Clinical and anatomical comparisons were undertaken in 23 cases of mortality due to severe craniocerebral injuries. The set of clinical examinations included circulation and brain gas exchange studies. Cerebral circulatory hypoxy was revealed in all the patients, but in cases of its compensated form all signs of brain stem injury were lacking, while in cases of its non-compensated form foci of brain stem injury could be revealed at autopsy. Timely elimination of brain stem compression in cases of its anatomic integrity preserved helps to convert the non-compensated form of cerebral circulatory hypoxy into its compensated form.
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Transl Psychiatry
January 2025
Department of Neurosurgery, General Hospital of Northern Theater Command, Postgraduate Training Base of General Hospital of Northern Theater Command of Jinzhou Medical University, Shenyang, Liaoning, China.
Traumatic brain injury (TBI) is identified as a risk factor for Parkinson's disease (PD), which is a neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra (SN). However, the precise mechanism by which chronic TBI initiates PD pathogenesis is not yet fully understood. In our present study, we assessed the chronic progression and pathogenesis of PD-like behavior at different intervals in TBI mice.
View Article and Find Full Text PDFDev Cell
January 2025
Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Toronto, ON M5G 0A4, Canada; Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, Toronto, ON M5G 0A4, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON M5S 1A8, Canada. Electronic address:
Distinguishing tumor maintenance genes from initiation, progression, and passenger genes is critical for developing effective therapies. We employed a functional genomic approach using the Lazy Piggy transposon to identify tumor maintenance genes in vivo and applied this to sonic hedgehog (SHH) medulloblastoma (MB). Combining Lazy Piggy screening in mice and transcriptomic profiling of human MB, we identified the voltage-gated potassium channel KCNB2 as a candidate maintenance driver.
View Article and Find Full Text PDFPharmaceutics
December 2024
Joint Department of Biomedical Engineering, The University of North Carolina at Chapel Hill and North Carolina State University, Chapel Hill, NC 27599, USA.
Background/objectives: Glioblastoma multiforme (GBM) is the most common high-grade primary brain cancer in adults. Despite efforts to advance treatment, GBM remains treatment resistant and inevitably progresses after first-line therapy. Induced neural stem cell (iNSC) therapy is a promising, personalized cell therapy approach that has been explored to circumvent challenges associated with the current GBM treatment.
View Article and Find Full Text PDFLife (Basel)
December 2024
Department of Tissue Engineering and Regenerative Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia, Cheras, Kuala Lumpur 56000, Malaysia.
Fetal bovine serum (FBS) has long been the standard supplement in cell culture media, providing essential growth factors and proteins that support cell growth and differentiation. However, ethical concerns and rising costs associated with FBS have driven researchers to explore alternatives, particularly human platelet lysate (HPL). Among these alternatives, fibrinogen-depleted HPL (FD-HPL) has gained attention due to its reduced thrombogenicity, which minimizes the risk of clot formation in cell cultures and enhances the safety of therapeutic applications.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Neuroregeneration, Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Meibergdreef 47, 1105 BA Amsterdam, The Netherlands.
Semaphorin 3A (Sema3A) is an axon guidance molecule, which is also abundant in the adult central nervous system (CNS), particularly in perineuronal nets (PNNs). PNNs are extracellular matrix structures that restrict plasticity. The cellular sources of Sema3A in PNNs are unknown.
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