维普中文期刊产品整合服务
488篇 您的检索式:作者名="Danese"
    题名 作者 年代 出处 被引量
1Etiopathogenesis of inflammatory bowel diseases显示文摘理论解释煽动性的肠疾病(IBD ) 的发病机理自从 Crohn 的疾病(CD ) 和 ulcerative (UC ) 被建议了作为疾病的二种主要形式被认出。尽管在 CD 和 UC 的织物损坏的准确原因和机制还得完全被理解,足够的进步发生了作为有效接受下列假设:IBD 是在环境因素,微生物引起的因素,和肠的免疫系统之中作为一个复杂相互作用的结果发生在遗传上易受影响的个人的不恰当的有免疫力的回答。在环境因素的一张几乎无穷的表之中,吸烟为 UC 为 CD 和一个保护的因素作为一个风险因素被识别了。在微生物引起的因素之中,没有有说服力的证据显示古典传染代理人引起 IBD,当作为具有中央重要性对正常伤寒植物群装证据点到反常有免疫力的回答时。内脏发炎被天生以及适应的免疫系统的房间调停,与非有免疫力的房间的另外的贡献,例如上皮,间充质并且 endothelial,和血小板。Silvio Danese Claudio Fiocchi 2006World Journal of Gastroenterology2006,12,30:61
2Intestinal microbiota in inflammatory bowel disease:Friend of foe?显示文摘Inflammatory bowel disease(IBD) arises from disruption of immune tolerance to the gut commensal microbiota,leading to chronic intestinal inflammation and mucosal damage in genetically predisposed hosts.In healthy individuals the intestinal microbiota have a symbiotic relationship with the host organism and possess important and unique functions,including a metabolic function(i.e.digestion of dietary compounds and xenobiotics,fermentation of undigestible carbohydrates with production of short chain fatty acids),a mucosal barrier function(i.e.by inhibiting pathogen invasion and strengthening epithelial barrier integrity),and an immune modulatory function(i.e.mucosal immune system priming and maintenance of intestinal epithelium homeostasis).A fine balance regulates the mechanism that allows coexistence of mammals with their commensal bacteria.In IBD this mechanism of immune tolerance is impaired because of several potential causative factors.The gut microbiota composition and activity of IBD patients are abnormal,with a decreased prevalence of dominant members of the human commensal microbiota(i.e.Clostridium Ⅸa and Ⅳ groups,Bacteroides,bifidobacteria) and a concomitant increase in detrimental bacteria(i.e.sulphate-reducing bacteria,Escherichia coli).The observed dysbiosis is concomitant with defective innate immunity and bacterial killing(i.e.reduced mucosal defensins and IgA,malfunctioning phagocytosis) and overaggressive adaptive immune response(due to ineffective regulatory T cells and antigen presenting cells),which are considered the basis of IBD pathogenesis.However,we still do not know how the interplay between these parameters causes the disease.Studies looking at gut microbial composition,epithelial integrity and mucosal immune markers in genotyped IBD populations are therefore warranted to shed light on this obscure pathogenesis.Francesca Fava Silvio Danese 2011World Journal of Gastroenterology2011,17,5:30
3Extraintestinal manifestations in inflammatory bowel disease显示文摘Inflammatory bowel diseases (IBD) can be really considered to be systemic diseases since they are often associated with extraintestinal manifestations,complications, and other autoimmune disorders. Indeed,physicians who care for patients with ulcerative colitis and Crohn's disease, the two major forms of IBD, face a new clinical challenge every day, worsened by the very frequent rate of extraintestinal complications. The goal of this review is to provide an overview and an update on the extraintestinal complications occurring in IBD.Indeed, this paper highlights how virtually almost every organ system can be involved, principally eyes, skin,joints, kidneys, liver and biliary tracts, and vasculature (or vascular system) are the most common sites of systemic IBD and their involvement is dependent on different mechanisms.Silvio Danese Stefano Semeraro Alfredo Papa Italia Roberto Franco Scaldaferri Giuseppe Fedeli Giovanni Gasbarrini Antonio Gasbarrini 2005World Journal of Gastroenterology2005,11,46:24
