Objectives: Experimental animal models of brain death that mimic human conditions may be useful for investigating novel strategies that increase quality and quantity of organs for transplant.
Materials And Methods: Brain death was induced by increasing intracranial pressure by inflating an intracranial placed balloon catheter. Brain death was confirmed by flatline electroencephalogram, physical signs of apnea, and absence of brain stem reflexes. Donor management was done after brain death. Intracranial pressure and physiologic variables were continually monitored during 9 hours' follow-up.
Results: Ninety percent of brain dead animals showed typical signs of brain death such as diabetes insipidus, hypertensive, and hypotensive periods. Donor care was performed for 9 hours after brain death, and the mean arterial pressure was maintained above 60 mm Hg.
Conclusions: We conclude that the rat model of brain death can be performed in a standardized, reproducible, and successful way.
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http://dx.doi.org/10.6002/ect.2013.0229 | DOI Listing |
Gene
January 2025
Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province 150081, PR China. Electronic address:
Currently, the pathogenesis of epilepsy remains poorly understood. Although there is evidence indicating that iron death might play a significant role, its molecular immunological mechanisms are largely unknown. This study was designed to analyze and explore the molecular mechanisms and immunological characteristics of iron death-related genes in epilepsy.
View Article and Find Full Text PDFNeurocrit Care
January 2025
Division of Neurocritical Care, Departments of Neurology and Neurosurgery, New York University Langone Medical Center, 530 First Avenue, MSB-2-206, New York, NY, 10016, USA.
Background: The Uniform Determination of Death Act requires brain death/death by neurologic criteria (BD/DNC) determination to be in accordance with "accepted medical standards." The medical organizations responsible for delineating these guidelines are only specified statutorily in two states. State health organizations (SHOs) are composed of policy experts and medical professionals who are responsible for addressing medical, ethical, and legislative problems related to health.
View Article and Find Full Text PDFNeurotherapeutics
January 2025
Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Chile. Electronic address:
Acute brain injuries (ABIs) encompass a broad spectrum of primary injuries such as ischemia, hypoxia, trauma, and hemorrhage that converge into secondary injury where some mechanisms show common determinants. In this regard, astroglial connexin and pannexin channels have been shown to play an important role. These channels are transmembrane proteins sharing similar topology and form gateways between adjacent cells named gap junctions (GJs) and pores into unopposed membranes named hemichannels (HCs).
View Article and Find Full Text PDFNeurosci Res
January 2025
Department of Cell Physiology, Graduate School of Medicine, Nagoya University, Nagoya 466-8550, Japan. Electronic address:
Sensorineural hearing loss causes cell death in central auditory neurons, but molecular mechanisms of triggering this process are not fully understood. We report here that loss of afferent activity promotes cell death by facilitating proBDNF-p75NTR signals in cochlear nucleus of chicks around hatch. RNA-seq analyses revealed up-regulation of genes related to proBDNF-p75NTR-JNK signals as well as apoptosis at the nucleus within 24hours after unilateral cochlea deprivation.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Department of Pharmacology, University of Michigan Medical School, Ann Arbor, United States of America.
Dravet syndrome (DS) is a developmental and epileptic encephalopathy (DEE) that begins in the first year of life. While most cases of DS are caused by variants in SCN1A, variants in SCN1B, encoding voltage-gated sodium channel β1 subunits, are also linked to DS or to the more severe early infantile DEE. Both disorders fall under the OMIM term DEE52.
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