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    题名 作者 年代 出处 被引量
1A nuclear import inhibitory peptide ameliorates the severity of cholecystokinin-induced acute pancreatitis显示文摘AIM: To assess the effect of our novel cell-permeable nuclear factor-kappaB (NF-κB) inhibitor peptide PN50 in an experimental model of acute pancreatitis. PN50 was produced by conjugating the cell-penetrating penetratin peptide with the nuclear localization signal of the NF-κB p50 subunit.METHODS: Pancreatitis was induced in male Wistar rats by administering 2×100 μg/kg body weight of cholecystokininoctapeptide (CCK) intraperitoneally (IP) at an interval of 1 h. PN50-treated animals received 1 mg/kg of PN50 IP 30 min before or after the CCK injections. The animals were sacrificed 4 h after the first injection of CCK.RESULTS: All the examined laboratory (the pancreatic weight/body weight ratio, serum amylase activity,pancreatic levels of TNF-α and IL-6, degree of lipid peroxidation, reduced glutathione levels, NF-κB binding activity, pancreatic and lung myeloperoxidase activity) and morphological parameters of the disease were improved before and after treatment with the PN50 peptide.According to the histological findings, PN50 protected the animals against acute pancreatitis by favoring the induction of apoptotic, as opposed to necrotic acinar cell death associated with severe acute pancreatitis.CONCLUSION: Our study implies that reversible inhibitors of stress-responsive transcription factors like NF-κB might be clinically useful for the suppression of the severity of acute pancreatitis.Tamás Letoha Csaba Somlai Tamáas Takács Annamária Szabolcs Katalin Jármay Zoltán Rakonczay Jr Péter Hegyi Ilona Varga József Kaszaki István Krizbai Imre Boros Ern(?) Duda Erzsébet Kusz Botond Penke 2005World Journal of Gastroenterology2005,11,7:15
2Relevance of α-defensins(HNP1-3) and defensin β-1 in diabetes显示文摘AIM: To investigate the genetic background of human defensin expression in type 1 and 2 diabetes.METHODS: Associations between DEFA1/DEFA3 gene copy number polymorphism and diabetes as well as between the promoter polymorphisms of DEFB1 and diabetes were studied. The copy number variation of the DEFA1/DEFA3 genes was determined in 257 diabetic patients(117 patients with type 1 and 140 with type 2 diabetes). The control group consisted of 221 age- and gender-matched healthy blood donors. The cumulative copy numbers of the DEFA1/DEFA3 genes were detected by using quantitative PCR analysis. To evaluate the HNP 1-3(human neutrophil peptide 1-3 or α-defensin) levels in the circulation, plasma HNP 1-3 concentrations were measured by ELISA. The expression of DEFA1/A3 in peripheral leukocytes of the diabetic patients was measured by quantitative RT PCR analysis. Three SNPs of the human DEFB1(human defensin β-1) gene: DEFB1 G-20A(rs11362), DEFB1 C-44G(rs1800972) and DEFB1 G-52A(rs1799946) were genotyped by Custom TaqMan? Real Time PCR assay.RESULTS: Significant differences were observed in HNP1-3 levels between the healthy subjects and both groups of diabetic patients. The mean ± SE was 28.78 ± 4.2 ng/mL in type 1 diabetes, and 29.82 ± 5.36 ng/mL in type 2 diabetes, vs 11.94 ± 2.96 ng/mL in controls; P < 0.01 respectively. There was no significant difference between patients with type 1 and type 2 diabetes in the high plasma concentrations of HNP1-3. The highest concentrations of α-defensin were found in diabetic patients with nephropathy(49.4 ± 4.8 ng/mL), neuropathy(38.7 ± 4.8 ng/mL) or cardiovascular complications(45.6 ± 1.45 ng/L). There was no significant difference in the cumulative copy numbers of DEFA1/DEFA3 genes between controls and patients, or between patients with the two types of diabetes. Comparisons of HNP 1-3 plasma level and DEFA1/A3 copy number of the same patient did not reveal significant relationship between defensin-α levels and the gene copy numbers(r2 = 0.01). Similarly, no positive correlation was observed between the copy numbers and the mRNA expression levels of DEFA1/A3. Regarding the C-44G polymorphism of DEFB1, the GG 'protective' genotype was much less frequent(1%-2%) among both groups of patients than among controls(9%).CONCLUSION: Elevated HNP1-3 levels in diabetes are independent of DEFA1/DEFA3 copy numbers, but GG genotype of C-44G SNP in DEFB1 gene may result in decreased defensin β-1 production.Balázs Csaba Németh Tamás Várkonyi Ferenc Somogyvári Csaba Lengyel Katalin Fehértemplomi Szabolcs Nyiraty Péter Kempler Yvette Mándi 2014World Journal of Gastroenterology2014,20,27:4
