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James W. Lillard

Researcher at Morehouse School of Medicine

Publications -  141
Citations -  7945

James W. Lillard is an academic researcher from Morehouse School of Medicine. The author has contributed to research in topics: Cancer & Metastasis. The author has an hindex of 40, co-authored 128 publications receiving 6984 citations. Previous affiliations of James W. Lillard include University of Alabama & University of Louisville.

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Nanoparticle-based targeted drug delivery

TL;DR: This article presents an overview of nanotechnology for the biologist and discusses the attributes of the novel XPclad((c)) nanoparticle formulation that has shown efficacy in treating solid tumors, single dose vaccination, and oral delivery of therapeutic proteins.
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Ghrelin inhibits leptin- and activation-induced proinflammatory cytokine expression by human monocytes and T cells

TL;DR: This is the first report demonstrating that ghrelin functions as a key signal, coupling the metabolic axis to the immune system, and supporting the potential use of gh Relin and GHS-R agonists in the management of disease-associated cachexia.
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A Study of Effects of MultiCollinearity in the Multivariable Analysis.

TL;DR: This work aims to perform a simulation study with various scenarios of different collinearity structures to investigate the effects of coll inearity under various correlation structures amongst predictive and explanatory variables and to compare these results with existing guidelines to decide harmful collinairity.
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Mechanisms for induction of acquired host immunity by neutrophil peptide defensins

TL;DR: These studies show that defensins enhance systemic IgG, but not IgA, Ab responses through help provided by CD4(+) Th1- and Th2-type cytokines and foster B and T cell interactions to link innate immunity with the adaptive immune system.
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CXCL12-CXCR4 interactions modulate prostate cancer cell migration, metalloproteinase expression and invasion.

TL;DR: It is reported that functional CXCR4 is significantly expressed by prostate cancer cell lines, LNCaP and PC3, when compared with normal prostatic epithelial cells (PrEC), and anti-CX CR4 antibodies significantly impaired the migration and invasive potential of PC3 and L NCaP cells.