BackgroundGastrointestinal motility disturbances rank among the most frequently reported medical complications of spaceflight. Astronauts experience delayed gastric emptying, erratic small intestinal transit and reduced colonic propulsion. The underlying mechanisms are multifactorial. Microgravity alters intra-abdominal physical mechanics, disrupts autonomic and enteric neural circuits, shifts gastrointestinal hormone secretion profiles, inflicts oxidative stress upon effector cells, and perturbs gut microbial communities. Cross-model comparisons reveal substantial disagreement, suggesting that no single ground-based analog fully captures the pathophysiology of orbital flight.AimTo critically review how weightlessness affects gastric emptying, small intestinal transit and colonic motility; to critically evaluate contradictory findings across simulation platforms; and to delineate the neural, humoral, cellular and microbiological mechanisms involved.MethodsWe searched PubMed, Web of Science and the NASA Technical Reports Server for articles published between January 1990 and June 2026 (last search 30 June 2026). Search terms included: “microgravity”, “weightlessness”, “spaceflight”, “gastrointestinal motility”, “gastric emptying”, “intestinal transit”, “gut microbiome”, “interstitial cells of Cajal” and “oxidative stress”. Studies using head-down bed rest, hindlimb unloading, clinorotation, parabolic flight and actual spaceflight were included. The review follows a critical narrative design; the full search strategy and the framework used to appraise the evidence are described in Section 1.1.ResultsAltered-gravity studies suggest that gastrointestinal dysmotility may involve neurohumoral dysregulation, oxidative injury to interstitial cells of Cajal and smooth muscle, barrier dysfunction and altered enteric signaling; however, most mechanistic evidence derives from simulated models and has not been directly validated during human spaceflight. Direct human motility measurements remain sparse, and the evidence comprises a mixture of direct observations, model-dependent inferences and testable hypotheses. Cross-study agreement is poor: some head-down bed rest trials report accelerated small-bowel transit, whereas tail-suspension models and limited flight observations suggest motor suppression. These divergences may reflect model-specific confounding rather than a uniform effect of microgravity.ConclusionCurrent ground-based models each capture only partial aspects of orbital GI pathophysiology. Future work should combine multi-omics profiling with next-generation simulation platforms to develop evidence-based countermeasures for long-duration missions.

Raman and Brillouin scattering are sensitive approaches to detect chemical composition and mechanical elasticity pathology of cells in cancer development and their medical treatment researches.The application is,however,suffering from the lack of ability to synchronously acquire the scattering signals following three-dimensional(3D)cell morphology with reasonable spatial resolution and signal-to-noise ratio.Herein,we propose a divided-aperture laser differential confocal 3D Geometry-Raman-Brillouin microscopic detection technology,by which reflection,Raman,and Brillouin scattering signals are simultaneously in situ collected in real time with an axial focusing accuracy up to 1 nm,in the height range of 200 μm.The divided aperture improves the anti-noise capability of the system,and the noise influence depth of Raman detection reduces by 35.4％,and the Brillouin extinction ratio increases by 22 dB.A high-precision multichannel microspectroscopic system containing these functions is developed,which is utilized to study gastric cancer tissue.As a result,a 25％reduction of collagen concentration,42％increase of DNA substances,17％and 9％decrease in viscosity and elasticity are finely resolved from the 3D mappings.These findings indicate that our system can be a powerful tool to study cancer development new therapies at the sub-cell level.

Abstract Background An increasing number of asymptomatic gastrointestinal stromal tumor (GIST) patients are being identified. The objective of this study was to examine the association between necroptosis-related genes and high-risk GIST, providing data to inform the treatment and follow-up guidelines of asymptomatic patients. Methods The GIST dataset was acquired and by analyzing the dataset of GIST patients in high-risk and low-risk groups, we identified differentially expressed genes (DEGs). We constructed a diagnostic model and used it to analyze the screened DEGs in order to identify key genes involved in GIST. We then constructed mRNA-miRNA and mRNA-TF interaction networks to predict the interaction networks of key genes. We employed immune infiltration analysis to examine the correlation between immune cells and key genes. Results A total of 15 necroptosis-related DEGs were identified by analyzing the datasets of high and low-risk GIST patients. A diagnostic model was developed utilizing five essential genes (CAPN1, DNM1L, H2AFZ, MYC, and UCHL1) for discriminating high-risk and low-risk for GIST. The key gene MYC exhibited the highest level of interaction with miRNA, while the key gene CAPN1 displayed the most interactions with TFs. Immune infiltration analysis showed that the key gene MYC has a significant positive correlation with eosinophils and memory B cells. Conclusion The key genes MYC and CAPN1 may play crucial roles in the progression of GIST disease.

