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Oxidative/Nitrosative Stress and Brain Involvement in Sepsis: A Relationship Supported by Immunohistochemistry.
Medicina (Kaunas)
November 2024
SIC Medicina Legale, Via Potito Petrone, 85100 Potenza, Italy.
: A large amount of recent evidence suggests that cellular inability to consume oxygen could play a notable part in promoting sepsis as a consequence of mitochondrial dysfunction and oxidative stress. The latter could, in fact, represent a fundamental stage in the evolution of the "natural history" of sepsis. Following a study previously conducted by the same working group on heart samples, the present research project aims to evaluate, through an immunohistochemical study, the existence and/or extent of oxidative stress in the brains of subjects who died due to sepsis and define, after reviewing the literature, its contribution to the septic process to support the use of medications aimed at correcting redox anomalies in the management of septic patients.
View Article and Find Full Text PDFCorrection of aberrant splicing of ELP1 pre-mRNA by kinetin derivatives - A structure activity relationship study.
Eur J Med Chem
December 2024
Laboratory of Experimental Biology, Faculty of Science, Palacký University, Šlechtitelů 27, CZ-78371 Olomouc, Czech Republic; Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacký University, Hněvotínská 3, 775 15 Olomouc, Czech Republic. Electronic address:
Familial dysautonomia is a debilitating congenital neurodegenerative disorder with no causative therapy. It is caused by a homozygous mutation in ELP1 gene, resulting in the production of the transcript lacking exon 20. The compounds studied as potential treatments include the clinical candidate kinetin, a plant hormone from the cytokinin family.
View Article and Find Full Text PDFThe Neuroprotective Effects of Caffeine in a Neonatal Hypoxia-Ischemia Model are Regulated through the AMPK/mTOR Pathway.
Int J Biol Sci
January 2025
Department of Neonatology and Pediatric Intensive Care, Children's Hospital University of Bonn, Bonn, Germany.
Article Synopsis
- Neonatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of death and disability in newborns, and caffeine has shown promise in mitigating its effects.
- In a neonatal rat model, caffeine administration post-injury reduced brain damage and inflammation compared to controls, highlighting its potential benefits.
- The study found that caffeine influences the AMPK/mTOR pathway, suggesting that targeting this pathway could enhance neuroprotection and improve outcomes for HIE, especially in regions lacking sufficient resources for treatment.
[The role of drug Cytoflavin in the correction of dysautonomia in patients with post-COVID syndrome].
Zh Nevrol Psikhiatr Im S S Korsakova
December 2024
Saint Petersburg State University, St. Petersburg, Russia.
Objective: To evaluate the autonomic dysfunction of cardiovascular system (CVS) in patients with post-COVID syndrome with the help of active orthotest and heart rate variability methods.
Material And Methods: 70 patients with PCOS were examined, who were divided into 2 groups. Group 1 patients received standard therapy and Cytoflavin for 35 days, Group 2 patients received only standard therapy.
Effect of Acute Hypoxia Exposure on the Availability of A Adenosine Receptors and Perfusion in the Human Brain.
J Nucl Med
January 2025
Institute of Neuroscience and Medicine, Molecular Organization of the Brain (INM-2), Forschungszentrum Jülich, Jülich, Germany;
In animal studies it has been observed that the inhibitory neuromodulator adenosine is released into the cerebral interstitial space during hypoxic challenges. Adenosine's actions on the A adenosine receptor (AAR) protect the brain from oxygen deprivation and overexertion through adjustments in cerebral blood flow, metabolism, and electric activity. Using 8-cyclopentyl-3-(3-[F]fluoropropyl)-1-propylxanthine ([F]CPFPX), a PET tracer for the AAR, we tested the hypothesis that hypoxia-induced adenosine release reduces AAR availability in the human brain.
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