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Full-Text Articles in Respiratory System

The Effects Of A Four-Week Whole-Body High-Intensity Training Program On Female Athletes 2015, Lindsey Taylor May 2015

The Effects Of A Four-Week Whole-Body High-Intensity Training Program On Female Athletes 2015, Lindsey Taylor

Master's Theses

Purpose: The purpose of this study was to examine the aerobic benefits and changes in running economy (RE) following a fourweek whole-body high-intensity interval training (HIIT) program on an athletic female population. Participants: Fourteen female student-athletes volunteered to participate in the study. Design: Participants reported on two occasions for VO2max and RE testing and were divided into two training groups based upon baseline VO2max: Endurance (END; n=6) and HIIT (n=8). Participants completed 12 total training sessions. During each session, END completed 30 minutes of vigorous-intensity running, while HIIT completed a total of four minutes of whole-body intervals. Measures: Maximal oxygen …


Histone Deacetylase Inhibitors Prevent Pulmonary Endothelial Hyperpermeability And Acute Lung Injury By Regulating Heat Shock Protein 90 Function, Atul D. Joshi, Nektarios Barabutis, Charalampos Birmpas, Christiana Dimitropoulou, Gagan Thangjam, Mary Cherian-Shaw, John Dennison, John D. Catravas Jan 2015

Histone Deacetylase Inhibitors Prevent Pulmonary Endothelial Hyperpermeability And Acute Lung Injury By Regulating Heat Shock Protein 90 Function, Atul D. Joshi, Nektarios Barabutis, Charalampos Birmpas, Christiana Dimitropoulou, Gagan Thangjam, Mary Cherian-Shaw, John Dennison, John D. Catravas

Bioelectrics Publications

Transendothelial hyperpermeability caused by numerous agonists is dependent on heat shock protein 90 (Hsp90) and leads to endothelial barrier dysfunction (EBD). Inhibition of Hsp90 protects and restores transendothelial permeability. Hyperacetylation of Hsp90, as by inhibitors of histone deacetylase (HDAC), suppresses its chaperone function and mimics the effects of Hsp90 inhibitors. In this study we assessed the role of HDAC in mediating lipopolysaccharide (LPS)-induced transendothelial hyperpermeability and acute lung injury (ALI). We demonstrate that HDAC inhibition protects against LPS-mediated EBD. Inhibition of multiple HDAC by the general inhibitors panobinostat or trichostatin provided protection against LPS-induced transendothelial hyperpermeability, acetylated and suppressed Hsp90 …