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| 1 | 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 |
| 2 | 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 |
| 3 | 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 |
| 4 | 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 |
| 5 | 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 |
| 6 | 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 |
| 7 | 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 |
| 8 | Hirschsprung's disease显示文摘 | Kenny S E Tam P K H Garcia-Barcelo M | 2010 | Semin Pedlatr Surg2010，19，3： | 1 |
| 9 | 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 |
| 10 | Accumulation of miR-155 and BIC RNA in human B cell lymphomas显示文摘 | Eis P S Tam W Sun L | 2005 | Proc Natl Acad Sci U S A2005，102，10： | 1 |
| 11 | Modified Intelligent Driver Model显示文摘 | Oussama Derbel Tamás Péter | 2012 | Periodica Polytechnica2012，40，2： | 1 |
| 12 | X-chromosome activity of the mouse primordial germ cells revealed by the expression of an X-linked lacZ transgene显示文摘 | Zhou S X Tan S S | 1994 | Development1994，120，： | 1 |
| 13 | Products of ozone-initiated chemistry in a simulated aircraft environment显示文摘 | Wisthaler A Tamás G Wyon D P Strφm-Tejsen P Space D Beauchamp J Hansel A M(a)rk T D Weschler C J | | 0，，13： | 1 |
| 14 | Human eosinophils induce mucin production in airway epithelial cells via epidermal growth factor receptor activation显示文摘 | Burgel P R Lazarus S C Tam D C | 2001 | J Immunol2001，167，： | 1 |
| 15 | Suppressor of cytokine signalling gene expression is elevated in breast carcinoma显示文摘 | Raccurt M Tam S P Lau P | 2003 | Br J Cancer2003，89，： | 1 |
| 16 | Human mast cell tryptase: multiple cDNAs and genes reveal a multigene ser- ine protease family显示文摘 | Vanderslice P Ballinger S M Tam E K | 1990 | Proc Natl Acad Sci USA1990，87，10： | 1 |
| 17 | Algal growth and nutrient removal in Hong Kong domestic wastewater显示文摘 | TAM N P Y WONG Y S LIONG E | 1989 | Environs Pollute1989，58，： | 1 |
| 18 | Gustatory 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 | 2012 | Brain Research2012，，： | 1 |
| 19 | Design of Gram-negative selective antimicrobial peptides显示文摘 | Muhle S A Tam J P | | 0，，19： | 1 |
| 20 | Accumulation of miR-155 and BIC RNA in human B cell lymphomas显示文摘 | Eis P S Tam W Sun L | 2005 | Proc Natl Acad Sci USA2005，102，： | 1 |
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