Evaluation of stress status using the stress map for guide dog candidates in the training stage using variations in the serum cortisol with nerve growth factor and magnesium ions.

Most studies on guide dogs for the blind were conducted to investigate the appropriateness of the animals, including in terms of their breeding, constitution, and temperament. However, research to comprehend the stress status of guide dog candidates in response to their training has been unclear. In this study, the levels of serum cortisol, nerve growth factor (NGF), and magnesium ion (Mg) levels of guide dog candidates during the three training stages-the elementary, intermediate, and advanced classes-were examined.

Analysis of serum magnesium ions in dogs exposed to external stress: A pilot study.

Magnesium ions (Mg) are essential for various enzymatic reactions in the body associated with energy production and activation of the muscles and nerves. Mg is also involved in blood pressure regulation, maintenance of body temperature, and glucose metabolism. Although various factors including foods and physical conditions have been reported to change serum Mg status in humans, serum Mg in dogs exposed to external stress has been unclear.

Effects of candesartan on electrical remodeling in the hearts of inherited dilated cardiomyopathy model mice.

Inherited dilated cardiomyopathy (DCM) is characterized by dilatation and dysfunction of the ventricles, and often results in sudden death or heart failure (HF). Although angiotensin receptor blockers (ARBs) have been used for the treatment of HF, little is known about the effects on postulated electrical remodeling that occurs in inherited DCM. The aim of this study was to examine the effects of candesartan, one of the ARBs, on cardiac function and electrical remodeling in the hearts of inherited DCM model mice (TNNT2 ΔK210).

Multistep ion channel remodeling and lethal arrhythmia precede heart failure in a mouse model of inherited dilated cardiomyopathy.

Background: Patients with inherited dilated cardiomyopathy (DCM) frequently die with severe heart failure (HF) or die suddenly with arrhythmias, although these symptoms are not always observed at birth. It remains unclear how and when HF and arrhythmogenic changes develop in these DCM mutation carriers. In order to address this issue, properties of the myocardium and underlying gene expressions were studied using a knock-in mouse model of human inherited DCM caused by a deletion mutation ΔK210 in cardiac troponinT.

Pathophysiological remodeling of mouse cardiac myocytes expressing dominant negative mutant of neuron restrictive silencing factor.

Background: It has been previously reported that the transgenic mouse expressing the dominant negative mutant of the neuron restrictive silencing factor (dnNRSF) in the heart died from lethal arrhythmia, so the present study aimed to clarify the electrophysiological alteration of the ventricular myocyte isolated from the dnNRSF mouse.

Methods And Results: The action potential (AP) and membrane currents were recorded using the whole-cell patch-clamp method. Intracellular Ca(2+) was measured with Indo-1AM.

Causes of abnormal Ca2+ transients in Guinea pig pathophysiological ventricular muscle revealed by Ca2+ and action potential imaging at cellular level.

Background: Abnormal Ca(2+) transients are often observed in heart muscles under a variety of pathophysiological conditions including ventricular tachycardia. To clarify whether these abnormal Ca(2+) transients can be attributed to abnormal action potential generation or abnormal Ca(2+) handling/excitation-contraction (EC) coupling, we developed a procedure to determine Ca(2+) and action potential signals at the cellular level in isolated heart tissues.

Methodology/principal Findings: After loading ventricular papillary muscle with rhod-2 and di-4-ANEPPS, mono-wavelength fluorescence images from rhod-2 and ratiometric images of two wavelengths of emission from di-4-ANEPPS were sequentially obtained.

Altered KCNQ3 potassium channel function caused by the W309R pore-helix mutation found in human epilepsy.

The second tryptophan (W) residue of the conserved WW motif in the pore helix of many K+ channel subunit is thought to interact with the tyrosine (Y) residues of the selectivity filter. A missense mutation causing the replacement of the corresponding residues with an arginine (W309R) occurs in KCNQ3 subunits forming part of M-channels. In this study, we examined the functional consequences of the W309R mutation in heterogously expressed KCNQ channels.

A simple technique for isolating healthy heart cells from mouse models.

Single heart cells of mouse models provide powerful tools for heart research. However, their isolation is not easy, and it imposes a significant bottleneck on their use in cellular studies of the heart. Aiming to overcome this problem, this report introduces a novel technique that reproducibly isolates healthy heart cells from mouse models.

Different cation sensitivities and binding site domains of Na+-Ca2+-K+ and Na+-Ca2+ exchangers.

We examined inhibitory effects of external multivalent cations Ni(2+), Co(2+), Cd(2+), La(3+), Mg(2+), and Mn(2+) on reverse-mode exchange of the K(+)-dependent Na(+)/Ca(2+) exchanger NCKX2 and the K(+)-independent exchanger NCX1 expressed in CCL-39 cells by measuring the rate of Ca(2+) uptake with radioisotope tracer and electrophysiological techniques. The apparent affinities for block of Ca(2+) uptake by multivalent cations was higher in NCKX2 than NCX1, and the rank order of inhibitory potencies among these cations was different. Additional experiments also showed that external Li(+) stimulated reverse-mode exchange by NCX1, but not NCKX2 in the presence of 5 mM K(+).

Cell-volume regulation by swelling-activated chloride current in guinea-pig ventricular myocytes.

The cell-volume regulation by swelling-activated Cl- current (I(Cl,swell)) was studied in guinea pig ventricular myocytes, using a microscopic video-image analysis. We have previously shown that in ventricular cells depolarized in high-K+ ([K+]o>45 mM) solution, an activation of the cyclic AMP-dependent Cl- current (I(Cl,cAMP)) leads to cell swelling. We first investigated the mechanism underlying the I(Cl,cAMP)-independent recovery (shrinkage) of the swollen cells.