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| 1 | Effects of octreotide on acute necrotizing pancreatitis in rabbits显示文摘AIM: To assess the role of oxygen-derived free radicals and cytokines in the pathogenesis of taurocholic acid-induced acute pancreatitis, and to evaluate the preventive effects of octreotide towards the development of acute pancreatitis. METHODS: Acute pancreatitis was induced in male New Zealand white rabbits by retrograde injection of 0.8 mL/kg·b·m, of 50 g/L sodium taurocholate(NaTC) in the pancreatic duct. Sham-operated animals served as control. Octreotide 1 mglkg·b.m.was administered subcutaneously before the induction of pancreatitis. Blood was taken from the jugular vein before and at 1, 3, 6, 12 and 24 h after pancreatitis induction.Serum activities of amylase, IL-6 and TNF-α and levels of malonyl dialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GPx), catalase and superoxide dismutase (Mn-,Cu-,and Zn-SOD) in pancreatic tissue were measured.RESULTS: Serum TNF-α and IL-6 levels increased significantly 3 h after the onset of pancreatitis, and then returned to control level. The tissue concentration of MDA was significantly elevated at 24 h, while the GSH level and GP-x, catalase, Mn-SOD, Cu-, Zn-SOD activities were all significantly decreased in animals with pancreatitis as compared to the control. Octreotide pretreatment significantly reversed the changes in cytokines and reactive oxygen metabolites. Octreotide treatment did not alter the serum amylase activity and did not have any beneficial effects on the development of histopathological changes.CONCLUSION: Oxygen-derived free radicals and proinflammatory cytokines are generated at an early stage of NaTc-induced acute pancreatitis in rabbits. Prophylac ticoctreotide treatment can prevent release of cytokines and generation of reactive oxygen metabolites, but does not have any beneficial effects on the development of necrotizing pancreatitis. | Lászl6Czakó PéterHegyi TamásTakács CsabaGóg AndrásFarkas YvetteMándy Ilona Sz.Varga LászlóTiszlavicz JánosLonovics | 2004 | World Journal of Gastroenterology2004，10，14： | 21 |
| 2 | A 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 | 2005 | World Journal of Gastroenterology2005，11，7： | 15 |
| 3 | L-arginine-induced experimental pancreatitis显示文摘Despite medical treatment, the lethality of severe acute pancreatitis is still high (20-30%). Therefore, it is very important to find good animal models to characterise the events of this severe disease. In 1984, Mizunuma et. al. developed a new type of experimental necrotizing pancreatitis by intraperitoneal administration of a high dose of L-arginine in rats. This non-invasive model is highly reproducible and produces selective, dose-dependent acinar cell necrosis.Not only is this a good model to study the pathomechanisne of acute necrotizing pancreatitis, but it is also excellent to observe and influence the time course changes of the disease. By writing this review we iluminate some new aspects of cell physiology and pathology of acute necrotizing pancreatitis. Unfortunately, the reviews about acute experimental pancreatitis usually did not discuss this model.Therefore, the aim of this manuscript was to summarise the observations and address some challenges for the future in L-arginine-induced pancreatitis. | PéterHegyi ZoltánRakonczayJr RékaSári CsabaGóg JánosLonovics TamásTakács LászlóCzakó | 2004 | World Journal of Gastroenterology2004，10，14： | 7 |
| 4 | Activation of human fibroblast-like synoviocytes by uric acid crystals in rheumatoid arthritis显示文摘Hyperuricemia-mediated uric acid crystal formation may cause joint inflammation and provoke the destruction of joints through the activation of inflammasome-mediated innate immune responses.However,the immunopathological effects and underlying intracellular regulatory mechanisms of uric acid crystal-mediated activation of fibroblast-like synoviocytes(FLS)in rheumatoid arthritis(RA)have not been elucidated.Therefore,we investigated the in vitro effects of monosodium urate crystals,alone or in combination with the inflammatory cytokines tumor-necrosis factor(TNF)-a or interleukin(IL)-1b,on the activation of human FLS from RA patients and normal control subjects and the underlying intracellular signaling mechanisms of treatment with these crystals.Monosodium urate crystals were able to significantly increase the release of the inflammatory cytokine IL-6,the chemokine CXCL8 and the matrix metalloproteinase(MMP)-1 from both normal and RA-FLS(all P,0.05).Moreover,the additive or synergistic effect on the release of IL-6,CXCL8 and MMP-1 from both normal and RA-FLS was observed following the combined treatment with