Search bioRxiv⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/677609

Improving Sensitivity of the Digits-in-Noise Test using Antiphasic Stimuli

De Sousa, K. C.·Swanepoel, D. W.·Moore, D. R.·Myburgh, H.·Smits, C.
View original source ↗Export metadata ↓

Abstract

ObjectiveThe digits-in-noise test (DIN) has become increasingly popular as a consumer-based method to screen for hearing loss. Current versions of all DINs either test ears monaurally or present identical stimuli binaurally (i.e., diotic noise and speech, NoSo). Unfortunately, presentation of identical stimuli to each ear inhibits detection of unilateral sensorineural hearing loss (SNHL), and neither diotic nor monaural presentation sensitively detects conductive hearing loss (CHL). Following an earlier finding of enhanced sensitivity in normally hearing listeners, this study tested the hypothesis that interaural antiphasic digit presentation (NoS{pi}) would improve sensitivity to hearing loss caused by unilateral or asymmetric SNHL, symmetric SNHL, or CHL.\n\nDesignThis cross-sectional study, recruited adults (18-84 years) with various levels of hearing, based on a four-frequency pure tone average (PTA) at 0.5, 1, 2 and 4kHz. The study sample was comprised of listeners with normal hearing (n=41; PTA [≤] 25 dB HL in both ears), symmetric SNHL (n=57; PTA > 25 dB HL), unilateral or asymmetric SNHL (n=24; PTA > 25 dB HL in the poorer ear) and CHL (n=23; PTA > 25 dB HL and PTA air-bone gap [≥] 20 dB HL in the poorer ear). Antiphasic and diotic speech reception thresholds (SRTs) were compared using a repeated-measures design.\n\nResultsAntiphasic DIN was significantly more sensitive to all three forms of hearing loss than the diotic DIN. SRT test-retest reliability was high for all tests (ICC r > 0.89). Area under the receiver operating characteristics (ROC) curve for detection of hearing loss (> 25 dB HL) was higher for antiphasic DIN (0.94) than for diotic DIN (0.77) presentation. After correcting for age, PTA of listeners with normal hearing or symmetric SNHL was more strongly correlated with antiphasic (rpartial[96]=0.69) than diotic (rpartial=0.54) SRTs. Slope of fitted regression lines predicting SRT from PTA was significantly steeper for antiphasic than diotic DIN. For listeners with normal hearing or CHL, antiphasic SRTs were more strongly correlated with PTA (rpartial[62]=0.92) than diotic SRTs (rpartial[62]=0.64). Slope of regression line with PTA was also significantly steeper for antiphasic than diotic DIN. Severity of asymmetric hearing loss (poorer ear PTA) was unrelated to SRT. No effect of self-reported English competence on either antiphasic or diotic DIN among the mixed first-language participants was observed\n\nConclusionsAntiphasic digit presentation markedly improved the sensitivity of the DIN test to detect SNHL, either symmetric or asymmetric, while keeping test duration to a minimum by testing binaurally. In addition, the antiphasic DIN was able to detect CHL, a shortcoming of previous monaural or binaurally diotic DIN versions. The antiphasic DIN is thus a powerful tool for population-based screening. This enhanced functionality combined with smartphone delivery could make the antiphasic DIN suitable as a primary screen that is accessible to a large global audience.

Source connections

Explore related subjects

pathologyPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

De Sousa, K. C., Swanepoel, D. W., Moore, D. R., Myburgh, H., Smits, C.. 2019-06-21. Improving Sensitivity of the Digits-in-Noise Test using Antiphasic Stimuli. https://doi.org/10.1101/677609

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Midlife nonlinearities across scale in Biondi body amyloid formation in the human choroid plexus

Human choroid plexus epithelial cells (CPECs), which produce cerebrospinal fluid and form the blood-cerebrospinal fluid barrier, accumulate discrete intracellular amyloid inclusions called Biondi bodies (BBs). Using systematic manual and machine learning approaches on the choroid plexus glomus, we determined the percentages of CPECs containing thioflavin S-stained BBs as well as BB load and spatial distributions in whole slide images from 77 cases across the human lifespan. On average, BB prevalence was near zero until age 40, rose steeply in the 5th and 6th decades, and exceeded 50% after age 70. As prevalence plateaued, BB load continued to rise with age. Accelerated BB accumulation was seen in two cases of diabetic ketoacidosis, including a 16-year-old, while an 85-year-old with the relatively rare APOE2/E2 genotype had fewer BBs than expected. BB prevalence in the choroid plexus glomus was not associated with Alzheimer's disease, but was lower in females than males. Notably, spatial clustering of BBs was universal across cases while nearest-neighbor analyses suggested cell-to-cell, prion-like BB spread that can account for the nonlinearities seen at tissue and population scales. The abrupt, nonlinear BB accumulation during midlife coincides with or precedes other common aging-associated neuropathologies of the human brain, consistent with broad BB and choroid plexus contributions to brain aging and disease.

