Ocular diseases are closely related to the physiological changes in the eye sphere and its contents. Using biomechanical methods to explore the relationship between the structure and function of ocular tissue is beneficial to reveal the pathological processes. Studying the pathogenesis of various ocular diseases will be helpful for the diagnosis and treatment of ocular diseases. We provide a critical review of recent biomechanical analysis of ocular diseases including glaucoma, high myopia, and diabetes. And try to summarize the research about the biomechanical changes in ocular tissues (e.g., optic nerve head, sclera, cornea, etc.) associated with those diseases. The methods of ocular biomechanics research in vitro in recent years are also reviewed, including the measurement of biomechanics by ophthalmic equipment, finite element modeling, and biomechanical analysis methods. And the preparation and application of microfluidic eye chips that emerged in recent years were summarized. It provides new inspiration and opportunity for the pathogenesis of eye diseases and personalized and precise treatment.
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http://dx.doi.org/10.1186/s12938-022-01019-1 | DOI Listing |
Retin Cases Brief Rep
December 2024
Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, USA.
Purpose: To report the clinical presentation, treatment course, and outcome of a case of bilateral frosted branch angiitis (FBA) and neuroretinitis associated with acute Epstein-Barr virus (EBV) infection in a pediatric patient with Turner Syndrome.
Methods: Case report with multimodal ocular imaging and extensive systemic workup.
Results: A 16-year-old female with Turner syndrome presented with acute bilateral vision loss, hearing loss, and ataxia.
Ophthalmol Ther
January 2025
Division of Rheumatology, University of Colorado School of Medicine, Aurora, CO, USA.
Introduction: Combined uveitis-rheumatology clinics (combined clinics) are a relatively recent clinical care model. Here we report the demographics, ocular and systemic disease characteristics, and medications utilized in patients seen in a combined clinic at a tertiary care hospital in the USA.
Methods: Medical records were reviewed of patients seen at the Combined Clinic at the University of Colorado Hospital between January 1, 2016 and November 1, 2023.
J Neurooncol
January 2025
National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Purpose: This study explores the effects of mifepristone on the proliferation, motility, and invasion of malignant and benign meningioma cells, aiming to identify mifepristone-sensitive types and investigate the underlying molecular mechanisms.
Methods: IOMM-Lee and HBL-52 meningioma cells were treated with 0, vehicle control (VC), 5, 10, 20, 40, and 80 μM of mifepristone for 12, 24, 48, 72, and 96 h. Proliferation was assessed via CCK8 assay, while motility and invasion were measured using wound scratch and transwell assays.
Alzheimers Dement
December 2024
The University of British Columbia, Vancouver, BC, Canada.
Background: An imbalance between the production and clearance of amyloid beta (Aß) has emerged as a major cause of sporadic Alzheimer's disease (AD). Retinal wholemount studies can identify cell-specific involvement in Aß clearance mechanisms which cannot be accomplished in the brain ex vivo.
Methods: Eye cross-sections of double transgenic (Tg, APP-PS1) and non-carrier sibling female mice (n = 16, 4 per group) at 3- and 9- month ages were probed with antibodies 6E10 (Aβ1-16 amino-acid residues, soluble and insoluble species), ionized calcium-binding adapter molecule 1 (IBA1, microglia/macrophage), glial fibrillary acidic protein (GFAP, astrocytes), glutamine synthetase (GS, Müller cells) and aquaporin-4 (AQP4, membrane water channel) using immunofluorescence.
Alzheimers Dement
December 2024
Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, Sydney, NSW, Australia.
Background: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a rare, hereditary cerebrovascular disease which causes stroke, complex migraine, and cognitive impairment. Given its monogenic nature, CADASIL is considered a 'pure' model of small vessel disease and vascular dementia. CADASIL is caused by NOTCH3 pathogenic variants with a broad resulting phenotypic spectrum.
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