Objective Options for management of unilateral hearing loss (UHL) in children include conventional hearing aids, bone-conduction hearing devices, contralateral routing of signal (CROS) aids, and frequency-modulating (FM) systems. The objective of this study was to systematically review the current literature to characterize auditory outcomes of hearing rehabilitation options in UHL. Data Sources PubMed, EMBASE, Medline, CINAHL, and Cochrane Library were searched from inception to January 2016. Manual searches of bibliographies were also performed. Review Methods Studies analyzing auditory outcomes of hearing amplification in children with UHL were included. Outcome measures included functional and objective auditory results. Two independent reviewers evaluated each abstract and article. Results Of the 249 articles identified, 12 met inclusion criteria. Seven articles solely focused on outcomes with bone-conduction hearing devices. Outcomes favored improved pure-tone averages, speech recognition thresholds, and sound localization in implanted patients. Five studies focused on FM systems, conventional hearing aids, or CROS hearing aids. Limited data are available but suggest a trend toward improvement in speech perception with hearing aids. FM systems were shown to have the most benefit for speech recognition in noise. Studies evaluating CROS hearing aids demonstrated variable outcomes. Conclusions Data evaluating functional and objective auditory measures following hearing amplification in children with UHL are limited. Most studies do suggest improvement in speech perception, speech recognition in noise, and sound localization with a hearing rehabilitation device.
Background:Findings from a small clinical study suggested that statins may counteract the ther-
Steroid hormone receptors including estrogen receptors (ER) classically function as ligand-regulated transcription factors. However, estrogens also elicit cellular effects through binding to extra-nuclear ER (ERα, ERβ, and G protein-coupled ER or GPER) that are coupled to kinases. How extra-nuclear ER actions impact cardiac ischemia-reperfusion (I/R) injury is unknown. We treated ovariectomized wild-type female mice with estradiol (E2) or an estrogen-dendrimer conjugate (EDC), which selectively activates extra-nuclear ER, or vehicle interventions for two weeks. I/R injury was then evaluated in isolated Langendorff perfused hearts. Two weeks of treatment with E2 significantly decreased infarct size and improved post-ischemic contractile function. Similarly, EDC treatment significantly decreased infarct size and increased post-ischemic functional recovery compared to vehicle-treated hearts. EDC also caused an increase in myocardial protein S-nitrosylation, consistent with previous studies showing a role for this post-translational modification in cardioprotection. In further support of a role for S-nitrosylation, inhibition of nitric oxide synthase, but not soluble guanylyl cyclase blocks the EDC mediated protection. The administration of ICI182,780, which is an agonist of G-protein coupled estrogen receptor (GPER) and an antagonist of ERα and ERβ, did not result in protection; however, ICI182,780 significantly blocked EDC-mediated cardioprotection, indicating participation of ERα and/or ERβ. In studies determining the specific ER subtype and cellular target involved, EDC decreased infarct size and improved functional recovery in mice lacking ERα in cardiomyocytes. In contrast, protection was lost in mice deficient in endothelial cell ERα. Thus, extra-nuclear ERα activation in endothelium reduces cardiac I/R injury in mice, and this likely entails increased protein S-nitrosylation. Since EDC does not stimulate uterine growth, in the clinical setting EDC-like compounds may provide myocardial protection without undesired uterotrophic and cancer-promoting effects.
Type I IFNs are used for treating viral, neoplastic, and inflammatory disorders. The protein products encoded by IFN-stimulated genes (ISGs) likely mediate clinical effects of IFN in patients. Macroarray assays, used for studying ISG induction in IFN-treated patients, comprise genes identified predominantly through analysis of long-term cell lines. To discover genes induced selectively by IFN-beta in PBMC, we exposed whole blood to physiological concentrations of IFN-beta. PBMC were prepared, and RNA was extracted, reverse-transcribed, and hybridized to cDNA microarrays, and microarray analysis identified 39 ISGs and 20 IFN-repressed genes (IRGs). Thirty-three ISGs were known previously, and six ISGs were novel. New ISGs included GTP cyclohydrolase 1; hypothetical protein LOC129607; hypothetical protein FLJ38348; leucine aminopeptidase 3; squalene epoxidase; and GTP-binding protein overexpressed in skeletal muscle. Twenty IRGs included IL-1beta and CXCL8, which had been identified earlier. CXCL1 was a novel IRG identified in the current study. PCR analysis demonstrated the regulation of six novel ISGs and CXCL1 as an IRG in PBMC and astrocytoma cells. Results were validated using RNA obtained ex vivo from blood of patients after injection with IFN-beta. Identification of new ISGs and IRGs in primary PBMC will enhance macroarray assays for monitoring IFN responsiveness.
These findings indicate that for children with special health care needs, enrollment in a multidisciplinary aerodigestive clinic may improve health care outcomes by decreasing technical direct cost by 70% and significantly decreasing patient hospital days by an estimated 1 week per year. Furthermore, coordinated aerodigestive care in a medical home setting may lower health care expenditures from a systems-based perspective.
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