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Figure 1. Human oligodendrocytes. A. Cartoon of oligodendrocyte myelination of neuronal axons. B-D. Oligodendrocytes grown in a dish (cell culture). E,F. Oligodendrocyte excitotoxicity. G. Peroxynitrite (ONOO) formation and protein damage. H. Oligodendrocyte excitotoxicity with quinolinic acid (QA) causes formation of toxic forms of α-synuclein as monomer (arrow) and oligomers. Ponceau shows equal protein loading in the lanes.

iPSCs and NSCs model newborn brain injury

This article discusses research by Dr. Lee J. Martin and his team on HIE, a leading cause of neonatal mortality. They use human induced pluripotent stem cells (iPSCs) and neural stem cells (NSCs) and emphasize the vulnerability of oligodendrocytes, sharing how these cells can accumulate toxic misfolded proteins, potentially causing severe neural damage and long-term cognitive disabilities in affected infants.
Johns Hopkins University School of Medicine

Department of Pathology at the Johns Hopkins University School of Medicine

The Division of Neuropathology is a cornerstone of the Department of Pathology at the Johns Hopkins University School of Medicine, with its historical championing of human clinical neuropathology and large and small animal models of human neuropathology.
Figure 1. HIE vulnerable human brain regions.

Protecting infants from brain damage: A focus on HIE

Lee J. Martin, PhD from Johns Hopkins University School of Medicine, discusses the pathology of infant hypoxic-ischemic encephalopathy (HIE), and the research he and his team are conducting to understand cell death mechanisms related to HIE and therefore identify new therapies.

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