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Winfred W. Williams

Researcher at Harvard University

Publications -  87
Citations -  8522

Winfred W. Williams is an academic researcher from Harvard University. The author has contributed to research in topics: Transplantation & Kidney transplantation. The author has an hindex of 38, co-authored 83 publications receiving 8027 citations. Previous affiliations of Winfred W. Williams include University Hospital of Lausanne & Brown University.

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HLA-Mismatched Renal Transplantation without Maintenance Immunosuppression

TL;DR: Five patients with end-stage renal disease received combined bone marrow and kidney transplants from HLA single-haplotype mismatched living related donors, with the use of a nonmyeloablative preparative regimen, and it was possible to discontinue all immunosuppressive therapy 9 to 14 months after the transplantation.
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Intercellular adhesion molecule-1-deficient mice are protected against ischemic renal injury.

TL;DR: It is reported that renal ICAM-1 mRNA levels and systemic levels of the cytokines IL-1 and TNF-alpha increase 1 h after ischemia/ reperfusion in the mouse, likely acting via potentiation of neutrophilendothelial interactions.
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Complement activation in acute humoral renal allograft rejection: diagnostic significance of C4d deposits in peritubular capillaries.

TL;DR: C4d in peritubular capillary walls distinguishes AHR from ACR, is more specific and sensitive than traditional criteria, and is a potentially valuable adjunct in the diagnosis of graft dysfunction.
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Acute Humoral Rejection in Kidney Transplantation: II. Morphology, Immunopathology, and Pathologic Classification

TL;DR: The incidence of acute humoral rejection in renal allograft biopsies has been difficult to determine because widely accepted diagnostic criteria have not been established and non-HLA antibodies or subthreshold levels of DSA were detected in posttransplant recipient sera.
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Chronic Humoral Rejection: Identification of Antibody-Mediated Chronic Renal Allograft Rejection by C4d Deposits in Peritubular Capillaries

TL;DR: C4d can be used to separate this group of CR from the nonspecific category of chronic allograft nephropathy and may have the potential to guide successful therapeutic intervention and support the hypothesis that a substantial fraction of CR is mediated by antibody (immunologically active).