|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Regulation of hepatic blood flow:The hepatic arterial buffer response revisited显示文摘The interest in the liver dates back to ancient times when it was considered to be the seat of life processes. The liver is indeed essential to life,not only due to its complex functions in biosynthesis,metabolism and clearance,but also its dramatic role as the blood volume reservoir. Among parenchymal organs,blood flow to the liver is unique due to the dual supply from the portal vein and the hepatic artery. Knowledge of the mutual communication of both the hepatic artery and the portal vein is essential to understand hepatic physiology and pathophysiology. To distinguish the individual importance of each of these inflows in normal and abnormal states is still a challenging task and the subject of on-going research. A central mechanism that controls and allows constancy of hepatic blood flow is the hepatic arterial buffer response. The current paper reviews the relevance of this intimate hepatic blood flow regulatory system in health and disease. We exclusively focus on the endogenous interrelationship between the hepatic arterial and portal venous inflow circuits in liver resection and transplantation,as well as inflammatory and chronic liver diseases. We do not consider the hepatic microvascular anatomy,as this has been the subject of another recent review. | Christian Eipel Kerstin Abshagen Brigitte Vollmar | 2010 | World Journal of Gastroenterology2010，16，48： | 49 |
| 2 | 标准参数、铋屏蔽、部分CT扫描和管电流调制在胸部CT检查中减少女性乳腺放射剂量的对照性研究显示文摘评价3种不同的技术[铋屏蔽、部分CT扫描和球管电流调制(TCM)]在胸部CT检查中降低女性乳腺放射剂量的可能性。使用带有乳腺的半拟人胸部模体,在64层CT设备上对剂量和影像质量进行测量和模拟。采用蒙特卡洛(MC)方法计算三维剂量分布。通过测量和模拟确定噪声。铋屏蔽使乳腺放射剂量减少约50%。噪声增加40%,影像质量因伪影而受损。在部分CT扫描中,未直接照射乳腺,乳腺放射剂量减少50%。为维持恒定的噪声水平,增加前后位的照射量导致脊柱放射剂量增加。 | S. V. Vollmar W.A. Kalender 秦乃姗(译) 唐光健(校) | 2008 | 国际医学放射学杂志2008，31，5： | 8 |
| 3 | Stimulation of p38 MAPK by hormal preconditioning with atrial natriuretic peptide显示文摘AIM:Stress-activated signaling pathways responsible for hepatic ischemia reperfusion injury and their modulation by protective interventions are widely unknown.Preconditioning of rat livers with Atrial Natriuretic Peptide(ANP)attenuates ischemia reperfusion injury(Gerbes et al.Hepatology1998,18:1309-1317),SinANP has recently been shown to be a regulator of the p38MAPKpathway in endothelial cells(Kiemer et al.CircRes2002,90:874-881).aim of this thudy was to investigate activities of MAPK during ischemia and reperfusion and effects of ANP on MAPK.METHODS:Rat livers were perfused with KH-buffer in the presence or absence of ANP for 20min,kept in cold UWsloution for 24h,and reperfused forupto120min,Activities of p38MAPKand JNKwas determined by in vitro phosphorylation assays using MBP and c-jun as substrates.After SDS/PAGE electrophoresis,gels were quantified by phosphorimaging.RESULTS:Activity of p38MAPKin control organs decreased in the course of ischemia and reperfusion by85%,whereas ANPincreased p38 activity by up to 30-fold.JNKactivation of control livers increased in the course of ischemia and reperfusion by up to three-fold.This increase in JNK activrity was slightly elevated in ANP preconditioned organs.CONCLUSION:This work represents a systematic investigation of MAPK activation during liver ischemia and reperfusion.Employing ANP,for the first time a pharmacological approach to modulate these central signal transduction molecules is presented. | Alexandra K. Kiemer Stefanie Kulhanek-Heinze Tobias Gerwig Alexander L. Gerbes Angelika M. Vollmar | 2002 | World Journal of Gastroenterology2002，8，4： | 7 |