4Familial aggregation in inflammatory bowel disease:Is it genes or environment?显示文摘Inflammatory bowel disease (IBD) develops in genetically susceptible individuals due to the influence of environmental factors, leading to an abnormal recognition of microbiota antigens by the innate immune system which triggers an exaggerated immune response and subsequent bowel tissue damage. IBD has been more frequently found in families, an observation that could be due to either genetic, environmental or both types of factors present in these families. In addition to expanding our knowledge on IBD pathogenesis, defining the specific contribution to familial IBD of each one of these factors might have also clinical usefulness. We review the available evidence on familial IBD pathogenesis.Tiago Nunes Gionata Fiorino Silvio Danese Miquel Sans 2011World Journal of Gastroenterology2011,17,22:9
5Narrow-band imaging endoscopy to assess mucosal angiogenesis in inflammatory bowel disease: A pilot study显示文摘AIM: To investigate whether narrow band imaging (NBI) is a useful tool for the in vivo detection of angiogenesis in inflammatory bowel disease (IBD) patients. METHODS: Conventional and NBI colonoscopy was performed in 14 patients with colonic inflammation (8 ulcerative colitis and 6 Crohn’s disease). Biopsy samples were taken and CD31 expression was assayed immuno- histochemically; microvascular density was assessed by vessel count. RESULTS: In areas that were endoscopically normal but positive on NBI, there was a significant (P < 0.05) increase in angiogenesis (12 ± 1 vessels/field vs 18 ± 2 vessels/field) compared with areas negative on NBI. In addition, in areas that were inflamed on white light endoscopy and positive on NBI, there was a significant (P < 0.01) increase in vessel density (24 ± 7 vessels/f ield) compared with NBI-negative areas.CONCLUSION: NBI may allow in vivo imaging of intestinal angiogenesis in IBD patients.Silvio Danese Gionata Fiorino Erika Angelucci Stefania Vetrano Nico Pagano Giacomo Rando Antonino Spinelli Alberto Malesci Alessandro Repici 2010World Journal of Gastroenterology2010,16,19:9
6Calcium supplementation for the prevention of colorectal adenomas: a systematic review and meta-analysis of randomized controlled trials显示文摘AIM: To determine the efficacy of calcium supplementation in reducing the recurrence of colorectal adenomas.METHODS: We conducted a systematic review and meta-analysis of published studies. We searched Pub Med, Scopus, the Cochrane Library, the WHO International Clinical Trials Registry Platform, and the Clinical Trials.gov website, through December 2015. Randomized, placebo-controlled trials assessing supplemental calcium intake for the prevention of recurrence of adenomas were eligible for inclusion. Two reviewers independently selected studies based on predefined criteria, extracted data and outcomes(recurrence of colorectal adenomas, and advanced or 'high-risk' adenomas), and rated each trial's riskof-bias. Between-study heterogeneity was assessed, and pooled risk ratio(RR) estimates with their 95% confidence intervals(95%CI) were calculated using fixed- and random-effects models. To express the treatment effect in clinical terms, we calculated the number needed to treat(NNT) to prevent one adenoma recurrence. We also assessed the quality of evidence using GRADE.RESULTS: Four randomized, placebo-controlled trials met the eligibility criteria and were included. Daily doses of elemental calcium ranged from 1200 to 2000 mg, while the duration of treatment and follow-up of participants ranged from 36 to 60 mo. Synthesis of intention-to-treat data, for participants who had undergone follow-up colonoscopies, indicated a modest protective effect of calcium in prevention of adenomas(fixed-effects, RR = 0.89, 95%CI: 0.82-0.96; randomeffects, RR = 0.87, 95%CI: 