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| 1 | Cellular and molecular mechanisms of intestinal fibrosis显示文摘Fibrosis is a chronic and progressive process characterized by an excessive accumulation of extracellular matrix (ECM) leading to stiffening and/or scarring of the involved tissue. Intestinal fibrosis may develop in several different enteropathies, including inflammatory bowel disease. It develops through complex cell, extracellular matrix, cytokine and growth factor interactions. Distinct cell types are involved in intestinal fibrosis, such as resident mesenchymal cells (fibroblasts, myofibroblasts and smooth muscle cells) but also ECM-producing cells derived from epithelial and endothelial cells (through a process termed epithelialand endothelial-mesenchymal transition), stellate cells, pericytes, local or bone marrow-derived stem cells. The most important soluble factors that regulate the activation of these cells include cytokines, chemokines, growth factors, components of the renin-angiotensin system, angiogenic factors, peroxisome proliferator-activated receptors, mammalian target of rapamycin, and products of oxidative stress. It soon becomes clear that although inflammation is responsible for triggering the onset of the fibrotic proc-ess, it only plays a minor role in the progression of this condition, as fibrosis may advance in a self-perpetuating fashion. Definition of the cellular and molecular mechanisms involved in intestinal fibrosis may provide the key to developing new therapeutic approaches. | Silvia Speca Ilaria Giusti Florian Rieder Giovanni Latella | 2012 | World Journal of Gastroenterology2012，18，28： | 32 |
| 2 | Role of nitric oxide in the impairment of circular muscle contractility of distended, uninflamed mid-colon in TNBS-induced acute distal colitis in rats显示文摘AIM: To evaluate the role of nitric oxide (NO) in the motor disorders of the dilated uninflamed mid-colon (DUMC)from trinitrobenzene sulfonic acid (TNBS)-induced acute distal colitis in rats.METHODS: Colitis was induced in male Sprague-Dawley rats by a single intracolonic administration of TNBS.Control rats received an enema of 0.9% saline. The rats were killed 48 h after TNBS or saline administration.Macroscopic and histologic lesions of the colon were evaluated. Myeloperoxidase (MPO) and nitric oxide synthase (NOS) activity were measured on the colonic tissue. In TNBS rats, we evaluated spontaneous and evoked contractile activity in circular muscle strips derived from DUMC in comparison to the same colonic segment of control rats, both in the presence and in the absence of a non-selective NOS isoforms inhibitor N-nitro-Larginine (L-NNA). Pharmacological characterization of electric field stimulation (EFS)-evoked contractile responses was also performed.RESULTS: In TNBS rats, the distal colon showed severe histological lesions and a high MPO activity, while the DUMC exhibited normal histology and MPO activity.Constitutive NOS activity was similar in TNBS and control rats, whereas inducible NOS activity was significantly increased only in the injured distal colon of TNBS rats.Isometrically recorded mechanical activity of circular muscle strips from DUMC of TNBS rats showed a marked reduction of the force and frequency of spontaneous contractions compared to controls, as well as of the contractile responses to a contracting stimulus. In the presence of L-NNA, the contractile activity and responses displayed a significantly greater enhancement compared to controls. The pharmacological characterization of EFS contractile responses showed that a cooperative-like interaction between cholinergic muscarinic and tachykinergic neurokinin 1 and 2 receptors mediated transmission in DUMC of TNBS rats vs a simple additive interaction in controls.CONCLUSION: The results of this study show that, during TNBS-induced acute distal colitis, circular muscle intrinsic contractile mechanisms and possible enteric neural excitatory activity are inhibited in the distended uninflamed mid-colon. Suppression of NO synthesis markedly improves spontaneous and evokes muscle contractions, in spite of any evident change in local NO activity. | Luciano Onori Annalisa Aggio Simona D'Alo' Paola Muzi Maria Grazia Cifone Gabriella Mellillo Rachele Ciccocioppo Gennaro Taddei Giuseppe Frieri Giovanni Latella | 2005 | World Journal of Gastroenterology2005，11，36： | 7 |
