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| 1 | 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 |
| 2 | Sclerostin activity plays a key role in the negative effect of glucocorticoid signaling on osteoblast function in mice显示文摘Stress during prenatal development is correlated with detrimental cognitive and behavioral outcomes in offspring. However, the long-term impact of prenatal stress(PS) and disrupted glucocorticoid signaling on bone mass and strength is not understood. In contrast, the detrimental effect of lead(Pb) on skeletal health is well documented. As stress and Pb act on common biological targets via glucocorticoid signaling pathways and co-occur in the environment, this study first sought to assess the combined effect of stress and Pb on bone quality in association with alterations in glucocorticoid signaling. Bone parameters were evaluated using microCT, histomorphometry, and strength determination in 8-month-old male mouse offspring subjected to PS on gestational days 16 and 17, lifetime Pb exposure(100 p.p.m. Pb in drinking water), or to both. Pb reduced trabecular bone mass and, when combined with PS, Pb unmasked an exaggerated decrement in bone mass and tensile strength. Next, to characterize a mechanism of glucocorticoid effect on bone, prednisolone was implanted subcutaneously(controlled-release pellet, 5 mg·kg^(-1) per day) in 5-month-old mice that decreased osteoblastic activity and increased sclerostin and leptin levels. Furthermore, the synthetic glucocorticoid dexamethasone alters the anabolic Wnt signaling pathway. The Wnt pathway inhibitor sclerostin has several glucocorticoid response elements, and dexamethasone administration to osteoblastic cells induces sclerostin expression. Dexamethasone treatment of isolated bone marrow cells decreased bone nodule formation, whereas removal of sclerostin protected against this decrement in mineralization.Collectively, these findings suggest that bone loss associated with steroid-induced osteoporosis is a consequence of sclerostin-mediated restriction of Wnt signaling, which may mechanistically facilitate glucocorticoid toxicity in bone. | Eric E Beier Tzong-Jen Sheu Emily A Resseguie Masahiko Takahata Hani A Awad Deborah A Cory-Slechta J Edward Puzas | 2017 | Bone Research2017，5，2： | 3 |
| 3 | Portal vein thrombosis after splenectomy显示文摘 | Emily R Winslow L.Michael Brunt Jeffery A Drebin Nathaniel J Soper Mary E Klingensmith | 2002 | The American Journal of Surgery2002，，6： | 3 |
| 4 | Histopathological characteristics and causes of kidney graft failure in the current era of immunosuppression显示文摘BACKGROUND The histopathological findings on the failing kidney allograft in the modern era is not well studied. In this study, we present our experience working with kidney transplant recipients with graft failure within one year of the biopsy.AIM To report the histopathological characteristics of failed kidney allografts in the current era of immunosuppression based on the time after transplant, cause of the end-stage renal disease and induction immunosuppressive medications.METHODS In a single-center observational study, we characterized the histopathological findings of allograft biopsies in kidney transplant recipients with graft failure within one year after the biopsy.RESULTS We identified 329 patients with graft failure that met the selection criteria between January 1, 2006 and December 31, 2016. The three most common biopsy findings were interstitial fibrosis and tubular atrophy(IFTA, 53%), acute rejection (AR, 43%) and transplant glomerulopathy(TG, 33%). Similarly, the three most common causes of graft failure based on the primary diagnosis were AR(40%),TG(17%), and IFTA(13%). Most grafts failed within two years of post-transplant(36%). Subsequently, approximately 10%-15% of grafts failed every two years: >2-4 years(16%), > 4-6 years(13%), > 6-8 years(11%), > 8-10 years(9%) and > 10 years(16%). AR was the most common cause of graft failure in the first six years(48%), whereas TG was the most prevalent cause of graft failure after 6 years(32%) of transplant.CONCLUSION In the current era of immunosuppression, AR is still the most common cause of early graft failure, while TG is the most prevalent cause of late graft failure. | Sandesh Parajuli Fahad Aziz Neetika Garg Sarah E Panzer Emily Joachim Brenda Muth Maha Mohamed Justin Blazel Weixiong Zhong Brad C Astor Didier A Mandelbrot Arjang Djamali | 2019 | World Journal of Transplantation2019，9，6： | 2 |
