58 results about "HL - Hearing loss" patented technology

Provided are compositions and method for prophylaxis and / or therapy of hearing loss or related dysfunctions, including but not limited to tinnitus, that could be ameliorated by restoring central nervous system inhibitory synapses. The compositions include polynucleotides and viral vectors that are used to express at least one GABA receptor component which may be a GABAA receptor alpha 1 subunit or GABAR receptor Ib subunit. Expression of the GABA receptor may be under control of a CaMKII promoter.

The present disclosure provides a construct comprising a coding sequence operably linked to a promoter, wherein the coding sequence encodes a vascular endothelial growth factor (VEGF) binding agent or a portion thereof. In some embodiments, a construct is an AAV construct. In some embodiments, an AAV construct is a part of an AAV particle. Compositions comprising constructs and AAV particles described herein can be useful in treating hearing loss, for example, hearing loss associated with vestibular schwannoma.

Provided herein are compositions that include at least two different nucleic acid vectors, where each of the at least two different vectors includes a coding sequence that encodes a different portion of an otoferlin protein, and the use of these compositions to treat hearing loss in a subject.

The present invention relates to a mitochondrial permeability transition pore (mPTP)-targeting composition for treating hearing loss, and, more specifically, uses a compound, or a pharmaceutically / sitologically acceptable salt thereof, which targets the mitochondrial permeability transition pore (mPTP) to inhibit the activity or opening thereof, and thus can effectively prevent, alleviate, or treat hearing loss caused by mPTP opening.

The invention relates to a method for associating gene mutation points with specific physiological characteristics. The method comprises the following steps: receiving a sequenced test gene sequence from a human gene database; taking out a test sequence fragment with the gene length equal to the window length from the test gene sequence by adopting a sliding window with the window length; analyzing the test sequence fragments by using the prediction model; based on the analysis, determining whether the test sequence fragment is associated with a specific physiological feature; and determining that the test gene locus located at the center of the test sequence fragment is a gene mutation point associated with the specific physiological feature in response to judging that the test sequence fragment is associated with the specific physiological feature.

This invention relates to a recombinant adeno-associated virus (rAAV) vector encoding connexin 26 (CX26). The invention further relates to the use of the AAV vector in the treatment of hereditary hearing loss.

The invention discloses an application of an ECM related gene in treatment of hearing loss. Specifically, the invention provides an application of an active ingredient, and the active ingredient is used for preparing a composition for treating hearing loss. And the active ingredient comprises a down-regulating agent of an ECM-related gene selected from the group consisting of Col6a3, Ogn, Col3a1, or a combination thereof. The composition disclosed by the invention can be used for effectively treating sensorineural hearing loss caused by excessive ECM deposition.

Provided herein are compositions that include at least two different nucleic acid vectors, where each of the at least two different vectors includes a coding sequence that encodes a different portion of an otoferlin protein, and the use of these compositions to treat hearing loss in a subject.

The present invention relates to a viral vector comprising an EF1a promoter and expressing MPZL2, and a pharmaceutical composition for preventing or treating hearing loss comprising the same. The application of the recombinant virus vector provides a fundamental treatment strategy for hereditary hearing loss caused by Mpzl2 mutation in the absence of an effective treatment method at present.

The invention discloses an application of harpagide in preparation of a medicine for inhibiting STUB1. The harpagide can be used as a specific inhibitor of E3 ubiquitin ligase STUB1. By inhibiting the STUB1, the harpagide can effectively block the GR ubiquitination process mediated by the STUB1, so that the GR is prevented from being degraded by the proteasome, and the stability of the GR protein level is finally realized. Through combined application of harpagide and glucocorticoid, the treatment effect of hormone in a noise-induced hearing loss animal model can be remarkably improved, and the treatment effect is better than that of treatment by independently using hormone.

The present disclosure provides methods of preventing and / or treating hearing loss in an individual comprising administering to the individual a composition comprising an agent that increases the expression and / or activity of a Pou4f3 protein. The present disclosure also provides methods of preventing and / or treating a vestibular disorder in an individual comprising administering to the individual a composition comprising an agent that increases the expression and / or activity of a Pou4f3 protein.

The present application relates to the technical field of biological medicine, and particularly relates to a composition for protecting cochlear spiral ganglion neurons and application thereof. The composition comprises Panax notoginseng saponins (PNS) and Polygonatum sibiricum polysaccharide (PSP). Research shows that the composition can significantly improve the survival rate of neurons, promote neurite growth, reduce the level of reactive oxygen species, inhibit cell apoptosis, and promote autophagy by regulating the PI3K / AKT signaling pathway, thereby effectively resisting ototoxicity damage induced by aminoglycoside antibiotics. The present application further provides the use of the composition in the preparation of a drug for preventing or treating sensorineural hearing loss.

