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Hearing Disorders: HELP
Articles by Jeffrey D. Ohmen
Based on 8 articles published since 2009
(Why 8 articles?)
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Between 2009 and 2019, Jeff Ohmen wrote the following 8 articles about Hearing Disorders.
 
+ Citations + Abstracts
1 Article Large-scale phenotyping of noise-induced hearing loss in 100 strains of mice. 2016

Myint, Anthony / White, Cory H / Ohmen, Jeffrey D / Li, Xin / Wang, Juemei / Lavinsky, Joel / Salehi, Pezhman / Crow, Amanda L / Ohyama, Takahiro / Friedman, Rick A. ·Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, 1501 San Pablo Street, Los Angeles, CA 90089-2821, USA. · Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, 1501 San Pablo Street, Los Angeles, CA 90089-2821, USA; Bioinformatics and Systems Biology Program, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0419, USA. · Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, 1501 San Pablo Street, Los Angeles, CA 90089-2821, USA; Department of Cell Biology and Genetics, House Research Institute, Los Angeles, CA 90057, USA. · Department of Preventive Medicine, Keck School of Medicine of USC, 2250 Alcazar St, Los Angeles, CA 90089-9073, USA. · Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, 1501 San Pablo Street, Los Angeles, CA 90089-2821, USA; Department of Cell Biology and Genetics, House Research Institute, Los Angeles, CA 90057, USA. Electronic address: rick.friedman@med.usc.edu. ·Hear Res · Pubmed #26706709.

ABSTRACT: A cornerstone technique in the study of hearing is the Auditory Brainstem Response (ABR), an electrophysiologic technique that can be used as a quantitative measure of hearing function. Previous studies have published databases of baseline ABR thresholds for mouse strains, providing a valuable resource for the study of baseline hearing function and genetic mapping of hearing traits in mice. In this study, we further expand upon the existing literature by characterizing the baseline ABR characteristics of 100 inbred mouse strains, 47 of which are newly characterized for hearing function. We identify several distinct patterns of baseline hearing deficits and provide potential avenues for further investigation. Additionally, we characterize the sensitivity of the same 100 strains to noise exposure using permanent thresholds shifts, identifying several distinct patterns of noise-sensitivity. The resulting data provides a new resource for studying hearing loss and noise-sensitivity in mice.

2 Article A comprehensive catalogue of the coding and non-coding transcripts of the human inner ear. 2016

Schrauwen, Isabelle / Hasin-Brumshtein, Yehudit / Corneveaux, Jason J / Ohmen, Jeffrey / White, Cory / Allen, April N / Lusis, Aldons J / Van Camp, Guy / Huentelman, Matthew J / Friedman, Rick A. ·Department of Medical Genetics, University of Antwerp, 2610 Antwerp, Belgium. · Neurogenomics Division and The Dorrance Center for Rare Childhood Disorders, Translational Genomics Research Institute, 85004 Phoenix, AZ. · Department of Medicine/Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA. · House Ear Institute, Los Angeles 90057, CA, United States. · Keck School of Medicine, USC, Los Angeles, CA, United States. ·Hear Res · Pubmed #26341477.

ABSTRACT: The mammalian inner ear consists of the cochlea and the vestibular labyrinth (utricle, saccule, and semicircular canals), which participate in both hearing and balance. Proper development and life-long function of these structures involves a highly complex coordinated system of spatial and temporal gene expression. The characterization of the inner ear transcriptome is likely important for the functional study of auditory and vestibular components, yet, primarily due to tissue unavailability, detailed expression catalogues of the human inner ear remain largely incomplete. We report here, for the first time, comprehensive transcriptome characterization of the adult human cochlea, ampulla, saccule and utricle of the vestibule obtained from patients without hearing abnormalities. Using RNA-Seq, we measured the expression of >50,000 predicted genes corresponding to approximately 200,000 transcripts, in the adult inner ear and compared it to 32 other human tissues. First, we identified genes preferentially expressed in the inner ear, and unique either to the vestibule or cochlea. Next, we examined expression levels of specific groups of potentially interesting RNAs, such as genes implicated in hearing loss, long non-coding RNAs, pseudogenes and transcripts subject to nonsense mediated decay (NMD). We uncover the spatial specificity of expression of these RNAs in the hearing/balance system, and reveal evidence of tissue specific NMD. Lastly, we investigated the non-syndromic deafness loci to which no gene has been mapped, and narrow the list of potential candidates for each locus. These data represent the first high-resolution transcriptome catalogue of the adult human inner ear. A comprehensive identification of coding and non-coding RNAs in the inner ear will enable pathways of auditory and vestibular function to be further defined in the study of hearing and balance. Expression data are freely accessible at https://www.tgen.org/home/research/research-divisions/neurogenomics/supplementary-data/inner-ear-transcriptome.aspx.

