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19篇 您的检索式:作者名="Jaster M"
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1Impact 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 2018World Journal of Gastroenterology2018,24,28:3
2Bivalirudin inhibits peripro- cedural platelet function and tissue factor expression of human smooth muscle ceils显示文摘Pepke W Eisenreich A Jaster M 2013Cardiovasc Ther2013,31,2:1
3Bivalirudin inhibits periprocedural plateIet function and tissue factor expression of human smooth muscle cells显示文摘Pepke W Eisenreich A Jaster M 2013Cardiovasc Ther2013,31,2:1
4Randomized comparison of platelet-leukocyte aggregates and platelet in blood: heparin coated coiled wire stent implantation versus balloon angioplasty in acute myocardial infarction 显示文摘Jaster M Schwimmbeck P Spencker S 2003Thromb Res2003,112,56:1
5Bivalirudin inhib- its periprocedural platelet function and tissue factor ex- pression of human smooth muscle cells显示文摘Pepke W Eisenreich A Jaster M 2013Cardiovasc T- her2013,31,2:1
6The amount of flbrinogen - positive platelets predicts the occurrence of instent restenosis显示文摘JASTER M HORSTKOTFE D WILLICH T 2008Atherosclerosis2008,197,1:1
7Bivalirudin inhibits periproce-dural platelet function and tissue factor expression of human smoothmuscle cells显示文摘Pepke W Eisenreich A Jaster M 2013Cardiovasc Ther2013,31,2:1
8An emphasis on accuracy-meeting the many challenges of large gear inspection显示文摘JASTER M 2011Gear Technology2011,6,:1
9Randomized comparison of platelet-leukocyte aggregates and platelet in blood:heparin coated coiled wire stent implantation versus balloon angioplasty in acute myocardial infarction显示文摘 SP Spencker S 2003Thromb Res2003,12,56:1
10The amount of fibrinogen-positive platelets predicts the occurrence of in-stent restenosis 显示文摘Jaster M Horstkotte D Willich T 2008Atherosclerosis2008,197,1:1
11Bivalimdin inhibits periprocedural platelet function and tissue factor expression of hu- man smooth muscle cells显示文摘Pepke W Eisenreich A Jaster M 2013Cardiovasc Ther2013,31,2:1
12An emphasis on accuracy-meeting the many challenges of large gear inspection显示文摘JASTER M 2011Gear Technology2011,6,:1
13The amount offibrinogen-positive platelets predicts the occurrence of in-stent restenosis显示文摘Jaster M Horstkotte D Willich T 2008Atherosclerosis2008,197,1:1
14Effects of varying particles size of forage on digestion and chewing behavior of dairy heifers 显示文摘Jaster E H Murphy M R 1983Dairy Sci1983,66,:1
15Bivalirudin inhibits periprocedural platelet function and tissue factor expression of human smooth muscle eells显示文摘Pepke W Eisenreieh A Jaster M 2013Cardiovase Ther2013,31,2:1
16Bivalirudin inhibits peripmcedural platalet function and tissue factor expression of human smooth muscle cells 显示文摘Pepke W Eisenreich A Jaster M 2013Cardiovasc Ther2013,31,2:1
17Ran-domized comparison of platelet-leukocyte aggregates and platelet activation in blood:heparin-coated coiled wire stent implantation versus balloon angioplasty in acute myocardial infarction显示文摘Jaster M Schwimmbeck P Spencker S 2003Thromb Res2003,112,56:1
18Feeding supplemental niacin for milk production in six dairy herds显示文摘Jaster E H Rakes G F Hutjens M F 1983J Dairy Sci1983,66,:1
19Uncoupling protein 2 deficiency of non-cancerous tissues inhibits the progression of pancreatic cancer in mice显示文摘Background: Pancreatic ductal adenocarcinoma(PDAC) is a disease of the elderly mostly because its development from preneoplastic lesions depends on the accumulation of gene mutations and epigenetic alterations over time. How aging of non-cancerous tissues of the host affects tumor progression, however, remains largely unknown. Methods: We took advantage of a model of accelerated aging, uncoupling protein 2-deficient( Ucp2 knockout, Ucp2 KO) mice, to investigate the growth of orthotopically transplanted Ucp2 wild-type(WT) PDAC cells(cell lines Panc02 and 6606PDA) in vivo and to study strain-dependent differences of the PDAC microenvironment. Results: Measurements of tumor weights and quantification of proliferating cells indicated a significant growth advantage of Panc02 and 6606PDA cells in WT mice compared to Ucp2 KO mice. In tumors in the knockout strain, higher levels of interferon-γ m RNA despite similar numbers of tumor-infiltrating T cells were observed. 6606PDA cells triggered a stronger stromal reaction in Ucp2 KO mice than in WT animals. Accordingly, pancreatic stellate cells from Ucp2 KO mice proliferated at a higher rate than cells of the WT strain when they were incubated with conditioned media from PDAC cells. Conclusions: Ucp2 modulates PDAC microenvironment in a way that favors tumor progression and implicates an altered stromal response as one of the underlying mechanisms.Denis Revskij Jakob Runst Camilla Umstätter Luise Ehlers Sarah Rohde Dietmar Zechner Manuela Bastian Brigitte Müller-Hilke Georg Fuellen Larissa Henze Hugo Murua Escobar Christian Junghanss Axel Kowald Uwe Walter Rüdiger Köhling Olaf Wolkenhauer Robert Jaster 2023Hepatobiliary & Pancreatic Diseases International2023,22,2:0
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