J
James G. Cronin
Researcher at Swansea University
Publications - 50
Citations - 2935
James G. Cronin is an academic researcher from Swansea University. The author has contributed to research in topics: Innate immune system & Inflammation. The author has an hindex of 23, co-authored 46 publications receiving 2331 citations. Previous affiliations of James G. Cronin include University of London & Ludwig Maximilian University of Munich.
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Journal ArticleDOI
Defining Postpartum Uterine Disease and the Mechanisms of Infection and Immunity in the Female Reproductive Tract in Cattle
TL;DR: Advances in knowledge about infection and immunity in the female genital tract should be exploited to develop new therapeutics for uterine disease.
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Toll-Like Receptor 4 and MYD88-Dependent Signaling Mechanisms of the Innate Immune System Are Essential for the Response to Lipopolysaccharide by Epithelial and Stromal Cells of the Bovine Endometrium
TL;DR: Endometrial epithelial and stromal cells have an intrinsic role in innate immune surveillance in the endometrium, and in the case of LPS this recognition occurs via TLR4- and MYD88-dependent cell signaling pathways.
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Mechanisms of Infertility Associated with Clinical and Subclinical Endometritis in High Producing Dairy Cattle
Iain Martin Sheldon,S B Price,James G. Cronin,Robert O. Gilbert,John E. Gadsby,John E. Gadsby +5 more
TL;DR: LPS impairs the function of the hypothalamus and pituitary, and directly perturbs ovarian granulosa cells steroidogenesis, providing mechanisms to explain the association between uterine disease and anovulatory anoestrus.
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Dynasore - not just a dynamin inhibitor
TL;DR: Evidence is revealed that dynasore reduces labile cholesterol in the plasma membrane, and disrupts lipid raft organization, in a dynamin-independent manner, to explore the regulation of cholesterol in plasma membranes.
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p16INK4a and p14ARF tumor suppressor genes are commonly inactivated in cutaneous squamous cell carcinoma
TL;DR: The p16(INK4a) and p14(ARF) tumor suppressor genes (TSGs) are encoded within the CDKN2A locus on chromosome 9p21 and function as cell cycle regulatory proteins in the p53 and RB pathways and promoter methylation is the commonest mechanism of gene inactivation.