3 Article The Genetic Architecture of Hearing Impairment in Mice: Evidence for Frequency-Specific Genetic Determinants. 2015

Crow, Amanda L / Ohmen, Jeffrey / Wang, Juemei / Lavinsky, Joel / Hartiala, Jaana / Li, Qingzhong / Li, Xin / Salehide, Pezhman / Eskin, Eleazar / Pan, Calvin / Lusis, Aldons J / Allayee, Hooman / Friedman, Rick A. ·Department of Preventive Medicine and Institute for Genetic Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California 90033. · House Ear Institute, Los Angeles, California 90057. · Department of Otolaryngology and Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California 90033. · Department of Otolaryngology, Head and Neck Surgery, Eye & ENT Hospital of Fudan University, Shanghai 200031, China. · Clinical Laboratory Department, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province 330006, China. · Department of Computer Science and Inter-Departmental Program in Bioinformatics, University of California, Los Angeles, California 90095. · Departments of Human Genetics, Medicine, and Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine at UCLA, Los Angeles, California 90095. · Department of Otolaryngology and Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California 90033 rick.friedman@med.usc.edu. ·G3 (Bethesda) · Pubmed #26342000.

ABSTRACT: Genome-wide association studies (GWAS) have been successfully applied in humans for the study of many complex phenotypes. However, identification of the genetic determinants of hearing in adults has been hampered, in part, by the relative inability to control for environmental factors that might affect hearing throughout the lifetime, as well as a large degree of phenotypic heterogeneity. These and other factors have limited the number of large-scale studies performed in humans that have identified candidate genes that contribute to the etiology of this complex trait. To address these limitations, we performed a GWAS analysis using a set of inbred mouse strains from the Hybrid Mouse Diversity Panel. Among 99 strains characterized, we observed approximately two-fold to five-fold variation in hearing at six different frequencies, which are differentiated biologically from each other by the location in the cochlea where each frequency is registered. Among all frequencies tested, we identified a total of nine significant loci, several of which contained promising candidate genes for follow-up study. Taken together, our results indicate the existence of both genes that affect global cochlear function, as well as anatomical- and frequency-specific genes, and further demonstrate the complex nature of mammalian hearing variation.

4 Article Genome-wide association analysis demonstrates the highly polygenic character of age-related hearing impairment. 2015

Fransen, Erik / Bonneux, Sarah / Corneveaux, Jason J / Schrauwen, Isabelle / Di Berardino, Federica / White, Cory H / Ohmen, Jeffrey D / Van de Heyning, Paul / Ambrosetti, Umberto / Huentelman, Matthew J / Van Camp, Guy / Friedman, Rick A. ·1] Center for Medical Genetics, University of Antwerp, Antwerp, Belgium [2] StatUa Center for Statistics, University of Antwerp, Antwerp, Belgium. · Center for Medical Genetics, University of Antwerp, Antwerp, Belgium. · Neurogenomics Division, The Translational Genomics Research Institute, Phoenix, AZ, USA. · 1] Center for Medical Genetics, University of Antwerp, Antwerp, Belgium [2] StatUa Center for Statistics, University of Antwerp, Antwerp, Belgium [3] Neurogenomics Division, The Translational Genomics Research Institute, Phoenix, AZ, USA. · 1] Audiology Unit, Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy [2] Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy. · Cell Biology and Genetics Division, House Research Institute, Los Angeles, CA, USA. · Department of Otolaryngology, University Hospital of Antwerp, Edegem, Belgium. ·Eur J Hum Genet · Pubmed #24939585.

