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9篇 您的检索式:作者名="M.Ghobrial"
    题名 作者 年代 出处 被引量
1Chronic allograft rejection:A significant hurdle to transplant success显示文摘The state-of-the-art immunosuppression drugs do not ensure indefi nite transplant survival,and most transplants are continuously lost to chronic rejection even years posttransplantation.This form of rejection is responsible for long-term failure of transplanted organs.The mechanisms involved in development of chronic rejection are not well-understood.One of the main features of chronic rejection is progressive luminal narrowing of graft vessels,which results in compromised blood flow,ischemia,cell death,and finally graft failure.All the existing immunosuppressive regimens are targeting acute rejection,and at present there is no available therapy for prevention of chronic rejection.Chronic rejection involves two major,but interrelated responses:The first is the host immune response against the transplant mediated primarily by alloreactive T and B cells,and the second is injury and repair of the graft(vasculopathy of graft vessels).Here we focus on recent advances in understanding the cellular and molecular aspects of chronic transplant vasculopathy and function of macrophages,topics pivotal for development of novel antichronic rejection therapies.Malgorzata Kloc Rafik M.Ghobrial 2014Burns & Trauma2014,2,1:2
2Recipient Morbidity After Living and Deceased Donor Liver Transplantation: Findings from the A2ALL Retrospective Cohort Study?显示文摘C. E.Freise B. W.Gillespie A. J.Koffron A. S. F.Lok T. L.Pruett J. C.Emond J. H.Fair R. A.Fisher K. M.Olthoff J. F.Trotter R. M.Ghobrial J. E.Everhart 2008American Journal of Transplantation2008,,12:2
3Targeting Apoptosis Pathways in Cancer Therapy显示文摘Irene M.Ghobrial Thomas E.Witzig Alex A.Adjei 2009CA: A Cancer Journal for Clinicians2009,,3:1
4Recipient Morbidity After Living and Deceased Donor Liver Transplantation: Findings from the A2ALL Retrospective Cohort Study<sup>?</sup>显示文摘C. E.Freise B. W.Gillespie A. J.Koffron A. S. F.Lok T. L.Pruett J. C.Emond J. H.Fair R. A.Fisher K. M.Olthoff J. F.Trotter R. M.Ghobrial J. E.Everhart 2008American Journal of Transplantation2008,,12:1
5Targeting Apoptosis Pathways in Cancer Therapy显示文摘Irene M.Ghobrial Thomas E.Witzig Alex A.Adjei 2009CA: A Cancer Journal for Clinicians2009,,3:1
6Recipient Morbidity After Living and Deceased Donor Liver Transplantation: Findings from the A2ALL Retrospective Cohort Study<sup>?</sup>显示文摘C. E.Freise B. W.Gillespie A. J.Koffron A. S. F.Lok T. L.Pruett J. C.Emond J. H.Fair R. A.Fisher K. M.Olthoff J. F.Trotter R. M.Ghobrial J. E.Everhart 2008American Journal of Transplantation2008,,12:1
7An Early Regional Experience with Expansion of Milan Criteria for Liver Transplant Recipients显示文摘J. J.Guiteau R. T.Cotton W. K.Washburn A.Harper C. A.O’Mahony A.Sebastian S.Cheng G.Klintmalm M.Ghobrial G.Halff L.Mieles J.Goss 2010American Journal of Transplantation2010,,9:1
8Hepatitis C Positive Grafts may be used in Orthotopic Liver Transplantation: A Matched Analysis显示文摘SammySaab Rafik M.Ghobrial Ayman B.Ibrahim GreggKunder FranciscoDurazo StevenHan Douglas G.Farmer HasanYersiz Leonard I.Goldstein Ronald W.Busuttil 2003American Journal of Transplantation2003,,9:1
9The RNA helicase DHX15 is a critical regulator of natural killer-cell homeostasis and functions显示文摘The RNA helicase DHX15 is widely expressed in immune cells and traditionally thought to be an RNA splicing factor or a viral RNA sensor.However,the role of DHX15 in NK-cell activities has not been studied thus far.Here,we generated Dhx15-floxed mice and found that conditional deletion of Dhx15 in NK cells(Ncr1CreDhx15fl/fl mice)resulted in a marked reduction in NK cells in the periphery and that the remaining Dhx15-deleted NK cells failed to acquire a mature phenotype.As a result,Dhx15-deleted NK cells exhibited profound defects in their cytolytic functions.We also found that deletion of Dhx15 in NK cells abrogated their responsiveness to IL-15,which was associated with inhibition of IL-2/IL-15Rβ(CD122)expression and IL-15R signaling.The defects in Dhx15-deleted NK cells were rescued by ectopic expression of a constitutively active form of STAT5.Mechanistically,DHX15 did not affect CD122 mRNA splicing and stability in NK cells but instead facilitated the surface expression of CD122,likely through interaction with its 3′UTR,which was dependent on the ATPase domain of DHX15 rather than its splicing domain.Collectively,our data identify a key role for DHX15 in regulating NK-cell activities and provide novel mechanistic insights into how DHX15 regulates the IL-15 signaling pathway in NK cells.Guangchuan Wang Xiang Xiao Yixuan Wang Xiufeng Chu Yaling Dou Laurie J.Minze Rafik M.Ghobrial Zhiqiang Zhang Xian C.Li 2022Cellular & Molecular Immunology2022,19,6:0
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