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| 1 | IgA肾病的免疫抑制与强化支持治疗显示文摘IgA肾病是最常见的肾小球肾炎类型。数个研究结果表明,针对肾小球系膜的IgA沉积和循环的IgA抗体,可以使用免疫抑制疗法。改善全球肾脏病预后(KDIGO)指南推荐,使用肾素血管紧张素系统(RAS)阻滞剂,即血管紧张素转换酶抑制剂(ACEI)或血管紧张素Ⅱ受体阻断剂(ARB),治疗每日尿蛋白排泄量超过1克的IgA肾病患者。KDIGO指南还建议。 | Rauen T Eitner F Fitzner C 王建中 | 2015 | 中华肾病研究电子杂志2015，4，6： | 46 |
| 2 | IgA肾病的强化支持和免疫抑制疗法显示文摘IgA肾病患者在强化支持治疗的基础上,如果加上免疫抑制疗法,其临床结果尚不清楚。最近德国学者进行了一项多中心、非盲、随机对照试验,两组平行、序贯设计。在6个月的磨合期,支持治疗(特别是阻断肾素一血管紧张素系统)根据蛋白尿的量而调整。 | Rauen T Eitner F Fitzner C 王建中 | 2016 | 中华肾病研究电子杂志2016，5，1： | 9 |
| 3 | 纯Ti和Ti-Pd合金在有、无添加H_2O_2的磷酸盐缓冲溶液中的耐腐蚀性能(英文)显示文摘采用动电位和电化学阻抗谱技术研究了纯Ti(2级)和Ti-Pd合金(7级)的耐腐蚀性能。实验温度为36.6℃,实验溶液包括模拟的健康人体条件的pH7.4的PBS溶液和添加了H2O2(0.015mol/L)的pH5.2的炎症状态的PBS溶液。Ti-Pd合金(7级Ti),在含H2O2的PBS溶液中,其耐腐蚀性能比纯Ti的好(较低的腐蚀电流密度),表明其是一种很好的骨科植入材料。 | P. HANDZLIK phandzli@agh.edu.pl K. FITZNER | 2013 | Transactions of Nonferrous Metals Society of China2013，23，3： | 6 |
| 4 | Molecular determinants of the antitumor effects of trichostatin A in pancreatic cancer cells显示文摘AIM:To gain molecular insights into the action of the histone deacetylase inhibitor(HDACI) trichostatin-A(TSA) in pancreatic cancer(PC) cells.METHODS:Three PC cell lines,BxPC-3,AsPC-1 and CAPAN-1,were treated with various concentrations of TSA for def ined periods of time.DNA synthesis was assessed by measuring the incorporation of 5-bromo-2'deoxyuridine.Gene expression at the level of mRNA was quantif ied by real-time polymerase chain reaction.Expression and phosphorylation of proteins was monitored by immunoblotting,applying an infrared imaging technology.To study the role of p38 MAP kinase,the specif ic enzyme inhibitor SB202190 and an inactive control substance,SB202474,were employed.RESULTS:TSA most eff iciently inhibited BrdU incorporation in BxPC-3 cells,while CAPAN-1 cells displayed the lowest and AsPC-1 cells an intermediate sensitivity.The biological response of the cell lines correlated with the increase of histone H3 acetylation after TSA application.In BxPC-3 cells(which are wild-type for KRAS),TSA strongly inhibited phosphorylation of ERK 1/2 and AKT.In contrast,activities of ERK and AKT in AsPC-1 and CAPAN-1 cells(both expressing oncogenic KRAS) were not or were only modestly affected by TSA treatment.In all three cell lines,but most pronounced in BxPC-3 cells,TSA exposure induced an activation of the MAP kinase p38.Inhibition of p38 by SB202190 slightly but signif icantly diminished the antiproliferative effect of TSA in BxPC-3 cells.Interestingly,only BxPC-3 cells responded to TSA treatment by a signif icant increase of the mRNA levels of bax,a pro-apoptotic member of the BCL gene family.Finally,in BxPC-3 and AsPC-1 cells,but not in the cell line CAPAN-1,signif icantly higher levels of the cell cycle inhibitor protein p21Waf1 were observed after TSA application.CONCLUSION:The biological effect of TSA in PC cells correlates with the increase of acetyl-H3,p21Waf1,phospho-p38 and bax levels,and the decrease of phosphoERK 1/2 and phospho-AKT. | Elisabeth Emonds Brit Fitzner Robert Jaster | 2010 | World Journal of Gastroenterology2010，16，16： | 5 |