ABSTRACT: We performed a genome-wide association study (GWAS) to identify the genes responsible for age-related hearing impairment (ARHI), the most common form of hearing impairment in the elderly. Analysis of common variants, with and without adjustment for stratification and environmental covariates, rare variants and interactions, as well as gene-set enrichment analysis, showed no variants with genome-wide significance. No evidence for replication of any previously reported genes was found. A study of the genetic architecture indicates for the first time that ARHI is highly polygenic in nature, with probably no major genes involved. The phenotype depends on the aggregated effect of a large number of SNPs, of which the individual effects are undetectable in a modestly powered GWAS. We estimated that 22% of the variance in our data set can be explained by the collective effect of all genotyped SNPs. A score analysis showed a modest enrichment in causative SNPs among the SNPs with a P-value below 0.01.

5 Article Genome-wide association study for age-related hearing loss (AHL) in the mouse: a meta-analysis. 2014

Ohmen, Jeffrey / Kang, Eun Yong / Li, Xin / Joo, Jong Wha / Hormozdiari, Farhad / Zheng, Qing Yin / Davis, Richard C / Lusis, Aldons J / Eskin, Eleazar / Friedman, Rick A. ·Department of Cell and Molecular Biology and Genetics, House Research Institute, Los Angeles, CA, USA. ·J Assoc Res Otolaryngol · Pubmed #24570207.

ABSTRACT: Age-related hearing loss (AHL) is characterized by a symmetric sensorineural hearing loss primarily in high frequencies and individuals have different levels of susceptibility to AHL. Heritability studies have shown that the sources of this variance are both genetic and environmental, with approximately half of the variance attributable to hereditary factors as reported by Huag and Tang (Eur Arch Otorhinolaryngol 267(8):1179-1191, 2010). Only a limited number of large-scale association studies for AHL have been undertaken in humans, to date. An alternate and complementary approach to these human studies is through the use of mouse models. Advantages of mouse models include that the environment can be more carefully controlled, measurements can be replicated in genetically identical animals, and the proportion of the variability explained by genetic variation is increased. Complex traits in mouse strains have been shown to have higher heritability and genetic loci often have stronger effects on the trait compared to humans. Motivated by these advantages, we have performed the first genome-wide association study of its kind in the mouse by combining several data sets in a meta-analysis to identify loci associated with age-related hearing loss. We identified five genome-wide significant loci (<10(-6)). One of these loci confirmed a previously identified locus (ahl8) on distal chromosome 11 and greatly narrowed the candidate region. Specifically, the most significant associated SNP is located 450 kb upstream of Fscn2. These data confirm the utility of this approach and provide new high-resolution mapping information about variation within the mouse genome associated with hearing loss.

6 Article Functional variants of MIF, INFG and TFNA genes are not associated with disease susceptibility or hearing loss progression in patients with Ménière's disease. 2013

Gázquez, Irene / Moreno, Antonia / Requena, Teresa / Ohmen, Jeff / Santos-Perez, Sofia / Aran, Ismael / Soto-Varela, Andres / Pérez-Garrigues, Herminio / López-Nevot, Alicia / Batuecas, Angel / Friedman, Rick A / López-Nevot, Miguel A / López-Escamez, Jose A. ·Otology and Neurotology Group CTS495, Centro de Genómica e Investigación Oncológica Pfizer-Universidad de Granada-Junta de Andalucía (GENyO), Avda. de la Ilustración, 114, 18014 Granada, Spain. ·Eur Arch Otorhinolaryngol · Pubmed #23179933.

