Purpose: We evaluate visual outcomes in patients with EVO/EVO+™ (posterior chamber phakic intraocular lens with a central port) within approved United States (US) age and refractive range indications.
Patients And Methods: This single-center retrospective study evaluated one-month, single-center postoperative data for 225 eyes meeting inclusion criteria and undergoing EVO/EVO+ implantation from April to October 2022. Data included lens size (mm), lens power (diopters of spherical and cylindrical power), preoperative best corrected visual acuity, preoperative spherical equivalent from manifest refraction, achieved postoperative uncorrected visual acuity, postoperative refraction, intraocular pressure (mmHg), and adverse events.
Purpose: To evaluate the safety and efficacy of a sustained-release intracanalicular dexamethasone insert for postoperative inflammation and pain implanted in a clinical setting preoperatively or on postoperative day 1.
Methods: Single-site, retrospective, contralateral eye study of patients undergoing cataract surgery. Included were subjects with a dexamethasone intracanalicular insert implanted in the clinic immediately prior to surgery in one eye (same-day) and on postoperative day 1 (POD1) in the contralateral eye.
Bacterial infection is one known etiology of prostatic inflammation. Prostatic inflammation is associated with prostatic collagen accumulation and both are linked to progressive lower urinary tract symptoms in men. We characterized a model of prostatic inflammation using transurethral instillations of UTI89 in C57BL/6J male mice with the goal of determining the optimal instillation conditions, understanding the impact of instillation conditions on urinary physiology, and identifying ideal prostatic lobes and collagen 1a1 prostatic cell types for further analysis.
View Article and Find Full Text PDFWe genetically engineered expression of an activated form of P110 alpha, the catalytic subunit of PI3K, in mouse prostate epithelium to create a mouse model of direct PI3K activation (Pbsn-cre4Prb;PI3K ). We hypothesized that direct activation would cause rapid neoplasia and cancer progression. Pbsn-cre4Prb;PI3K mice developed widespread prostate intraepithelial hyperplasia, but stromal invasion was limited and overall progression was slower than anticipated.
View Article and Find Full Text PDFThe purpose of this symposium report is to summarize information from a session 3 oral presentation at the Society of Toxicologic Pathology Annual Symposium in Raleigh, North Carolina. Mice are genetically tractable and are likely to play an important role in elucidating environmental, genetic, and aging-related mechanisms of urinary dysfunction in men. We and others have made significant strides in developing quantitative methods for assessing mouse urinary function and our collaborators recently showed that aging male mice, like men, develop urinary dysfunction.
View Article and Find Full Text PDFLaboratory mice are used to identify causes of urinary dysfunction including prostate-related mechanisms of lower urinary tract symptoms. Effective use of mice for this purpose requires a clear understanding of molecular, cellular, anatomic, and endocrine contributions to voiding function. Whether the prostate influences baseline voiding function has not been specifically evaluated, in part because most methods that alter prostate mass also change circulating testosterone concentrations.
View Article and Find Full Text PDFBeta-catenin (CTNNB1) directs ectodermal appendage spacing by activating ectodysplasin A receptor (EDAR) transcription, but whether CTNNB1 acts by a similar mechanism in the prostate, an endoderm-derived tissue, is unclear. Here we examined the expression, function, and CTNNB1 dependence of the EDAR pathway during prostate development. hybridization studies reveal EDAR pathway components including in the developing prostate and localize these factors to prostatic bud epithelium where CTNNB1 target genes are co-expressed.
View Article and Find Full Text PDFSubperiosteal extension of a subgaleal hematoma (SGH) to the orbit is a reported, but rare complication of trauma. This report details a 13-year-old African-American male who originally presented to the emergency department after trauma with headache and was found on CT imaging to have a contained subgaleal hemorrhage. He presented 2 days later with increased pain and proptosis of the left eye with findings of decreased visual acuity, elevated intraocular pressure, proptosis, and complete external ophthalmoplegia.
View Article and Find Full Text PDFPurpose: The purpose of the current study was to assess the potential involvement of acid-sensing ion channel 1 (ASIC1) in retinal ganglion cell (RGC) death and investigate the neuroprotective effects of inhibitors of ASICs in promoting RGC survival following optic nerve crush (ONC).
Results: ASIC1 protein was significantly increased in optic nerve extracts at day 7 following ONC in rats. Activated calpain-1 increased at 2 and 7 days following ONC as evidenced by increased degradation of α-fodrin, known substrate of calpain.
Purpose: Understanding the role of mitochondria in retinal ganglion cells (RGCs) is relevant to human disease as studies have shown mitochondrial abnormalities in primary open-angle glaucoma patients. This study seeks to determine the effects of the sigma-1 receptor (σ-1r) and its agonists on mitochondrial function in oxygen- and glucose- deprived (OGD) purified neonatal RGCs.