Objective:To study the efficacy and influencing factors of ursodeoxycholic acid (UDCA) in the treatment of cholesterol gallstone, so as to provide reference for the treatment of cholesterol gallstone by internal medicine.Methods:From March 1, 2017 to March 31, 2018, at outpatient department of gastroenterology of 9 Beijing medical centers including Peking University People′s Hospital, the Sixth Medical Center of PLA General Hospital, Beijing Huaxin Hospital, PLA Rocket Force Characteristic Medical Center, Peking University Aerospace Center Hospital, Beijing Youan Hospital of Capital Medical University and Beijing Tiantan Hospital of Capital Medical University, Beijing Tongren Hospital of Capital Medical University, and Beijing Shijitan Hospital of Capital Medical University, the data of patients with cholesterol gallstone treated by UDCA were collected. The inclusion criteria were that the largest diameter of stone was ≤10 mm and the stone was not detected under X-ray. The treatment plan was taking UDCA orally for 6 months at a dose of 10 mg·kg -1·d -1. The basic information of patients, the ultrasound examination results before treatment and 6 months after treatment, and scores of biliary abdominal pain and dyspepsia symptom were collected. Univariate and multivariate logistic regression were used to analyze the influencing factors of the efficacy in gallstrone dissolution by UDCA, and Wilcoxon signed rank test was used for statistical analysis. Results:A total of 215 patients were enrolled. The complete dissolution rate of gallstone was 19.5% (42/215) and partial dissolution rate was 50.7% (109/215), and the total effective rate was 70.2% (151/215). The complete dissolution rate of sandy stone was significantly higher than that of lumped stones (37.0%(17/46) vs. 14.8%(25/169); OR=3.377, 95% confidence interval (95% CI) 1.621 to 7.035, P=0.001). In lumped stones, the complete dissolution rate of the stones with diameter ≤5 mm was significantly higher than that of the stones with diameter >5 mm (37.5%(9/24) vs. 11.0%(16/145); OR=4.837, 95% CI 1.823 to 12.839, P=0.002). The complete dissolution rate of patients with higher body mass index ( OR=0.872, 95% CI 0.764 to 0.995, P=0.043) and longer disease course ( OR=0.942, 95% CI 0.912 to 0.973, P<0.001) was low. The results of multivariate logistic analysis indicated that long disease course of gallstone ( OR=0.940, 95% CI 0.908 to 0.974, P=0.001), rough gallbladder wall ( OR=0.438, 95% CI 0.200 to 0.962, P=0.040) and lumped stone ( OR=0.236, 95% CI 0.101 to 0.550, P=0.001) were independent risk factors of influencing the efficacy of stone dissolution by UDCA. As for lumped stones, the independent risk factors included long disease course of gallstone ( OR=0.926, 95% CI 0.877 to 0.978, P=0.006) and stone diameter >5 mm ( OR=0.142, 95% CI 0.043 to 0.470, P=0.001). After 6 months of UDCA treatment, score of biliary abdominal pain decreased from 0 (0 to 6) to 0 (0 to 0) and the score of dyspepsia symptom decreased from 1 (0 to 2) to 0 (0 to 0), and the differences between before treatment and after treatment were statistically significant ( Z=-8.50, and -9.13, both P<0.001). Conclusions:UDCA has a certain efficacy in cholesterol gallstone dissolution and can ease biliary abdominal pain and dyspepsia symptom. Long disease course of gallstone, rough gallbladder wall and stone diameter >5 mm are independent risk factors of poor efficacy in gallstone dissolution by UDCA.

