Anti-hypertrophic effect of NHE-1 inhibition involves GSK-3beta-dependent attenuation of mitochondrial dysfunction.

Although Na(+)-H(+) exchanger 1 (NHE-1) inhibition has been demonstrated to have anti-hypertrophic effect indirectly through mitochondria, the detailed cellular mechanisms mediating this effect remain elusive. In this study we sought to determine whether NHE-1 inhibition exerts an anti-hypertrophic effect by modulating the mitochondrial permeability transition pore (mPTP) opening through the AMP-activated protein kinase (AMPK)/glycogen synthase kinase 3beta (GSK-3beta) pathway during hypertrophy in cardiomyocytes. An in vivo model of hypertrophy was induced in male Sprague-Dawley rats by subjecting them to 3, 7 or 28 days of coronary artery ligation (CAL).

NHE-1 inhibition-induced cardioprotection against ischaemia/reperfusion is associated with attenuation of the mitochondrial permeability transition.

Aims: The possible contribution of the cardiac mitochondrial permeability transition pore (PTP) towards the cardioprotective effects of Na(+)-H(+) exchanger-1 (NHE-1) inhibition was studied in hearts subjected to ischaemia/reperfusion (IR).

Methods And Results: Langendorff-perfused rat hearts were subjected to 40 min of global ischaemia and 60 min of reperfusion in the presence or absence of the NHE-1 specific inhibitor AVE-4890 (AVE, 5 microM). Mitochondrial PTP opening was determined in the intact heart using 2-deoxy-[(3)H]-glucose entrapment and in isolated mitochondria by monitoring the decrease of the calcium-induced light scattering.

Clinical validity of the Chinese version of Mattis Dementia Rating Scale in differentiating dementia of Alzheimer's type in Hong Kong.

The present study aimed to examine the clinical validity and applicability of the Chinese version of Mattis Dementia Rating Scale (CDRS) for elderly Chinese individuals. The scale was found to have good reliability with internal consistency ranging from 0.7 to 0.