| 5 | Impact of hyperglycemia on autoimmune pancreatitis and regulatory T-cells显示文摘AIM To evaluate the influence of hyperglycemia on the progression of autoimmune pancreatitis.METHODS We induced hyperglycemia by repetitive intraperitoneal(ip) injection of 50 mg/kg streptozotocin in MRL/Mp J mice, which develop autoimmune pancreatitis due to a genetic predisposition. We compared the extent of inflammation(histological score, CD3^+ lymphocytes, CD8^+ T-cells, CD4^+ T-cells, Foxp3^+ T-helper cells) in the pancreas of hyperglycemic and normoglycemic mice. We also analyzed the number of leukocytes, lymphocytes, granulocytes and monocytes in the blood. In addition, we determined the percentage of CD3^+ lymphocytes, CD8^+ T-cells, CD4^+ T-cells, Foxp3^+ T-helper cells, Foxp3^+ CD25^+ T-helper and Foxp3^+T-helper cells in the spleen by flow cytometry.RESULTS Treatment with streptozotocin caused a strong induction of hyperglycemia and a reduction in body weight(P < 0.001). Severe hyperglycemia did not, however, lead to an aggravation, but rather to a slight attenuation of autoimmune pancreatitis. In the pancreas, both the histological score of the pancreas as well as the number of CD3+ lymphocytes(P < 0.053) were decreased by hyperglycemia. No major changes in the percentage of CD8^+ T-cells, CD4^+ T-cells, Foxp3^+ T-helper cells were observed between hyperglycemic and normoglycemic mice. Hyperglycemia increased the numbers of leukocytes(P < 0.001), lymphocytes(P = 0.016), granulocytes and monocytes(P = 0.001) in the blood. Hyperglycemia also moderately reduced the percentage of CD3^+ lymphocytes(P = 0.057), significantly increased the percentage of Foxp3^+ T-helper cells(P = 0.018) and Foxp3^+ CD25^+ T-helper cells(P = 0.021) and reduced the percentage of Foxp3^+T-helper cells(P = 0.034) in the spleen. CONCLUSION Hyperglycemia does not aggravate but moderately attenuates autoimmune pancreatitis, possibly by increasing the percentage of regulatory T-cells in the spleen. | Franz-Tassilo Müller-Graff Brit Fitzner Robert Jaster Brigitte Vollmar Dietmar Zechner | 2018 | World Journal of Gastroenterology2018，24，28： | 3 |
| 6 | Distinct antifibrogenic effects of erlotinib,sunitinib and sorafenib on rat pancreatic stellate cells显示文摘AIM:To study if three clinically available small molecule kinase inhibitors(SMI),erlotinib,sunitinib and sorafenib,exert antifibrogenic effects on pancreatic stellate cells(PSC)and analyze the basis of their action.METHODS:Cultured rat PSC were exposed to SMI.Cell proliferation and viability were assessed employing 5-bromo-2’-deoxyuridine incorporation assay and flow cytometry,respectively.2-Deoxy-2-[18F]fluoroglucose(18F-FDG)uptake was measured to study metabolic activity.Exhibition of the myofibroblastic PSC phenotype was monitored by immunofluorescence analysis ofα-smooth muscle actin(α-SMA)expression.Levels of mRNA were determined by real-time PCR,while protein expression and phosphorylation were analyzed by immunoblotting.Transforming growth factor-β1 (TGF-β1)levels in culture supernatants were quantified by ELISA.RESULTS:All three SMI inhibited cell proliferation and18F-FDG uptake in a dose-dependent manner and without significant cytotoxic effects.Furthermore,additive effects of the drugs were observed.Immunoblot analysis showed that sorafenib and sunitib,but not erlotinib,efficiently blocked activation