3Increased duodenal expression of mi R-146a and-155 in pediatric Crohn's disease显示文摘AIM: To evaluate the role of micro RNA(mi R)-146 a,-155 and-122 in the duodenal mucosa of pediatric patients with Crohn's disease(CD) and the effect of transforming growth factor-β(TGF-β) on these mi Rs in duodenal epithelial and fibroblast cells.METHODS: Formalin-fixed, paraffin-embedded biopsies derived from the macroscopically inflamed(CD inflamed: n = 10) and intact(CD intact: n = 10) duodenal mucosa of pediatric CD patients and control children(C: n = 10) were examined. Expression of mi R-146 a,-155 and-122 was determined by realtime polymerase-chain reaction(PCR). The expression of the above mi Rs was investigated in recombinant human TGF-β(1 nmol/L, 24 h) or vehicle treated small intestinal epithelial cells(CCL-241) and primary duodenal fibroblast cells derived from healthy children as well.RESULTS: Expression of mi R-146 a was significantly higher in the inflamed duodenal mucosa compared to the intact duodenal mucosa of children with CD(CD inflamed: 3.21 ± 0.50 vs CD intact: 0.62 ± 0.26, p ≤ 0.01) and to the control group(CD inflamed: 3.21 ± 0.50 vs C: 1.00 ± 0.33, p ≤ 0.05). The expression of mi R-155 was significantly increased in the inflamed region of the duodenum compared to the control group(CD inflamed: 4.87 ± 1.02 vs Control: 1.00 ± 0.40, p ≤ 0.001). The expression of mi R-122 was unchanged in the inflamed or intact mucosa of CD patients compared to controls. TGF-β treatment significantly decreased the expression of mi R-155 in small intestinal epithelial cells(TGF-β: 0.7 ± 0.083 vs Control: 1 ± 0.09, p ≤ 0.05) and also the expression of mi R-146a(TGF-β: 0.67 ± 0.04 vs Control: 1 ± 0.15, p ≤ 0.01) and mi R-155(TGF-β: 0.72 ± 0.09 vs Control: 1 ± 0.06, p ≤ 0.05) in primary duodenal fibroblasts compared to corresponding vehicle treated controls. TGF-β treatment did not influence the expression of mi R-122.CONCLUSION: The elevated expression of mi R-146 a and-155 in the inflamed duodenal mucosa of CD patients suggests the role of these mi Rs in the pathomechanism of inflammatory bowel disease. Antiinflammatory TGF-β plays an important role in the regulation of the expression of these mi Rs.Dániel Szucs Nóra Judit Béres Réka Rokonay Kriszta Boros Katalin Borka Zoltán Kiss András Arató Attila J Szabó ádám Vannay Erna Sziksz Csaba Bereczki Gábor Veres 2016World Journal of Gastroenterology2016,22,26:2
4Risks and Predictors of Blood Transfusion in Pediatric Patients Undergoing Open Heart Operations显示文摘Andrea Székely Zsuzsanna Cserép Erzsébet Sápi Tamás Breuer Csaba A. Nagy Péter Vargha István Hartyánszky András Szatmári András Treszl 2009The Annals of Thoracic Surgery2009,,1:2
5PLGA: poloxamer and PLGA: poloxamine blend nanostructures as carriers for nasal gene delivery显示文摘Csaba N Sanchez A Alonso MJ 2006J Control Release2006,113,2:1
6lonically crosslinked chitosan/tripolyphosphate nanoparticles for oligonucleotide and plasmid DNA delivery 显示文摘Csaba N Koping-Hoggard M Alonso MJ 2009lnt J Pharm2009,382,1:1
7Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: role of nitric oxide and CGRP?显示文摘P. Ferdinandy Tamás Csont Csaba Csonka Marianna T?r?k Mária Dux József Németh László I. Horváth László Dux Zoltán Szilvássy Gábor Jancsó 1997Naunyn - Schmiedeberg’s Archives of Pharmacology1997,,3:1
8The effects of vitamin E on tissue oxidation in nephrotoxic (anti-glomerular basement membrane) nephritis显示文摘Em?ke Endreffy Sándor Túri Zoltán Lászik Csaba Bereczki Katalin Kása 1991Pediatric Nephrology1991,,3:1
9Production of a defensin-like antifungal protein NFAP from Neosartorya fischeri in Pichia pastoris and its antifungal activity against filamentous fungal isolates from human infections显示文摘Máté Virágh Dóra V?r?s Zoltán Kele Laura Kovács ádám Fizil Gergely Lakatos Gergely Maróti Gyula Batta Csaba Vágv?lgyi László Galgóczy 2014Protein Expression and Purification2014,,:1