Background: Deoxyribonucleic acid (DNA) methyltransferase inhibitors, such as decitabine, have made great advances in cancer therapy as combinational drugs. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has an obvious anti-tumor effect; however, some gastric cancer (GC) cells are resistant to TRAIL-induced cell death. This study sought to explore the synergistic anti-tumor effect of TRAIL and decitabine, and the potential synergetic mechanism. Methods: The cell growth inhibition effect was monitored by the IncuCyte ZOOM Live-Cell Analysis System, and cell viability was determined by Cell Counting Kit- 8 assays. Apoptosis was detected by Annexin V/Propidium Iodide double staining. Death receptor 4 (DR4) was knocked down by ribonucleic acid (RNA) interference, and the effect of DR4 deletion on TRAIL sensitivity was analyzed. Methylationspecific polymerase chain reaction (PCR) was applied to determine the methylation status of DR4. The messenger RNA (mRNA) and protein expression levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. The expression of the DRs on the cell membrane surfaces was analyzed by flow cytometry. Results: The combined use of decitabine and TRAIL synergistically inhibited cell growth in 2 TRAILresistant cell lines. Further, decitabine augmented TRAIL-induced apoptosis in a caspase-dependent manner. The co-application of decitabine and TRAIL facilitated the activation of caspase-7, -8, -9, and poly ADPribose polymerase (PARP). Notably, decitabine increased the expression of DR4 at the transcriptional and post-transcriptional levels. DR4 expression on the cell membrane surfaces was also upregulated after decitabine exposure. The depletion of DR4 by specific inhibitors attenuated TRAIL-induced apoptosis and weakened the synergistic effects of decitabine and TRAIL. In addition, DR4 gene presented methylation status in SNU-1 cells. The low mRNA and protein expression of DR4 were also detected in SNU-1 cells. Conclusions: Decitabine enhances the effect of TRAIL by inhibiting the growth and inducing the apoptosis of GC cells. This is achieved by the epigenetic modification of decitabine, which upregulates DR4. Decitabine may act as a sensitizing agent of TRAIL. The combined use of decitabine and TRAIL may provide a novel idea for GC treatment.

In this report, we show that Epstein–Barr virus (EBV)-infected lymphoblastoid cell lines (LCL) express Fas and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 and that LCL are lysed following engagement of these receptors by agonist Fas and TRAIL receptor-specific monoclonal antibodies (MAb). We also show that EBV-specific CD4+ T cells mediate bystander lysis of susceptible targets through both the Fas/Fas ligand (FasL) and the TRAIL pathways, but find that the dominant mechanism of lysis following cognate, HLA class II-restricted recognition of LCL is the perforin/granzyme pathway. Killing of LCL by EBV-specific CD4+ T cells was strongly inhibited by concanamycin A, an agent that elevates granule pH, resulting in accelerated destabilization and degradation of perforin. In contrast, blocking anti-FasL MAb showed only limited inhibition of LCL killing. Blocking anti-TRAIL MAb had no effect on lysis of LCL by EBV-specific CD4+ T cells. We further show that culture of EBV-specific CD4+ T cells in the presence of interleukin 4 markedly abrogates effector cytotoxic function against LCL through direct depletion of intracellular perforin, with no evidence of a Th1 to Th2 shift in patterns of cytokine expression.