| 3 | Crucial steps in the natural history of inflammatory bowel disease显示文摘Inflammatory bowel diseases(IBD),including ulcerative colitis(UC) and Crohn's disease(CD),are chronic,progressive and disabling disorders.Over the last few decades,new therapeutic approaches have been introduced which have led not only to a reduction in the mortality rate but also offered the possibility of a favorable modification in the natural history of IBD.The identification of clinical,genetic and serological prognostic factors has permitted a better stratification of the disease,thus allowing the opportunity to indicate the most appropriate therapy.Early treatment with immunosuppressive drugs and biologics has offered the opportunity to change,at least in the short term,the course of the disease by reducing,in a subset of patients with IBD,hospitalization and the need for surgery.In this review,the crucial steps in the natural history of both UC and CD will be discussed,as well as the factors that may change their clinical course.The methodological requirements for high quality studies on the course and prognosis of IBD,the true impact of environmental and dietary factors on the clinical course of IBD,the clinical,serological and genetic predictors of the IBD course(in particular,which of these are rel-evant and appropriate for use in clinical practice),the impact of the various forms of medical treatment on the IBD complication rate,the role of surgery for IBD in the biologic era,the true magnitude of risk of colorectal cancer associated with IBD,as well as the mortality rate related to IBD will be stressed;all topics that are extensively discussed in separate reviews included in this issue of World Journal of Gastroenterology. | Giovanni Latella Claudio Papi | 2012 | World Journal of Gastroenterology2012，18，29： | 7 |
| 4 | Smad3 knock-out mice as a useful model to study intestinal fibrogenesis显示文摘瞄准:为了在形态学和免疫评估可能的差别, CD3,转变生长因素 beta1 (TGF-beta1 ) , Smad7, alpha 光滑的肌肉肌动朊(alpha-Sma ) ,和骨胶原的组织化学的表示打 I-VII 小并且在 Smad3 空、野类型的老鼠的大肠。方法:十 0 和十只野类型的成年老鼠在年龄和机关的 4 瞬间被牺牲(食管,小、大的肠,输尿管) 为组织学被收集(苏木精和曙红,马森 thrichrome,染色的银) ,形态测定法和免疫组织化学分析。肠的织物 homogenates 的 TGF-beta1 层次被 ELISA 估计。结果:没有宏观的肠的损害在空、野类型的老鼠两个都被检测。组织学并且 morphometric 评估在肌肉层厚度揭示了重要减小小并且在空老鼠的大肠同样与野类型的老鼠相比。Immunohistochemistry 评估显示出染色在的 CD3+ T 房间, TGF-beta1 和 Smad7 的重要增加小并且 Smad3 空老鼠的大肠粘膜同样与野类型的老鼠相比。染色的 Alpha-Sma 和骨胶原 I-VII 小并且大肠没在二组老鼠之间不同。结肠的织物 homogenates 的 TGF-beta1 层次比在野类型的老鼠在空老鼠是显著地更高的。在初步的实验,导致 TNBS 的肠的纤维变性的重要减小作为与野类型的老鼠相比在空老鼠被观察。结论:Smad3 空老鼠是一个有用模型调查在肠的发炎和纤维变性表明小径的 TGF-beta/Smad 的在活体内角色。 | Giuliana Zanninelli Antonella Vetuschi Roberta Sferra Angela D'Angelo Amato Fratticci Maria Adelaide Continenza Maria Chiaramonte Eugenio Gaudio Renzo Caprilli Giovanni Latella | 2006 | World Journal of Gastroenterology2006，12，8： | 3 |
| 5 | News from the “5th international meeting on inflammatory bowel diseases” CAPRI 2010显示文摘 | Giovanni Latella Claudio Fiocchi Renzo Caprili | 2010 | Journal of Crohn’s and Colitis2010，，6： | 1 |
| 6 | Rifaximin improves symptoms of acquired uncomplicated diverticular disease of the colon显示文摘 | Giovanni Latella Maria Pimpo Sandra Sottili Maddalena Zippi Angelo Viscido Maria Chiaramonte Giuseppe Frieri | 2003 | International Journal of Colorectal Disease2003，，1： | 1 |
| 7 | Results of the 4th scientific workshop of the ECCO (I): Pathophysiology of intestinal fibrosis in IBD显示文摘 | Giovanni Latella Gerhard Rogler Giorgos Bamias Christine Breynaert Jon Florholmen Gianluca Pellino Shimon Reif Silvia Speca Ian C. Lawrance | 2014 | Journal of Crohn’s and Colitis2014，，： | 1 |
| 8 | Nanotechnology in the treatment of inflammatory bowel diseases显示文摘 | Angelo Viscido Annalisa Capannolo Giovanni Latella Renzo Caprilli Giuseppe Frieri | 2014 | Journal of Crohn’s and Colitis2014，，： | 1 |
| 9 | Mechanisms of initiation and progression of intestinal fibrosis in IBD显示文摘 | Giovanni Latella Jacopo Di Gregorio Vincenzo Flati Florian Rieder Ian C. Lawrance | 2014 | Scandinavian Journal of Gastroenterology2014，，1： | 1 |
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