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Biology subjects

Chou, T.-Y.

Publications and source records attributed to Chou, T.-Y..

2 recordsLinked to original sources

Quantitative Gait Analysis in a Sheep Model of In-Utero Spina Bifida Repair

Objective: To evaluate quantitative gait analysis in a sheep model (Ovis aries) of in-utero spina bifida repair. Method: Using a 3D marker-based motion capture system, we quantified spatiotemporal gait parameters and hindlimb joint angles in a sheep model of in-utero spina bifida repair and normal controls. A linear support vector machine classifier, trained and tested on subject-disjoint partitions with individual gait cycles as the unit of analysis, evaluated the relationship between hindlimb joint angles and clinician-assigned Texas Spinal Cord Injury Scale scores. Linear mixed-effects models compared spatiotemporal parameters, hoof height, and hip drop across 3- to 6-month evaluations and between groups. Results: In treated (n=14) and control (n=3) lambs, front- and hindlimb gait speed differed by timepoint (both p=0.025). Across 1,632 left and 1,661 right hindlimb gait cycles, held-out classification accuracy was 85.9% and 88.6% (Cohen's {kappa}=0.78 and 0.84) for left and right hindlimbs, respectively, against majority-class proportions of 76.5% and 75%. Left hindlimb hip drop differed between treated lambs and controls ({Delta}=0.8 cm, p=0.027). Between-group contrasts were considered exploratory given the small control group. Conclusion: Quantitative gait analysis was feasible in an in-utero spina bifida repair model. Hindlimb kinematic profiles classified clinical ambulation scores above the majority-class baseline.

bioengineering↗

Unraveling the immunological roles of serum amyloid A3 in aortic immune cell subsets during atherosclerosis progression

Atherosclerosis is a growing concern in developed nations, necessitating the identification of therapeutic targets for advancing personalized medicine. Serum amyloid A3 (Saa3) has been linked to accelerated plaque progression by affecting cholesterol metabolism and modulation of inflammation. We hypothesize that knocking out Saa3 (Saa3-/-) could mitigate plaque development by regulating aortic immune cell compositions during atherosclerosis progression. Using a murine model, we induced atherosclerosis via a gain-of-function mutant PCSK9-encoding adeno-associated viral vector (AAVmPCSK9) in female wild-type (WT) and Saa3-/- mice. Saa3-/- mice developed smaller plaques than WT mice, and single-cell RNA sequencing revealed significant differences in aortic immune cell populations, particularly among aortic macrophages. Aortic macrophages in atherosclerotic Saa3-/-mice represent an anti-inflammatory and tissue-repairing phenotype and the Trem2hi macrophages, characterized by high Gpnmb, Lpl, and Spp1 expressions, predominated over the typical foamy macrophages in Saa3-/- compared to WT mice. Notably, SAA3 regulates cholesterol metabolism and inflammatory responses in foamy macrophages. Our study highlights Saa3 as a key modulator of aortic immune cells that impact atherosclerosis progression.

immunology↗