Objective:To investigate the expression changes of farnesoid X receptor (FXR) in the evolution of normal intestinal mucosa, colorectal adenoma (CRA) and colorectal cancer (CRC), and the correlation of FXR expression with clinicopathological features and prognosis of patients with colorectal tumors.Methods:The UALCAN website tool was used to analyze the expression level of FXR gene transcripts of CRC and normal colorectal tissues in The Cancer Genome Atlas (TCGA) database. The patients undergoing colonoscopy and treatment in the Aerospace Center Hospital from January 2019 to September 2020 were selected, and the immunohistochemistry was used to detect the expression of FXR protein in 100 CRA tissues, 47 CRC tissues and 11 normal colonic mucosal tissues from healthy people (healthy control). Combining with clinical data, the relationship between FXR protein expression and clinicopathological characteristics of patients with colorectal tumors was analyzed. According to the Kaplan-Meier Plotter online database, the median expression level of FXR gene transcripts in CRC patients was analyzed, and the patients were divided into FXR low-expression group and high-expression group, the relationship between the expression of FXR gene and prognosis of CRC patients was investigated.Results:The analysis of data from TCGA database showed that the expression level of FXR gene transcripts in CRC tissues was lower than that in normal colorectal tissues ( P < 0.01). Immunohistochemical examination of the collected tissues showed that the positive rate of FXR protein gradually decreased from the cecum to the rectum. The positive rates of FXR protein in healthy control, CRA patients and CRC patients were 90.9% (10/11), 24.0% (24/100), 6.3% (3/47), and the difference was statistically significant ( χ2 = 35.56, P < 0.01); the positive rate of FXR protein in cancer tissues from CRC patients was lower than that in normal tissues adjacent to cancer [6.3% (3/47) vs. 65.2% (15/23)], and the difference was statistically significant ( χ2 = 27.98, P < 0.01). There was no statistical difference in the positive rate of FXR among CRA patients with different gender, age, maximum diameter of adenoma, and aggression (all P > 0.05). There was also no statistical difference in the positive rate of FXR among CRC patients with different gender, age, tumor site, maximum diameter of tumor, degree of differentiation, TNM staging, and vascular tumor thrombus (all P > 0.05). According to the survival analysis of Kaplan-Meier Plotter online database, the recurrence-free survival of CRC patients with high expression of FXR was better than that of patients with low expression of FXR ( P = 0.003). Conclusions:The expression level of FXR gradually decreases in the intestinal tissues of healthy people, CRA patients and CRC patients. The prognosis of CRC patients with low FXR expression is poor.

Objective To profile gut microbiome-associated metabolites in serum and investigate whether these metabolites could distinguish individuals with colorectal cancer (CRC) or adenoma from normal healthy individuals. Design Integrated analysis of untargeted serum metabolomics by liquid chromatography-mass spectrometry and metagenome sequencing of paired faecal samples was applied to identify gut microbiome-associated metabolites with significantly altered abundance in patients with CRC and adenoma. The ability of these metabolites to discriminate between CRC and colorectal adenoma was tested by targeted metabolomic analysis. A model based on gut microbiome-associated metabolites was established and evaluated in an independent validation cohort. Results In total, 885 serum metabolites were significantly altered in both CRC and adenoma, including eight gut microbiome-associated serum metabolites (GMSM panel) that were reproducibly detected by both targeted and untargeted metabolomics analysis and accurately discriminated CRC and adenoma from normal samples. A GMSM panel-based model to predict CRC and colorectal adenoma yielded an area under the curve (AUC) of 0.98 (95% CI 0.94 to 1.00) in the modelling cohort and an AUC of 0.92 (83.5% sensitivity, 84.9% specificity) in the validation cohort. The GMSM model was significantly superior to the clinical marker carcinoembryonic antigen among samples within the validation cohort (AUC 0.92 vs 0.72) and also showed promising diagnostic accuracy for adenomas (AUC=0.84) and early-stage CRC (AUC=0.93). Conclusion Gut microbiome reprogramming in patients with CRC is associated with alterations of the serum metabolome, and GMSMs have potential applications for CRC and adenoma detection.

目的 检测肿瘤坏死因子相关凋亡诱导配体(TRAIL)对胃癌细胞的杀伤作用及其受体在胃癌细胞中的表达情况,评估TRAIL信号在胃癌治疗中的可行性.方法 研究选取11株胃癌细胞进行实验,采用实时荧光定量PCR方法检测胃癌细胞中TRAIL相关受体(DR4、DR5、DcR1、DcR2)mRNA表达.采用Cell Counting Kit-8(CCK-8)法检测TRAIL抑制胃癌细胞生长,Annexin V/PI双染色法测定TRAIL诱导细胞凋亡,Western blot检测TRAIL介导Caspase裂解.结果 死亡受体DR4、DR5在11株胃癌细胞内普遍高表达,表达水平显著高于诱骗受体DcR1、DcR2.TRAIL对9株胃癌细胞有不同程度的生长抑制作用,SNU-16、NUGC3、NCI-N87和SNU-1灵敏度最高,抑制作用呈时间和剂量依赖性.TRAIL通过诱导细胞凋亡发挥肿瘤杀伤作用,低浓度TRAIL(200 ng/ml)作用24 h后50％以上细胞发生凋亡.Caspase-3、-8、-9和PARP的裂解水平与凋亡程度相关.结论 TRAIL对胃癌细胞具有不同程度的生长抑制和凋亡诱导作用,在胃癌中具有潜在应用价值.

