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Prech Uapinyoying on Muck Rack

Prech Uapinyoying

As seen in: Nature, BioRxiv
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Articles

Use of organ transplant solution to preserve skeletal muscle for cellular and spatial transcriptomic analyses

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By Prech Uapinyoying, Aiping Zhang, Pamela Barraza-Flores, Won Dong Lee, Angela N. Viaene, Sanda Alexandrescu, Casie Genetti, Yi-Wen Chen, Alan H. Beggs, Carsten G. Bönnemann, Monkol Lek, Jyoti Jaiswal, Nhu Chau
| Nature Verified
Abstract Single-cell and spatial transcriptomic technologies have revolutionized human cell and tissue research. Success of these methods critically depends on the preservation of RNA integrity, cellular viability, and structure of the explanted tissues—features that are impacted by tissue storage conditions, and pose challenges in research settings, where tissues are often collected in the operating room and transported to distant laboratories.
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Failure to resolve inflammation contributes to juvenile onset cardiac damage in a mouse model of Duchenne muscular dystrophy - Cell Death & Disease

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By James S. Novak, Prech Uapinyoying
| Nature Verified
Abstract Absence of dystrophin protein causes cardiac dysfunction in patients with Duchenne muscular dystrophy (DMD). Unlike boys with DMD, the common mouse model of DMD (B10-mdx) does not manifest cardiac deficits until late adulthood. This has limited our understanding of the mechanism and therapeutic approaches to target the pediatric onset of cardiac pathology in DMD. Here we show that the mdx mouse model on the DBA/2 J genetic background (D2-mdx) displays juvenile-onset cardiac degeneration.
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Failure to resolve inflammation contributes to juvenile onset cardiac damage in a mouse model of Duchenne Muscular Dystrophy

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By James S. Novak, Amy Lischin, Prech Uapinyoying, Ravi Hindupur
| BioRxiv
Abstract Absence of dystrophin protein causes cardiac dysfunction in patients with Duchenne muscular dystrophy (DMD). Unlike boys with DMD, the common mouse model of DMD (B10-mdx) does not manifest cardiac deficits until late adulthood. This has limited our understanding of the mechanism and therapeutic approaches to target the pediatric onset of cardiac pathology in DMD. Here we show that the mdx mouse model on the DBA/2J genetic background (D2-mdx) displays juvenile-onset cardiac degeneration.
Open in Who Shared Issue with article?
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