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William R. Swindell

Researcher at Jewish Hospital

Publications -  78
Citations -  4889

William R. Swindell is an academic researcher from Jewish Hospital. The author has contributed to research in topics: Psoriasis & Gene expression profiling. The author has an hindex of 32, co-authored 72 publications receiving 3851 citations. Previous affiliations of William R. Swindell include University of Michigan & Heritage College of Osteopathic Medicine.

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Modulation of Epidermal Transcription Circuits in Psoriasis: New Links between Inflammation and Hyperproliferation

TL;DR: A new approach for delineating epidermis-specific pathways and regulatory mechanisms that underlie altered gene expression in psoriasis is developed and highlights previously unrecognized “transcription circuits” that can provide targets for development of non-systemic therapies.
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Indicators of "Healthy Aging" in older women (65-69 years of age). A data-mining approach based on prediction of long-term survival

TL;DR: The multivariable model developed characterizes a "healthy aging" phenotype based upon an integration of measures that together reflect multiple dimensions of an aging adult (65-69 years of age) and may be of value as biomarkers in human studies that evaluate anti-aging interventions.
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Cellular dissection of psoriasis for transcriptome analyses and the post-GWAS era

TL;DR: This paper identified differentially expressed genes (DEGs) with altered expression in psoriasis lesions (n = 216 patients), as well as candidate genes near susceptibility loci from GWAS studies, and proposed an approach for generating hypotheses to explain GWAS hits at intergenic loci.
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A GRHL3-regulated repair pathway suppresses immune-mediated epidermal hyperplasia

TL;DR: It is determined that the prodifferentiation transcription factor grainyhead-like 3 (GRHL3), which is essential during epidermal development, is dispensable for adult skin homeostasis, but required for barrier repair after adult epidersmal injury.
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Early tissue responses in psoriasis to the antitumour necrosis factor-α biologic etanercept suggest reduced interleukin-17 receptor expression and signalling.

TL;DR: Antitumour necrosis factor (anti‐TNF)‐α therapy has made a significant impact on the treatment of psoriasis despite these agents being designed to neutralize TNF‐α activity.