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45 results for “Ototoxicity”

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geo20/100

Effect of subchronic ototoxic exposure on the vestibular epithelium

GEO Series GSE292474. Mus musculus; Rattus norvegicus. 27 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenSep 2025View details →
geo20/100

Effect of subchronic ototoxicity on the vestibular ganglion in rodents

GEO Series GSE226517. Rattus norvegicus; Mus musculus. 12 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenDec 2023View details →
ClinicalTrials.gov20/100

Ototoxicity of Artemether / Lumefantrine (Coartem) and Other Antimalarials

ClinicalTrials.gov study NCT00451139. IPD Sharing: Not stated. Countries: 1. Publications: 0.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov20/100

Multicenter, Prospective Observational Study for Early Diagnosis, and Development of Follow-up Protocol and Hearing Rehabilitation Program for Ototoxic Hearing Loss After Chemotherapy for Pediatric So

ClinicalTrials.gov study NCT05633719. IPD Sharing: Not stated. Countries: 0. Publications: 0.

restrictedIPD-UNDECIDEDFeb 2026View details →
zenodo16/100

Pterostilbene Protects Cochlea from Ototoxicity in Streptozotocin-Induced Diabetic Rats by Inhibiting Apoptosis

<p>Diabetes mellitus (DM) causes ototoxicity by inducing oxidative stress, microangiopathy, and apoptosis in the cochlear sensory hair cells. The natural anti-oxidant pterostilbene (PTS) (trans-3,5-dimethoxy-4-hydroxystylbene) has been reported to relieve oxidative stress and apoptosis in DM, but its role in diabetic-induced ototoxicity is unclear. This study aimed to investigate the effects of dose-dependent PTS on the cochlear cells of <em>streptozotocin</em> (STZ)-induced diabetic rats. The study included 30 albino male Wistar rats that were randomized into five groups: non-diabetic control (Control), diabetic control (DM), and diabetic rats treated with intraperitoneal PTS at 10, 20, or 40 mg/kg/day during the four-week experimental period (DM + PTS10, DM + PTS20, and DM + PTS40). Distortion product otoacoustic emission (DPOAE) tests were performed at the beginning and end of the study. At the end of the experimental period, apoptosis in the rat cochlea was investigated using caspase-8, cytochrome-c, and terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin end labeling (TUNEL). Quantitative real-time polymerase chain reaction was used to assess the mRNA expression levels of the following genes: <em>CASP-3</em>, BCL-associated X protein (<em>BAX</em>), and<em> BCL-2</em>. Body weight, blood glucose, serum insulin, and malondialdehyde (MDA) levels in the rat groups were evaluated. The mean DPOAE amplitude in the DM group was significantly lower than the means of the other groups (0.9&ndash;8 kHz; P &lt; 0.001 for all). A dose-dependent increase of the mean DPOAE amplitudes was observed with PTS treatment (P &lt; 0.05 for all). The Caspase-8 and Cytochrome-c protein expressions and the number of TUNEL-positive cells in the hair cells of the Corti organs of the DM rat group were significantly higher than those of the PTS treatment and control groups (DM &gt; DM + PTS10 &gt; DM + PTS20 &gt; DM + PTS40 &gt; Control; P &lt; 0.05 for all). PTS treatment also reduced cell apoptosis in a dose-dependent manner by increasing the mRNA expression of the anti-apoptosis <em>BCL2</em> gene and by decreasing the mRNA expressions of both the pro-apoptosis <em>BAX</em> gene and its effector <em>CASP-3</em> and the ratio of <em>BAX/BCL-2</em> in a dose-dependent manner (P &lt; 0.05 compared to DM for all). PTS treatment significantly improved the metabolic parameters of the diabetic rats, such as body weight, blood glucose, serum insulin, and MDA levels, consistent with our other findings (P &lt; 0.05 compared to DM for all). PTS decreased the cochlear damage caused by diabetes, as confirmed by DPOAE, biochemical, histopathological, immunohistochemical, and molecular findings. This study reports the first in vivo findings to suggest that PTS may be a protective therapeutic agent against diabetes-induced ototoxicity.</p>

restrictedMay 2020View details →

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Last verified 2026-04-30Open record

DANDI Archive for NWB datasets

DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.

dandi-nwb
electrophysiologyopenPublished Dandiset metadata and archive endpoints are available through the production DANDI API.
Last verified 2026-04-30Open record

International Brain Laboratory public data

The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.

ibl
behavioral-neuroscienceopenPublic sessions can be searched and loaded from the IBL public data server through ONE.
Last verified 2026-04-29Open record

OpenNeuro

OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.

openneuro
neuroscienceopenPublished datasets are available on demand over the internet.
Last verified 2026-04-29Open record