Background: The aim of the present study was to compare the rates of change in Ganglion Cell- Inner Plexiform Layer (GCIPL) and Retinal Nerve Fiber Layer (RNFL) thickness, as measured by Optical Coherence Tomography (OCT) Guided Progression Analysis (GPA) program in control group, Primary Open Angle Glaucoma (POAG) and Pseudoexfoliation Glaucoma (PXG) eyes.
Methods: 60 POAG and 60 PXG patients and 30 control group patients were included in the study. Patients diagnosed with glaucoma were divided into two groups as mild (Mean deviation (MD) > -6.00) and moderate-severe (MD < -6.00). The average, superior and inferior quadrant thinning rates (expressed in micrometers per year) of GCIPL and RNFL in the OCT GPA program were compared between groups.
Results: Average GCIPL thinning rates were -0.23 ± 0.21 μm/year in the control group, -0.64 ± 0.54 μm/year in POAG patients, and -1.06 ± 1.16 μm/year in PXG patients (ANOVA, p < 0.001). Average RNFL thinning rates were -0.33 ± 0.44 μm/year in the control group, -0.86 ± 0.73 μm/year in POAG patients, and -1.33 ± 1.4 μm/year in PXG patients (ANOVA, p < 0.001).
Conclusions: The rates of GCIPL and RNFL thinning were highest in patients with PXG. We found that the glaucoma stage did not affect the rate of RNFL and GCIPL thinning.
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http://dx.doi.org/10.1186/s12886-024-03837-4 | DOI Listing |
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694462 | PMC |
Acta Neuropathol Commun
January 2025
Department of Neurology, Peking Union Medical College Hospital, Peking Union Medical College (PUMC) and Chinese Academy of Medical Science (CAMS), Beijing, China.
Mutations in the ANXA11 gene, encoding an RNA-binding protein, have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), but the underlying in vivo mechanisms remain unclear. This study examines the clinical features of ALS patients harboring the ANXA11 hotspot mutation p.P36R, characterized by late-onset motor neuron disease and occasional multi-system involvement.
View Article and Find Full Text PDFJ Hematol Oncol
January 2025
Department of Radiation Oncology, Henan Provincial Key Laboratory of Radiation Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, People's Republic of China.
Background: Targeting glucose uptake by glucose transporter (GLUT) inhibitors is a therapeutic opportunity, but efforts on GLUT inhibitors have not been successful in the clinic and the underlying mechanism remains unclear. We aim to identify the key metabolic changes responsible for cancer cell survival from glucose limitation and elucidate its mechanism.
Methods: The level of phosphorylated YAP was analyzed with Western blotting and Phos-tag immunoblotting.
Mol Cell Endocrinol
January 2025
Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY,11439, USA. Electronic address:
Liver fibrosis is potentially a reversible form of liver disease that evolved from the early stage of liver scarring as a consequence of chronic liver injuries. Recurrent injuries in the liver without any appropriate medication cause the injuries to get intense and deeper, which gradually leads to the progression of irreversible cirrhosis or carcinoma. Unfortunately, there are no approved treatment strategies for reversing hepatic fibrosis, making it one of the significant risk factors for developing advanced liver disorders and liver disease-associated mortality.
View Article and Find Full Text PDFESMO Open
January 2025
Dana-Farber Cancer Institute, Boston. Electronic address:
Background: Brain metastases (BMs) are common in human epidermal growth factor receptor 2 (HER2)-positive advanced breast cancer, increasing morbidity and mortality. Systemic therapy for BMs can be effective, with the triple combination of trastuzumab, capecitabine, and tucatinib being a potential standard. More recently, intracranial activity of antibody-drug conjugates has been reported, but the size of individual studies has been small.
View Article and Find Full Text PDFCurr Cardiol Rep
January 2025
Johns Hopkins University Division of Cardiology, Baltimore, MD, USA.
Purpose Of Review: The present review aims to address systemic sclerosis (SSc)-associated myocardial disease, a significant cause of morbidity and mortality, by examining the mechanisms of inflammation, microvascular dysfunction, and fibrosis that drive cardiac involvement. The objective is to elucidate critical risk factors and explore advanced diagnostic tools for early detection, enhancing patient outcomes by identifying those at highest risk.
Recent Findings: Recent studies underscore the importance of specific autoantibody profiles, disease duration, and cardiovascular comorbidities as key risk factors for severe cardiac manifestations in SSc.
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