目的 通过回顾电子结肠镜检出结肠憩室患者的资料,分析结肠憩室发病特点及其与伴发疾病的相关性.方法 回顾性分析2014年6月-2019年5月该院13638例行电子结肠镜检查的内镜资料,采用SPSS 19.0统计软件分析结肠憩室患者检出情况及内镜下组织表现,以及其与伴发疾病的相关性.结果 共发现结肠憩室379例,检出率为2.78％,呈逐年升高趋势,由1.79％增长至3.35％,第5年较第1年检出率明显提高(P<0.05).结肠憩室发病与结肠息肉、结肠癌、结肠脂肪瘤、结肠黏膜黑变病和肠道手术史呈正相关(P<0.05),与缺血性结肠炎无明显相关性(P>0.05).结论 5年间电子结肠镜下结肠憩室检出率明显升高,结肠憩室检出率与结肠息肉、结肠癌、结肠脂肪瘤、结肠黑变病及肠道手术史均有相关性.

目的 评估2014年《中国早期胃癌筛查及内镜诊治共识意见》关于胃癌高危人群筛查在不同地区的适用性及有效性.方法 选取2018年1月至2018年6月就诊于安阳市人民医院和航天中心医院消化内科的患者,通过问卷调查方式采集胃癌相关高危因素信息,根据《共识意见》分为高危组及低危组,经胃镜及病理检查确认,比较两组患者胃癌、癌前疾病及癌前病变的检出情况,并分析胃癌高危因素.结果 384例患者根据《共识意见》分为胃癌高危组265例(69.0％)、低危组119例(31.0％).高危组患者胃癌、癌前病变检出率均为9.4％(25/265),显著高于低危组胃癌(1.7％,2/119)和癌前病变检出率(3.4％,4/119)(P<0.01),《共识意见》对胃癌的敏感性为92.6％,特异性为32.8％;高危组患者问卷调查中危险因素符合项数主要体现为2～3项,其中胃癌前疾病史及不良饮食习惯是胃癌发病的独立危险因素.结论 2014年《中国早期胃癌筛查及内镜诊治共识意见》在不同地区医院内筛查胃癌高危人群的适用性相同,其敏感性高而特异性及总符合率较低.与其他高危因素相比,既往癌前疾病史、吃饭速度快及饮食不规律与胃部疾病相关性更高.

目的:探讨健康体检人群消化道疾病的患病情况及胃肠镜联合检查的必要性.方法:回顾性分析笔者所在医院2016年5月-2017年12月2889例自愿接受胃肠镜联合检查的无症状健康体检者检查结果.结果:胃镜检查前三位消化道疾病分别为慢性非萎缩性胃炎(1587例,54.93％)、反流性食管炎(386例,13.36％)和胃息肉(252例,8.72％);慢性非萎缩性胃炎、胃息肉、反流性食管炎、慢性萎缩性胃炎、消化性溃疡和上消化道癌症检出率随着年龄的增长呈上升趋势(P<0.05);男性慢性非萎缩性胃炎和胃息肉的检出率明显低于女性(P<0.05);而慢性萎缩性胃炎、消化性溃疡和上消化道癌症检出率明显高于女性(P<0.05).结肠镜检查前三位病变分别为结直肠息肉(623例,21.56％)、结直肠炎(452例,15.65％)和溃疡性结肠炎(58例,2.01％);结直肠息肉和结直肠癌检出率随着年龄的增长呈上升趋势(P<0.05),而结直肠炎检出率随着年龄的增长呈下降趋势(P<0.05);男性结直肠息肉检出率明显高于女性(P<0.05),而结直肠炎检出率明显低于女性(P<0.05).结论:健康体检人群消化道疾病的发病率较高,胃肠镜联合检查有助于提高上消化道癌症和结直肠癌及癌前病变的检出率,有助于提高治疗效果,改善患者预后.

