Changes in retinal vasculature and ocular circulation may play an important role in the glaucoma development and progression. We evaluated the vertical asymmetry across the temporal raphe of the deep retinal layer vessel density, using swept-source optical coherence tomography angiography (SS-OCTA), and its relationship with the central visual field (VF) loss. Thirty-four eyes of 27 patients with open-angle glaucoma were included. SS-OCTA macular scanning was performed within a 3 × 3 mm (300 × 300 pixels) volume, centred on the fovea. The relationships between the vertical asymmetrical deep retinal vessel density reduction (ADRVD) across the temporal raphe and various ocular parameters were analysed. Twenty-two glaucomatous eyes with ADRVDs had central VF loss. Contrarily, ADRVDs were not found in any of the 12 eyes without central VF loss. Thirteen eyes (59.1%) with central VF loss had ADRVDs topographically corresponding to the central VF loss and macular ganglion cell complex thinning. The glaucomatous eyes with ADRVDs exhibited inferior rather than superior central VF loss (P = 0.032). Thus, ADRVD specifically indicates the glaucomatous central visual loss. Further analysis of ADRVD may improve our understanding on glaucoma pathogenesis, offering new treatment insights.
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http://dx.doi.org/10.1038/s41598-020-63931-7 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Department of Immunology and Regenerative Biology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Malignant gliomas are heterogeneous tumors, mostly incurable, arising in the central nervous system (CNS) driven by genetic, epigenetic, and metabolic aberrations. Mutations in isocitrate dehydrogenase (IDH1/2) enzymes are predominantly found in low-grade gliomas and secondary high-grade gliomas, with IDH1 mutations being more prevalent. Mutant-IDH1/2 confers a gain-of-function activity that favors the conversion of a-ketoglutarate (α-KG) to the oncometabolite 2-hydroxyglutarate (2-HG), resulting in an aberrant hypermethylation phenotype.
View Article and Find Full Text PDFExp Physiol
January 2025
Department of Physiology, School of Medicine, University College Cork, Cork, Ireland.
Absence of the structural protein, dystrophin, results in the neuromuscular disorder Duchenne Muscular Dystrophy (DMD). In addition to progressive skeletal muscle dysfunction, this multisystemic disorder can also result in cognitive deficits and behavioural changes that are likely to be consequences of dystrophin loss from central neurons and astrocytes. Dystrophin-deficient mdx mice exhibit decreases in grey matter volume in the hippocampus, the brain region that encodes and consolidates memories, and this is exacerbated with ageing.
View Article and Find Full Text PDFJ Magn Reson Imaging
January 2025
Department of Neurology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Background: Central arterial stiffening is associated with brain white matter (WM) damage and gray matter (GM) volume loss in older adults, but little is known about this association from an adult lifespan perspective.
Purpose: To investigate the associations of central arterial stiffness with WM microstructural organization, WM lesion load, cortical thickness, and GM volume in healthy adults across the lifespan.
Study Type: This is a cross-sectional study.
J Assist Reprod Genet
January 2025
Department of Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Pregnancy complications pose challenges for both pregnant women and obstetricians globally, with the pathogenesis of many remaining poorly understood. Recently coined as a mode of cell death, cuproptosis has been proposed but remains largely unexplored. This process involves copper overload, resulting in the accumulation of fatty acylated proteins and subsequent loss of iron-sulfur cluster proteins.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Eye Center, Xiangya Hospital, Central South University, Changsha, China.
Fatty acid binding proteins (FABPs) are a class of small molecular mass intracellular lipid chaperone proteins that bind to hydrophobic ligands, such as long-chain fatty acids. FABP5 expression was significantly upregulated in the N-methyl-d-aspartic acid (NMDA) model, the microbead-induced chronic glaucoma model, and the DBA/2J mice. Previous studies have demonstrated that FABP5 can mediate mitochondrial dysfunction and oxidative stress in ischemic neurons, but the role of FABP5 in oxidative stress and cell death in retina NMDA injury models is unclear.
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