritis in rats

AIM: To study the effects of He-Ne laser irradiation on experimental chronic atrophic gastritis (CAG) in rats. METHODS: Sixty-three male adult Wistar rats were randomly divided into five groups including normal control group, model control group and three different dosages He-Ne laser groups. The chronic atrophic gastritis (CAG) model in rats was made by pouring medicine which was a kind of mixed liquor including 2% sodium salicylate and 30% alcohol down the throat for 8 wk to stimulate rat gastric mucosa, combining with irregular fasting and compulsive sporting as pathogenic factors; 3.36, 4.80, and 6.24 J/cm2 doses of He-Ne laser were used, respectively for three different treatment groups, once a day for 20 d. The pH value of diluted gastric acid was determined by acidimeter, the histopathological changes such as the inflammatory degrees in gastric mucosa, the morphology and structure of parietal cells were observed, and the thickness of mucosa was measured by micrometer under optical microscope. RESULTS: In model control group, the secretion of gastric acid was little, pathologic morphological changes in gastric mucosa such as thinner mucous, atrophic glands, notable inflammatory infiltration were found. After 3.36 J/cm2 dose of He-Ne laser treatment for 20 d, the secretion of gastric acid was increased (P<0.05), the thickness of gastric mucosa was significantly thicker than that in model control group (P<0.01), the gastric mucosal inflammation cells were decreased (P<0.05). Morphology, structure and volume of the parietal cells all recuperated or were closed to normal. CONCLUSION: 3.36 J/cm2 dose of He-Ne laser has a significant effect on CAG in rats.     

大鼠慢性萎缩性胃炎时粘膜血管病变与胃癌的关系

目的慢性萎缩性胃炎是否发生癌变是一个争论的问题．为了研究慢性萎缩性胃炎胃粘膜血管病变的发生与胃癌的关系,应用大鼠进行实验观察胃粘膜的改变．方法应用ＭＮＮＧ（１５０ｍｇ／Ｌ）在诱癌（ｎ＝１５０）过程中动态观察胃粘膜间质组织形态学改变及ＶｉｔＤ３的作用．并用墨汁主动脉灌注以观察粘膜血管的改变．结果局限性血管内皮细胞增大、数量增多是导致粘膜组织有效的血液循环减少,引起粘膜组织萎缩的主要因素．经主动脉灌注墨汁表明粘膜腺体萎缩区血管明显减少,粘膜组织呈现一个功能低落,组织变性消失的过程．结论慢性萎缩性胃炎不是胃癌的直接相关性病变．     

鼠慢性萎缩性胃炎胃黏膜形态特征和细胞增殖调控因子变化研究

目的　研究鼠慢性萎缩性胃炎 (CAG)的病理变化和细胞增殖分子调控变化 ,探讨CAG发生的可能机制。方法　综合采用 6 0 %乙醇或 2 %水杨酸钠、2 0mmol/L去氧胆酸钠和 0 .1%氨水建立大鼠CAG模型。观察大鼠胃黏膜病理组织变化和黏液分泌功能。测定大鼠血清表皮生长因子 (EGF)和前列腺素E2 (PGE2 )水平 ,免疫组化分析EGF受体 (EGFR)、C erbB2、P5 3、P16和Bcl 2蛋白的表达。结果　鼠CAG胃窦黏膜的炎症改变明显 ,腺体数目和厚度显著降低 ,部分大鼠出现肠上皮化生。扫描电镜可见胃黏膜破溃、细胞脱落。鼠CAG胃黏膜氨基己糖和血清PGE2较正常组显著下降 (P <0 .0 5 )。CAG大鼠血清EGF水平为 (2 .2 4± 0 .83) μg/L ,较正常大鼠的 (0 .6 1± 0 .2 8) μg/L显著升高 (P <0 .0 5 )。鼠CAG胃组织EGFR和C erbB2阳性表达率分别为 4 5 %和 70 % ,正常大鼠均无表达 (P <0 .0 5 )。正常大鼠P16蛋白表达率为 75 % ,显著高于模型大鼠的 10 % (P <0 .0 5 ) ,模型大鼠Bcl 2蛋白表达率为5 0 % ,高于正常大鼠的 10 % (P <0 .0 5 )。CAG和正常大鼠的P5 3蛋白表达率分别为 30 %和 10 % ,差异无显著性 (P >0 .0 5 )。结论　鼠CAG的发生与多种致病因素破坏胃黏膜屏障 ,胃黏膜细胞增殖和凋亡失衡有关。