ABSTRACT: Variability in acute immune response genes could determine susceptibility or prognosis for Ménière's disease (MD). The cytokines tumor necrosis factor α (TNFα), macrophage migration inhibitory factor (MIF) and interferon γ (INFγ) are proinflammatory cytokines of the innate immune response. These cytokines mediate inflammation and have been previously associated with the inflammatory process in several autoimmune diseases. We investigated the association between functional allelic variants of MIF (rs35688089), IFNG (rs2234688) and TNFA (rs1800629) in patients with MD. In addition to testing these variants for an association with disease, we also tested for an association with clinical aspects of disease progression, such as persistence of vertigo and the sensorineural hearing loss. A total of 580 patients with diagnosis of definite MD, according to the diagnostic scale of the American Academy of Otolaryngology-Head and Neck Surgery, and 552 healthy controls were included. DNA samples from a set of 291 American patients were used to confirm the results obtained in the MIF gene in our Spanish cohort. Although we found a significant association with the allele containing five repeats of CATT within the MIF gene in patients with MD in the Spanish cohort [corrected p = 0.008, OR = 0.69 (95 % CI, 0.54-0.88)], this finding could not be replicated in the American set. Moreover, no genetic associations for variants in either the TNFA or IFNG genes and MD were found. These results support the conclusion that functional variants of MIF, INFG, and TFNA genes are not associated with disease susceptibility or hearing loss progression in patients with MD.

7 Article GRM7 variants associated with age-related hearing loss based on auditory perception. 2012

Newman, Dina L / Fisher, Laurel M / Ohmen, Jeffrey / Parody, Robert / Fong, Chin-To / Frisina, Susan T / Mapes, Frances / Eddins, David A / Robert Frisina, D / Frisina, Robert D / Friedman, Rick A. ·Thomas H. Gosnell School of Life Sciences, Rochester Institute of Technology, 153 Lomb Memorial Dr. Rochester, NY 14623, USA. dina.newman@rit.edu ·Hear Res · Pubmed #23102807.

ABSTRACT: Age-related hearing impairment (ARHI), or presbycusis, is a common condition of the elderly that results in significant communication difficulties in daily life. Clinically, it has been defined as a progressive loss of sensitivity to sound, starting at the high frequencies, inability to understand speech, lengthening of the minimum discernable temporal gap in sounds, and a decrease in the ability to filter out background noise. The causes of presbycusis are likely a combination of environmental and genetic factors. Previous research into the genetics of presbycusis has focused solely on hearing as measured by pure-tone thresholds. A few loci have been identified, based on a best ear pure-tone average phenotype, as having a likely role in susceptibility to this type of hearing loss; and GRM7 is the only gene that has achieved genome-wide significance. We examined the association of GRM7 variants identified from the previous study, which used an European cohort with Z-scores based on pure-tone thresholds, in a European-American population from Rochester, NY (N = 687), and used novel phenotypes of presbycusis. In the present study mixed modeling analyses were used to explore the relationship of GRM7 haplotype and SNP genotypes with various measures of auditory perception. Here we show that GRM7 alleles are associated primarily with peripheral measures of hearing loss, and particularly with speech detection in older adults.

8 Article Genome-wide screening for genetic loci associated with noise-induced hearing loss. 2009

White, Cory H / Ohmen, Jeffrey D / Sheth, Sonal / Zebboudj, Amina F / McHugh, Richard K / Hoffman, Larry F / Lusis, Aldons J / Davis, Richard C / Friedman, Rick A. ·Department of Cell Biology and Genetics, House Ear Institute, Gonda Center for Cellular and Molecular Biology, 2100 West 3rd Street, Los Angeles, CA 90057, USA. cwhite@hei.org ·Mamm Genome · Pubmed #19337678.

ABSTRACT: Noise-induced hearing loss (NIHL) is one of the more common sources of environmentally induced hearing loss in adults. In a mouse model, Castaneous (CAST/Ei) is an inbred strain that is resistant to NIHL, while the C57BL/6J strain is susceptible. We have used the genome-tagged mice (GTM) library of congenic strains, carrying defined segments of the CAST/Ei genome introgressed onto the C57BL/6J background, to search for loci modifying the noise-induced damage seen in the C57BL/6J strain. NIHL was induced by exposing 6-8-week old mice to 108 dB SPL intensity noise. We tested the hearing of each mouse strain up to 23 days after noise exposure using auditory brainstem response (ABR). This study identifies a number of genetic loci that modify the initial response to damaging noise, as well as long-term recovery. The data suggest that multiple alleles within the CAST/Ei genome modify the pathogenesis of NIHL and that screening congenic libraries for loci that underlie traits of interest can be easily carried out in a high-throughput fashion.