University of Tennessee Health Science Center

About: University of Tennessee Health Science Center is a education organization based out in Memphis, Tennessee, United States. It is known for research contribution in the topics: Population & Transplantation. The organization has 15716 authors who have published 26884 publications receiving 1176697 citations.

Spontaneous firing patterns and axonal projections of single corticostriatal neurons in the rat medial agranular cortex

Abstract: 1. Spontaneous fluctuations of membrane potential, patterns of spontaneous firing, dendritic branching patterns, and intracortical and striatal axonal arborizations were compared for two types of c...

The Possibilities and Pitfalls of Doing a Secondary Analysis of a Qualitative Data Set

Abstract: The purpose of this article is to identify the general methodologic and data set-specific challenges that must be overcome when attempting a secondary analysis of qualitative data Two separate examples of secondary analyses of qualitative data sets are also described, including one unsuccessful beginning

Myofibroblast-mediated mechanisms of pathological remodelling of the heart

Abstract: The syncytium of cardiomyocytes in the heart is tethered within a matrix composed principally of type I fibrillar collagen The matrix has diverse mechanical functions that ensure the optimal contractile efficiency of this muscular pump In the diseased heart, cardiomyocytes are lost to necrotic cell death, and phenotypically transformed fibroblast-like cells-termed 'myofibroblasts'-are activated to initiate a 'reparative' fibrosis The structural integrity of the myocardium is preserved by this scar tissue, although at the expense of its remodelled architecture, which has increased tissue stiffness and propensity to arrhythmias A persisting population of activated myofibroblasts turns this fibrous tissue into a living 'secretome' that generates angiotensin II and its type 1 receptor, and fibrogenic growth factors (such as transforming growth factor-β), all of which collectively act as a signal-transducer-effector signalling pathway to type I collagen synthesis and, therefore, fibrosis Persistent myofibroblasts, and the resultant fibrous tissue they produce, cause progressive adverse myocardial remodelling, a pathological hallmark of the failing heart irrespective of its etiologic origin Herein, we review relevant cellular, subcellular, and molecular mechanisms integral to cardiac fibrosis and consequent remodelling of atria and ventricles with a heterogeneity in cardiomyocyte size Signalling pathways that antagonize collagen fibrillogenesis provide novel strategies for cardioprotection