The present application relates to a composition using an endothelin B receptor agonist, such as Sovastatin (N-succinyl-[Glu9, Ala11, 15] endothelin 1, IRL-1620), for promoting cell proliferation and protecting the original neuroepithelium of cochlear and vestibular cells located within the ear sac. The pharmaceutical composition is systemically administered by means of tympanic membrane puncture, cochleostomy or intravenous or intramuscular injection. A pharmaceutical composition for the treatment of sensorineural hearing loss and vestibular disorders caused by inner ear cell degeneration, the pharmaceutical composition comprising a compound of an endothelin analogue, the use being treated by the neuroprotection and neurogenesis mechanism of cochlear vestibular hair cells and synapses.

In certain embodiments the present invention provides a method of treating hearing loss comprising: (a) administering a gene suppression agent that suppresses both copies of an endogenous gene causing the hearing loss; and (b) administering an exogenous wild-type allele engineered to resist suppression by the gene suppression agent.The present invention provides in certain embodiments a method of treating a genetic hearing loss (GHL) in a patient in need thereof comprising: (a) identifying a mutation in a GHL-causing gene, wherein the mutation causes GHL in the patient; and (b) administering to the patient a pharmaceutical composition comprising a therapeutic miRNA and a pharmaceutically acceptable carrier, wherein the GHL therapeutic miRNA is of 18 to 25 nucleotides in length and knocks-down the GHL-causing gene function at a higher level than it knocks-down gene function in a corresponding wild-type gene.

The present disclosure provides methods for inducing cell cycle reentry of postmitotic cell. The present disclosure further provides cells and compositions for treating diseases, such as cardiovascular diseases, neural disorders, hearing loss, and diabetes.

The present invention relates to a recombinant adeno-associated virus (rAAV) vector encoding a connexin 26 (CX26). The invention also relates to the use of said AAV vector in the treatment of hereditary hearing loss.

The present disclosure provides compositions and methods for treating subjects at risk for or with sensorineural hearing loss by modulating the rate of Atoh1 protein degradation to increase levels of Atoh1 protein.

The invention provides an application of an expression inhibitor of Gadd45a in preparation of a medicine for preventing or reducing the ototoxicity of cis-platinum. In-vivo and in-vitro experiments prove that by locally applying the Gadd45a inhibitor, cochlea hair cells and auditory functions can be effectively protected by activating autophagy, inhibiting an NF-kappaB1 inflammation pathway and regulating JNK-mediated apoptosis, so that hearing loss caused by cis-platinum is relieved. The invention provides a brand-new effective medicine product and a treatment strategy for clinically preventing and treating the ototoxicity of cis-platinum, and has important clinical application value for preventing or relieving the ototoxicity of a patient receiving cis-platinum chemotherapy.

The application discloses application of an Rps14 gene, a medicine and a construction method of a mouse model, belongs to the technical field of biotechnology, and the nucleotide sequence of the Rps14 gene is shown as SEQ NO. 1; compared with the prior art, the specific Rps14 transgenic mouse with a loxp site provided in the application can be used for specifically studying functions and effects of Rps14 overexpression at different sites. Specific overexpression of Rps14 in Lgr5 positive inner ear stem cells can promote significant increase of ectopic hair cells, and effective effects can be used for promoting structural and functional repair after hair cell damage and for improving hearing loss. Rps14 can be synergistically regulated with other reported inner ear genes, for example, Atoh1, Gfi1, Pou3f4 and the like, and effectively promote more ectopic hair cell proliferation and functional maturation.

A method for treating hearing loss in a subject in need thereof is provided. The method includes providing a combination of transcription factors to induce generation of a hair cell-like cell, thereby treating the hearing loss in the subject. The generated hair cell-like cells exhibit characteristic of mature functional cells that is useful in cell replacement therapy for autologous transplantation.

The present invention relates to a brain-derived neural factor (BDNF) for use in the prevention of hearing loss induced by a platinum-based chemotherapeutic drug in a subject wherein the BDNF is administered intratympanically to the subject.

N-(3-Substituted thiazol-2(3H)-ylidene)-1H-pyrrolo[2,3-b]pyridine-3-carboxamides and N-(3-substituted oxazol-2(3H)-ylidene)-1H-pyrrolo[2,3-b]pyridine-3-carboxamidesare disclosed. The compounds activate Yap and inhibit Lats kinases. They are therefore useful for treating hearing loss.

Provided is an expression cassette for expressing GJB2 protein, which comprises a cochlear supporting cell and cochlear lateral wall-specific promoter and a nucleic acid encoding GJB2 protein. Also provided is a recombinant adeno-associated viral vector, the genome of which comprises an expression cassette for expressing GJB2 protein inserted between two ITR sequences; and a combination of at least two recombinant adeno-associated viral vectors. The recombinant adeno-associated viral vector or combination thereof can be used for treating or preventing hearing loss associated with defects in the GJB2 gene.

