Most sphingolipids and ceramides (except a few unique to a specific donor TM group) were found to be common in the control and POAG TM. Latent commensalism by Fusarium was suggested by identification of Fusarium-specific lipids, which was supported further by PCR amplification and sequencing of DNA.

Purpose: To determine the differential profiles of sphingomyelin, sphingoid base, sphingoid base-1-phosphate, and ceramide and their quantitative differences between trabecular meshwork (TM) derived from normotensive and hypertensive intraocular pressure states of DBA/2J mice. Methods: Normotensive and hypertensive state TM were collected from mice and analyzed. Lipid extraction was performed using the Bligh and Dyer method, and the protein concentrations were determined using the Bradford method. The lipids were identified and quantified using appropriate standards with a TSQ Quantum Access Max triple quadrupole mass spectrometer applying class-specific lipid identification settings. Results: The comparative profiles of sphingomyelin, sphingoid base, sphingoid base-1-phosphate, and ceramide between normotensive and hypertensive TM showed several species unique to a phase and as well common between states. Conclusion: The presence or absence of several sphingolipids and ceramides in the normotensive or hypertensive states may contribute to better understanding of the glaucomas.

The expression of cochlin in the trabecular meshwork (TM) precedes the clinical glaucoma symptoms in DBA/2J mice. The ability to quantify cochlin in the local tissue (TM) offers potential diagnostic and prognostic values. We present two (spectroscopic and magnetomotive) optical coherence tomography (OCT) approaches for in vivo cochlin quantification in a periodic manner. The cochlin-antibody OCT signal remains stable for up to 24 hours as seen at 3.5 hours after injection allowing for repeated quantification in the living mouse eyes.

Vitamin D deficiency has been associated with the risk for immune-mediated inflammatory reactions in various respiratory infections. Our study investigated the association between vitamin D deficiency and coronavirus disease 2019 (COVID-19) patients' outcomes. We included 545 patients who were admitted to a tertiary center in Jeddah, Saudi Arabia from March 2020 to July 2021 with a vitamin D serum test result at the time of infection or prior to disease onset. The data were extracted retrospectively using a data collection sheet. Our primary outcomes were intensive care unit (ICU) admission and in-hospital mortality. The cut-off values for vitamin D were <25, 25-49, and 50-250 for deficient, suboptimal, and optimal levels respectively. Our result revealed that there is no association between vitamin D serum levels deficiency and ICU admission (OR=1.08, p=0.75) or in-hospital mortality (OR=1.74, p=0.97). ICU admission and in-hospital mortality percentages in patients with vitamin D deficiency were 14.1% and 6.4%, respectively. In comparison, percentages for patients with optimal levels were 16.67% and 6.15% for ICU admission and inhospital mortality, respectively. Smoking was not associated with ICU admission (p=0.05) or in-hospital mortality (p=0.38). Our study does not support a relationship between vitamin D deficiency and COVID-19 patients' outcomes. Future studies should be directed toward conducting randomized clinical trials to determine whether vitamin D has an effective role in reducing COVID-19 severity.