Noise-induced nitrotyrosine increase and outer hair cell death in guinea pig cochlea / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>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.</p><p><b>METHOD</b>Thirty guinea pigs were used in this study. The experimental animals were either exposed for 4 hours per day to broadband noise at 122 dB SPL (A-weighted) for 2 consecutive days or perfused cochleae with 5 mg/ml of the SIN1 solutions, an exogenous NO and superoxide donor, for 30 minutes. Then the cochleae of the animals were dissected. Propidium iodide (PI), a DNA intercalating fluorescent probe, was used to trace morphological changes in OHC nuclei. The distribution of nitrotyrosine (NT) in the organ of Corti and the cochlear lateral wall tissue from the guinea pigs were examined using fluorescence immunohistochemistry method. Whole mounts of organ of Corti were prepared. Morphological and fluorescent changes were examined under a confocal microscope.</p><p><b>RESULTS</b>Either after noise exposure or after SIN1 perfusion, outer hair cells (OHCs) death with characteristics of both apoptotic and necrotic degradation appeared. Nitrotyrosine immunolabeling could be observed in the OHCs from the control animals. After noise exposure, NT immunostaining became much greater than the control animals in OHCs. The apoptotic OHC has significant increase of nitrotyrosine in and around the nucleus following noise exposure. In the normal later wall of cochleae, relatively weak nitrotyrosine immunolabeling could be observed. After noise exposure, nitrotyrosine immunoactivity became stronger in stria vascularis.</p><p><b>CONCLUSION</b>Noise exposure induced increase of nitrotyrosine production is associated with OHCs death suggesting reactive nitrogen species participation in the cochlear pathophysiology of noise-induced hearing loss.</p>

The primary evaluation of minimal prepared ceramic veneer in anterior teeth for clinical application / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To evaluate the clinical application value of minimal prepared ceramic veneer in anterior teeth, by analyzing the esthetic effects and success rates.</p><p><b>METHODS</b>Forty-four anterior teeth in 30 patients with minor esthetic defect were included in this study. Less than 0.5 mm preparation or no preparaion technique was used in the clinical procedure. Glass ceramics veneers were delivered and 3M Relyx Veneer were used as the adhesive. The final appearance of each restoration was evaluated by patients on visual analogue scales (VAS) and by professional prosthodontists. Evaluation criteria included margin effects, color, shape and translucency. The success rate of all the restoration were analyzed in 6, 12 and 24 month after the treatment.</p><p><b>RESULTS</b>The patients' degree of satisfaction was 9.2 ± 0.4, while the excellent rate of esthetic effect of margin effect, color, shape and translucency was 89% (39/44), 91% (40/44), 98% (43/44) and 93% (41/44) by professional prosthodontist. The success rate of 6, 12 and 24 month were 100% (44/44), 98% (43/44) and 91% (40/44).</p><p><b>CONCLUSIONS</b>The minimal prepared venneers have a good esthetic effect and a satisfactory success rate, and is a suitable technique in esthetic treatment under the critical indications.</p>

Caspase 3 activation and apoptosis inducing factor translocation in noise exposure induced out hair cells apoptosis / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To investigate the pathway and mechanism of noise exposure induced out hair cells (OHC) apoptosis.</p><p><b>METHODS</b>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. The apoptosis inducing factor (AIF) translocation from mitochondria in OHC were further examined by immunohistology method. The nuclei were labeled with PI and the mitochondrion was labeled with Mito-tracker. Whole mount organ of Corti was prepared. Morphological and fluorescent change was observed use confocal microscope.</p><p><b>RESULTS</b>In the normal OHC, AIF is distributed where the mitochondria were located and no activated caspase 3 was observed. After the animals exposed to broadband noise at 122 dB in 4 h/day for 2 days, both apoptosis and necrosis were appeared in OHC. AIF translocated from mitochondrion to nuclei in apoptotic and necrotic OHC following noise exposure. The noise exposure triggered activation of caspase 3 in apoptic hair cells. But no caspase 3 activation appeared in necrotic OHC.</p><p><b>CONCLUSIONS</b>These findings indicated that the caspase-dependent pathway is an important pathway in noise exposure induced apoptosis. And AIF also involves OHC death pathway following noise exposure.</p>