Methods: Retinal ganglion cells were isolated from rat pups and subjected to OGD in varying conditions in the presence or absence of σ-1r agonist and antagonist and following addition of an AAV2-σ-1r vector that was used to increase σ-1r expression.
A 52-year-old woman presented with painless vision loss for 3 months. She was in custody for allegedly robbing a bank and had recently been diagnosed with paranoid schizophrenia. She had 20/100 VA OD, a 2+RAPD, and optic atrophy.
View Article and Find Full Text PDFRecently, in a poll by Research America, a significant number of individuals placed losing their eyesight as having the greatest impact on their lives more so than other conditions, such as limb loss or memory loss. When they were also asked to rank which is the worst disease that could happen to them, blindness was ranked first by African-Americans and second by Caucasians, Hispanics, and Asians. Therefore, understanding the mechanisms of disease progression in the eye is extremely important if we want to make a difference in people's lives.
View Article and Find Full Text PDFJ Orthop Sports Phys Ther
February 2016
There is a growing body of evidence surrounding the pathology and treatment of meniscal root tears. As surgical techniques are being developed and refined, rehabilitation protocols for meniscal root repairs must be defined and tested. Little information has been published regarding specific rehabilitation parameters for meniscal root repairs through all phases of rehabilitation.
View Article and Find Full Text PDFThe ionotropic glutamate receptors (iGLuR) have been hypothesized to play a role in neuronal pathogenesis by mediating excitotoxic death. Previous studies on iGluR in the retina have focused on two broad classes of receptors: NMDA and non-NMDA receptors including the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor (AMPAR) and kainate receptor. In this study, we examined the role of receptor desensitization on the specific excitotoxic effects of AMPAR activation on primary retinal ganglion cells (RGCs).
View Article and Find Full Text PDFPurpose: Glaucoma is an optic neuropathy commonly associated with elevated intraocular pressure (IOP), leading to optic nerve head (ONH) cupping, axon loss, and apoptosis of retinal ganglion cells (RGCs), which could ultimately result in blindness. Brn3b is a class-4 POU domain transcription factor that plays a key role in RGC development, axon outgrowth, and pathfinding. Previous studies suggest that a decrease in Brn3b levels occurs in animal models of glaucoma.
View Article and Find Full Text PDFSigma-1 receptor (σ-1) activation and mitogen-activated protein kinases (MAPKs) have been shown to protect retinal ganglion cells (RGCs) from cell death. The purpose of this study was to determine if σ-1 receptor stimulation with pentazocine could promote neuroprotection under conditions of an ischemia-like insult (oxygen glucose deprivation (OGD)) through the phosphorylation of extracellular signal regulated kinase (pERK)1/2. Primary RGCs were isolated from P3-P7 Sprague-Dawley rats and purified by sequential immunopanning using Thy1.
View Article and Find Full Text PDFSigma-1 receptors (σ-1rs) exert neuroprotective effects on retinal ganglion cells (RGCs) both in vivo and in vitro. This receptor has unique properties through its actions on several voltage-gated and ligand-gated channels. The purpose of this study was to investigate the role that σ-1rs play in regulating cell calcium dynamics through activated L-type Voltage Gated Calcium Channels (L-type VGCCs) in purified RGCs.
View Article and Find Full Text PDFGlaucoma is an optic neuropathy, commonly associated with elevated intraocular pressure (IOP) characterized by optic nerve degeneration, cupping of the optic disc, and loss of retinal ganglion cells which could lead to loss of vision. Endothelin-1 (ET-1) is a 21-amino acid vasoactive peptide that plays a key role in the pathogenesis of glaucoma; however, the receptors mediating these effects have not been defined. In the current study, endothelin B (ET(B)) receptor expression was assessed in vivo, in the Morrison's ocular hypertension model of glaucoma in rats.
View Article and Find Full Text PDFInvest Ophthalmol Vis Sci
July 2012
Purpose: Glaucoma is a progressive optic neuropathy characterized by loss of retinal ganglion cells (RGCs) and optic nerve degradation. Existing treatments focus on lowering IOP; however, vision loss may still progress. Neuroprotective drugs may be useful as an adjunct approach to prevent further loss of RGCs, although efficacious drugs are lacking.
View Article and Find Full Text PDFGenetic deletion or mutations of presenilin genes (PS1/PS2) cause familial Alzheimer's disease and calcium (Ca²⁺) signaling abnormalities. PS1/PS2 act as endoplasmic reticulum (ER) Ca²⁺ leak channels that facilitate passive Ca²⁺ leak across ER membrane. Studies with PS1/PS2 double knockout (PS1/PS2-DKO) mouse embryonic fibroblasts showed that PS1/PS2 were responsible for 80% of passive Ca²⁺ leak from the lumen of endoplasmic reticulum to cytosol.
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