Topiramate-Induced Aqueous Misdirection in a Nanophthalmic Eye

A 51-year-old female was referred to the emergency department with a one-day history of severe right eye pain, blurry vision, and conjunctival injection. A review of past ocular history was notable for nanophthalmos and narrow angles with patent peripheral iridotomies. Anterior segment exam findings were consistent with aqueous misdirection and a review of medications indicated recent topiramate initiation for headaches and depression. The acute attack was initially controlled with medical management and plans for future surgical intervention were made. Although ocular screening prior to initiation of topiramate is not recommended, this case highlights the importance of pre-screening in a patient with a pre-existing condition such as nanophthalmos. Additionally, this case addresses the ocular side effects of anti-depressants and the emerging relationship between glaucoma and depression. Appropriately addressing these issues and coordinating care with behavioral health providers has the potential to prevent optic nerve damage and loss of vision

Surface Acoustic Wave devices for ocular drug delivery

In this work we are reporting on the development of a novel SurfaceAcoustic Wave (SAW) device based on MEMS technology for drug delivery in thetreatment of ocular diseases. The miniaturized SAW drug delivery device will beplaced on the eye surface to allow non-invasive long-term drug application basedon the programmed timeline and electronic control of a drug regiment. Thisnovel drug delivery method is expected to lead to better clinical outcomes inthe treatment of various eye diseases, and improved patient compliance withtherapy. The device can be programmed for delivery of precise amounts of drugsat predetermined times over several months, and will use acoustic streaming topush the drug outside of the reservoir. Our modeling results were obtained usingCOMSOL multiphysics program and Coventor microfluidic simulator. Differentforce values were applied to investigate the force necessary to push the drugthrough the outlet. © 2010 IEEE

Twentieth Symposium on COVID-19: COVID-19 as of July 14, 2022: What Have We Learned? How Can We Use What We Have Learned?

Opening Remarks and Moderator: Edward C. Halperin, M.D., M.A. Chancellor/CEO, New York Medical College, Professor of Radiation Oncology, Pediatrics, and History, Provost for Biomedical Affairs, Touro University, The Miriam Popack Chair in Biomedical Ethics After the Holocaust How Does COVID-19 Infection Affect the Eye? (About 10% of Infected Individuals Have Eye Symptoms.) Sankara Mahesh, M.D., FRCS Program Director, Ophthalmology, Westchester Medical Center, Advanced Eye Specialty Services, Associate Professor of Ophthalmology, New York Medical College How Does COVID-19 Infection and Vaccination Affect Hearing? Katrina R. Stidham, M.D. Director, Balance Center, Cochlear Implant Center, Maria Fareri Children\u27s Hospital, Westchester Medical Center, Associate Professor of Otolaryngology, New York Medical College Monkeypox: What is It? What Causes It? How Do We Manage It? Should I Be Worried About It? David Revelli, Ph.D. Research Scientist, Lovelace Biomedical Research Institute With the Evolving Data Coming In, Which of My Children Need the Vaccine and/or Booster Shots Now? Tami Hendriksz, DO, FACOP, FAAP Dean and Chief Academic Officer, Professor of Pediatrics, Touro University California College of Osteopathic Medicine Am I Just Sick and Tired of This Pandemic and the News on Television or Am I Depressed? I Don\u27t Feel Like Going Back to the Office or to Shows or Weddings Like I Used to. Ronnie Swift, M.D. Professor and Associate Chairman of Psychiatry and Behavioral Health, New York Medical College, Chief of Psychiatry, Metropolitan Hospital and Medical Center Q & A Hosted by: Edward C. Halperin, M.D., M.A. Chancellor/CEO, New York Medical College, Professor of Radiation Oncology, Pediatrics, and History, Provost for Biomedical Affairs, Touro University, The Miriam Popack Chair in Biomedical Ethics After the Holocaus

Carbenoxolone treatment ameliorated metabolic syndrome in WNIN/Ob obese rats, but induced severe fat loss and glucose intolerance in lean rats.