| 4 | PI 3-kinase pathway is responsible for antiapoptotic effects of atrial natriuretic peptide in rat liver transplantation显示文摘AIM:To investigate the in vivo effect of atrial natriureticpeptide(ANP)and its signaling pathway during ortho-topic rat liver transplantation.METHODS:Rats were infused with NaCl,ANP(5 μg/kg),wortmannin(WM,16 μg/kg),or a combination ofboth for 20 min.Livers were stored in UW solution(4°C)for 24 h,transplanted and reperfused.Apoptosis wasexamined by caspase-3 activity and TUNEL staining.Phosphorylation of Akt and Bad was visualized by West-ern blotting and phospho-Akt-localization by confocalmicroscopy.RESULTS:ANP-pretreatment decreased caspase-3activity and TUNEL-positive cells after cold ischemia,indicating antiapoptotic effects of ANP in vivo.The an-tiapoptotic signaling of ANP was most likely caused byphosphorylation of Akt and Bad,since pretreatment withPI 3-kinase inhibitor WM abrogated the ANP-inducedreduction of caspase-3 activity.Interestingly,analysis ofliver tissue by confocal microscopy showed translocationof phosphorylated Akt to the plasma membrane of hepa-tocytes evoked by ANP.CONCLUSION:ANP activates the PI-3-kinase pathwayin the liver in vivo leading to phosphorylation of Bad, an event triggering antiapoptotic signaling cascade inischemic liver. | Uwe Grutzner Melanie Keller Michael Bach Alexandra K Kiemer Herbert Meissner Manfred Bilzer Stefan Zahler Alexander L Gerbes Angelika M Vollmar | 2006 | World Journal of Gastroenterology2006，12，7： | 3 |
| 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 | 从中医阴阳气血理论浅析满月与不寐显示文摘本文从中医阴阳气血理论入手,从病因病机、气血阴阳、现代研究几个角度对月相盈亏与不寐之间的关系进行了理论阐述,说明月节律对人体的影响是不容忽视的,并详细阐述了中国古代医家利用月节律治疗不寐的理论依据,以期为临床治疗不寐提供更多理论依据和更好的治疗方法。 | Vollmar Jing 任宏珊 刘彬冰 赵凌 梁繁荣 | 2016 | 湖南中医杂志2016，32，4： | 3 |
| 7 | Combined inhibition of vascular endothelial growth factor (VEGF),fibroblast growth factor and platelet-derived growth factor,but not inhibition of VEGF alone,effectively suppresses angiogenesis and vessel maturation in endometriosis lesion显示文摘 | Elitzsch A Vollmar B | 2006 | Hum Reprod2006，21，1： | 1 |
| 8 | Leukocytes contribute to hepatic ischemia/reperfusion in injury Via inter cellular adhesion molecule-1 mediated venular adherence显示文摘 | Vollmar B Glasz J | 1995 | Surgery1995，117，2： | 1 |
| 9 | Revaseularization and microcirculation of freshly grafted islets of Langerhans 显示文摘 | Menger MD Yamauchi J-I Vollmar B | 2001 | World J Surg2001，25，4： | 1 |
| 10 | Hydroxyethyl starch (130 kD),but not crystalloid volume supportimproves microcirculation during normotensive endotoxemia显示文摘 | Hoffmann JN Vollmar B Laschke MW | | 0，，02： | 1 |
| 11 | Rat model of femur fracture and cecal ligation and puncture显示文摘 | Menger MD Vollmar B | 2005 | J Trauma2005，59，3： | 1 |
| 12 | Microhemodynamicand cellular mechanisms of activated protein C action duringendotoxemia 显示文摘 | Hoffmann JN Vollmar B Laschke MW | 2004 | Crit Care Med2004，32，4： | 1 |
| 13 | Hydroxyethyl starch (130kD), but not crystalloid volume support, improves microcirculation during normotensive endotoxemia显示文摘 | Hoffmann J N Vollmar B Laschke M W | 2002 | Anesthesiology2002，97，2： | 1 |
| 14 | Microcirculation and excretory function of the liver under conditions of carbon dioxide pneumoperitoneum显示文摘 | Leister l Schüler P Vollmar B | 2004 | Surg Endosc2004，18，9： | 1 |
| 15 | Tne atrial natriuretic peptide regulates the production of inflammatory mediators in macrophages 显示文摘 | Kiemer AK Vollmar AM | 2001 | Ann Rheum Dis2001，60，3： | 1 |
| 16 | Hepatic microcirculatory perfu- sion failure is a determinant of liver dysfunction in warm ischemia- reperfusion显示文摘 | Vollmar B Glasz J Leiderer R | 1994 | Am J Pathol1994，145，6： | 1 |
| 17 | In vivo analysis of microcirculation following closed soft-tissue injury显示文摘 | Vollmar B Menger MD | 1999 | J Orthop Res1999，17，5： | 1 |
| 18 | Surface cooling inhibits tumor necrosis factor-alpha -induced microvascular perfusion failure, leukocyte adhesion, and apoptoSis in the striated muscle显示文摘 | Westermann S Vollmar B Thorlacius H | 1999 | Surgery1999，126，： | 1 |
| 19 | Endothelins like immunoreactivity in plasma of patients 显示文摘 | Gerbes AL Vollmar AM | 1992 | Life Sci1992，51，14： | 1 |
| 20 | Systemic and Regional Hemodynamics of Isoflurane and Sevoflurane in Rats 显示文摘 | Conzen P F Vollmar B Habazettl H | 1992 | Anesth Analg1992，74，： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员