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| 1 | Alleviated mucosal and neuronal damage in a rat model of Crohn's disease显示文摘AIM:To establish a rat model suitable to investigate the repetitive relapsing inflammations(RRI)characteristic to Crohn’s disease.METHODS:Colitis was induced by 2,4,6-trinitrobenzenesulfonic acid(TNBS).RRI were mimicked by repeating administrations of TNBS.Tissue samples were taken from control,once,twice and three times treated rats from the inflamed and adjacent non-inflamed colonic segments at different timepoints during the acute intestinal inflammation.The means of the ulcerated area were measured to evaluate the macroscopic mu-cosal damage.The density of myenteric neurons was determined on whole mounts by Hu C/Hu D immunohistochemistry.Heme oxygenase-1(HO-1)expression was evaluated by molecular biological techniques.RESULTS:TNBS-treated rats displayed severe colitis,but the mortality was negligible,and an increase of body weight was characteristic throughout the experimental period.The widespread loss of myenteric neurons,and marked but transient HO-1 up-regulation were demonstrated after the first TNBS administration.After repeated doses the length of the recovery time and extent of the ulcerous colonic segments were markedly decreased,and the neuronal loss was on a smaller scale and was limited to the inflamed area.HO-1 m RNA level was notably greater than after a single dose and overexpression was sustained throughout the timepoints examined.Nevertheless,the HO-1protein up-regulation after the second TNBS treatment proved to be transient.Following the third treatment HO-1 protein expression could not be detected.CONCLUSION:Experimentally provoked RRI may exert a protective preconditioning effect against the mucosal and neuronal damage.The persistent up-regulation of HO-1 m RNA expression may correlate with this. | Petra Talapka Lajos István Nagy Alexandra Pál Marietta Zita Poles Anikó Berkó Mária Bagyánszki László Géza Puskás éva Fekete Nikolett Bódi | 2014 | World Journal of Gastroenterology2014,20,44: | 3 |
| 2 | Structural and molecular features of intestinal strictures in rats with Crohn's-like disease显示文摘AIM: To develop a new rat model we wanted to gain a better understanding of stricture formation in Crohn's disease(CD).METHODS: Chronic colitis was induced locally by the administration of 2,4,6-trinitrobenzenesulfonic acid(TNBS). The relapsing inflammation characteristic to CD was mimicked by repeated TNBS treatments. Animals were randomly divided into control, once, twice and three times TNBS-treated groups. Control animals received an enema of saline. Tissue samples were taken from the strictured colonic segments and also adjacent proximally and distally to its 60, 90 or 120 d after the last TNBS or saline administrations. The frequency and macroscopic extent of the strictures were measured on digital photographs. The structural features of strictured gut wall were studied by light- and electron microscopy. Inflammation related alterations in TGF-beta 2 and 3, matrix metalloproteinases 9(MMP9) and TIMP1 m RNA and protein expression were determined by quantitative real-time PCR and western blot analysis. The quantitative distribution of caspase 9 was determined by post-embedding immunohistochemistry.RESULTS: Intestinal strictures first appeared 60 d after TNBS treatments and the frequency of them increased up to day 120. From day 90 an intact lamina epithelialis, reversible thickening of lamina muscularis mucosae and irreversible thickening of the muscularis externa were demonstrated in the strictured colonic segments. Nevertheless the morphological signs of apoptosis were frequently seen and excess extracellular matrix deposition was recorded between smooth muscle cells(SMCs). Enhanced caspase 9 expression on day 90 in the SMCs and on day 120 also in myenteric neurons indicated the induction of apoptosis. The m RNA expression profile of TGF-betas after repeated TNBS doses was characteristic to CD, TGF-beta 2, but not TGF-beta 3 was up-regulated. Overexpression of MMP9 and down-regulation of TIMP1 were demonstrated. The progressive increase in the amount of MMP9 protein in the strictures was also obvious between days 90 and 120 but TIMP1 protein was practically undetectable at this time.CONCLUSION: These findings indicate that aligned structural and molecular changes in the gut wall rather than neuronal cell death play the primary role in stricture formation. | Petra Talapka Anikó Berkó Lajos István Nagy Lalitha Chandrakumar Mária Bagyánszki László Géza Puskás éva Fekete Nikolett Bódi | 2016 | World Journal of Gastroenterology2016,22,22: | 3 |