BACKGROUND: 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regulates local glucocorticoid action in tissues by catalysing conversion of inactive glucocorticoids to active glucocorticoids. 11β-HSD1 inhibition ameliorates obesity and associated co-morbidities. Here, we tested the effect of 11β-HSD inhibitor, carbenoxolone (CBX) on obesity and associated comorbidities in obese rats of WNIN/Ob strain, a new animal model for genetic obesity. METHODOLOGY/PRINCIPAL FINDINGS: Subcutaneous injection of CBX (50 mg/kg body weight) or volume-matched vehicle was given once daily for four weeks to three month-old WNIN/Ob lean and obese rats (n = 6 for each phenotype and for each treatment). Body composition, plasma lipids and hormones were assayed. Hepatic steatosis, adipose tissue morphology, inflammation and fibrosis were also studied. Insulin resistance and glucose intolerance were determined along with tissue glycogen content. Gene expressions were determined in liver and adipose tissue. CBX significantly inhibited 11β-HSD1 activity in liver and adipose tissue of WNIN/Ob lean and obese rats. CBX significantly decreased body fat percentage, hypertriglyceridemia, hypercholesterolemia, insulin resistance in obese rats. CBX ameliorated hepatic steatosis, adipocyte hypertrophy, adipose tissue inflammation and fibrosis in obese rats. Tissue glycogen content was significantly decreased by CBX in liver and adipose tissue of obese rats. Severe fat loss and glucose- intolerance were observed in lean rats after CBX treatment. CONCLUSIONS/SIGNIFICANCE: We conclude that 11β-HSD1 inhibition by CBX decreases obesity and associated co-morbidities in WNIN/Ob obese rats. Our study supports the hypothesis that inhibition of 11β-HSD1 is a key strategy to treat metabolic syndrome. Severe fat loss and glucose -intolerance by CBX treatment in lean rats suggest that chronic 11β-HSD1 inhibition may lead to insulin resistance in normal conditions

Carbenoxolone Treatment Ameliorated Metabolic Syndrome in WNN/Ob Obese Rats but induced Severe Fat Loss and Glucose Intolerance in Learn Rats

not cop

Effect of carbenoxolone on food intake, body weight and organ weights in WNIN/Ob lean and obese rats.

<p>Values represent means ± SEM of 6 rats per group. LC, Lean control; OC, Obese control; LT, Lean- treated; OT, Obese- treated. Parameters were measured after four weeks of treatment with carbenoxolone (50 mg/kg/body weight/day) or vehicle (same volume of phosphate buffer saline).</p>#<p><i>p</i><0.05,</p>##<p><i>p</i><0.01 and ### <i>p</i><0.001 comparing vehicle-treated lean and obese rats.</p>*<p><i>p</i><0.05,</p>**<p><i>p</i><0.01 and *** <i>p</i><0.001 comparing carbenoxolone- treated animals with vehicle-treated animals of the same phenotype. </p

Effect of carbenoxolone on plasma biochemical parameters in WNIN/Ob lean and obese rats.

<p>(A). Fed-state corticosterone. (B). Fasting corticosterone. (C). Fed-state triglycerides. (D). Fasting triglycerides. (E). Fed-state total cholesterol. (F). Fasting total cholesterol. (G). Fed-state HDL cholesterol. (H). Fasting HDL cholesterol. Plasma parameters were measured after 4weeks of treatment with carbenoxolone or vehicle (50 mg/kg bodyweight/day). Empty bars indicate lean phenotype where as filled bars indicate obese phenotype. Values are means ± SEM for 6 animals for group. #<i>p</i><0.05, ##<i>p</i><0.01 and ### <i>p</i><0.001 comparing vehicle-treated lean and obese rats. *<i>p</i><0.05, **<i>p</i><0.01 and *** <i>p</i><0.001 comparing carbenoxolone-treated animals with vehicle-treated animals of the same phenotype.</p

Effect of carbenoxolone on adipose tissue gene expression quantified by semi quantitative reverse transcription PCR.

<p>(A). Stearoyl CoA desaturase 1 (SCD1). (B). Malic enzyme 1 (ME1). (C). Macrophage expressed gene (MPEG). (D). Lysosomal acid lipase (LIPA). (E). Beta3-Adrenergic receptor (β3-AR). Parameters were measured after 4weeks of treatment with carbenoxolone or vehicle (50 mg/kg body weight/day). Empty bars indicate lean phenotype where as filled bars indicate obese phenotype. Relative gene expression was measured using calnexin gene as internal control. Relative expression of gene of interest in lean control was taken as 1. Values are means ± SEM for 4 animals for group. . #<i>p</i><0.05, ##<i>p</i><0.01 and ### <i>p</i><0.001 comparing vehicle-treated lean and obese rats. *<i>p</i><0.05, **<i>p</i><0.01 and *** <i>p</i><0.001 comparing carbenoxolone-treated animals with vehicle-treated animals of the same phenotype.</p

Effect of carbenoxolone on body composition of WNIN/Ob lean and obese rats.

<p>(A). fat percentage. (B). Lean body mass. (C). Fat free mass. Body composition was measured by TOBEC after 4weeks of treatment with carbenoxolone or vehicle (50 mg/kg body weight/day). Empty bars indicate lean phenotype where as filled bars indicate obese phenotype. Values are means ± SEM for 6 animals for group. #<i>p</i><0.05, ##<i>p</i><0.01 and ### <i>p</i><0.001 comparing vehicle-treated lean and obese rats. *<i>p</i><0.05, **<i>p</i><0.01 and *** <i>p</i><0.001 comparing carbenoxolone-treated animals with vehicle-treated animals of the same phenotype.</p