Distribution and change of peroxynitrite in the guinea pig cochlea following noise exposure.

Nitric oxide (NO)-mediated pathology depends on the formation of reactive intermediates, such as the peroxynitrite (ONOO). ONOO can nitrate free tyrosine and tyrosine residues of proteins. Therefore, increases in tyrosine nitration reflect the amount of ONOO produced by oxidative stress.

A mutation in SLC22A4 encoding an organic cation transporter expressed in the cochlea strial endothelium causes human recessive non-syndromic hearing loss DFNB60.

The high prevalence/incidence of hearing loss (HL) in humans makes it the most common sensory defect. The majority of the cases are of genetic origin. Non-syndromic hereditary HL is extremely heterogeneous.

Diverse Kir expression contributes to distinct bimodal distribution of resting potentials and vasotone responses of arterioles.

The resting membrane potential (RP) of vascular smooth muscle cells (VSMCs) is a major determinant of cytosolic calcium concentration and vascular tone. The heterogeneity of RPs and its underlying mechanism among different vascular beds remain poorly understood. We compared the RPs and vasomotion properties between the guinea pig spiral modiolar artery (SMA), brain arterioles (BA) and mesenteric arteries (MA).

Noise-induced nitrotyrosine increase and outer hair cell death in guinea pig cochlea.

Background: Modern research has provided new insights into the biological mechanisms of noise-induced hearing loss, and a number of studies showed the appearance of increased reactive oxygen species (ROS) and reactive nitrogen species (RNS) during and after noise exposure. This study was designed to investigate the noise exposure induced nitrotyrosine change and the mechanism of outer hair cells death in guinea pig cochlea.

Method: Thirty guinea pigs were used in this study.

[The primary evaluation of minimal prepared ceramic veneer in anterior teeth for clinical application].

Objective: To evaluate the clinical application value of minimal prepared ceramic veneer in anterior teeth, by analyzing the esthetic effects and success rates.

Methods: Forty-four anterior teeth in 30 patients with minor esthetic defect were included in this study. Less than 0.

[The influence of toothguide training box on shade matching veracity].

Purpose: The aim of the study was to evaluate the influence of toothguide training box(TTB) on shade matching veracity, and compare the differences of influence on shade matching veracity of tabs of shadeguide and on that of tabs out of shadeguide.

Methods: 31 graduated students who had 1 to 5-year clinical experience without color blindness were trained by TTB once a week for 3 weeks. Elapsed time and scores from the training system were recorded each time.

[Caspase 3 activation and apoptosis inducing factor translocation in noise exposure induced out hair cells apoptosis].

Objective: To investigate the pathway and mechanism of noise exposure induced out hair cells (OHC) apoptosis.

Methods: The cochleae of control and noise exposure group were dissected. The activity of caspase 3, an important mediator of apoptosis, in OHC, was examined with carboxyfluorescein-labeled fluoromethyl ketone (FMK)-peptide inhibitors.

Dihydropyridines inhibit acetylcholine-induced hyperpolarization in cochlear artery via blockade of intermediate-conductance calcium-activated potassium channels.

Acetylcholine (ACh) induces hyperpolarization and dilation in a variety of blood vessels, including the cochlear spiral modiolar artery (SMA) via the endothelium-derived hyperpolarization factor (EDHF). We demonstrated previously that the ACh-induced hyperpolarization in the SMA originated in the endothelial cells (ECs) by activating a Ca(2+)-activated K(+) channel (K(Ca)); the hyperpolarization in smooth muscle cells was mainly an electrotonic spread via gap junction coupling. In the present study, using intracellular recording, immunohistology, and vascular diameter tracking techniques on in vitro SMA preparations, we found that 1) ACh-induced hyperpolarization was suppressed by intermediate-conductance K(Ca) (IK) blockers clotrimazole (IC(50) = 116 nM) and nitrendipine and by the calmodulin antagonist trifluoperazine, but it was not suppressed by the big-conductance K(Ca) blocker iberiotoxin.