Evaluation of the vitreous microbial contamination rate in office-based three-port microincision vitrectomy surgery using Retrector technology

Background: To perform a microbiological contamination analysis of the vitreous during office-based micro-incision vitrectomy surgery (MIVS) assessing whether the bacteria detected correlated with patient's ocular conjunctival flora. Methods: This is a prospective, interventional, nonrandomized case series of patients undergoing office-based MIVS, anti-VEGF, and dexamethasone intravitreal injections (triple therapy) for the treatment of wet age-related macular degeneration (AMD) and diabetic macular edema (DME). All patients were operated at a small procedure room in an ambulatory clinic of the Department of Ophthalmology, University of Montreal, Quebec, Canada. Conjunctival samples were done before placing the sclerotomies. The MIVS was done with a 23-gauge retractable vitrector, a 27-gauge infusion line, and a 29-gauge chandelier. Undiluted and diluted vitreous were collected for aerobic, anaerobic and fungal cultures. Outcomes measured were bacterial species identification within samples collected from the conjunctiva and the vitreous. Results: Thirty-seven patients (37 eyes) were recruited and completed over 17 months of follow-up. Twenty-eight had wet AMD and nine had DME. There were 13 men and 24 women, with a mean age of 78 years. Eighteen patients (46%) had culture positive conjunctival flora. Twenty-six bacterial colonies were tabulated in total from the conjunctival swabs. All bacteria detected were gram-positive bacteria (100%), most commonly: Staphylococcus epidermitis in 11 (42%) and Corynebacterium sp. in 6 (23%). Only 1/18 patients had more than 3 species isolated, 6/18 patients had 2 species and 11/18 patients had 1 species identified on the conjunctival swab. Only 1 of the 37 undiluted midvitreous samples was culture positive, equating to a contamination rate of 2.7%. None of the diluted vitreous samples were culture positive. All cultures were negative for fungus. No serious postoperative complications occurred, including bacterial endophthalmitis, choroidal detachment, and retinal detachment. Conclusion: This preliminary study of office-based MIVS gives us insights on the ocular surface microbial profile and vitreous contamination rate of performing such procedures outside the OR-controlled environment. Our initial results seem to indicate that there is little risk of bacterial translocation and contamination from the conjunctiva into the vitreous. Therefore, if endophthalmitis occurs post-operatively, the source may likely arise after the procedure. Larger studies are needed to confirm our data

In Vivo Comparison of 23-and 25-Gauge Sutureless Vitrectomy Incision Architecture Using Spectral Domain Optical Coherence Tomography

Purpose. To investigate the in vivo incision architecture using spectral domain optical coherence tomography (SD-OCT) in 23-gauge and 25-gauge transconjunctival sutureless pars plana vitrectomy (TSPPV). Methods. A prospective observational study of 22 eyes of 22 patients that underwent three-port 25-gauge (10 eyes) or 23-gauge (12 eyes) TSPPV was performed. the three sclerotomies sites in each eye were analyzed by Corneal Adapter Model (CAM) RTVue SD-OCT (Optovue Inc., Fremont, CA, USA) with wound cross-section images (longitudinal and transversal) on days 1, 7, and 30 postoperatively. Transversal and longitudinal length, location, angle between the conjunctival surface tangent and the incision plane, and architecture deformations were evaluated. Results. All patients (22 eyes) completed the study and surgeries lasted less than 60 minutes. All wounds were obliquely performed, 23-gauge mean angle was 23 +/- 5 degrees, and 25-gauge angule was 21 +/- 4 degrees. Twenty-three-gauge sclerotomy transversal mean length was 1122 +/- 242 mu m and 25-gauge transversal sclerotomy mean length was 977 +/- 174 mu m; 23-gauge longitudinal mean length was 363 +/- 42 mu m and 25-gauge longitudinal sclerotomy mean length was 234 +/- 19 mu m; 23-gauge open wound thickness mean was 61 +/- 28 mu m and 25-gauge open wound thickness mean was 22 +/- 6 mu m. All results were statistically significant (P < 0.05). No vitreous incarceration or silicone oil residue was observed in incision sites with both gauges. Conclusions. the 23-gauge and 25-gauge architectural wound constructions were well visualized using CAM SD-OCT. Statistical differences between the two gauges were observed throughout the study period.Teixeira Oftalmol, BR-70392901 Brasilia, DF, BrazilUniversidade Federal de São Paulo, Dept Ophthalmol, São Paulo, BrazilUniv Catolica Brasilia, Dept Ophthalmol, Brasilia, DF, BrazilUniv Montreal, Dept Ophthalmol, Hop Maisonneuve Rosemont, Montreal, PQ, CanadaPontificia Univ Catolica Rio de Janeiro, Dept Ophthalmol, Rio de Janeiro, RJ, BrazilUniv Illinois, Dept Ophthalmol, Chicago, IL 60680 USAUniversidade Federal de São Paulo, Dept Ophthalmol, São Paulo, BrazilWeb of Scienc