Photocatalytic nitrogen fixation is a promising sustainable and green strategy for NH3 synthesis.

[目的]探讨替诺福韦联合苦参素胶囊对乙型肝炎肝硬化患者临床效果、炎症反应及细胞免疫功能的影响,为临床治疗提供理论依据.[方法]选取2014-01-2016-01于我院消化内科就诊的乙型肝炎肝硬化患者256例,按照随机数字表法分为替诺福韦组(128例)和联合组(128例),2组患者在常规治疗的基础上分别服用替诺福韦、替诺福韦联合苦参素胶囊,治疗48周.观察2组患者治疗前后肝功能、血清HBV DNA水平、HBV DNA转阴率、炎性因子、细胞免疫功能的变化情况.[结果]治疗第48周,联合组总体疗效明显高于替诺福韦组(93.75％vs.85.16％,P＜0.05);而联合组血清AST、ALT和TBIL水平明显低于替诺福韦组(P＜0.05),联合组患者血清HBV DNA转阴率高于替诺福韦组(88.28％ vs.78.91％,P＜0.05).治疗第48周,联合组血清HBV DNA、IL-6、TNF-α和TGF-β1水平低于替诺福韦组(P＜0.05);而联合组血清CD4+水平和CD4+/CD8+比值明显高于替诺福韦组(P＜0.05).[结论]替诺福韦联合苦参素可以降低乙型肝炎肝硬化患者血清HBV DNA的水平,改善患者肝功能,增强患者细胞免疫功能,具有良好的临床疗效.

Metastatic neoplasm of the small intestine is uncommonly encountered. We herein reported a case of 66-year-old female patient with a history of cervical carcinoma presented as a spell of digestive symptoms. Imaging examination revealed disseminated disease involving her proximal jejunum. Endoscopic biopsy was performed showing metastatic squamous cell carcinoma with the same characteristics of cervical lesion. Although the clinical presentation of enteral metastases is extremely rare, awareness of such metastatic pattern of cervical cancer is necessary for diagnostic practices and therapeutic decisions.

Objective: Some neoplasms are missed in colonoscopy procedures make the colonic adenoma surveillance intervals difficult to put into practice. Our research tried to avoid the influence of missed neoplasms, analyzed the adenoma recurrence and provided surveillance suggestion for patients after polypectomy or other endoscopic therapy. Methods: A total of 303 patients with colonic adenoma and lesions remove between 2005 and 2009 were respectively analyzed, all patients were suggested colonoscopy within 6 months after initial colonoscopy and removed missed adenomas. Every patient underwent surveillance colonoscopies every 1-2 years to detect the adenomas recurrence. Results: The median recurrence time was 23 months, male patients, patients older than 60 years, patients with extracolonic tumor history; with alcohol history and patients with >= 3 adenomas has high risk of adenoma recurrence. Conclusions: The first surveillance colonscopy are suggested 24 months after initial colonscopy, if patients are male patients, older than 60 years, with extracolonic tumor history or drinking history in the mean time, shorter surveillance interval are suggested.

Objective To investigate the relationship between general clinical characteristics,different stages of adenomas,metabolic syndrome (MetS) factors of patients with colorectal adenoma (CRA) and cyclooxygenase-2 (COX-2)expression in colonic mucosa.Methods Samples of normal mucosa in left colon from 51 CRA patients(CRA group) and 8 patients(control group,without CRA or any MetS factors) were collected.The expression of COX-2 in colonic mucosa was detected by immunohistochemnistry (IHC).COX-2 IHC staining scores and percentages of samples identified as COX-2 positive in epithelial layer,together with numbers of lamina propria COX-2 positive cells were assessed.The relationship between these 3 indexes and general clinical characteristics such as sex,age,smoking history,alcohol history,history of gallbladder removal,history of gastrointestinal neoplasms,and family history of colorectal neoplasms,were analyzed.CRA patients were divided into two groups based on whether they were with advanced adenomas or MetS factors,and two groups were compared with each other.Results No general clinical characteristics were significantly associated with COX-2 expression in colonic normal mucosa(P＞0.05).Numbers of lamina propria COX-2 positive cells in patients with advanced adenomas were significantly higher than control group (P＜ 0.05).All 3 indexes above-mentioned in CRA patients with MetS factors were significantly higher than those without any MetS factors (P＜0.01).Conclusion COX-2 expression in colonic mucosa of patients with CRA is significantly associated with MetS factors.

