3D cell cultures are widely used in biomedical research for the recapitulation of microenvironments. Viability assessment and monitoring of these intricate conformations remain an open problem as standard cell viability protocols based on colorimetry or microscopy are not directly applicable to intact 3D samples. Optical coherence tomography (OCT) has been explored extensively for subsurface structural and quasi-functional analysis of 3D cell cultures and tissue.
View Article and Find Full Text PDFConvenient tools to assess canine skeletal muscle health would be useful for a variety of applications, including standard veterinary assessments of dog fitness, as well as studies of muscle deterioration due to age or disease. One technology that can be applied conveniently to awake dogs with minimal restraint is electrical impedance myography (EIM). In EIM, a weak electrical current is applied surface electrodes to a muscle of interest and consequent impedance characteristics of the muscle are obtained, providing insight into muscle condition and composition.
View Article and Find Full Text PDFBackground: Degenerative myelopathy (DM) in dogs shares similarities with superoxide dismutase 1-associated human amyotrophic lateral sclerosis (ALS). Brain microstructural lesions are quantified using diffusion tensor imaging (DTI) in ALS patients.
Objective: Characterize brain neurodegenerative changes in DM-affected dogs using DTI.
CLN2 neuronal ceroid lipofuscinosis is a rare recessive hereditary retinal and neurodegenerative disease resulting from deleterious sequence variants in TPP1 that encodes the soluble lysosomal enzyme tripeptidyl peptidase-1 (TPP1). Children with this disorder develop normally, but starting at 2-4 years of age begin to exhibit neurological signs and visual deficits. Vision loss that progresses to blindness is associated with progressive retinal degeneration and impairment of retinal function.
View Article and Find Full Text PDFCLN2 neuronal ceroid lipofuscinosis is a hereditary neurodegenerative disorder characterized by progressive vision loss, neurological decline, and seizures. CLN2 disease results from mutations in TPP1 that encodes the lysosomal enzyme tripeptidyl peptidase-1 (TPP1). Children with CLN2 neuronal ceroid lipofuscinosis experience ocular disease, characterized by progressive retinal degeneration associated with impaired retinal function and gradual vision loss culminating in total blindness.
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