monosodium urate crystals and TNF-a or IL-1b.Further experiments showed that the release of the measured inflammatory cytokine,chemokine and MMP-1 stimulated by monosodium urate crystals were differentially regulated by the intracellular activation of extracellular signal-regulated kinase and c-Jun N-terminal kinase pathways but not the p38 mitogen-activated protein kinase pathway.Our results therefore provide a new insight into the uric acid crystal-activated immunopathological mechanisms mediated by distinct intracellular signal transduction pathways leading to joint inflammation in RA. | Da P Chen Chun K Wong Lai S Tam Edmund K Li Christopher WK Lam | 2011 | Cellular & Molecular Immunology2011，8，6： | 5 |
| 5 | Relevance 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 | 2014 | World Journal of Gastroenterology2014，20，27： | 4 |
| 6 | 查看详情显示文摘 | W C Huang H Y Tam P K A Wai X Y Dong H Ming J P Xie | | 中国物理快报(英文版)0，，： | 4 |
| 7 | 神经连接蛋白-3缺乏可阻止高分级神经胶质瘤生长显示文摘在一项新的研究中,来自美国国家卫生研究院、斯坦福大学、达纳法伯癌症研究所和哈佛医学院的研究人员发现某些侵袭性脑瘤的生长能够通过切断它们获取大脑中神经细胞产生的一种信号分子加以阻止.这些研究人员发现当这种被称作神经连接蛋白-3(neuroligin-3,NLGN3)的信号分子缺乏时,或者当利用药物干扰这种信号分子时,人高分级神经胶质瘤不能够在小鼠大脑中扩散. | Venkatesh H S Tam L T Woo P J | 2017 | 临床误诊误治2017，30，11： | 3 |
| 8 | Frequency and prognostic role of mucosal healing in patients with Crohn's disease and ulcerative colitis after one-year of biological therapy显示文摘AIM:To assess the endoscopic activity before and after a one-year period of biological therapy and to evaluate the frequency of relapses and need for retreatment after stopping the biologicals in patients with Crohn’s disease(CD)and ulcerative colitis(UC).METHODS:The data from 41 patients with CD and 22 patients with UC were assessed.Twenty-four CD patients received infliximab,and 17 received adalimumab.The endoscopic severity of CD was quantified with the simplified endoscopic activity score for Crohn’s disease in CD and with the Mayo endoscopic subscore in UC.RESULTS:Mucosal healing was achieved in 23 CD and7 UC patients.Biological therapy had to be restarted in78%of patients achieving complete mucosal healing with CD and in 100%of patients with UC.Neither clinical remission nor mucosal healing was associated with the time to restarting the biological therapy in either CD or UC.CONCLUSION:Mucosal healing did not predict sustained clinical remission in patients in whom the biological therapies had been stopped. | Klaudia Farkas Péter László Lakatos Mónika Szcs va Pallagi-Kunstár Anita Bálint Ferenc Nagy Zoltán Szepes Noémi Vass Lajos S Kiss Tibor Wittmann Tamás Molnár | 2014 | World Journal of Gastroenterology2014，20，11： | 2 |
| 9 | Risks 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 | 2009 | The Annals of Thoracic Surgery2009，，1： | 2 |
| 10 | Accumulation of miR-155 and BIC RNA in human B cell lyrephomas 显示文摘 | Eis P S Tam W Sun L | 2005 | Proc Nail Acad Sci USA2005，102，10： | 1 |
| 11 | Cell cycle arrest and apoptosis induced by the coronavirus infectious bronchitis virus in the absence of p53显示文摘 | U F Q TAM J P LIU D X | 2007 | Virology2007，365，2： | 1 |
| 12 | Wound-induced migration of rat hepatic stellate cells is modulated by endothelin-1 through rho-kinasemediated alterations in the acto-myosin cytoskeleton显示文摘 | Tangkijvanich P Tam SP Yee Jr HF | 2001 | Hepatology2001，33，1： | 1 |
| 13 | Motivating Knowledge Worker - the Challenge for the 1990s 显示文摘 | i TAM P M | 1993 | Long Range Planning1993，26，3： | 1 |
| 14 | Bone mineral density and its correlation with clinical and laborato- ry factors in chronic peritoneal dialysis patients显示文摘 | Ersoy FF Passadakis SP Tam P | 2006 | J Bone Miner Metab2006，24，1： | 1 |
| 15 | Association behavior of poly( methacrylic acid)-block-poly( methyl methacrylate) in aqueous medium : potentiometric and laser light scattering studies显示文摘 | Ravi P WANG C Tam K C | 2003 | Macromolecules2003，36，： | 1 |
| 16 | Machine fault diagnosis through an effective exact wavelet analysis 显示文摘 | Tse P W Yang W X Tam H Y | 2004 | Journal of Sound and Vibration2004，277，45： | 1 |
| 17 | A biological survey of' ballast water in container ships entering Hong Kong显示文摘 | CHU K H TAM P F FUNG C H | 1997 | Hydrobiologia1997，352，1： | 1 |
| 18 | Effects of Matrine on proliferation and differentiation in K-562 cells显示文摘 | ZHANG L P JIANG J K TAM J W | 2001 | Leuk Res2001，25，9： | 1 |
| 19 | Hirschsprung's disease显示文摘 | Kenny S E Tam P K H Garcia-Barcelo M | 2010 | Semin Pedlatr Surg2010，19，3： | 1 |
| 20 | Miniaturized Micros-Trip Low Pass Filter with Wide Stop-Band Using Double Equilateral U- Shaped Defected Ground Structure 显示文摘 | Ting S W Tam K W Martins R P | 2006 | IEEE Microwave and Wireless Components Letters2006，16，5： | 1 |
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