Profile of Producers and Production of Dry-Aged Beef in Brazil

No information is currently available on the profile of producers and production process of dry-aged beef in Brazil, to the best of the authors’ knowledge. We surveyed 37 Brazilian companies that were producing dry-aged beef in 2020 to investigate this market. The absolute and relative frequency of responses was calculated to obtain the sum, average, minimum, and maximum values. From the respondents, dry-aged beef was first produced in 2009, and most producers are located in big cities. Most respondents control and monitor chamber temperature; however, humidity and air velocity only are monitored. The aging period (mostly between 22 to 60 days) was the main indicator of product readiness. The process losses (water loss and crust trimming) can reach 65%. Some producers perform microbiological analyses to ensure product safety and others use tools such as GMP and SOP. The results of this survey may help governmental institutions to develop a standardized industrial protocol for producing dry-aged beef in Brazil

Neuron-Derived Semaphorin 3A Is an Early Inducer of Vascular Permeability in Diabetic Retinopathy via Neuropilin-1

SummaryThe deterioration of the inner blood-retinal barrier and consequent macular edema is a cardinal manifestation of diabetic retinopathy (DR) and the clinical feature most closely associated with loss of sight. We provide evidence from both human and animal studies for the critical role of the classical neuronal guidance cue, semaphorin 3A, in instigating pathological vascular permeability in diabetic retinas via its cognate receptor neuropilin-1. We reveal that semaphorin 3A is induced in early hyperglycemic phases of diabetes within the neuronal retina and precipitates initial breakdown of endothelial barrier function. We demonstrate, by a series of orthogonal approaches, that neutralization of semaphorin 3A efficiently prevents diabetes-induced retinal vascular leakage in a stage of the disease when vascular endothelial growth factor neutralization is inefficient. These observations were corroborated in TgCre-Esr1/Nrp1flox/flox conditional knockout mice. Our findings identify a therapeutic target for macular edema and provide further evidence for neurovascular crosstalk in the pathogenesis of DR

MicroRNA signatures in vitreous humour and plasma of patients with exudative AMD

Age-related macular degeneration (AMD) is a leading cause of blindness worldwide affecting individuals over the age of 50. The neovascular form (NV AMD) is characterized by choroidal neovascularization (CNV) and responsible for the majority of central vision impairment. Using non-biased microRNA arrays and individual TaqMan qPCRs, we profiled miRNAs in the vitreous humour and plasma of patients with NV AMD. We identified a disease-associated increase in miR-146a and a decrease in miR-106b and miR-152 in the vitreous humour which was reproducible in plasma. Moreover, miR-146a/miR-106b ratios discriminated patients with NV AMD with an area under the Receiver Operating Characteristic curve (ROC AUC) of 0,977 in vitreous humour and 0,915 in plasma suggesting potential for a blood-based diagnostic. Furthermore, using the AMD Gene Consortium (AGC) we mapped a NV AMD-associated SNP (rs1063320) in a binding site for miR-152-3p in the HLA-G gene. The relationship between our detected miRNAs and NV AMD related genes was also investigated using gene sets derived from the Ingenuity Pathway Analysis (IPA). To our knowledge, our study is the first to correlate vitreal and plasma miRNA signatures with NV AMD, highlighting potential future worth as biomarkers and providing insight on NV AMD pathogenesis

Retinal lipid and glucose metabolism dictates angiogenesis through the lipid sensor Ffar1

Tissues with high metabolic rates often use lipids, as well as glucose, for energy, conferring a survival advantage during feast and famine1. Current dogma suggests that high-energy–consuming photoreceptors depend on glucose2, 3. Here we show that the retina also uses fatty acid β-oxidation for energy. Moreover, we identify a lipid sensor, free fatty acid receptor 1 (Ffar1), that curbs glucose uptake when fatty acids are available. Very-low-density lipoprotein receptor (Vldlr), which is present in photoreceptors4 and is expressed in other tissues with a high metabolic rate, facilitates the uptake of triglyceride-derived fatty acid5, 6. In the retinas of Vldlr−/− mice with low fatty acid uptake6 but high circulating lipid levels, we found that Ffar1 suppresses expression of the glucose transporter Glut1. Impaired glucose entry into photoreceptors results in a dual (lipid and glucose) fuel shortage and a reduction in the levels of the Krebs cycle intermediate α-ketoglutarate (α-KG). Low α-KG levels promotes stabilization of hypoxia-induced factor 1a (Hif1a) and secretion of vascular endothelial growth factor A (Vegfa) by starved Vldlr−/− photoreceptors, leading to neovascularization. The aberrant vessels in the Vldlr−/− retinas, which invade normally avascular photoreceptors, are reminiscent of the vascular defects in retinal angiomatous proliferation, a subset of neovascular age-related macular degeneration (AMD)7, which is associated with high vitreous VEGFA levels in humans. Dysregulated lipid and glucose photoreceptor energy metabolism may therefore be a driving force in macular telangiectasia, neovascular AMD and other retinal diseases