| 3 | Lipotoxicity in the liver显示文摘Obesity due to excessive food intake and the lack of physical activity is becoming one of the most serious public health problems of the 21stcentury. With the increasing prevalence of obesity, non-alcoholic fatty liver disease is also emerging as a pandemic. While previously this pathophysiological condition was mainly attributed to triglyceride accumulation in hepatocytes,recent data show that the development of oxidative stress, lipid peroxidation, cell death, inflammation and fibrosis are mostly due to accumulation of fatty acids,and the altered composition of membrane phospholipids. In fact, triglyceride accumulation might play a protective role, and the higher toxicity of saturated or trans fatty acids seems to be the consequence of a blockade in triglyceride synthesis. Increased membrane saturation can profoundly disturb cellular homeostasis by impairing the function of membrane receptors,channels and transporters. However, it also inducesendoplasmic reticulum stress via novel sensing mechanisms of the organelle's stress receptors. The triggered signaling pathways in turn largely contribute to the development of insulin resistance and apoptosis. These findings have substantiated the lipotoxic liver injury hypothesis for the pathomechanism of hepatosteatosis.This minireview focuses on the metabolic and redox aspects of lipotoxicity and lipoapoptosis, with special regards on the involvement of endoplasmic reticulum stress responses. | Veronika Zámbó Laura Simon-Szabó Péter Szelényi va Kereszturi Gábor Bánhegyi Miklós Csala | 2013 | World Journal of Hepatology2013,5,10: | 3 |
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| 7 | Haploinsufficiency of delta- like 4 ligand results in embryonic lethality due to ma:or defects in arterial and vascular development显示文摘 | Gale N W Dominguez M G Noguera I Pan L Hughes V Va]enzuela D M | 2004 | Proc Natl Acad Sci USA2004,101,15: | 1 |
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| 12 | Conserved and variable functions of the oE stress response in related genomes显示文摘 | Rhodias VA Sub WC Nonaka G | 2006 | PLoS Biol2006,4,1: | 1 |
| 13 | Improving tribological properties of sputtered boron carbide coatings by process modifications 显示文摘 | Eckardt T Bewilogua K Va der Kolk G | 2000 | Surface & Coatings Technology2000,126,1: | 1 |
| 14 | Detection of deviation in performance of battery cells by data compression and similarity analysis 显示文摘 | VA HKOV G BYTINER S SVENSSON M | 2014 | International Journal of Intelligent Systems2014,29,3: | 1 |
| 15 | International guidelines for the diagnosis and management of hereditary haem- orrhagic telangiectasia显示文摘 | FAUGHNAN ME PALDA VA GARCIA-TSAO G HHT Foundation International-Guidelines Working Group | 2011 | J Med Genet2011,48,: | 1 |
| 16 | A meta analysis显示文摘 | Dhamidharka VA Kwoncstevens G | | 0,,02: | 1 |
| 17 | Werfel,Suppression of interleukin-12 production by human monocytes after preincubation with lipopolysaccharide显示文摘 | Wittmann VA Larsson P Schmidt G | 1999 | Blood1999,94,: | 1 |
| 18 | Overexpression of heat-shock proteins reduces survival of Mycobacterium tuberculosis in the chronic phase of infection显示文摘 | Stewart GR Snewin VA Walzl G | 2001 | Nat Med2001,7,: | 1 |
| 19 | Analysis of apoptosis during hair follicle regression(catogen)显示文摘 | Lindner G Botchkarev VA Botehkareva NV | 1997 | Am J Pathol1997,151,6: | 1 |
| 20 | Long-term effect of antiangio- genic therapy for retinopathy of prematurity up to 5 years of follow-up显示文摘 | MARTINEZ-CASTTELLANOS MA SCHWAKRTS HERNaNDEZ- ROJAS ML KON-JARA VA GARCIA-AGUIRRE G GUER- RERO-NARANJO JL | 2013 | Retina2013,33,2: | 1 |