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Erwin W. Gelfand
Researcher at University of Colorado Denver
Publications - 679
Citations - 37565
Erwin W. Gelfand is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Immunoglobulin E & T cell. The author has an hindex of 99, co-authored 675 publications receiving 36059 citations. Previous affiliations of Erwin W. Gelfand include University of Colorado Hospital & University of Virginia.
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Ethanol inhibits ligand‐activated Ca2+ channels in human B lymphocytes
TL;DR: The inhibitory effects of ethanol on ligand‐activated Ca2+ channels and subsequent induction of c‐fos may provide the basis for its immunosuppressive action.
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Use of IGIV in the treatment of immune-mediated dermatologic disorders.
TL;DR: IGIV has shown benefit in reducing symptoms and the need for cortecosteroids or cytotaxic drugs in a number of dermatologic conditions and in many of these diseases the initial benefits seen in open-labeled trials must be confirmed in controlled clinical trials.
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Heterozygous IKKβ activation loop mutation results in a complex immunodeficiency syndrome.
Jordan K. Abbott,Jordan K. Abbott,Angelica C. Ehler,Divya Jayaraman,Paul R. Reynolds,Kanao Otsu,Laurie Manka,Erwin W. Gelfand +7 more
TL;DR: The identified in an adult with ectodermal dysplasia and immunodeficiency a germline, gain-of-function mutation, K171R, in IKBKB, suggesting it underlies a novel immunodficiency syndrome.
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Altered Purine and Pyrimidine Metabolism in Erythrocytes with Purine Nucleoside Phosphorylase Deficiency
Irving H. Fox,Jan Kaminska,N. Lawrence Edwards,Erwin W. Gelfand,Kenneth Rich,William N. Arnold +5 more
TL;DR: Two hypotheses to account for the associated immunodeficiency—that the enzyme deficiency leads to a block of PP-ribose-P synthesis or inhibition of pyrimidine synthesis—could not be supported by observations in erythrocytes from both enzyme-deficient families.
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Coding-region alterations in BTK do not universally cause X-linked agammaglobulinemia.
TL;DR: Because of the known anti-inflammatory role of MKP-1, GILZ, and TTP, their reduced transactivation could be a mechanism by which relative glucocorticoid insensitivity occurs in patients with nasal polyps and asthma.