| 5 | Tissue structure and connexin expression of cannie pulmonary veins显示文摘 | Sander V Emily E | 2002 | Cardiovasc Res2002，55，： | 1 |
| 6 | The cytoplasmic tails of infectious bronchitis virus E and M proteins mediate their interaction显示文摘 | EMILY C CAROLYN E M | 2003 | Virology2003，312，： | 1 |
| 7 | Computer image analysisand classification of giant ragweed seeds显示文摘 | Sako Y Emilie E R Daoust T et a1 | 2001 | Weed Sci2001，49，： | 1 |
| 8 | A pilot study of a thiazolidinedione, troglitazone, in nonalcoholic steatohepatitis显示文摘 | Stephen H Caldwell Elizabeth E Hespenheide Jan A Redick Julia C Iezzoni Emily H Battle Bonnie L Sheppard | 2001 | The American Journal of Gastroenterology2001，，2： | 1 |
| 9 | Frey Procedure in Patients with Chronic Pancreatitis: Short and Long-term Outcome from a Prospective Study显示文摘 | Alexandra Roch Dorothée Brachet Emilie Lermite Patrick Pessaux Jean-Pierre Arnaud | 2012 | Journal of Gastrointestinal Surgery2012，，7： | 1 |
| 10 | Differential radiometers using Fabry-Perot interferometric technique for remote sensing of greenhouse gases显示文摘 | E M Georgieva W S Heaps Emily L Wilson | 2008 | IEEE Transactions on Geoscienceand Remote sensing2008，46，10： | 1 |
| 11 | The structure ofgrowing social networks 显示文摘 | EMILY M J MICHELLE Q NEWMAN M E J | 2001 | Physical Review Letters E2001，64，04： | 1 |
| 12 | Bosco, Rb in breast cancer显示文摘 | Emily E | 2007 | Cell Cycle2007，6，6： | 1 |
| 13 | 4-Phenylbutyric Acid Treatment Rescues Trafficking and Processing of a Mutant Surfactant Protein-C显示文摘 | Stewart Gareth A Ridsdale Ross Martin Emily P Na Cheng-Lun Xu Yan Mandapaka Karunyakanth Weaver Timothy E | 2012 | EN2012，，3： | 1 |
| 14 | Bosco, Elizabeth Kramer 显示文摘 | Sarah L Seeley Emily E | 2007 | Cancer letters2007，245，： | 1 |
| 15 | Genomic variation in the MAP3K5 gene is associated with &bgr;-thalassemia disease severity and hydroxyurea treatment efficacy显示文摘 | Christina Tafrali Arsinoi Paizi Joseph Borg Milena Radmilovic Marina Bartsakoulia Emily Giannopoulou Olga Giannakopoulou Maja Stojiljkovic-Petrovic Branka Zukic Konstantinos Poulas Eleana F Stavrou Polyxeni Lambropoulou Alexandra Kourakli Alexander E Feli | 2013 | Pharmacogenomics2013，，5： | 1 |
| 16 | Systematic analysis of bacterialeffectorpostsynaptic density 95/disc large/zonula occludens-1(PDZ)domain interactions demonstrates Shigella Osp E proteinpromotes protein kinase C activation via PDLIM proteins显示文摘 | Chae-ryun Yi John E Allen Brian Russo Soo Young Lee Jason E Heindl Leigh A Baxt Bobby Brooke Herrera Emily Kahoud Gavin Mac Beath Marcia B Goldberg | 2014 | The Journal of biological chemistry2014，289，30： | 1 |
| 17 | Living with Ma'i Suka: Individual, Familial, Cultural, and Environmental Stress a- mong Patients with Type 2 Diabetes Melliitus and Their Caregivers in American Samoa显示文摘 | Emily E Corabelle T Stephen T | 2008 | Prev Chronic Dis2008，5，3： | 1 |
| 18 | Total and labile soil organic matter in organic and conventional farming systems显示文摘 | EMILY E MARRIOTT MICHELLE M | 2006 | Soil Science Society of America Journal2006，70，6： | 1 |
| 19 | Biodegradation and environmental behavior of biodiesel mixtures in the sea: an initial study 显示文摘 | Jared A DeMello Catherine A Cannichael Emily E Peacock | 2007 | Marine Pollution Bulletin2007，，7： | 1 |
| 20 | Amniotic fluid concentrations of interleukin-1β, interleukin-6 and TNFα in chorioamnionitis before 32 weeks of gestation:histological associations and neonatal outcome显示文摘 | Baud O Emilie D Pelletier E | 1999 | Br J Obstetrics Gynec1999，106，1： | 1 |
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