肠道黏膜免疫应答在腹泻型肠易激综合征中的作用机制研究进展

肠易激综合征（IBS）是一组以腹痛、腹胀、腹部不适、排便习惯改变为主要症状，伴随一系列如焦虑、抑郁、头痛、失眠等次要并发症的胃肠道功能紊乱性疾病。以肠道动力改变和主要症状为依据，IBS分为腹泻型、便秘型、混合型。IBS在全球范围内因国家和年龄的不同，发病率为10%~20%，欧美国家发病率为10%~15%，女性发病率是男性的2倍[1]。虽然IBS的作用机制仍不清楚，但近年来随着免疫学与肠道疾病相关研究增多，肠道黏膜免疫应答在腹泻型肠易激综合征（IBS-D）发病中起着重要作用。本文针对肠道黏膜免疫应答在IBS-D中的异常作用和可能作用机制进行综述。

清热化湿方对脾胃湿热证患者胃黏膜AQP3、AQP4蛋白表达的影响

目的:探讨脾胃湿热证与胃黏膜水通道蛋白(AQP3)、AQP4表达的关系俄语及中药清热化湿方的作用机制。方法:选择慢性浅表性胃炎患者68例,其中脾胃湿热证53例(湿重于热19例,热重于湿14例,湿热并重20例),脾虚证15例;另选正常健康体检者10例为正常对照组。脾胃湿热证患者予中药清热化湿方,并采用免疫组化方法检测入选者胃黏膜 AQP3、AQP4表达情况。结果:AQP3、AQP4在脾胃湿热证组的表达明显强于正常对照组(P<0.05);脾虚证组与正常组比较差异无显著性(P>0.05);各亚型之间呈湿重于热>湿热并重>热重于湿的趋势,但差异无显著性(P>0.05)。治疗后,脾胃湿热证组 AQP3、AQP4表达水平显著下降(P<0.01),与正常对照组及脾虚证组比较差异无显著性(P>0.05)。结论:AQP3、AQP4的异常表达可能是脾胃湿热证的发生机制之一,中药清热化湿方可能通过影响 AQP3、AQP4的表达而发挥治疗作用。

女性下生殖道HPV感染和HPV相关的宫颈肿瘤

子宫颈病变是女性最常见的疾患之一。在女性癌瘤中 ,宫颈癌的发病率仅次于乳腺癌。人乳头状瘤病毒(HPV)感染在宫颈肿瘤的发病机制中起着重要的作用 ,许多学者关注HPV疫苗的预防和治疗。在女性生殖道HPV传播及继发性感染是局部性的 ,因此 。

Classification of submucosal tumors in the gastrointestinal tract

This review is part two of three, which will present an update on the classification of gastrointestinal submucosal tumors. Part one treats of the diagnosis and part three of the therapeutic methods regarding gastrointestinal submucosal tumors. In the past there has been some confusion as to the classification of gastrointestinal submucosal tumors. Changes in classifications have emerged due to recent advances in mainly immunohistochemistry and electron microscopy. The aim of this paper is to update the reader on the current classification. Literature searches were performed to find information related to classification of gastrointestinal submucosal tumors. Based on these searches the twelve most frequent submucosal tumor types were chosen for description of their classification. The factors that indicate whether tumors are benign or malignant are mainly size and number of mitotic counts. Gastrointestinal stromal tumors are defined mainly by their CD117 positivity. In the future, there should be no more confusion between gastrointestinal stromal tumors and other types of submucosal tumors.

Expression of matrix metalloproteinase-1 and tumor necrosis factor-α in ulcerative colitis

AIM： To examine the expression of matrix metalloproteinase-1 （MMP-1） and tumor necrosis factor-α （TNF-~~） in the colon mucosa of patients with ulcerative colitis （UC）.METHODS： Reverse transcription-polymerase chain reaction （RT-PCR） and immunohistochemistry were used to examine the expression of MMP-1 and TNF-α at both mRNA and protein levels in the colon mucosa of patients with UC. Correlation between MMP-1 and TNF-α and their correlation with the severity of the disease were also analyzed statistically.RESULTS： The expression of MMP-1 and TNF-α in the ulcerated and inflamed colon mucosa of patients with UC was significantly higher than that in the non-inflamed mucosa of normal controls at both mRNA and protein levels. Furthermore, the expression of MMP-1 and TNF-α in the ulcerated area was significantly higher than that in the inflamed area of patients with UC （0.9797 ± 0.1433 vs 0.6746 ± 0.0373, 0.8669 ± 0.0746 vs 0.5227 ± 0.0435, P 〈 0.05）. There was no statistically significant difference in the non-inflamed area of normal controls. There was a significant correlation between MMP-1 and TNF-c~ expression （0.9797 ± 0.1433 vs 0.8669 ± 0.0746, P 〈 0.05）, the correlating factor was 0.877. MMP-1 and TNF-α showed a significant correlation with the severity of the disease （0.0915 ：e 0.0044 vs 0.0749 vs 0.0032, 0.0932 ± 0.0019 vs 0.0724 ± 0.0043, P 〈 0.05）, their correlating factors were 0.942 and 0.890, respectively.CONCLUSION： Excessively expressed MMP-1 directly damages the colon mucosa by degrading extracellular matrix （ECM） in patients with UC. While damaging colon mucosa, excessively expressed TNF-α stimulates MMPs secreting cells to produce more MMP-1 and aggravates the mucosa damage. MMP-1 promotes secretion of TNF-α in a positive feedback manner to cause further injury in the colon mucosa. MMP-1 and TNF-α correlate well with the severity of the disease, and therefore, can be used clinically as biological markers to judge the severity of UC.

程序性细胞死亡因子4基因对川崎病血清诱导血管内皮细胞凋亡的影响

目的研究程序性细胞死亡因子4(PDCD4)对川崎病病人血清诱导的血管内皮细胞凋亡的作用。方法研究时间为2017年3月至2018年4月。采集邵阳学院附属第一医院川崎病病人血清,处理血管内皮细胞,实时荧光定量PCR(realtime PCR)和蛋白质印迹法检测细胞中PDCD4 mRNA和蛋白表达水平。在血管内皮细胞中转染PDCD4 siRNA,用川崎病血清培养,以Realtime PCR和蛋白质印迹法检测细胞中PDCD4表达水平。MTT方法检测细胞增殖,流式细胞术检测细胞凋亡,蛋白质印迹法检测细胞中活化型半胱氨酸天冬氨酸蛋白酶3(C-Caspase-3)、活化型Caspase-9(C-Caspase-9)蛋白水平。结果川崎病病人血清处理后的血管内皮细胞中PDCD4表达上调[mRNA:(1.00±0.01)比(3.51±0.36);蛋白:(0.26±0.08)比(0.57±0.06)]。PDCD4 siRNA可以下调川崎病病人血清诱导的血管内皮细胞中PDCD4表达水平[mRNA:(0.91±0.09)比(0.41±0.06);蛋白:(0.65±0.08)比(0.30±0.05)]。川崎病病人血清处理后的血管内皮细胞增殖能力降低[(100.00±0.00)%比(72.01±7.32)%],细胞凋亡率升高[(6.32±0.58)%比(21.26±2.31)%],细胞中的C-Caspase-3、C-Caspase-9蛋白水平升高。下调PDCD4可以提高川崎病血清条件下血管内皮细胞增殖能力[(71.57±9.05)%比(89.52±6.80)%],减少细胞凋亡[(22.58±1.79)%比(16.47±1.24)%]和细胞中C-Caspase-3、C-Caspase-9蛋白表达。结论下调PDCD4减少川崎病病人血清诱导的血管内皮细胞凋亡。