|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | MELD Score as a Predictor of Early Death in Patients Undergoing Elective Transjugular Intrahepatic Portosystemic Shunt (TIPS) Procedures显示文摘 | Aaron Montgomery Hector Ferral Rajiv Vasan Darren W. Postoak | 2005 | CardioVascular and Interventional Radiology2005，，3： | 2 |
| 2 | Distal embolic protection during femoropopliteal atherectomy显示文摘 | Suri R Wholey MH Postoak D | 2006 | Catheter Cardiovasc Inter2006，67，3： | 1 |
| 3 | Survival after elective transjugular intrahepatic portosystemic shunt creation: prediction with model for end-stage liver disease score显示文摘 | Ferral H Gamboa P Postoak DW | 2004 | Radiology2004，231，1： | 1 |
| 4 | Tools of the subclavian trade显示文摘 | Wholey MH Postoak D Suri R | 2006 | Endovascular Today2006，5，： | 1 |
| 5 | Tools of the subclavian trade显示文摘 | Wholey MH Postoak D Sufi R | 2006 | Endovascular Today2006，，5： | 1 |
| 6 | Survival after elective transjugular intrahepatic portosystemic shunt creation:prediction with model for end-stage liver disease score显示文摘 | Ferral H Gamboa P Postoak D W | 2004 | Radiology2004，，27： | 1 |
| 7 | Tools of the Subclavian Trade显示文摘 | Wholey M H Postoak D Suri R | 2006 | Endovascular Today2006，5，4： | 1 |
| 8 | Survival after elective transjugular intrahepatic portosystemic shunt creation: prediction with model for end-stage liver disease score 显示文摘 | Ferral H Gamboa P Postoak DW | 2004 | Radiology2004，231，1： | 1 |
| 9 | Distal embolic protectionduring femoropopliteal atherectomy显示文摘 | Suri R Wholey MH Postoak D | | 0，，3： | 1 |
| 10 | Pik3c3 deficiency in myeloid cells imparts partial resistance to experimental autoimmune encephalomyelitis associated with reduced IL-1βproduction显示文摘The PIK3C3/VPS34 subunit of the class III phosphatidylinositol 3-kinase(PtdIns3K)complex plays a role in both canonical and noncanonical autophagy,key processes that control immune-cell responsiveness to a variety of stimuli.Our previous studies found that PIK3C3 is a critical regulator that controls the development,homeostasis,and function of dendritic and T cells.In this study,we investigated the role of PIK3C3 in myeloid cell biology using myeloid cell-specific Pik3c3-deficient mice.We found that Pik3c3-deficient macrophages express increased surface levels of major histocompatibility complex(MHC)class I and class II molecules.In addition,myeloid cell-specific Pik3c3 ablation in mice caused a partial impairment in the homeostatic maintenance of macrophages expressing the apoptotic cell uptake receptor TIM-4.Pik3c3 deficiency caused phenotypic changes in myeloid cells that were dependent on the early machinery(initiation/nucleation)of the classical autophagy pathway.Consequently,myeloid cell-specific Pik3c3-deficient animals showed significantly reduced severity of experimental autoimmune encephalomyelitis(EAE),a primarily CD4^(^(+))T-cell-mediated mouse model of multiple sclerosis(MS).This disease protection was associated with reduced accumulation of myelin-specific CD4^(^(+))T cells in the central nervous system and decreased myeloid cell IL-1βproduction.Further,administration of SAR405,a selective PIK3C3 inhibitor,delayed disease progression.Collectively,our studies establish PIK3C3 as an important regulator of macrophage functions and myeloid cell-mediated regulation of EAE.Our findings also have important implications for the development of small-molecule inhibitors of PIK3C3 as therapeutic modulators of MS and other autoimmune diseases. | Guan Yang Wenqiang Song Jielin Xu JLuke Postoak Feixiong Cheng Jennifer Martinez Jianhua Zhang Lan Wu Luc Van Kaer | 2021 | Cellular & Molecular Immunology2021，18，8： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员