0.77-0.98; high quality of evidence). The NNT was 20(95%CI: 12-61) to prevent one colorectal adenoma recurrence within a period of 3 to 5 years. On the other hand, the association between calcium treatment and advanced adenomas did not reach statistical significance(fixed-effects, RR = 0.92, 95%CI: 0.75-1.13; random-effects, RR = 0.92, 95%CI: 0.71-1.18; moderate quality of evidence). CONCLUSION: Our results suggest a modest chemopreventive effect of calcium supplements against recurrent colorectal adenomas over a period of 36 to 60 mo. Further research is warranted.Stefanos Bonovas Gionata Fiorino Theodore Lytras Alberto Malesci Silvio Danese 2016World Journal of Gastroenterology2016,22,18:6
7Combination Therapy With Infliximab and Azathioprine Is Superior to Monotherapy With Either Agent in Ulcerative Colitis显示文摘Remo Panaccione Subrata Ghosh Stephen Middleton Juan R. Márquez Boyd B. Scott Laurence Flint Hubert JF. van Hoogstraten Annie C. Chen Hanzhe Zheng Silvio Danese Paul Rutgeerts 2013Gastroenterology2013,,:5
8Identification of serum and tissue micro‐ RNA expression profiles in different stages of inflammatory bowel disease显示文摘M. Iborra F. Bernuzzi C. Correale S. Vetrano G. Fiorino B. Beltrán F. Marabita M. Locati A. Spinelli P. Nos P. Invernizzi S. Danese 2013Clin Exp Immunol2013,,2:4
9Mucosal biomarkers in inflammatory bowel disease:Key pathogenic players or disease predictors?显示文摘Inflammatory bowel diseases(IBDs) are chronic inflammatory disorders of the bowel,including ulcerative colitis and Crohn's disease.A single etiology has not been identified,but rather the pathogenesis of IBD is very complex and involves several major and minor contributors,employing different inflammatory pathways which have different roles in different patients.Although new and powerful medical treatments are available,many are biological drugs or immunosuppressants,which are associated with significant side effects and elevated costs.As a result,the need for predicting disease course and response to therapy is essential.Major attempts have been made at identifying clinical characteristics,concurrent medical therapy,and serological and genetic markers as predictors of response to biological agents.Only few reports exist on how mucosal/tissue markers are able to predict clinical behavior of the disease or its response to therapy.The aim of this paper therefore is to review the little information available regarding tissue markers as predictors of response to therapy,and reevaluate the role of tissue factors associated with disease severity,which can eventually be ranked as 'tissue factor predictors'.Five main categories are assessed,including mucosal cytokines and chemokines,adhesion molecules and markers of activation,immune and non-immune cells,and other mucosal components.Improvement in the design and specificity of clinical studies are mandatory to be able to classify tissue markers as predictors of disease course and response to specific therapy,obtain the goal of achieving 'personalized pathogenesisoriented therapy' in IBD.Franco Scaldaferrii Carmen Correale Antonio Gasbarrini Silvio Danese 2010World Journal of Gastroenterology2010,16,21:4
10Risk of postoperative recurrence and postoperative management of Crohn's disease显示文摘Crohn's disease (CD) is a chronic inflammatory disease of the digestive tract with systemic manifestations. Etiology is unknown, even if immunological, genetic and environmental factors are involved. The majority of CD patients require surgery during their lifetime due to progressive bowel damage, but, even when all macroscopic lesions have been removed by surgery, the disease recurs in most cases. Postoperative management represents therefore a crucial mean for preventing recurrence. Several