Passive lower-limb cycling represents an elegant, cost-effective and widely accessible therapeutic strategy that may reduce the clinical cardiovascular burden imposed by spinal cord injury and other neurological disorders. Spinal cord injury (SCI) causes Crenigacestat in vivo altered autonomic control and severe physical deconditioning that converge to drive maladaptive cardiac remodelling. We used a clinically relevant experimental model to investigate
the cardio-metabolic responses to SCI and to establish whether passive hind-limb cycling elicits a cardio-protective effect. Initially, 21 male Wistar rats were evenly assigned to three groups: uninjured control (CON), T3 complete SCI (SCI) or T3 complete SCI
plus passive hind-limb cycling (SCI-EX; 2x30minday(-1), 5daysweek(-1) for 4weeks beginning 6days post-SCI). On day 32, cardio-metabolic function was assessed using in vivo echocardiography, learn more ex vivo working heart assessments, cardiac histology/molecular biology and blood lipid profiles. Twelve additional rats (n=6 SCI and n=6 SCI-EX) underwent in vivo echocardiography and basal haemodynamic assessments pre-SCI and at days 7, 14 and 32 post-SCI to track temporal cardiovascular changes. Compared with CON, SCI exhibited a rapid and sustained reduction in left ventricular dimensions and function that ultimately manifested as reduced contractility, increased myocardial collagen deposition and an up-regulation of transforming growth factor beta-1 (TGF beta(1)) and mothers against decapentaplegic homolog 3 (Smad3) mRNA. For SCI-EX, the initial reduction in left ventricular dimensions and function at day 7 post-SCI was completely reversed by day 32 post-SCI, and there were no differences MK-8931 in myocardial contractility between SCI-EX and CON. Collagen
deposition was similar between SCI-EX and CON. TGF beta(1) and Smad3 were down-regulated in SCI-EX. Blood lipid profiles were improved in SCI-EX versus SCI. We provide compelling novel evidence that passive hind-limb cycling prevents cardiac dysfunction and reduces cardiovascular disease risk in experimental SCI.”
“Objective: Our objective was to report and describe a case of psychosocial short stature in an adolescent girl with psychotic features. Psychosocial short stature is a rare condition in which emotional stress or deprivation in childhood profoundly reduces growth, leading to persistent short stature. This disorder is variably known as psychosocial dwarfism, hyperphagic short stature or maternal deprivation dwarfism. In the literature, psychosocial short stature has not been associated previously with psychosis.