7 research outputs found
Effects of a pulmonary rehabilitation program on physical capacity, peripheral muscle function and inflammatory markers in asthmatic children and adolescents: study protocol for a randomized controlled trial
RELATIONSHIP BETWEEN SCHOOLCHILDREN’S LEVELS OF PHYSICAL ACTIVITY, ANTHROPOMETRIC INDICES AND PULMONARY FUNCTION
Chronic Physiological Effects of Swim Training Interventions in Non-Elite Swimmers: A Systematic Review and Meta-Analysis
Background Swimming is a popular and potentially health-enhancing exercise, but has received less scientific attention compared with other exercise modes. Objective The objective of the study was to determine the chronic (long-term) effect of pool swim training on physiological outcomes in non-elite or non-competitive swimming participants
Differential regulation of clusterin isoforms by the androgen receptor
Clusterin (CLU) was initially reported as an androgen-repressed gene which is now shown to be an androgen-regulated ATP-independent cytoprotective molecular chaperone. CLU binds to a wide variety of client proteins to potently inhibit stress-induced protein aggregation and chaperone or stabilise conformations of proteins at times of cell stress. CLU is an enigmatic protein, being ascribed both pro- and anti-apoptotic roles. Recent evidence has shown that both secreted (sCLU) and nuclear (nCLU) isoforms can be produced, and that protein function is dependent on the sub-cellular localisation. We and others have shown that sCLU is cytoprotective, while nCLU is pro-apoptotic. It now seems likely that the apparently dichotomous functions of CLU result from the expression of different but related CLU isoforms and splice variants, and that cell survival depends in part on the relative expression of pro- versus anti-apoptotic CLU proteins. In cancer cells, increased sCLU expression is associated with increased resistance to apoptotic triggers and treatment resistance. CLU is a stress-induced protein upregulated after apoptotic triggers like androgen ablation and chemotherapy. Treatment strategies targeting stress-associated increases in sCLU expression enhance treatment-induced apoptosis and delay the emergence of androgen independence. Differential regulation of CLU isoforms and splice variants by androgens may be a pathway whereby cancer cells develop treatment resistance and evade apoptosis