PURPOSE: To evaluate the efficacy and complication of autologous plasmin (AP) injected before vitrectomy for rhegmatogenous retinal detachment (RRD). METHODS: Intravitreal AP injection (0.2 ml) was performed on the eyes without posterior vitreous detachment (PVD) 20 minutes before the vitrectomy for RRD. The extent of PVD was evaluated intraoperatively. Surgical PVD induction was performed and the ease of the procedure was graded. The extent of PVD, ease of PVD induction, and complications (including incidence of iatrogenic retinal break) were compared to those of the control eyes. In order to evaluate complications and measure activated partial thromboplastin time, a microbial culture of injected AP was performed and the rate of postoperative intraocular hemorrhage was investigated. Change in visual acuity and the rate of retinal reattachment were compared in order to evaluate the long-term surgical outcome. RESULTS: The extent of PVD was greater in the AP group than in the control group, and vitreal separation was facilitated by intravitreal AP injection. However, ease of PVD induction and frequency of iatrogenic retinal break found were not significantly different between cases and controls. Neither postoperative intraocular hemorrhage nor systemic coagulation abnormality occurred. Postoperative endophthalmitis and positive microbial culture of the AP solution were also not reported. There was no significant difference in the change in visual acuity and the rate of retinal reattachment between the two groups. CONCLUSIONS: Intravitreal AP injection can facilitate vitrectomy for RRD and has no effect on the rate of retinal reattachment.
Endophthalmitis ; Eye ; Fibrinolysin ; Hemorrhage ; Incidence ; Partial Thromboplastin Time ; Retinal Detachment ; Retinal Perforations ; Retinaldehyde ; Visual Acuity ; Vitrectomy ; Vitreous Detachment

This study aims to explore the impact of distributional changes in coronavirus disease 2019 (COVID-19) infection fear with sex differences. A quota sampling strategy was followed and 483 Korean adults were surveyed in a community sample. Self-report questionnaires were used to assess COVID-19 infection fear, depressive symptoms, and general characteristics.Quantile regression was used to explore the regression relationship of COVID-19 infection fear and an individual’s sex. There was a significant difference in COVID-19 infection fear (P= 0.001) and depression (P = 0.008) between the sexes - male and female. The differences between sexes at the 20th and 30th percentiles were significant (β = 2.04, P = 0.006; β = 1.5, P = 0.004, respectively). The results demonstrate that sex significantly predicts COVID-19 infection fear and women had significantly greater fear than men in the mild-level of COVID-19 infection fear.

Peroxisome proliferator-activated receptor gamma (PPARgamma) was identified as a cell-intrinsic regulator of Th17 cell differentiation. Th17 cells have been associated with several autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE), inflammatory bowel disease (IBD), and collagen-induced arthritis. In this study, we confirmed PPARgamma-mediated inhibition of Th17 cell differentiation and cytokine production at an early stage. Treatment with ciglitazone, a PPARgamma ligand, reduced both IL-1beta-mediated enhancement of Th17 differentiation and activation of Th17 cells after polarization. For Th17 cell differentiation, we found that ciglitazone-treated cells had a relatively low proliferative activity and produced a lower amount of cytokines, regardless of the presence of IL-1beta. The inhibitory activity of ciglitazone might be due to decrease of CCNB1 expression, which regulates the cell cycle in T cells. Hence, we postulate that a pharmaceutical PPARgamma activator might be a potent candidate for treatment of Th17-mediated autoimmune disease patients.
Arthritis, Experimental ; Autoimmune Diseases ; Cell Cycle ; Cell Proliferation ; Cytokines ; Encephalomyelitis, Autoimmune, Experimental ; Humans ; Inflammatory Bowel Diseases ; Interleukin-17 ; PPAR gamma* ; T-Lymphocytes ; Th17 Cells*