10Gustatory perception alterations in obesity: An fMRI study显示文摘Csaba Szalay Mihály Aradi Attila Schwarcz Gergely Orsi Gábor Perlaki Lívia Németh Sophia Hanna Gábor Takács István Szabó László Bajnok András Vereczkei Tamás Dóczi József Janszky Sámuel Komoly Péter ?rs Horváth László Lénárd Zoltán Karadi 2012Brain Research2012,,:1
11Ionically crosslinked chitosan/tripolyphosphate nanoparticles for oligonucleotide and plasmid DNA delivery显示文摘Csaba N Koping-Haggurd M Alonso M J 2009Int J Pharm2009,382,12:1
12Preparation of chitosan particles suitable for enzyme immobilization显示文摘EMESE B AGNES S N CSABA S 2008Biochem Biophys Methods2008,70,6:1
13PLGA:poloxamer and PLGA: poloxamine blend nanostructures as carriers for nasal gene delivery 显示文摘Csaba N Sanchez A Alonso MJ 2006J Control Release2006,113,:1
14PLGA:poloxamer and PLGA:poloxamine blend nanostructures as carriers for nasal gene delivery显示文摘Csaba N Sanchez A 2006Control Release2006,113,2:1
15The effect of exercise and nettle supplementation on oxidative stress markers in the rat brain显示文摘Anna Toldy Krisztián Stadler Mária Sasvári Judit Jakus Kyung J. Jung Hae Y. Chung István Berkes Csaba Nyakas Zsolt Radák 2005Brain Research Bulletin2005,,6:1
16Polyamines: molecules with regulatory functions in plant abiotic stress tolerance显示文摘Rubén Alcázar Teresa Altabella Francisco Marco Cristina Bortolotti Matthieu Reymond Csaba Koncz Pedro Carrasco Antonio F. Tiburcio 2010Planta2010,,6:1
17The performance of nanocarriers for transmucosal drug deliver显示文摘Csaba N Garcia-Fuentes M Alonso MJ 2006Expert Opin Drug Deliv2006,3,4:1
18Prenatal sonographic findings in 207 fetuses with trisomy 21显示文摘Csaba Papp Zoltán Bán Zsanett Szigeti ákos Csaba Levente Lázár Gy. Richard Nagy Zoltán Papp 2006European Journal of Obstetrics and Gynecology2006,,2:1
19Characterization of packed beds of plant materials processed by supercritical fluid extraction 显示文摘BENCE N BELA S CSABA D A Journal of Food Engineering0,88,1:1
20Insulin is necessary for the hypertrophic effect of cholecystokinin-octapeptide following acute necrotizing experimental pancreatitis显示文摘AIM: In previous experiments we have demonstrated that by administering low doses of cholecystokinin-octapeptide (CCK-8), the process of regeneration following L-arginine (Arg)-induced pancreatitis is accelerated. In rats that were also diabetic (induced by streptozotocin, STZ), pancreatic regeneration was not observed. The aim of this study was to deduce whether the administration of exogenous insulin could in fact restore the hypertrophic effect of CCK-8 in diabetic-pancreatitic rats.METHODS: Male Wistar rats were used for the experiments.Diabetes mellitus was induced by administering 60 mg/kg body mass of STZ intraperitoneally (i.p.), then, on d 8, pancreatitis was induced by 200 mg/100 g body mass Argi.p. twice at an interval of 1 h. The animals were injected subcutaneously twice daily (at 7 a.m. and 7 p.m.) with 1 μglkg of CCK-8 and/or 2 IU mixed insulin (300 g/L shortaction and 700 g/L intermediate-action insulin) for 14 d after pancreatitis induction. Following this the animals were killed and the serum amylase, glucose and insulin levels as well as the plasma glucagon levels, the pancreatic mass/body mass ratio (pm/bm), the pancreatic contents of DNA, protein, amylase, lipase and trypsinogen were measured. Pancreatic tissue samples were examined by light microscopy on paraffin-embedded sections.RESULTS: In the diabetic-pancreatitic rats treatment with insulin and CCK-8 significantly elevated pw/bm and the pancreatic contents of protein, amylase and lipase vs the rats receiving only CCK-8 treatment. CCK-8 administered in combination with insulin also elevated the number of acinar cells with mitotic activities, whereas CCK-8 alone had no effect on laboratory parameters or the mitotic activities in diabetic-pancreatitic rats.CONCLUSION: Despite the hypertrophic effect of CCK-8 being absent following acute pancreatitis in diabetic-rats,the simultaneous administration of exogenous insulin restored this effect. Our results clearly demonstrate that insulin is necessary for the hypertrophic effect of low-doses of CCK-8 following acute pancreatitis.Péter Hegyi Zoltán RakonczayJr Réka Sári László Czakó Norbert Farkas Csaba Góg József Németh János Lonovics Tamás Takács 2004World Journal of Gastroenterology2004,10,15:1
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