The present invention relates to brain derived nerve factor (BDNF) for use in the prevention or treatment of sensorineural hearing loss in a subject, wherein said BDNF is administered intranasally to said subject.

This application provides a method and apparatus for constructing a dataset for the prevention and treatment of occupational hearing loss. The method includes obtaining fused data by data association and matching from raw data from different sources, and incorporating medical theory into various stages such as feature selection and data preprocessing of the fused data. This makes the preprocessing results more targeted, supporting the task of preventing and treating occupational hearing loss. By performing multi-factor correlation analysis on a standard dataset, a subset of key features most strongly associated with hearing loss is selected. The standard dataset is oversampled and balanced to obtain a balanced dataset, which is then used to construct and train multiple machine learning models to select the optimal model. The high-precision performance of the optimal model on the test set verifies that the standard dataset has the ability to support highly robust predictions. Furthermore, using a suitable feature importance quantification method, the optimal model is verified to be consistent with medical theoretical expectations, thereby enhancing the credibility and interpretability of the prediction results.

To provide a new therapy targeting hair cells for the treatment of sensorineural hearing loss or vestibular dysfunction.SOLUTION: The present disclose provides polynucleotides containing a region of the myosin 15 (Myo15) promoter, as well as vectors containing the same, which can be used to promote expression of a transgene specifically in hair cells. The polynucleotides described herein can be operably linked to a transgene, such as a transgene encoding a therapeutic protein, to facilitate hair cell-specific expression of the transgene. The polynucleotides described herein can be operably linked to a therapeutic transgene and used in the treatment of a subject having or at risk of developing hearing loss or vestibular dysfunction.SELECTED DRAWING: Figure 1

Diagnosing and treating presbycusis (age related hearing loss) includes measuring basilar membrane stiffness. In an example, a low frequency component of an electrocochleogram stimulation signal is used to bias a region of the basilar membrane, the results of which are used basilar membrane stiffness. The resulting measurement is used to measure a subcomponent of presbycusis. Further, the measurement can be combined with known diagnostic methods to reveal or distinguish other origins of hearing loss such as strial presbycusis, sensory presbycusis, neural presbycusis, and cochlea conductive presbycusis. The relative contributions for each of the diagnosed origins of hearing loss can be determined.

The present invention relates to a pharmaceutical composition for preventing or treating hearing loss or tinnitus, comprising visomitin as an active ingredient. In the present invention, visomitin significantly inhibited ROS production induced by gentamicin or cisplatin treatment. In particular, visomitin exhibited an effect of inhibiting the cytotoxicity of gentamicin in an HEI-OC1 cell line and in cochleas extracted from mice in vitro experiments. In addition, in an in vivo experiment using zebrafish, visomitin significantly inhibited ROS generation in hair cells and apoptosis of hair cells caused by gentamicin treatment. The results demonstrate a superior improvement effect compared to antioxidants used as control drugs, and it is considered that visomitin can be used for preventing or treating hearing loss caused by toxicity of antibiotics or anticancer drugs.

The disclosure provides SL26A4 enhancers and SLC26A4 promoters, as well as vectors containing the same, that can increase gene expression in SLC26A4-expressing cells, such as interdental cells, root cells, spiral prominence cells, and vestibular supporting cells. The SLC26A4 enhancers and SLC26A4 promoters described herein may be operably linked to a polynucleotide, such as a transgene, encoding an expression product and used for the treatment of subjects having or at risk of developing hearing loss or vestibular dysfunction.

Compositions and methods for treating neuromuscular, neuromuscular degenerative, neurodegenerative, autoimmune, developmental, traumatic, hearing loss-related, and / or metabolic diseases including Spinal Muscular Atrophy (SMA) syndrome (SMA1, SMA2, SMA3, and SMA4, also known as Types I, II, III, and IV), Traumatic Brain Injury (TBI), concussion, keratoconjunctivitis sicca (dry eye disease), glaucoma, Sjogren's syndrome, rheumatoid arthritis, post-LASIK, antidepressant use, Wolfram syndrome, and Wolcott-Rallison syndrome. The compositions are selected from 2,3-DNP, 2,4-DNP, 2,5-DNP, 2,6-DNP, 3,4-DNP, or 3,5-DNP, bis 2,3-dinitrophenol, 2,4-dinitrophenol, 2,5-dinitrophenol, 2,6-dinitrophenol, 3,4-dinitrophenol, or 3,5-dinitrophenol (2,3-DNP, 2,4-DNP, 2,5-DNP, 2,6-DNP, 3,4-DNP, or 3,5-DNP) prodrugs; bisprodrug, bioprecursor molecules, and combinations thereof.