This report explores the consequences of acoustic overexposures on hearing in noisy environments for two macaque monkeys trained to perform a reaction time detection task using a Go/No-Go lever release paradigm. Behavioral and non-invasive physiological assessments were obtained before and after narrowband noise exposure. Physiological measurements showed elevated auditory brainstem response (ABR) thresholds and absent distortion product otoacoustic emissions (DPOAEs) post-exposure relative to pre-exposure. Audiograms revealed frequency specific increases in tone detection thresholds, with the greatest increases at the exposure band frequency and higher. Masked detection was affected in a similar frequency specific manner: threshold shift rates (change of masked threshold per dB increase in noise level) were lower than pre-exposure values at frequencies higher than the exposure band. Detection thresholds in sinusoidally amplitude modulated (SAM) noise post-exposure showed no difference from those in unmodulated noise, whereas pre-exposure masked detection thresholds were lower in the presence of SAM noise compared to unmodulated noise. These frequency-dependent results were correlated with cochlear histopathological changes in monkeys that underwent similar noise exposure. These results reveal that behavioral and physiological effects of noise exposure in macaques are similar to those seen in humans and provide preliminary information on the relationship between noise exposure, cochlear pathology and perceptual changes in hearing within individual subjects.
Introduction: Postoperative thrombosis is a common complication after congenital heart disease (CHD) surgery in children, and is associated with increased mortality and morbidity. Identification of risk factors may allow preventive therapy and improved outcomes. Hypothesis: We tested the hypothesis that genetic variants are associated with postoperative thrombosis after CHD surgery in children. Methods: Children with CHD were prospectively enrolled in an observational cohort study at the time of initial surgical repair/palliation. Clinically detected thrombosis within 30 days of surgery while in hospital was the primary outcome. Patients were genotyped on the Axiom Precision Medicine Research Array. Clinical and genetic (8 common variants in candidate genes) factors were assessed for association with the primary outcome with univariate and multivariate analysis. A two-tailed P-value of < 0.05 was considered statistically significant. Results: A total of 2,398 unique patients (median age 6 months, median weight 6.7 kg) had complete clinical and genetic data for analysis. Postoperative thrombosis occurred in 242 (10.1%). Patients with thrombosis were younger (P<0.001), with longer bypass time (P<0.001) and higher initial postoperative lactate (P<0.001). Thrombosis was also associated with longer hospital stay (50 ± 59 days vs 16 ± 31days, P<0.001) and mortality (15.3% vs 2.9%, P<0.001). One common variant near fibrinogen gamma ( FGG , rs7659024, NC_000004.12:g.154599778G>A) was associated with postoperative thrombosis, with a gene-dose effect (thrombosis observed in 8.9% GG, n=1370, 11% AG, n=869, 15.1% AA, n=159, P=0.025). In multivariate analysis age (per year older OR 0.7, 95% CI 0.61-0.79), bypass time (per hour OR 1.24, 95% CI 1.09-1.39), lactate (per mmol/L OR 1.15, 95% CI 1.19-1.32) and FGG genotype (GG reference, AG OR 1.51, 95% CI 1.09-2.08; AA OR 2.35, 95% CI 1.39-3.97) were each independently associated with postoperative thrombosis. Conclusions: A common variant near FGG previously associated with fibrinogen γ′ levels is an independent risk factor for postoperative thrombosis after CHD surgery. Preoperative genotyping with thromboprophylaxis for patients at sufficient risk may be considered.
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