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| 1 | Gut microbiota imbalance and colorectal cancer显示文摘The gut microbiota acts as a real organ. The symbiotic interactions between resident micro-organisms and the digestive tract highly contribute to maintain the gut homeostasis. However, alterations to the microbiome caused by environmental changes(e.g., infection, diet and/or lifestyle) can disturb this symbiotic relationship and promote disease, such as inflammatory bowel diseases and cancer. Colorectal cancer is a complex association of tumoral cells, non-neoplastic cells and a large amount of micro-organisms, and the involvement of the microbiota in colorectal carcinogenesis is becoming increasingly clear. Indeed, many changes in the bacterial composition of the gut microbiota have been reported in colorectal cancer, suggesting a major role of dysbiosis in colorectal carcinogenesis. Some bacterial species have been identified and suspected to play a role in colorectal carcinogenesis, such as Streptococcus bovis, Helicobacter pylori, Bacteroides fragilis, Enterococcus faecalis, Clostridium septicum, Fusobacterium spp. and Escherichia coli. The potential pro-carcinogenic effects of these bacteria are now better understood. In this review, we discuss the possible links between the bacterial microbiota and colorectal carcinogenesis, focusing on dysbiosis and the potential pro-carcinogenic properties of bacteria, such as genotoxicity and other virulence factors, inflammation, host defenses modulation, bacterial derived metabolism, oxidative stress and anti-oxidative defenses modulation. We lastly describe how bacterial microbiota modifications could represent novel prognosis markers and/or targets for innovative therapeutic strategies. | Johan Gagnière Jennifer Raisch Julie Veziant Nicolas Barnich Richard Bonnet Emmanuel Buc Marie-Agnès Bringer Denis Pezet Mathilde Bonnet | 2016 | World Journal of Gastroenterology2016，22，2： | 76 |
| 2 | Pre-diagnostic levels of adiponectin and soluble vascular cell adhesion molecule-1 are associated with colorectal cancer risk显示文摘AIM: To examine the relationships between pre-diagnostic biomarkers and colorectal cancer risk and assess their relevance in predictive models.METHODS: A nested case-control study was designed to include all first primary incident colorectal cancer cases diagnosed between inclusion in the SUpplémentation en VItamines et Minéraux AntioXydants cohort in 1994 and the end of follow-up in 2007. Cases (n = 50) were matched with two randomly selected controls (n = 100). Conditional logistic regression models were used to investigate the associations between pre-diagnostic levels of hs-CRP, adiponectin, leptin, soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1, E-selectin, monocyte chemoattractant protein-1 and colorectal cancer risk. Area under the receiver operating curves (AUC) and relative integrated discrimination improvement (RIDI) statistics were used to assess the discriminatory potential of the models. RESULTS: Plasma adiponectin level was associated with decreased colorectal cancer risk (P for linear trend = 0.03). Quartiles of sVCAM-1 were associated with increased colorectal cancer risk (P for linear trend = 0.02). No association was observed with any of the other biomarkers. Compared to standard models with known risk factors, those including both adiponectin and sVCAM-1 had substantially improved performance for colorectal cancer risk prediction (P for AUC improvement = 0.01, RIDI = 26.5%). CONCLUSION: These results suggest that pre-diagnostic plasma adiponectin and sVCAM-1 levels are associated with decreased and increased colorectal cancer risk, respectively. These relationships must be confirmed in large validation studies. | Mathilde Touvier Léopold Fezeu Namanjeet Ahluwalia Chantal Julia Nathalie Charnaux Angela Sutton Caroline Méjean Paule Latino-Martel Serge Hercberg Pilar Galan Sébastien Czernichow | 2012 | World Journal of Gastroenterology2012，18，22： | 15 |