of the AKT pathway,while all three drugs displayed little effect on phosphorylation of ERK1/2.Cells treated with sorafenib or sunitinib expressed less interleukin-6 mRNA as well as less collagen type 1 mRNA and protein.Sorafenib was the only drug that also upregulated the expression of matrix metalloproteinase-2 and reduced the secretion of TGF-β1 protein.All three drugs showed insignificant or discordant effects on the mRNA and protein levels ofα-SMA.CONCLUSION:The tested SMI,especially sorafenib,exert inhibitory effects on activated PSC,which should be further evaluated in preclinical studies. | Anne Elsner Falko Lange Brit Fitzner Martin Heuschkel Bernd Joachim Krause Robert Jaster | 2014 | World Journal of Gastroenterology2014，20，24： | 2 |
| 7 | Serum cardiac troponin T as a prognostic marker in early sepsis显示文摘 | Haude V Fitzner R | 1998 | Chest1998，113，： | 1 |
| 8 | Costs and benefits associated with diabetes education:a review of the literature显示文摘 | Bore SA Fitzner KA Panhalkar PS | 2009 | Diabetes Educ2009，35，1： | 1 |
| 9 | Pemxisome proliferator-aetivated receptor gamma overexpression inhibits profibrogenic activities of immortalised rat pancreatic stellate cells 显示文摘 | Jaster R Lichte P Fitzner B | 2007 | Cell Mol Med2007，9，3： | 1 |
| 10 | Galectin-1 is an inductor of pancreatic stellate cell activation显示文摘 | Fitzner B Walzel H Sparmann G | 2005 | Cell Signal2005，17，10： | 1 |
| 11 | In vitro investigation of titanium and hydroxyapatite dental implant surfaces using a rat bone marrow stromal cell culture system显示文摘 | Knabe C Klar F Fitzner R Radlanski RJ Gross U | | 0，，： | 1 |
| 12 | Control of oligodendroglial cell number by the miR-17-92 cluster显示文摘 | Budde H Schmitt S Fitzner D | 2010 | Development2010，137，13： | 1 |
| 13 | Identification of Polish RHDVa subtype strains based on the analysis of a high- ly variable part of VP60 gene显示文摘 | Fitzner A Niedbalski W Paprocka G | 2012 | Pol J Vet Sei2012，15，1： | 1 |
| 14 | In vitro investigation of titanium and hydroxyapatite dental implant surfaces using a rat bone marrow stromal cell culture system显示文摘 | Knabe C Klar F Fitzner R | 2002 | Biomaterial2002，15，4： | 1 |
| 15 | Health Care in Hong Kong and Mainland China: One Country, Two Systems?显示文摘 | Karen A Fitzner Sheryl Coughlin Cecilia Tomori Charles L Bennett | 2000 | Health Policy2000，，53： | 1 |
| 16 | Regulation of pancreatic stellate cell function in vitro: biological and molecular effects of all-trans retinoic acid显示文摘 | Jaster R Hilgandorf I Fitzner B | 2003 | Biochem Pharmacol2003，66，4： | 1 |
| 17 | Costs and benefits associated with diabetes education : a review of literature 显示文摘 | Boren SA Fitzner KA Panhalkar PS | 2008 | Diabetes Educ2008，35，1： | 1 |
| 18 | Control of oligoden- droglial cell number by the miR-17-92 cluster 显示文摘 | Budde H Schmitt S Fitzner D | 2010 | Devel- opment2010，137，13： | 1 |
| 19 | Chronic progressive multiple sclerosis:pathogenesis ofneurodegeneration and therapeutic strategies显示文摘 | Fitzner D Simons M | 2010 | Curr Neuropharmacol2010，8，： | 1 |
| 20 | Deposition of bo- ron nitride on graphite at 1300 K显示文摘 | PAWLAS-FORYST E FITZNER K | 1997 | Microchimica Acta1997，125，14： | 1 |
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