Biology subjects

Kita, A.

Publications and source records attributed to Kita, A..

3 recordsLinked to original sources

bioRxiv2026

Deep Learning-Assisted Evaluation of Laryngeal Mobility in a Rat Model

Vocal fold mobility is essential for normal laryngeal function and is often compromised following recurrent laryngeal nerve (RLN) or superior laryngeal nerve injuries. In a rat model of unilateral (RLN) injury, we quantitatively evaluate laryngeal mobility using advanced computer vision techniques. Adult male Long-Evans rats underwent direct laryngoscopy before and after RLN injury at the level of the 5th tracheal ring. High-resolution video recordings were analyzed with the open-source deep learning framework Social LEAP Estimates Animal Poses (SLEAP) to track key laryngeal landmarks. The displacement of the left and right arytenoid processes relative to the anatomical midpoint was measured frame-by-frame. Mean differences and 95% CI were computed for each arytenoid. A mean difference threshold of 0.42 differentiated laryngeal asymmetry from symmetry. This method offers a quantitative method of assessing laryngeal symmetry in a rat model.

bioengineering↗

bioRxiv2023

N-acetylcysteine Microparticles Reduce Cisplatin-induced RSC96 Schwann Cell Toxicity

ObjectivesCisplatin is known to cause inner ear dysfunction. There is growing evidence that cisplatin-induced demyelination of spiral or Scarpas ganglion neurons may play an additional role in drug-induced ototoxicity alongside afferent neuron injury. As Schwann cells produce myelin, there may be an opportunity to reduce ototoxic inner ear damage by promoting Schwann cell viability. This work describes a cellular model of cisplatin-induced Schwann cell injury and investigates the ability of the antioxidant N-acetylcysteine to promote Schwann cell viability. A local delivery system of drug-eluting microparticles was then fabricated, characterized, and investigated for bioactivity. MethodsRSC96 rat Schwann cells were dosed with varying concentrations of cisplatin to obtain a dose curve and identify the lethal concentration of 50% of the cells (LC50). In subsequent experiments, RSC96 cells were co-treated with cisplatin and both resuspended or eluted N-acetylcysteine. Cell viability was assessed with the CCK8 assay. ResultsThe LC50 dose of cisplatin was determined to be 3.76 M (p=2.2 x 10-16). When co-dosed with cisplatin and therapeutic concentration of resuspended or eluted N-acetylcysteine, Schwann cells had an increased viability compared to cells dosed with cisplatin alone. ConclusionRSC96 Schwann cell injury following cisplatin insult is characterized in this in vitro model. Cisplatin caused injury at physiologic concentrations and N-acetylcysteine improved cell viability and mitigated this injury. N-acetylcysteine was packaged into microparticles and eluted N-acetylcysteine retained its ability to increase cell viability, thus demonstrating promise as a therapeutic to offset cisplatin-induced ototoxicity. Lay SummaryCisplatin is a chemotherapeutic agent known to cause balance and hearing problems through damage to the inner ear. This project explored cisplatin injury in a Schwann cell culture model and packaged an antioxidant into microparticles suitable for future drug delivery applications.

bioengineering↗

bioRxiv2021

APOE ε4 allele advances the age-dependent decline of amyloid β clearance in the human cortex

IntroductionOur previous study indicated that the pericapillary clearance of amyloid {beta} (A{beta}) declines with age in APOE 3/3 subjects. Here, we examine whether the APOE {varepsilon}4 allele has an impact on this age-related decline. MethodsWe examined 69 autopsy brains of APOE {varepsilon}3/{varepsilon}4 or APOE {varepsilon}3/{varepsilon}3 individuals (30-65 years) for the immunohistochemical localization of intracellular, extracellular, and pericapillary A{beta} in the cerebral cortex. ResultsIn APOE {varepsilon}3/{varepsilon}4 individuals, the percentage of A{beta} positive pericapillary spaces began to decrease (p=0.030), and the number of extracellular A{beta} particles increased in the early 30s (p=0.0008). Those average values were significantly lower (p<0.0001) and higher (p<0.0001), respectively, compared to APOE {varepsilon}3/{varepsilon}3 individuals. DiscussionOur observations indicate that APOE {varepsilon}4 allele advances by one decade at the onset of age-related decline in A{beta} glymphatic clearance. This finding supports early clinical intervention and stratification by APOE genotype to prevent A{beta} deposition and AD progression.

pathology↗