drugs and approaches have been proposed to achieve this aim. Endoscopic inspection of the ileocolic anastomosis within 1 year from surgery is widely encouraged, given that endoscopic recurrence is one of the greatest predictors for clinical recurrence. A strategy should be planned only after stratifying patients according to their individual risk of recurrence, avoiding unnecessary therapies when possible benefits are reduced, and selecting high-risk patients for more aggressive intervention.Antonino Spinelli Matteo Sacchi Gionata Fiorino Silvio Danese Marco Montorsi 2011World Journal of Gastroenterology2011,17,27:4
11Microscopic features of colorectal neoplasia in inflammatory bowel diseases显示文摘The risk of developing dysplasia leading to colorectal cancer(CRC)is increased in both ulcerative colitis and Crohn’s disease.The prognosis of CRC may be poorer in patients with inflammatory bowel disease(IBD)than in those without IBD.Most CRCs,in general,develop from a dysplastic precursor lesion.The interpretation by the pathologist of the biopsy will guide decision making in clinical practice:colonoscopic surveillance or surgical management.This review summarizes features of dysplasia(or intraepithelial neoplasia)with macroscopic and microscopic characteristics.From an endoscopic(gross)point of view,dysplasia may be classified as flat or elevated(raised);from a histological point of view,dysplasia is separated into 3 distinct categories:negative for dysplasia,indefinite for dysplasia,and positive for dysplasia with low-or high-grade dysplasia.The morphologic criteria for dysplasia are based on a combination of cytologic(nuclear and cytoplasmic)and architectural aberrations of the crypt epithelium.Immunohistochemical and molecular markers for dysplasia are reviewed and may help with dysplasia diagnosis,although diagnosis is essentially based on morphological criteria.The clinical,epidemiologic,and pathologic characteristics of IBD-related cancers are,in many aspects,different from those that occur sporadically in the general population.Herein,we summarize macroscopic and microscopic features of IBD-related colorectal carcinoma.Aude Bressenot Virginie Cahn Silvio Danese Laurent Peyrin-Biroulet 2014World Journal of Gastroenterology2014,20,12:4
12Second European evidence-based consensus on the diagnosis and management of ulcerative colitis: Special situations显示文摘Gert Van Assche Axel Dignass Bernd Bokemeyer Silvio Danese Paolo Gionchetti Gabriele Moser Laurent Beaugerie Fernando Gomollón Winfried H?user Klaus Herrlinger Bas Oldenburg Julian Panes Francisco Portela Gerhard Rogler Jürgen Stein Herbert Tilg Simon Tra 2012Journal of Crohn’s and Colitis2012,,:4
13Characterization of genetically engineered mouse models carrying Col2a1-cre-induced deletions of Lrp5 and/or Lrp6显示文摘Mice carrying Collagen2a1-cre-mediated deletions of Lrp5 and/or Lrp6 were created and characterized.Mice lacking either gene alone were viable and fertile with normal knee morphology.Mice in which both Lrp5 and Lrp6 were conditionally ablated via Collagen2al-cre-mediated deletion displayed severe defects in skeletal development during embryogenesis.In addition,adult mice carrying Collagen2al-cre-mediated deletions of Lrp5 and/or Lrp6 displayed low bone mass suggesting that the Collagen2a1-cre transgene was active in cells that subsequently differentiated into osteoblasts.In both embryonic skeletal development and establishment of adult bone mass,Lrp5 and Lrp6 carry out redundant functions.Cassie A Schumacher Danese M Joiner Kennen D Less Melissa Oosterhouse Drewry Bart O Williams 2015Bone Research2015,3,4:3
14Review article: the role of anti‐TNF in the management of ulcerative colitis – past, present and future显示文摘S. Danese J.‐F. Colombel L. Peyrin‐Biroulet P. Rutgeerts W. Reinisch 2013Aliment Pharmacol Ther2013,,9:3
