Beyond Speech Intelligibility: Quantifying Behavioral and Perceived Listening Effort in Response to Dysarthric Speech.

Purpose: This study investigated whether listener processing of dysarthric speech requires the recruitment of more cognitive resources (i.e., higher levels of listening effort) than neurotypical speech.

A Clinical Pathway for the Care of Critically Ill Patients With Asthma in the Community Hospital Setting.

Objectives: The management of severe pediatric asthma exacerbations is variable. The use of clinical pathways has been shown to decrease time to clinical recovery and length of stay (LOS) for critically ill patients with asthma in freestanding children's hospitals. We sought to determine if implementing a clinical pathway for pediatric patients who are on continuous albuterol in a community hospital would decrease time to clinical recovery and LOS.

Familial hypertrophic cardiomyopathy and atrial fibrillation caused by Arg663His beta-cardiac myosin heavy chain mutation.

More than 40 different beta-cardiac myosin heavy chain (beta-MHC) missense mutations have been identified that cause familial hypertrophic cardiomyopathy (FHC). Some of these are recognized to have important clinical manifestations, such as an increased incidence of sudden death. We report that the beta-MHC missense mutation Arg663His causes predominant cardiac morphology and atrial fibrillation.

Regulation of calcium channel expression in neonatal myocytes by catecholamines.

Expression of the dihydropyridine (DHP) receptor (alpha 1 subunit of L-type calcium channel) in heart is regulated by differentiation and innervation and is altered in congestive heart failure. We examined the transmembrane signaling pathways by which norepinephrine regulates DHP receptor expression in cultured neonatal rat ventricular myocytes. Using a 1.

Acadesine improves tolerance to ischemic injury in rat cardiac myocytes.

The ability of acadesine to modulate injury in a myocyte model of simulated ischemia was studied. When freshly isolated adult rat ventricular myocytes were subjected to 10 min of simulated ischemia and reperfusion, greater that 75% of myocytes developed hypercontracture and the amplitude of contraction of the remaining, potentially viable myocytes was markedly depressed. When cells were pretreated with 50 microM acadesine for 5 min and exposed to acadesine during simulated ischemia and during 2-10 min of reperfusion, followed by reperfusion with control buffer, up to 90% of myocytes maintained normal morphology and could be stimulated to contract.