Faculty Bibliography

Abnormal serum lipid levels significantly increase the risk for cardiovascular disease. Furthermore, abnormal compositions of cholesterol in glandular secretions have been hypothesized as an etiology for meibomian gland dysfunction, yet this relationship has not been well studied in clinical settings. The primary purpose of this study was to determine if there is an association between dyslipidemia and meibomian gland dysfunction (MGD). The secondary purpose was to identify the factors, if any, that play a role in this association. A case-control study was performed between October 2013 and February 2015 which recruited 109 patients with MGD and 115 control patients without MGD. All participants were of Indian descent and had no history of dyslipidemia. Basic demographic information was collected as well as fasting levels of serum glucose, creatinine, triglycerides, total cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL). To calculate differences between groups, Z test or Student t test were used. A stepwise logistic regression model was used to calculate the estimates of odds ratios (ORs), where MGD was the dependent variable, making the independent variables consist of sex, age, body mass index (BMI), triglycerides ≥150 mg/dL, total cholesterol ≥200 mg/dL, LDL ≥130 mg/dL, or HDL ≤40 mg/dL, serum glucose, and serum creatinine. Dyslipidemia, defined by either a fasting total cholesterol level of ≥ 200 mg/dL, triglycerides ≥150 mg/dL, LDL ≥130 mg/dL, or HDL ≤40 mg/dL, was detected in 70 cases (64 %) and 21 controls (18 %), P < 0.001. Mean levels of triglycerides, total cholesterol, LDL, and HDL were 98.5 ± 42.1, 203.1 ± 13.2, 126.1 ± 10.2, and 53.3 ± 4.2 mg/dL, respectively, in cases and 82.3 ± 36.5, 156.6 ± 14.5, 92.2 ± 12.4, 45.8 ± 2.6 mg/dL, respectively, in controls. All differences were statistically significant (P < 0.05). MGD was significantly associated with age >65 years (OR 2.1; 95 % CI 1.2-3.2, P = 0.04), serum triglyceride concentration ≥150 mg/dL (OR 3.2; 95 % CI 1.9-4.4; P = 0.03), total cholesterol ≥200 mg/dL (OR 14.3; 95 % CI 8.2-20.7, P < 0.01), and LDL ≥130 mg/dL (OR 9.1; 95 % CI 6.6-13.2, P < 0.01). Adults from northern rural India with MGD are more likely to have abnormal serum lipid levels compared to age- and sex-matched adults without MGD. Eye care providers may have a role in discovering undiagnosed dyslipidemia, an important risk factor for cardiovascular illness.

IMPORTANCE/OBJECTIVE:This study shows that relocation of an academic ophthalmology residency program from an inpatient to an outpatient setting in western New York does not affect the consult volume but affects management patterns and follow-up rates. OBJECTIVE:To investigate the effects on the ophthalmology consultation service of an academic program with relocation from a Regional Level-1 Trauma center to an outpatient facility. DESIGN/METHODS:Consultation notes from 3 years before and 3 years after the University at Buffalo's (UB) Department of Ophthalmology relocation from a Regional Level-1 Trauma center (Erie County Medical Center) to an outpatient facility (Ross Eye Institute) were obtained from hospital electronic medical records and analyzed. SETTING/METHODS:Hospitalized care and institutional practice. PARTICIPANTS/METHODS:All inpatient or Emergency Room Ophthalmology consultation patients from the Department of Ophthalmology at UB from 2004 to 2010 (1,379 patients). EXPOSURES/METHODS:None, this was a retrospective chart review. MAIN OUTCOME MEASURES/METHODS:Patient demographics, reason for consult, diagnoses, and ophthalmic procedures performed by the UB Department of Ophthalmology before and after its relocation. RESULTS:Relocation to the outpatient facility did not affect consult volume (P=0.15). The number of consults focusing on ophthalmic conditions, as a percentage of the yearly total, rose 460% (P=0.0001), while systemic condition consults with ocular manifestations fell 83% (P=0.0001). Consults for ocular trauma decreased 65% (P=0.0034). Consults ending with a diagnosis of "normal exam" fell, as a percentage of the yearly total (56%, P=0.0023), while diagnoses of new ocular conditions rose 17% (P=0.00065). The percentage of consults for Medicaid patients fell 12% (P=0.0001), while those for privately insured patients rose 15% (P=0.0001). The number of ophthalmic procedures did not change, but postconsult patient follow-up fell from 23% at the Erie County Medical Center clinic to 2% after the move to Ross Eye Institute, a ≥97% decrease. CONCLUSION AND RELEVANCE/CONCLUSIONS:Relocation of UB's academic Ophthalmology program from an inpatient department to an outpatient facility had no effect on its consultation patient or procedure volume, but it significantly affected the nature of consult diagnoses and decreased outpatient follow-up by >90% at the latter location. Many hospitals are creating separate outpatient facilities that may experience similar obstacles.