15The second European evidence-based Consensus on the diagnosis and management of Crohn’s disease: Current management显示文摘A. Dignass G. Van Assche J.O. Lindsay M. Lémann J. S?derholm J.F. Colombel S. Danese A. D’Hoore M. Gassull F. Gomollón D.W. Hommes P. Michetti C. O’Morain T. ?resland A. Windsor E.F. Stange S.P.L. Travis 2010Journal of Crohn’s and Colitis2010,,1:2
16Balanced propofol sedation administered by nonanesthesiologists:The first Italian experience显示文摘AIM:To assess the efficacy and safety of a balanced approach using midazolam in combination with propofol,administered by nonanesthesiologists,in a large series of diagnostic colonoscopies.METHODS:Consecutive patients undergoing diagnostic colonoscopy were sedated with a single dose of midazolam(0.05 mg/kg)and lowdose propofol(starter bolus of 0.5 mg/kg and repeated boluses of 10 to 20 mg).Induction time and deepest level of sedation,adverse and serious adverse events,as well as recovery times,were prospectively assessed.Cecal intubation and adenoma detection rates were also collected.RESULTS:Overall,1593 eligible patients were included.The median dose of propofol administered was 70 mg(range:40120 mg),and the median dose of midazolam was 2.3 mg(range:24 mg).Median induction time of sedation was 3 min(range:14 min),and median recovery time was 23 min(range:1040 min).A moderate level of sedation was achieved in 1561(98%) patients,whilst a deep sedation occurred in 32(2%) cases.Transient oxygen desaturation requiring further oxygen supplementation occurred in 8(0.46%;95% CI:0.2%0.8%)patients.No serious adverse event was observed.Cecal intubation and adenoma detection rates were 93.5%and 23.4%(27.8%for male and 18.5%for female,subjects),respectively.CONCLUSION:A balanced sedation protocol provided a minimalization of the dose of propofol needed to target a moderate sedation for colonoscopy,resulting in a high safety profile for nonanesthesiologist propofol sedation.Alessandro Repici Nico Pagano Cesare Hassan Alessandra Carlino Giacomo Rando Giuseppe Strangio Fabio Romeo Angelo Zullo Elisa Ferrara Eva Vitetta Daniel de Paula Pessoa Ferreira Silvio Danese Massimo Arosio Alberto Malesci 2011World Journal of Gastroenterology2011,17,33:2
17Inflammatory bowel disease: the role of environmental factors显示文摘Silvio Danese Miquel Sans Claudio Fiocchi 2004Autoimmunity Reviews2004,,5:2
18Imaging techniques for assessment of inflammatory bowel disease: Joint ECCO and ESGAR evidence-based consensus guidelines显示文摘J. Panes Y. Bouhnik W. Reinisch J. Stoker S.A. Taylor D.C. Baumgart S. Danese S. Halligan B. Marincek C. Matos L. Peyrin-Biroulet J. Rimola G. Rogler G. van Assche S. Ardizzone A. Ba-Ssalamah M.A. Bali D. Bellini L. Biancone F. Castiglione R. Ehehalt R. G 2013Journal of Crohn’s and Colitis2013,,7:2
19Infliximab, Azathioprine, or Infliximab + Azathioprine for Treatment of Moderate to Severe Ulcerative Colitis: The UC Success Trial显示文摘Remo Panccione Subrata Ghosh Stephen Middleton Juan R. Marquez Igor Khalif Laurence Flint Hubert van Hoogstraten Hanzhe Zheng Silvio Danese Paul J. Rutgeerts 2011Gastroenterology2011,,5:2
20Early Diagnosis and Treatment of Postoperative Endoscopic Recurrence of Crohn’s Disease: Partial Benefit by Infliximab—A Pilot Study显示文摘Dario Sorrentino Giovanni Terrosu Alberto Paviotti Marco Geraci Claudio Avellini Giorgio Zoli Walter Fries Silvio Danese Pietro Occhipinti Tiziano Croatto Dimitra Zarifi 2012Digestive Diseases and Sciences2012,,5:2
返回顶部 每页显示:
共25页 首页 上一页 第1页 下一页 末页 /25 跳转

网站首页 | 关于我们 | 联系我们 | 产品服务 | 客服中心 | 广告服务 | 版权声明 | 网站联盟 | 友情链接 | 售卡网点

版权所有© 渝B2-20050021-1 渝公网安备 50019002500403号 违法和不良信息举报中心

互联网出版许可证 新出网证(渝)字10号 全国400电话 - 免长途话费