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One of the well-known causes of hearing loss is noise. Approximately 31.1% of Americans between the ages of 20 and 69 years (61.1 million people) have high-frequency hearing loss associated with noise exposure. In addition, recurrent noise exposure can accelerate age-related hearing loss. Phlorofucofuroeckol A (PFF-A) and dieckol, polyphenols extracted from the brown alga Ecklonia cava, are potent antioxidant agents. In this study, we investigated the effect of PFF-A and dieckol on the consequences of noise exposure in mice. In 1,1-diphenyl-2-picrylhydrazyl assay, dieckol and PFF-A both showed significant radical-scavenging activity. The mice were exposed to 115 dB SPL of noise one single time for 2 h. Auditory brainstem response(ABR) threshold shifts 4 h after 4 kHz noise exposure in mice that received dieckol were significantly lower than those in the saline with noise group. The high-PFF-A group showed a lower threshold shift at click and 16 kHz 1 day after noise exposure than the control group. The high-PFF-A group also showed higher hair cell survival than in the control at 3 days after exposure in the apical turn. These results suggest that noise-induced hair cell damage in cochlear and the ABR threshold shift can be alleviated by dieckol and PFF-A in the mouse. Derivatives of these compounds may be applied to individuals who are inevitably exposed to noise, contributing to the prevention of noise-induced hearing loss with a low probability of adverse effects. [ABSTRACT FROM AUTHOR]

Background and Objectives: We aim to explore the effects of residual auditory steady state response (ASSR) on cochlear implantation (CI) outcomes in children lacking auditory brainstem responses (ABRs)., Subjects and Methods: We retrospectively reviewed the data of child CI recipients lacking ABRs. All ears were divided into two groups: with residual ASSR and without ASSR. For each frequency, the T- and C-levels and the electrical dynamic ranges of postoperative 3-month and 1-year mappings were compared between the groups. To evaluate speech perception, patients who received simultaneous bilateral CIs were divided into two groups: group 1 exhibited responses at all frequencies in both ears; in group 2, at least one ear evidenced no response. The Categories of Auditory Perception (CAP) and Infant-Toddler Meaningful Auditory Integration Scale (IT-MAIS) scores were compared between the groups., Results: We enrolled 16 patients. At 2 kHz, the postoperative 3-month and 1-year T-levels of patients with residual hearing were lower than those of hearing loss group (p=0.001, p=0.035). In residual hearing group, the ASSR threshold correlated positively with the postoperative 1-year T-level (p=0.012, R2 =0.276) and C-level (p=0.002, R2 =0.374). Of 10 simultaneous bilateral CI recipients, 5 exhibited ASSRs at all frequencies and the other 5 showed no response at ≥1 frequency. The latter had higher CAP scores at the postoperative 1-year (p=0.018)., Conclusions: In children exhibiting hearing loss in ABR testing, residual hearing at 2 kHz ASSR correlated positively with the post-CI T-level. Those with ASSRs at all frequencies had significantly lower CAP scores at the postoperative 1year. CI should not be delayed when marginal residual hearing is evident in ASSR.

Two key virulence factors of Helicobacter pylori are the secreted virulent proteins of vacuolating toxin A (VacA) and cytotoxin associated protein A (CagA) which lead to damages of gastric epithelial cells. We previously identified that the cyanidin 3-O-glucoside (C3G) inhibits the secretion of both VacA and CagA. In the current report, we show that C3G inhibits VacA secretion in a dose-dependent manner by inhibiting secretion system subunit protein A (SecA) synthesis. As SecA is involved in translocation of bacterial proteins, we predicted that inhibition of the SecA pathway by C3G should decrease H. pylori-induced cell death. To test this hypothesis, the human gastric cell line KATO III cells were co-cultured with H. pylori 60190 (VacA(+)/CagA(+)) and C3G. We found that C3G treatment caused a decrease in activation of the pro-apoptotic proteins caspase-3/-8 in H. pylori-infected cells leading to a decrease in cell death. Our data suggest that consumption of foods containing anthocyanin may be beneficial in reducing cell damage due to H. pylori infection.

Anthocyanins have been studied as potential antimicrobial agents against Helicobacter pylori. We investigated whether the biosynthesis and secretion of cytotoxin-associated protein A (CagA) and vacuolating cytotoxin A (VacA) could be suppressed by anthocyanin treatment in vitro. H. pylori reference strain 60190 (CagA(+)/VacA(+)) was used in this study to investigate the inhibitory effects of anthocyanins; cyanidin 3-O-glucoside (C3G), peonidin 3-O-glucoside (Peo3G), pelargonidin 3-O-glucoside (Pel3G), and malvidin 3-O-glucoside (M3G) on expression and secretion of H. pylori toxins. Anthocyanins were added to bacterial cultures and Western blotting was used to determine secretion of CagA and VacA. Among them, we found that C3G inhibited secretion of CagA and VacA resulting in intracellular accumulation of CagA and VacA. C3G had no effect on cagA and vacA expression but suppressed secA transcription. As SecA is involved in translocation of bacterial proteins, the down-regulation of secA expression by C3G offers a mechanistic explanation for the inhibition of toxin secretion. To our knowledge, this is the first report suggesting that C3G inhibits secretion of the H. pylori toxins CagA and VacA via suppression of secA transcription.