| 3 | Colon cancer-associated B2 Escherichia coli colonize gut mucosa and promote cell proliferation显示文摘AIM:To provide further insight into the characterization of mucosa-associated Escherichia coli(E.coli)isolated from the colonic mucosa of cancer patients.METHODS:Phylogroups and the presence of cyclomodulin-encoding genes of mucosa-associated E.coli from colon cancer and diverticulosis specimens weredetermined by PCR.Adhesion and invasion experiments were performed with I-407 intestinal epithelial cells using gentamicin protection assay.Carcinoembryonic antigen-related cell adhesion molecule 6(CEACAM6)expression in T84 intestinal epithelial cells was measured by enzyme-linked immunosorbent assay and by Western Blot.Gut colonization,inflammation and procarcinogenic potential were assessed in a chronic infection model using CEABAC10 transgenic mice.Cell proliferation was analyzed by real-time mRNA quantification of PCNA and immunohistochemistry staining of Ki67.RESULTS:Analysis of mucosa-associated E.coli from colon cancer and diverticulosis specimens showed that whatever the origin of the E.coli strains,86%of cyclomodulin-positive E.coli belonged to B2 phylogroup and most harbored polyketide synthase(pks)island,which encodes colibactin,and/or cytotoxic necrotizing factor(cnf)genes.In vitro assays using I-407 intestinal epithelial cells revealed that mucosa-associated B2 E.coli strains were poorly adherent and invasive.However,mucosa-associated B2 E.coli similarly to Crohn’s disease-associated E.coli are able to induce CEACAM6expression in T84 intestinal epithelial cells.In addition,in vivo experiments using a chronic infection model of CEACAM6 expressing mice showed that B2 E.coli strain11G5 isolated from colon cancer is able to highly persist in the gut,and to induce colon inflammation,epithelial damages and cell proliferation.CONCLUSION:In conclusion,these data bring new insights into the ability of E.coli isolated from patients with colon cancer to establish persistent colonization,exacerbate inflammation and trigger carcinogenesis. | Jennifer Raisch Emmanuel Buc Mathilde Bonnet Pierre Sauvanet Emilie Vazeille Amélie de Vallée Pierre Déchelotte Claude Darcha Denis Pezet Richard Bonnet Marie-Agnès Bringer Arlette Darfeuille-Michaud | 2014 | World Journal of Gastroenterology2014，20，21： | 12 |
| 4 | Hepatitis C virus infection down-regulates the expression of peroxisome proliferator-activated receptor a and carnitine palmitoyl acyl-CoA transferase 1A显示文摘AIM: To elucidate the role of the peroxisome proliferator-activated receptor α (PPARα) and its target gene carnitine palmitoyl acyl-CoA transferase 1A (CPT1A)in the pathogenesis of hepatitis C virus (HCV) infection.METHODS: Liver samples were collected from the patients with chronic HCV infection and controls. HepG2cells were transfected with vector pEF352neo carrying.Two independent clones (clone N3 and N4) stably expressing HCV core protein were analyzed. Total RNA was extracted from cells and liver tissues. PPARα and CPT1A mRNAs were quantified by real-time polymerase chain reaction (PCR) using SYBR Green Master. Total extracted proteins were separated by polyacrylamide gel electrophoresis, and electroblotted. Membranes were incubated with the anti-PPARα antibody, then with a swine anti-rabbit IgG conjugated to horseradish peroxidase for PPARα. Protein bands were revealed by an enhanced chemiluminescence reaction for PPARα. For immunohistochemical staining of PPARα, sections were incubated with the primary goat polyclonal antibody directed against PPARα