OBJECTIVE To investigate the distribution of various bacteria in adenoma tissue of colorectal adenoma (T/CRA), normal colonic mucosa tissue adjacent to the adenoma (N/CRA), and healthy colonic mucosa tissue (N/H) by comparing the number of total bacteria, Bacteroides fragilis (BF), enterotoxigenic Bacteroides fragilis (ETBF), polyketide synthase (pks) gene-expressing Escherichia coli(E.coli)(pks(+) E. coli)among the above 3 types of tissues. METHODS A total of 36 patients diagnosed with colorectal adenoma by colonoscopy and pathology in Department of Gastroenterology, Peking University People's Hospital from September 2011 to September 2013 were selected into this study. T/CRA and N/CRA tissues from the 36 patients and N/H tissues from 18 healthy controls were collected for DNA extraction. The number of total bacteria, BF, ETBF, pks(+) E. coli was detected by quantitative real time PCR, and their correlation with colorectal adenoma was analyzed. RESULTS (1) The number of total bacteria decreased gradually from N/H, N/CRA, to T/CRA, with the median values being 3.18×10(8,) 1.57×10(8,) and 7.91×10(7) copies/g, respectively, and with significant difference among the three groups and between each two groups (all P<0.01). (2) The content of BF decreased gradually from N/H, N/CRA, to T/CRA, the median values being 6.03×10(5,) 4.28×10(4,) and 5.48×10(3) copies/g, respectively, and with significant difference among the three groups and between each two groups (all P<0.01). (3) The toxin content produced by ETBF increased from N/H, N/CRA, to T/CRA, the relative expression being 1.73±0.30, 6.15±1.52, and 8.54±1.80, respectively. Significant difference was found between the T/CRA and N/H tissue (P=0.003), but not between any other two groups. (4) The expression of clbB in pks(+) E.coli was highest in T/CRA colonic tissue (2.96±0.28), followed by the N/CRA (2.79±0.19) and N/H tissue (1.06±0.08). Significant difference was found between T/CRA and N/H tissues, as well as between N/CRA and N/H tissues (both P<0.001), but not between T/CRA and N/CRA tissues. CONCLUSIONS The number of total bacteria is markedly reduced in the colonic mucosa of CRA patients compared to normal people, while the expressions of ETBF and pks(+) E.coli are significantly increased. Such changes in total bacterial, ETBF and pks(+) E.coli concentrations in colonic mucosa may be related to the tumorigenesis of colorectal adenoma.

The fungal microbiota is an important component of the human gut microbiome and may be linked to gastrointestinal disease. In this study, the fungal microbiota of biopsy samples from adenomas and adjacent tissues was characterized by deep sequencing. Ascomycota, Glomeromycota and Basidiomycota were identified as the dominant phyla in both adenomas and adjacent tissues from all subjects. Among the 60 genera identified, the opportunist pathogens Phoma and Candida represented an average of 45% of the fungal microbiota. When analyzed at the operational taxonomic unit (OTU) level, however, a decreased diversity in adenomas was observed and three OTUs differed significantly from the adjacent tissues. Principal Component Analysis (PCA) revealed that the core OTUs formed separate clusters for advanced and non-advanced adenomas for which the abundance of four OTUs differed significantly. Moreover, the size of adenomas and the disease stage were closely related to changes in the fungal microbiota in subjects with adenomas. This study characterized the fungal microbiota profile of subjects with adenomas and identified potential diagnostic biomarkers closely related to different stages of adenomas.