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A Rare Case of Bilateral Foot Drop Following Cervical Decompression in Tandem Spinal Stenosis.
Cureus
December 2024
Orthopaedic Surgery, Ng Teng Fong General Hospital, Singapore, SGP.
This case report describes a 70-year-old male presenting with limb weakness, urinary retention and tandem cervical and lumbar spinal stenosis with complicating white cord syndrome, a rare reperfusion injury post decompression surgery. Initially admitted following an unwitnessed fall, the patient's neurological examination indicated that progressive weakness of the limbs and sensory loss etiology is cervical and lumbar spondylosis with severe spinal canal stenosis, confirmed by imaging. Due to rapid deterioration, he underwent C5 corpectomy, cervical decompression and fusion.
View Article and Find Full Text PDFM6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury.
Redox Rep
December 2025
Department of Cardiology, Fujian Medical University Union Hospital, Fuzhou, Fujian, People's Republic of China.
Objective: Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI and discovering new targets are crucial for the future treatment of MIRI.
Methods: We constructed the MIRI rat model and hypoxia/reoxygenation (H/R) injury cardiomyocytes model.
Protective activity of adipose-derived stem cell extracellular vesicles in ischemia and/or reperfusion.
World J Stem Cells
January 2025
Internal Medicine-II, Paracelsus Medical University Salzburg, Salzburg 5020, Austria.
Increasing evidence of the significant clinical value of protection against ischemia/reperfusion injury has contributed to the realization of the independent importance of this approach in improving prognosis and reducing cardiovascular mortality. Extracellular vesicles (EVs) derived by adipose mesenchymal stem cells may mediate the paracrine effects of stem cells and provide regenerative and anti-inflammatory properties, which are enhanced by γ-aminobutyric acid. The protective effects on cardiac myocytes may result from the EV embarked by miR-21-5p, which is a target for thioredoxin-interacting protein, regulating the formation of thioredoxin-interacting protein-thioredoxin complexes and subsequently enhancing the antioxidant activity of thioredoxin.
View Article and Find Full Text PDFBlockade of neddylation through targeted inhibition of DCN1 alleviates renal fibrosis.
Clin Sci (Lond)
January 2025
Zhengzhou University First Affiliated Hospital, Zhengzhou, China.
Neddylation is a process of attaching neuronal precursor cell-expressed developmentally downregulated protein 8 (NEDD8) to substrates for the protein function modulation via enzymatic cascades involving NEDD8-activating enzyme (E1), NEDD8-conjugating enzyme (E2), and NEDD8 ligase (E3). Defective in cullin neddylation 1 (DCN1) serves as a co-E3 ligase, that can simultaneously bind E2 UBE2M and cullin proteins to stabilize the catalytic center of the Cullin-Ring E3 ligase (CRL) complex, thereby promoting cullin neddylation. Neddylation is reported to be activated in diverse human diseases, and inhibition of protein neddylation has been regarded as a promising anticancer therapy.
View Article and Find Full Text PDFHigh expression of SERPINE1 and CTSL in keratinocytes in pressure injury caused by ischemia-reperfusion injury.
Tissue Cell
January 2025
Institute of Regenerative Medicine, Binzhou Medical University, Yantai, Shandong 264003, PR China; Department of Histology and Embryology, Binzhou Medical University, Yantai, Shandong 264003, PR China. Electronic address:
Introduction: Pressure Injury (PI) is a complex disease process which is influenced by multiple factors, among which ischemia-reperfusion (I/R) injury is closely related to the progression of PI. But its biomarkers are still unclearly. Understanding its physiological mechanisms and related molecular biomarkers is a key to developing effective prevention and therapeutic strategies.
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