pathology↗
bioRxiv2026

Systematic comparison of gliflozins identifies a selective anti-calcifying effect of canagliflozin beyond canonical SGLT2 inhibition

Background: Sodium-glucose cotransporter 2 inhibitors (SGLT2i) provide important cardiorenal benefits in chronic kidney disease (CKD), but their effects on vascular calcification remain conflicting. Whether potential anti-calcifying effects are shared across gliflozins or involve mechanisms beyond canonical SGLT2 inhibition is unknown. Methods: We systematically compared canagliflozin, dapagliflozin and empagliflozin in a high-phosphate diet-induced mouse model of vascular calcification and complementary ex vivo and in vitro models, including rodent and human vascular tissues and vascular smooth muscle cells (VSMCs). Aortic transcriptional response was investigated by RNA sequencing. VSMC calcification, proliferation, migration, viability, glucose uptake and bioenergetics were investigated using complementary cellular assays, including OsteoSense staining, Annexin V/propidium iodide staining, radiolabeled 2-deoxyglucose uptake and Seahorse ATP rate analysis. SGLT2/1 expression was examined by RT-qPCR, Western blotting and immunofluorescence. We also evaluated sotagliflozin, a dual SGLT1/2 inhibitor, and mizagliflozin, a selective SGLT1 inhibitor. Results: Among the three gliflozins, only canagliflozin significantly reduced aortic calcification in vivo. Its anti-calcifying effect was also observed in rodent aortic rings, human vascular explants, cultured VSMCs and aortic rings from diabetic db/db mice. Aortic RNA-seq revealed that canagliflozin partially reversed HPD-induced transcriptional alterations, including changes in pro-calcific signaling and cellular metabolism, while some endothelial and inflammatory responses were shared among gliflozins. In mouse VSMCs, canagliflozin reduced calcification across all tested concentrations, dose-dependently decreased osteogenic marker expression, and reduced proliferation and migration. Increased apoptotic and damaged cell fractions were observed at higher concentrations, but not at lower concentrations. Canagliflozin also reduced glucose uptake and mitochondrial ATP production, without significantly affecting glycolytic ATP production. Neither dapagliflozin nor empagliflozin reproduced these cellular and metabolic effects at any of the concentrations tested. SGLT2 and SGLT1 expression was low or undetectable in vascular tissues and cells, and neither sotagliflozin nor mizagliflozin reproduced the anti-calcifying effect of canagliflozin in vivo or in vitro. Conclusions: Canagliflozin exhibits a selective anti-calcifying profile among the gliflozins tested, associated with changes in VSMC responses and cellular metabolism. These findings suggest that its vascular protective effects may involve mechanisms beyond canonical SGLT2 inhibition.

pathology↗
bioRxiv2026

Failed allogeneic corneal lenticules show fibrosis and identity loss without dominant T cell rejection

Failed allogeneic corneal stromal lenticules develop progressive opacity, but the state of the implanted tissue is unknown. Here we show that six explants from three patients occupy a fibrotic integration-failure state with scar-matrix production and loss of corneal identity without a dominant T cell rejection program. Scar-matrix, transparency and corneal-identity programs separated every patient from eight unimplanted donor controls, the last defined by independent human single-cell references. Calibrated immune programs and repertoire reconstruction distinguished the explants from canonical adaptive rejection. Exchange reduced interface reflectivity initially, followed by recurrent opacity in two patients and corneal steepening with declining uncorrected acuity in the third. In non-scarring rabbit repair, identity moved toward the uninjured state as backscatter returned toward normal despite increasing similarity to the explant-derived expression signature. Within one culture experiment, marked scar suppression accompanied opposite identity responses. Tacrolimus and rapamycin likewise suppressed canonical rejection while moving identity in opposite directions. Resveratrol combined reduced scar-associated programs and increased identity with improved graft appearance in the source study. These findings establish classic-rejection activity and tissue integration as separable axes and direct treatment of failed lenticules from escalating immunosuppression toward control of stromal remodeling and preservation of corneal identity.

pathology↗