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http://dx.doi.org/10.1152/ajprenal.1993.265.3.F461 | DOI Listing |
Sci Rep
January 2025
Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Abassia, Cairo, Egypt.
Some patients with neuromyelitis optica spectrum disorder (NMOSD)-like symptoms test negative for anti-aquaporin-4 (anti-AQP4) antibodies. Among them, a subset has antibodies targeting myelin oligodendrocyte glycoprotein (MOG), a condition now termed MOG antibody-associated disease (MOGAD). MOGAD shares features with NMOSD, like optic neuritis and myelitis, but differs in pathophysiology, clinical presentation, imaging findings, and biomarkers.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Key Laboratory of Vegetable Legumes Germplasm Enhancement and Molecular Breeding in Southern China of Ministry of Agriculture and Rural Affairs, Institute of Vegetables, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China.
Plasma membrane intrinsic proteins (PIPs), one sub-family of aquaporins (AQPs), are responsible for plant abiotic stress responses. However, little information is currently available about the stress responsiveness of the promoter in vegetable pea. In the present study, one novel promoter of which shared high similarity to the -type from other plants, was isolated.
View Article and Find Full Text PDFFront Immunol
December 2024
Department of Neurology, University Hospital Ulm, Ulm, Germany.
Introduction: Very rarely, adult NMDAR antibody-associated encephalitis (NMDAR-E) leads to persistent cerebellar atrophy and ataxia. Transient cerebellar ataxia is common in pediatric NMDAR-E. Immune-mediated cerebellar ataxia may be associated with myelin oligodendrocyte glycoprotein (MOG), aquaporin-4 (AQP-4), kelch-like family member 11 (KLHL11), and glutamate kainate receptor subunit 2 (GluK2) antibodies, all of which may co-occur in NMDAR-E.
View Article and Find Full Text PDFAutophagy
December 2024
Laboratory of Metabolic and Molecular Biochemistry, Faculty of Medicine and Pharmacy, Research Institute for Health Sciences and Technology, University of Mons, Mons, Belgium.
Renal proximal tubules are a primary site of injury in metabolic diseases. In obese patients and animal models, proximal tubular epithelial cells (PTECs) display dysregulated lipid metabolism, organelle dysfunctions, and oxidative stress that contribute to interstitial inflammation, fibrosis and ultimately end-stage renal failure. Our research group previously pointed out AMP-activated protein kinase (AMPK) decline as a driver of obesity-induced renal disease.
View Article and Find Full Text PDFCell Mol Biol Lett
December 2024
School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction, Guangzhou Medical University, Guangzhou, 510140, China.
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