Corneal endothelial cells form a leaky barrier on the posterior surface of the cornea, allowing influx of nutrient-carrying aqueous humor through the paracellular space and efflux of excess fluid. Corneal edema arises when the density of these non-proliferative endothelial cells declines from endothelial disease or intraocular surgery. The cellular changes occurring at low densities are ill-defined. We therefore investigated the paracellular pathway of corneal endothelial cell monolayers of varying density to determine alterations occurring in paracellular permeability and monolayer morphology. Primary cultures of bovine corneal endothelial cells (BCECs) were passaged onto permeable supports under varying culture conditions to obtain confluent monolayers of <1000, 1000-1999 and >2000 cells/mm(2). Culture growth was monitored by transendothelial electrical resistance measurements. Diffusional permeability to sodium fluorescein, FITC-dextran MW 4000 or FITC-dextran MW 20,000 was measured. Confluent cultures were also analyzed by immunofluorescence localization of the tight junction protein ZO-1 and by transmission electron microscopy. For comparison, we evaluated ZO-1 for low and high density human corneal endothelium. Our results showed that all BCEC cultures grew to the same final transendothelial electrical resistance regardless of final density. In the diffusional permeability assay, permeability increased significantly only for the smallest tracer molecule (sodium fluorescein) in the lowest density monolayers (<1000 cells/mm(2)). ZO-1 immunofluorescence distinctly localized to intercellular junctions in high density BCEC cultures but had more diffuse localization at lower densities. Transmission electron microscopy imaging revealed cells with thinner cross-sectional profiles and longer overlapping intercellular processes at low density relative to high density cultures. Low density human corneal endothelium lacked the diffuse ZO-1 distribution seen in BCECs. Our data supports the hypothesis that barrier integrity is the primary function disrupted in low density corneal endothelial monolayers and contradicts the idea of a linear decline in barrier function with decreasing cell density.

Autism causes neuropathological changes in varied anatomical loci. A coherent neural mechanism to explain the spectrum of autistic symptomatology has not been proposed because most anatomical researchers focus on point-to-point functional neural systems (e.g., auditory and social networks) rather than considering global chemical neural systems. Serotonergic neurons have a global innervation pattern. Disorders Research Program, AS073234, Program Project (JW). Their cell bodies are found in the midbrain but they project their axons throughout the neural axis beginning in the fetal brain. This global system is implicated in autism by animal models and by biochemical, imaging, pharmacological, and genetics studies. However, no anatomical studies of the 5-HT innervation of autistic donors have been reported. Our review presents immunocytochemical evidence of an increase in 5-HT axons in postmortem brain tissue from autism donors aged 2.8-29 years relative to controls. This increase is observed in the principle ascending fiber bundles of the medial and lateral forebrain bundles, and in the innervation density of the amygdala and the piriform, superior temporal, and parahippocampal cortices. In autistic donors 8 years of age and up, several types of dystrophic 5-HT axons were seen in the termination fields. One class of these dystrophic axons, the thick heavily stained axons, was not seen in the brains of patients with neurodegenerative diseases. These findings provide morphological evidence for the involvement of serotonin neurons in the early etiology of autism, and suggest new therapies may be effective to blunt serotonin's trophic actions during early brain development in children

Imaging studies of serotonin transporter binding or tryptophan retention in autistic patients suggest that the brain serotonin system is decreased. However, treatment with drugs which increase serotonin (5-HT) levels, specific serotonin reuptake inhibitors (SSRIs), commonly produce a worsening of the symptoms. In this study we examined 5-HT axons that were immunoreactive to a serotonin transporter (5-HTT) antibody in a number of postmortem brains from autistic patients and controls with no known diagnosis who ranged in age from 2 to 29 years. Fine, highly branched, and thick straight fibers were found in forebrain pathways (e.g. medial forebrain bundle, stria terminalis and ansa lenticularis). Many immunoreactive varicose fine fibers were seen in target areas (e.g. globus pallidus, amygdala and temporal cortex). Morphometric analysis of the stained axons at all ages studied indicated that the number of serotonin axons was increased in both pathways and terminal regions in cortex from autism donors. Our findings provide morphological evidence to warrant caution when using serotonin enhancing drugs (e.g. SSRIs and receptor agonist) to treat autistic children. This article is part of a Special Issue entitled 'Trends in neuropharmacology: in memory of Erminio Costa'