at room temperature.RESULTS: Real-time PCR indicated that the PPARα level and expression level of CPT1A gene in hepatitis C patients lowered significantly as compared with the controls (1.8±2.8 vs 13±3.4, P = 0.0002; 1.1±1.5 vs 7.4+1, ,P = 0.004). Western blot results showed that the level of PPARα protein in the livers of hepatitis C patients was lower than that in controls (2.3±0.3 vs 3.6±0.2,P = 0.009). The immunohistochemical staining results in chronic hepatitis C patients indicated a decrease in PPARα staining in hepatocytes compared with those in the control livers. The in vitro studies found that in the N3 and N4 colon stably expressing HCV core protein, the PPARα mRNA levels were significantly lower than that in the controls.CONCLUSION: The impaired intrahepatic PPARα expression is associated with the pathogenic mechanism in hepatic injury during chronic HCV infection. HCV infection reduced the expression of PPARα and CPT1A at the level of not only mRNAs but also proteins. PPARα plays an important role in the pathogenesis of chronic HCV infection, but the impaired function of this nuclear receptor in HCV infection needs further studies. | Yang Cheng Sébastien Dharancy Mathilde Malapel Pierre Desreumaux | 2005 | World Journal of Gastroenterology2005，11，48： | 11 |
| 5 | Microbial markers in colorectal cancer detection and/or prognosis显示文摘Colorectal cancer(CRC) is the second leading cause of cancer worldwide. CRC is still associated with a poor prognosis among patients with advanced disease. On the contrary, due to its slow progression from detectable precancerous lesions, the prognosis for patients with early stages of CRC is encouraging. While most robust methods are invasive and costly, actual patient-friendly screening methods for CRC suffer of lack of sensitivity and specificity. Therefore, the development of sensitive, non-invasive and cost-effective methods for CRC detection and prognosis are necessary for increasing the chances of a cure. Beyond its beneficial functions for the host, increasing evidence suggests that the intestinal microbiota is a key factor associated with carcinogenesis. Many clinical studies have reported a disruption in the gut microbiota balance and an alteration in the faecal metabolome of CRC patients, suggesting the potential use of a microbialbased test as a non-invasive diagnostic and/or prognostic tool for CRC screening. This review aims to discuss the microbial signatures associated with CRC known to date, including dysbiosis and faecal metabolome alterations, andthe potential use of microbial variation markers for noninvasive early diagnosis and/or prognostic assessment of CRC and advanced adenomas. We will finally discuss the possible use of these markers as predicators for treatment response and their limitations. | Romain Villéger Amélie Lopès Julie Veziant Johan Gagnière Nicolas Barnich Elisabeth Billard Delphine Boucher Mathilde Bonnet | 2018 | World Journal of Gastroenterology2018，24，22： | 10 |
| 6 | Karyotype and Genome Size Estimation of Haliotis midae: Estimators to Assist Future Studies on the Evolutionary History of Haliotidae显示文摘 | PAOLO F RUHAN S MATHILDE V D M | 2010 | Journal of Shellfish Research2010，29，4： | 1 |
| 7 | Impaired expression of the peroxisome proliferator–activated receptor alpha during hepatitis C virus infection显示文摘 | Sébastien Dharancy Mathilde Malapel Gabriel Perlemuter Tania Roskams Yang Cheng Laurent Dubuquoy Philippe Podevin Filoména Conti Valérie Canva David Philippe Luc Gambiez Philippe Mathurin Jean-Claude Paris Kristina Schoonjans Yvon Calmus Stanislas Pol Joh | 2005 | Gastroenterology2005，，2： | 1 |
| 8 | Predicted Propo- fol effect-site concentration for induction and emergence of Anesthesia during early pregnancy 显示文摘 | Nicolas M Fr6d6rique S Mathilde P | 2009 | Anesth Analg2009，109，1： | 1 |
