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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 | 贵州喀斯特洞穴动物多样性及其生境研究——以黔西县红林地区为例显示文摘通过四次对青冈林洞、洗线洞和水响洞的调查,共获37种动物。各种类数量优势分别为有光带的蚁蛉幼虫、蕈蚊,弱光带和黑暗带水域的红点髭蟾蝌蚪以及洞壁的斑灶马。2001年10月和2003年3月,青冈林洞、洗线洞和水响洞分别有动物群落15、13和10种类型,优势群落为斑灶马、红点髭蟾蝌蚪和蚁蛉幼虫。动物的取食、隐蔽、繁殖、栖息等环境在不同时期的变换引起这一区域洞穴动物在种类、数量和空间分布等的变化,人类活动则加大了生境的差异。食物-陷阱法可用于部分动物的相对数量的调查。 | 陈浒 熊康宁 Leonardo Latella | 2005 | 中国岩溶2005，24，1： | 2 |
| 6 | Automatic verification of a behavioural subset of UML Statechart digrams using the SPIN model-checker显示文摘 | Latella D Majzik I Massink M | 1999 | Formal Aspects of Computing1999，11，6： | 1 |
| 7 | On the Use of Bio-PEPA for Modelling and Analysing Collective Behaviours in Swarm Robotics显示文摘 | Massink M Brambilla M Latella P | 2013 | Swarm Intelligence2013，7，2： | 1 |
| 8 | Current management of severe ulcerative colitis显示文摘 | Caprilli R Viscido A Latella G | 2007 | Nat Clin Pract Gastroenterol Hepatol2007，4，2： | 1 |
| 9 | GI distension in severe ulcerative colitis 显示文摘 | Latella G Vernia P Viscido A | 2002 | Am J Gastroenterol2002，97，5： | 1 |
| 10 | Rifaximin improves symptoms of acquired uncomplicated diverticular disease of the colon 显示文摘 | Latella G Pimpo MT Sottili S | 2003 | Int J Cotorectal Dis2003，18，1： | 1 |
| 11 | Smad3-null mice lack interstitial cells of Cajal in the colonic wall显示文摘 | Vetuschi A Sferra R Latella G | 2006 | Eur J Clin Invest2006，36，1： | 1 |
| 12 | Current manage- ment of severe ulcerative colitis 显示文摘 | Caprilli R Viscido A Latella G | 2007 | Nat Clin Pract Gas- troenterol Hepatol2007，4，2： | 1 |
| 13 | Current management of severe ulcerative colitis 显示文摘 | Caprilli R Viscido A Latella G | 2007 | Nat Clin Pract Gastroenterol Hepatol2007，4，2： | 1 |
| 14 | Outcome in chil- dren withpulmonary Langerhans cell Histioeytosis 显示文摘 | Braier J Latella A Balaneini B | 2004 | Pediatr BloodCaneer2004，43，7： | 1 |
| 15 | Long-term oral plus topical mesalazine in frequently relapsing ulcerative colitis显示文摘 | G. Frieri M. Pimpo B. Galletti G. Palumbo G. Corrao G. Latella M. Chiaramonte R. Caprilli | 2004 | Digestive and Liver Disease2004，，： | 1 |
| 16 | Reduction in corticospinal inhibition in the trained and untrained limb following unilat- eral leg strength training显示文摘 | Latella C Kidgell DJ Pearce AJ | 2012 | Eur J Appl Physiol2012，112，8： | 1 |
| 17 | Targeted disruption of Smad3 confers resistance to the development of dimethvlnitrosamine-induced hepatic fibrosis in mice显示文摘 | Latella G Vetuschi A Sferra R | 2009 | Liver Intemational2009，29，7： | 1 |
| 18 | Cholestasis, sclerosing cholan- gitis, and liver transplantation in Langerhans cell Histiocytosis显示文摘 | Braier J Ciocca M Latella A | 2002 | Med Pediatr Oncol2002，38，： | 1 |
| 19 | High temperature biaxial strength of porous mullite-alumina and mullite- zirconia ceramics显示文摘 | LATELLA B A MEHRTENS E G | 2007 | J Mater Sci2007，42，： | 1 |
| 20 | Long-term oral plus topical mesalazine in frequently relapsing ulcerative colitis显示文摘 | G. Frieri M. Pimpo B. Galletti G. Palumbo G. Corrao G. Latella M. Chiaramonte R. Caprilli | 2004 | Digestive and Liver Disease2004，，2： | 1 |
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