- 3D Printing in Biomedical Research
- Neurological diseases and metabolism
- Supramolecular Self-Assembly in Materials
- Atherosclerosis and Cardiovascular Diseases
- Nanofabrication and Lithography Techniques
- Neurological Disease Mechanisms and Treatments
- interferon and immune responses
- Neurological Disorders and Treatments
- Nerve injury and regeneration
- Systemic Lupus Erythematosus Research
- Kruppel-like factors research
- Microbial Metabolism and Applications
- Neurogenesis and neuroplasticity mechanisms
- Monoclonal and Polyclonal Antibodies Research
- Single-cell and spatial transcriptomics
- Nuclear Receptors and Signaling
- Pluripotent Stem Cells Research
- Credit Risk and Financial Regulations
- Hereditary Neurological Disorders
- Cell Adhesion Molecules Research
- Lysosomal Storage Disorders Research
New York Stem Cell Foundation
2022-2024
Infantile neuroaxonal dystrophy (INAD) is caused by recessive variants in PLA2G6 and a lethal pediatric neurodegenerative disorder. Loss of the Drosophila homolog PLA2G6, leads to ceramide accumulation, lysosome expansion, mitochondrial defects. Here, we report that retromer function, metabolism, endolysosomal pathway, morphology are affected INAD patient-derived neurons. We show mouse models, same features Purkinje cells, arguing neuropathological mechanisms evolutionary conserved these can...
The hypothalamus is a region of the brain that plays an important role in regulating body functions and behaviors. There growing interest human pluripotent stem cells (hPSCs) for modeling diseases affect hypothalamus. Here, we established hPSC-derived organoid differentiation protocol to model cellular diversity this region. Using hPSC line with tyrosine hydroxylase (TH)-TdTomato reporter dopaminergic neurons (DNs) other TH-expressing cells, interrogated DN-specific pathways...
Abstract Background Viral infection outcomes vary widely between individuals, ranging from mild symptoms to severe organ failure and death, it is clear that host genetic factors play a role in this variability. Type I interferon (IFN) critical anti-viral cytokine, we have previously noted differences type IFN levels world populations. Methods In study, investigate the interrelationship regional European ancestry, viral outcomes. Results cohorts of ancestry lupus patients living Europe,...
Dissociation of EBs using papain
Embryoid body formation is the aggregate of hPS cells in a three-dimensional format to differentiate into specific lineages. In this,protocol we would discuss some important steps ensure consistent EB using multiple cell lines.
This protocol is used to create adhesive and bioactive substrate for neural cell types, low high density nuerons, astrocytes, or organoids. It based on standard methods but includes several optimizations, use case recommendations, alternatives, advice.
Embryoid body formation is the aggregate of hPS cells in a three-dimensional format to differentiate into specific lineages. In this,protocol we would discuss some important steps ensure consistent EB using multiple cell lines.
This protocol is used to create adhesive and bioactive substrate for neural cell types, low high density nuerons, astrocytes, or organoids. It based on standard methods but includes several optimizations, use case recommendations, alternatives, advice.
hPSC Passaging and propagation using Laminin521 EDTA. Laminin actively supports survival, prevents spontaneous differentiation, increases plating efficiency, thus net expansion, enables 100% confluent single cell layer epithelial monolayer culture. EDTA-based (Gentle Cell Dissociation Reagent) minimizes stress enhances viability. lines require little or no adaptation.
Brain organoids are three-dimensional (3D) structures derived from human pluripotent stem cells (hPSCs) that reflect early brain organization. Compared with traditional cell cultures, offer a more accurate representation of development and function, rendering them suitable models for neurodevelopmental diseases. In this pilot to form using iPSCs, we focused on verifying successful approach our vmDA generated protocol, optimizing conditions maintain the (media, feeding schedule) as well...
Abstract Infantile Neuroaxonal Dystrophy (INAD) is caused by recessive variants in PLA2G6 and a lethal pediatric neurodegenerative disorder. Loss of the Drosophila homolog , leads to ceramide accumulation, lysosome expansion, mitochondrial defects. Here, we report that metabolism, endolysosomal pathway, morphology are affected INAD patient-derived neurons. We show mouse models same features glucosylceramides elevated dopaminergic neurons Purkinje cells, arguing neuropathological mechanisms...