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| http://dx.doi.org/10.7554/eLife.103278 | DOI Listing |
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Oxidative/Nitrosative Stress and Brain Involvement in Sepsis: A Relationship Supported by Immunohistochemistry.
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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 PDFDiagnosis and Management of Mitochondrial Encephalopathy, Lactic Acidosis, and Stroke-like Episodes Syndrome.
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Departments of Pediatrics, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul 06229, Republic of Korea.
Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a complex mitochondrial disorder characterized by a wide range of systemic manifestations. Key clinical features include recurrent stroke-like episodes, seizures, lactic acidosis, muscle weakness, exercise intolerance, sensorineural hearing loss, diabetes, and progressive neurological decline. MELAS is most commonly associated with mutations in mitochondrial DNA, particularly the m.
View Article and Find Full Text PDFErinacine A-Enriched Mycelium Ethanol Extract Lessens Cellular Damage in Cell and Models of Spinocerebellar Ataxia Type 3 by Improvement of Nrf2 Activation.
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December 2024
Department of Nutrition, Chung Shan Medical University, Taichung 402, Taiwan.
Spinocerebellar ataxia type 3 (SCA3), caused by the abnormal expansion of polyglutamine (polyQ) in the ataxin-3 protein, is one of the inherited polyQ neurodegenerative diseases that share similar genetic and molecular features. Mutant polyQ-expanded ataxin-3 protein is prone to aggregation in affected neurons and is predominantly degraded by autophagy, which is beneficial for neurodegenerative disease treatment. Not only does mutant polyQ-expanded ataxin-3 increase susceptibility to oxidative cytotoxicity, but it also hampers antioxidant potency in neuronal cells.
View Article and Find Full Text PDFA Genetic Make Up of Italian Lipizzan Horse Through Uniparental Markers to Preserve Historical Pedigrees.
Biology (Basel)
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Consiglio per la Ricerca in Agricoltura e l'Analisi dell'Economia Agraria (CREA), Research Centre for Animal Production and Aquaculture, Via Salaria 31, 00015 Monterotondo, Italy.
Lipizzan is a famous horse breed dating back to 1580 when the original stud of Lipica was established by the Hasburg Archduke Charles II. Currently, the Italian State Stud of Lipizzan Horses (ASCAL) is a conservation nucleus managed through strict mating rules where mitochondrial DNA sequences are used to verify the correct assignment of mares to a historical pedigree maternal lineage. Here, we analyzed the D-loop sequences of Lipizzan horses from the ASCAL in Monterotondo (Rome, Italy) in order to confirm their pedigree assignment to known female founder families.
View Article and Find Full Text PDFNew Insight into the Crayfish (Girard, 1852) (Crustacea, Cambaridae): A Morphometric Combined Approach to Describe the Case of a Mediterranean Population.
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Department of Veterinary Medicine, University of Sassari, Via Vienna 2, 07100 Sassari, SS, Italy.
We adopted a morphometric approach to provide statistical support for the description of two different morphotypes (I, reproductive, II, non-reproductive) firstly observed in specimens caught in a population from Sardinia Island (western Mediterranean). The morphometric study was preceded by molecular taxonomic identification using the mitochondrial Cytochrome C Oxidase subunit I (COI) gene. The presence or absence of the pathogen , responsible for the plague, was also investigated using the ribosomal Internal Transcribed Spacer (ITS) marker.
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