| 9 | What is the heritable component of spinal deformities in the European sea bass ( Dicentrarchus labrax )?显示文摘 | Agnès Bardon Marc Vandeputte Mathilde Dupont-Nivet Hervé Chavanne Pierrick Haffray Alain Vergnet Béatrice Chatain | 2009 | Aquaculture2009，，3： | 1 |
| 10 | Peptidoglycan maturation enzymes affect flagellar functionality in bacteria显示文摘 | Sophie Roure Mathilde Bonis Catherine Chaput Chantal Ecobichon Austin Mattox Charlotte Barrière Nina Geldmacher Stéphanie Guadagnini Christine Schmitt Marie‐Christine Prévost Agnès Labigne Steffen Backert Richard L. Ferrero Ivo G. Boneca | 2012 | Molecular Microbiology2012，，4： | 1 |
| 11 | An infant and child feedingindex is associated with the nutritional status of 6-to23-month-oldchildren in rural Burkina faso显示文摘 | Prosper SS Yves MP Mathilde S | 2006 | J Nutr2006，136，3： | 1 |
| 12 | HIV-associated pulmonary arterial hypertension: survival and prognostic factors in the modern therapeutic era显示文摘 | Bruno Degano Mathilde Guillaume Laurent Savale David Montani Xavier Ja?s Azzedine Yaici Jér?me Le Pavec Marc Humbert Gérald Simonneau Olivier Sitbon | 2010 | AIDS2010，，1： | 1 |
| 13 | Wavelength conversion in a highly nonlinear chalcogenide microstructured fiber 显示文摘 | DAT S L MATHILDE G LAURENT | 2012 | OPTICS LET- TERS2012，37，22： | 1 |
| 14 | An infant and child feeding index is associated with the nutritional status of 6-to 23-month-old children in rural burkina faso显示文摘 | Prosper SS Yves MP Mathilde S | 2006 | American Society for Nutrition J Nutr2006，136，3： | 1 |
| 15 | Plant secondary me tabolism glycosyltransferases: the emerging functional analysis 显示文摘 | Claire M M Mathilde L M Patrick S | 2005 | Trends in Plant Science2005，10，11： | 1 |
| 16 | The candidate gene approach in plant genetics:a review显示文摘 | Pflieger S Lefebvre V Mathilde C | 2001 | Mol Breed2001，7，： | 1 |
| 17 | Unintentional child home injury in- cidence and patterns in six countries in Europe显示文摘 | Mathilde S Robert B | 2008 | Interna- tional Journal of Injury Control and Safety Promotion2008，15，3： | 1 |
| 18 | A Pilot Study of Fecal Serine-Protease Activity: A Pathophysiologic Factor in Diarrhea-Predominant Irritable Bowel Syndrome显示文摘 | Richárd Róka András Rosztóczy Mathilde Leveque Ferenc Izbéki Ferenc Nagy Tamás Molnár János Lonovics Rafael Garcia–Villar Jean Fioramonti Tibor Wittmann Lionel Bueno | 2007 | Clinical Gastroenterology and Hepatology2007，，5： | 1 |
| 19 | 加工食品与心血管疾病发生风险:前瞻性队列研究(NutriNet-Santé)显示文摘目的评估食用超加工食品与心血管疾病发生风险的前瞻性关联。方法基于人群的队列研究。背景NutriNet-Santé队列,法国2009—2018年。参与者年龄≥18岁的105159位受试者。应用重复24小时的膳食记录(平均每人5.7小时)收集受试者饮食摄入情况,用以记录受试者日常对于3300种食品的摄入情况。根据加工程度利用NOVA分级将这些食品进行分类。主要结局测量在校正已知风险因素后,利用多变量Cox比例风险模型评估食用超加工食品与总体心血管疾病及冠状动脉性心脏病、脑血管疾病发生风险的关系。结果研究的中位随访时间为5.2年,其间食用超加工食品与总体心血管疾病[1409例患病,超加工食品在饮食中所占百分比绝对增加10%的危险比为1.12(95%可信区间为1.05~1.20);P<0.01,518208人年;食用超加工食品量最多的受试者(Q4)其总体心血管疾病发病率为277/10万人年,而在食用量最少的受试者(Q1)中为242/10万人年]、冠状动脉心脏病[665例患病;危险比1.13(1.02~1.24);P=0.02,520319人年;在超加工食品食用量最多和最少者的发病率分别为124/10万人年和109/10万人年]及脑血管疾病[829例患病;危险比1.11(1.01~1.21);P=0.02,520023人年;超加工食品食用量最多和最少者的发病率分别为163/10万人年和144/10万人年]的发病高风险有关。在校正了数种膳食营养质量标记(饱和脂肪酸、钠与糖摄入量、膳食纤维或者是来自主成分分析的健康饮食模式)的影响及大范围灵敏度分析后,这些结果仍存在统计学显著性。结论这项大型观察性研究发现,食用大量超加工食品与心血管疾病、冠状动脉性心脏病及脑血管疾病的高发病风险相关。这些结果仍需要在其他人群或研究单位进行验证,并且因果关系仍待确定。食品加工中的多种因素,如终产品的营养成分、添加剂、接触材料和新污染物,可能在这种联系中发挥某种作用,其各自作用的大小仍需要进一步研究。同时,几个国家的公共卫生当局近期已经开始鼓励人们食用未经加工或者经简单加工的食品,并且限制超加工食品的摄入。研究注册ClinicalTrials.gov NCT03335644。 | Méjean Caroline Bernard Srour Léopold K Fezeu Emmanuelle Kesse-Guyot Benjamin Allès Caroline Méjean Roland M Andrianasolo Eloi Chazelas Melanie Deschasaux Serge Hercberg Pilar Galan Carlos A Monteiro Chantal Julia Mathilde Touvier 霍永丰(译) | 2020 | 英国医学杂志中文版2020，23，1： | 0 |
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