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15篇 您的检索式:作者名="Felderbauer"
    题名 作者 年代 出处 被引量
1Pathophysi- ology and treatment of acute pancreatitis: New thera- peutic targets-a ray of hope 显示文摘Felderbauer P Muller C Bulut K 2005Basic & Clinical Phar- macology & Toxicology2005,97,:1
2Acquired pure megakaryocytic aplasia: a separate haematological disease entity or a syndrome with multiple causes? 显示文摘Felderbauer P Ritter PR Mattem D 2004Eur J Haemato12004,72,6:1
3Solid-pseudopapilary tumor of the pancreas (Frantz tumor) in children:report of four cases and review of the literature显示文摘Rebhandl W Felderbauer FX Puig S 2001J Surg Oncol2001,76,4:1
4Sensory neuropeptides and epithelial cell restitution : the relevance of SP-and CGRP-stimulated mast cells显示文摘Bulut K Felderbauer P Deters S 2008Int J Colorectal Dis2008,23,5:1
5Vascular endothelial growth factor (VEGF164) ameliorates intestinal epithelial injury in vitro in IEC -18 and Caco -2 monolayers via induction of TGFbeta release from epithelial cells 显示文摘Bulut K Pennartz C Felderbauer P 2006Scand Gastroentero2006,41,6:1
6Pancreatitis risk in primary hyperparathyroidism: relation to mutations in the SPINK1 trypsin inhibitor (N34S) and the cystic fi- brosis gene显示文摘Felderbauer P Karakas E Fendrich V 2008Am J Gastroenterol2008,103,2:1
7Pathophysiology and treatment of acute pancreatitis:new therapeutic targets-a my of hope显示文摘Felderbauer P Muller C Bulut K 0,,6:1
8Vascular endothelial growth factor (VEGF<sub>164</sub>) ameliorates intestinal epithelial injury in vitro in IEC-18 and Caco-2 monolayers via induction of TGF-&bgr; release from epithelial cells显示文摘K. Bulut C. Pennartz P. Felderbauer N. Ansorge M. Banasch F. Schmitz W. E. Schmidt P. Hoffmann 2006Scandinavian Journal of Gastroenterology2006,,6:1
9Solid pseudopapillary tumor of the pancreas in children:report of four cases and reviewof the literature显示文摘Rebhandl W Felderbauer FX Puig S 2001J Surg Oncol2001,76,4:1
10Solid-pseudopapillary tumor of the pancreas in children:report of four cases and review of the literature显示文摘Rebhandl W Felderbauer FX Puig S 2001J Surg Oncol2001,76,:1
11Pathophysiology and treatment of acute pancreatitis:new therapeutic targets-a ray of hope?显示文摘Felderbauer P Muller C Bulut K 2005Basic Clin Pharmacol Toxicol2005,97,:1
12Solid-pseudo papilary tumor of the pancreas (Frantz tumor) in children:report of four cases and review of the literature显示文摘Rebhandl W Felderbauer FX Puig S 2001J Surg Oncol2001,76,4:1
13Vascular endothelial growth factor (VEGF164) ameliorates intestinal epithelial injury in vitro in IEC-18 and Caco-2 monolayers via induction of TGF-β release from epithelial cells 显示文摘Bulut K Pennartz C Felderbauer P 2006Scand J Gastroenterol2006,41,6:1
14Pancreatitis risk in primary hyperparathyroidism:relation to mutations in the SPINK1 trypsin inhibitor( N34S ) and the cystic fibrosis gene 显示文摘Felderbauer P Karakas E Fendrich V 2008Am J Gastroentero12008,103,2:1
15钙敏感受体基因突变:慢性胰腺炎新的遗传危险因素显示文摘Objective.In 2003 we identified a family with familial hypocalciuric hypercalcemia(FHH)(heterozygous CASR gene mutation L173P)and a mutation in the pancreatic secretory trypsin inhibitor gene(SPINK1)(N34S).While family members with an isolated calcium-sensing receptor gene(CASR)mutation remained healthy,a combination of the CASR and SPINK1 gene mutation caused chronic pancreatitis(CP).We thus speculate that the combination of two genetic defects affecting calcium homeostasis and pancreatic enzyme activation might represent a novel approach in chronic inherited pancreatic disease.We therefore sought to explore whether CASR gene mutations were prevalent in a cohort of patients with CP and confirmed SPINK1 mutations.Material and methods.A cohort of 19 families(n = 170)with a history of idiopathic CP(ICP)was screened for mutations within the CASR gene;104 members of that cohort had a mutation(N34S)within the SPINK1 gene and 66 of those were suffering from CP.The entire CASR gene was screened for single strand conformation polymorphism under varying polyacrylamide gel conditions and subjected to direct dideoxy nucleotide sequencing of amplified cDNA.Results.Single-strand conformation polymorphisms were observed in 59 samples,clustering of exons 3,4 and 7.DNA sequence analysis revealed a yet unreported missense mutation in exon 7(R896H)and two conservative mutations in exon 4(F391F)and exon 7(E790E).Furthermore,an intronic polymorphism in nucleotide position 493-19 G > A was detected in 19 out of 170 members of that cohort.Conclusions.We identified three novel calcium-sensing receptor gene mutations(1 missense mutation,2 silent mutations and 1 intronic polymorphism)in a cohort of 19 families with ICP.In particular,the kindred with the R896H mutation presenting with a similar pedigree to the family described above may indicate a role for CASR gene mutations in SPINK1-related CP.Again,only the patient with the combination of both CASR and N34S SPINK1 gene mutation developed pancreatitis,whereas in the healthy parents and children only an isolated CASR or N34S SPINK1 gene mutation could be detected.We suggest that the CASR gene is a novel yet undetected co-factor in a multifactorial genetic setting of SPINK1-related pancreatitis that alters the susceptibility for pancreatitis in these patients.Felderbauer P. Klein W. Bulut K. 张欣 2006世界核心医学期刊文摘(胃肠病学分册)2006,2,9:0
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