Background: Hearing deficiency is the condition for which accession medical waivers are most commonly granted. The retention of individuals entering service with a waiver for hearing deficiency has not been previously studied.
Methods: Military retention among new enlistees with a medical waiver for hearing deficiency was compared with that among a matched comparison group of fully qualified enlistees. Comparisons according to branch of service over the first 3 years of service were performed with the Kaplan-Meier product-limit method and proportional-hazards model.
Results: Army subjects had significantly lower retention rates than did their fully qualified counterparts. In the adjusted model, Army and Navy enlistees with a waiver for hearing deficiency had a significantly lower likelihood of retention than did their matched counterparts.
Discussion: The increased likelihood of medical attrition in enlistees with a waiver for hearing loss provides no evidence to make the hearing accession standard more lenient and validates a selective hearing loss waiver policy.
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http://dx.doi.org/10.7205/milmed.172.1.63 | DOI Listing |
Hum Genet
January 2025
Division of Hearing and Balance Research, National Institute of Sensory Organs, NHO Tokyo Medical Center, 2-5-1 Higashigaoka, Meguro-Ku, Tokyo, 152-8902, Japan.
There are hundreds of rare syndromic diseases involving hearing loss, many of which are not targeted for clinical genetic testing. We systematically explored the genetic causes of undiagnosed syndromic hearing loss using a combination of whole exome sequencing (WES) and a phenotype similarity search system called PubCaseFinder. Fifty-five families with syndromic hearing loss of unknown cause were analyzed using WES after prescreening of several deafness genes depending on patient clinical features.
View Article and Find Full Text PDFCalcif Tissue Int
January 2025
Department of Paediatric Endocrinology, Alder Hey Children's Hospital, Liverpool, UK.
Autosomal recessive hypophosphatemic rickets type 2 (ARHR2) is an uncommon hereditary form of rickets characterised by chronic renal phosphate loss and impaired bone mineralisation. This results from compound heterozygous or homozygous pathogenic variants in ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), a key producer of extracellular inorganic pyrophosphate (PPi) and an inhibitor of fibroblast growth factor23 (FGF23). ENPP1 deficiency impacts FGF23 and increases its activity.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
School of Biosciences, University of Sheffield, Sheffield S10 2TN, United Kingdom.
Myosin-VIIA (MYO7A) is an unconventional myosin responsible for syndromic (Usher 1B) or nonsyndromic forms of deafness in humans when mutated. In the cochlea, MYO7A is expressed in hair cells, where it is believed to act as the motor protein tensioning the mechanoelectrical transducer (MET) channels, thus setting their resting open probability (). However, direct evidence for this unique role for an unconventional myosin in mature hair cells is lacking.
View Article and Find Full Text PDFAdv Sci (Weinh)
December 2024
Department of Otorhinolaryngology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
GJB2 encodes connexin 26 (Cx26), the most commonly mutated gene causing hereditary non-syndromic hearing loss. Cx26 is mainly expressed in supporting cells (SCs) and fibrocytes in the mammalian cochlea. Gene therapy is currently considered the most promising strategy for eradicating genetic diseases.
View Article and Find Full Text PDFJ Otol
July 2024
Department of Audiology, All India Institute of Speech and Hearing, Mysuru, Karnataka, India.
Purpose: The present systematic review examined imaging findings in the Auditory Neuropathy Spectrum Disorder (ANSD) population.
Methods: Electronic databases such as Pub Med, Google Scholar, J Gate, and Science Direct were used to conduct a literature search. The articles retrieved through the literature search were assessed in two stages.
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