No abstract

Using an extremely OSI versus a conventional sclerotomy incision reduces the incidence of wound leakage postoperatively because of its self-sealing effect. Other factors that contribute to wound leakage, such as increased surgical duration and nonmacular diagnosis, may be indirect measurements of extensive trocar rotation, causing wound leakage despite the use of an OSI.

Level IV, case series.

In neurons, intracellular membrane rafts are essential for specific actions of brain-derived neurotrophic factor (BDNF), which include the regulation of axon outgrowth, growth cone turning and synaptic transmission. Virtually all the actions of BDNF are mediated by binding to its receptor, TrkB. The association of TrkB with the tyrosine kinase, Fyn, is critical for its localization to intracellular membrane rafts. Here, we show that synapsins, a family of highly amphipathic neuronal phosphoproteins, regulate membrane raft lipid composition and consequently, the ability of BDNF to regulate axon/neurite development and potentiate synaptic transmission. In the brains of mice lacking all synapsins, the expression of both BDNF and TrkB were increased, suggesting that BDNF/TrkB-mediated signaling is impaired. Consistent with this finding, synapsin-depleted neurons exhibit altered raft lipid composition, deficient targeting of Fyn to rafts, attenuated TrkB activation, and abrogation of BDNF-stimulated axon outgrowth and synaptic potentiation. Conversely, overexpression of synapsins in neuroblastoma cells results in corresponding reciprocal changes in raft lipid composition, increased localization of Fyn to rafts, and promotion of BDNF-stimulated neurite formation. In the presence of synapsins, the ratio of cholesterol to estimated total phospholipids converged to 1, suggesting that synapsins act by regulating the ratio of lipids in intracellular membranes, thereby promoting lipid raft formation. These studies reveal a mechanistic link between BDNF and synapsins, impacting early development and synaptic transmission.

Strongyloidiasis is caused by the nematode Strongyloides stercoralis. The parasite has a unique life cycle that enables it to cause a hyperinfection syndrome in which pulmonary involvement is characteristic. We describe the case of a 68-yr-old Hispanic male from Puerto Rico with disseminated strongyloidiasis who developed intense granulomatous reaction in the lung associated with interlobular septal fibrosis. Granulomatous lung disease leading to fibrosis within the lung has been well demonstrated in schistosomiasis, another parasitic disease. This case represents the first report, as far as we are aware, of fibrosis within the lung and restrictive pulmonary disease in association with Strongyloides stercoralis.

Proliferative diabetic retinopathy is a potentially blinding sequela of uncontrolled diabetes that involves a complex interaction of pro-angiogenic and inflammatory pathways. In this study, we compared the levels of pro-angiogenic arachidonic acid-derived mediators in human vitreous humor obtained from eyes with high-risk proliferative diabetic retinopathy versus controls. The results indicated that lipoxygenase and cytochrome P450-derived eicosanoids were elevated (5-HETE, 12-HETE, 20-HETE, and 20-COOH-AA), and there appeared to be no differences in levels measured in eyes with tractional retinal detachments versus those without. These results provide further insight into the pathogenesis of this disease and for the development of future potential therapeutic agents that target arachidonic acid metabolites to treat diabetic retinopathy.

Objective Reasons for variations in atherosclerotic burden among individuals with similar levels of obesity are poorly understood, especially in African Americans (AA). This study examines whether high-sensitivity C-reactive protein (hsCRP) is useful for discriminating between benign and high-risk obesity phenotypes for subclinical atherosclerosis in AAs. Approach and Results Participants from the Jackson Heart Study (n=4682) were stratified into four phenotypes based on the presence of NHLBI definition of obesity or obesity-equivalent (BMI ≥30 or BMI 25-30 with waist circumference >102cm in men and >88cm in women) and inflammation by hsCRP ≥2 mg/L. Using multivariate regression models, we conducted cross-sectional analyses of the association between inflammatory obesity phenotypes and subclinical atherosclerosis determined by carotid intima-media thickness (cIMT) or coronary artery calcium scores (CAC). Gender specific analyses were conducted given significant interaction for gender (p=0.03). The prevalence of obesity or equivalent was 65%, of which 30% did not have inflammation. Conversely, 37% of non-obese individuals had inflammation. Among non-obese men, hsCRP ≥2mg/L identified a subset of individuals with higher cIMT (Adjusted-mean-difference= 0.05, 95% CI 0.02, 0.08 mm) compared to their non-inflammatory counterparts. Among obese men, hsCRP <2mg/L identified a subset of individuals with lower CAC compared to their inflammatory counterparts. Among women, associations between hsCRP and cIMT or CAC were not found. Conclusions In the largest AA population-based cohort to date, hsCRP was useful in identifying a subset of non-obese men with higher cIMT, but not in women. hsCRP did not identify a subset of obese individuals with less subclinical atherosclerosis.

Neoplastic infiltration of primary idiopathic myelofibrosis into the eye and surrounding structures, which is scantly described in the current literature, may be an early sign of new onset or relapsing primary myelofibrosis. Chemotherapy can be very effective in the ultimate treatment and remission of these ocular symptoms.