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Background: Atopic dermatitis (AD) is characterized by defective skin barrier and imbalance in T helper 1/T helper 2 (Th1/Th2) cytokine expression. Filaggrin (FLG) is the key protein to maintaining skin barrier function. Recent studies indicated that Th1/Th2 cytokines influence FLG expression in keratinocytes. However, the role of Th1/Th2 cytokines on FLG processing is not substantially documented. Our aim was to investigate the impact of Th1/Th2 cytokines on FLG processing. Methods: HaCaT cells and normal human keratinocytes were cultured in low and high calcium media and stimulated by either interleukin (IL)-4, 13 or interferon-γ (IFN-γ). FLG, its major processing proteases and key protease inhibitor lymphoepithelial Kazal-type-related inhibitor (LEKTI) were measured by both real-time quantitative polymerase chain reaction and Western blotting. Their expression was also evaluated in acute and chronic AD lesions by immunohistochemistry. Results: IL-4/13 significantly reduced, while IFN-γ significantly up-regulated FLG expression. IL-4/13 significantly increased, whereas IFN-γ significantly decreased the expression of kallikreins 5 and 7, matriptase and channel-activating serine protease 1. On the contrary, IL-4/13 significantly decreased, while IFN-γ increased the expression of LEKTI and caspase-14. Similar trends were observed in AD lesions. Conclusions: Our results suggested that Th1/Th2 cytokines differentially regulated the expression of major FLG processing enzymes. The imbalance between Th1 and Th2 polarized immune response seems to extend to FLG homeostasis, through the network of FLG processing enzymes.

It was well known that tangential vitreoretinal traction and epiretinal membrane play important roles during the formation of macular hole (MH) associated with retinal detachment (RD) in highly myopic eyes. But it was not clear about the correlations between anteroposterior traction, posterior vitreous cortex (PVC) and MH-RD. The vitreous status in highly myopic eyes were analyzed to explore the effect of PVC in the role of MH-RD formation.Sixteen consecutive highly myopic eyes with RD due to MH were retrospectively analyzed from January 2009 to April 2009. The preoperative examinations for detecting posterior vitreous detachment (PVD) and vitreoretinal traction included B-mode ultrasonography and optical coherence tomography (OCT). The residual PVC and PVD were confirmed intraoperatively during triamcinolone acetonide (TA) assisted vitrectomy.Under ultrasonography, the preoperative PVD patterns were stratified as: complete PVD in three (19%) eyes, partial PVD in eight (50%) eyes, and no PVD in five (31%) eyes. OCT confirmed vitreoretinal traction and no complete PVD in 10 (63%) eyes, including anteroposterior traction in four eyes and tangential traction in six eyes. During TA-assisted vitrectomy, it was confirmed that no complete PVD existed in 16 eyes, including six eyes (38%) finally diagnosed of partial PVD, and five (31%) eyes with vitreoschisis. Anteroposterior vitreoretinal traction around MH is always in conjunction with partial PVD (67%), and high proportion (80%) of vitreoschisis is associated with tangential vitreoretinal traction. Comparing with the precision of TA staining of PVD diagnosis, the coincidence rate of ultrasonography was 69% (P = 0.02), and that of OCT was 63% (P0.01).The residual PVC due to partial PVD or vitreoschisis may cause the anteroposterior or tangential traction of macular area, which contributes to the formation of MH and subsequent RD in highly myopic eyes. And it is necessary to realize the vitreoretinal relationship and assess the status of PVC synthetically for surgery by combined ultrasonography and OCT preoperatively and TA staining intraoperatively.

Idiopathic choroidal neovascularization (ICNV) is an uncommon disorder affecting primarily individuals younger than the age of 50 years. In CNV patients, no apparent cause can be determined. This study aimed to evaluate the functional and morphological change of the retina with ICNV in young adults.In this retrospective study, 32 eyes of 32 patients with subfoveal or juxta/extra foveal ICNV had been admitted into the Shanghai First People's Hospital from January 2009 to July 2010. The functional changes were evaluated using the best corrected visual acuity (BCVA) and the microperimetry in the macular area. The morphology changes were evaluated using optical coherence tomography (OCT), the color fundus photography and the fluorescein angiography.Seventeen patients with juxta/extra foveal and 15 subfoveal CNV were investigated. The mean logarithm of the minimum angle of resolution (LogMAR) BCVA was 0.39, the mean central retinal thickness (CRT) was 334 µm, and the mean sensitivity (MS) was 11.8 decibels (dB). In the subfoveal group, there was a strong correlation between CRT and BCVA (r = -0.675, F = 2.167, P0.01); as well as that between CRT and MS (r = -0.681, F = 22.91, P0.01). While in the juxta/extra foveal CNV group, the correlation of CRT and BCVA was not significant (r = -0.071, F = 1.018, P0.05); neither was the correlation of CRT and MS (r = -0.142, F = 36.54, P0.05). The microperimetry (MP-1) test revealed 17 (53%) patients with stable fixation, 9 (28%) with relatively unstable and 6 (19%) with unstable fixation. Fixation stability correlated positively with sensitivity in the central 2° diameter area (r = 0.380, F = 3.213, P0.05) and the duration of symptoms (r = 0.401, F = 7.933, P0.05).ICNV was associated with reduced total MS, unstable fixation and eccentric fixation. These findings emphasized functional change in ICNV is beyond the BCVA and regular morphology change, which provided additional information of functional evaluation in clinical practice.

Trans-arachidonic acids (TAAs), newly discovered markers of nitrative stress and the major products of nitrogen dioxide (NO2(·))-mediated isomerization of arachidonic acid (AA), represent a new mechanism of NO2(·)-induced toxicity. It has been reported that TAAs were generated in oxygen-induced microvascular degeneration model and TAAs were also generated in a diabetic retinopathy (DR) model. In this study, we examined high glucose-induced nitrative stress damage and TAAs levels and explored the possible mechanisms for DR caused by reactive nitrogen species.Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ) at 60 mg/kg. Bovine retinal capillary endothelial cells (BRECs) were selectively cultured and incubated with normal or high glucose. The serum TAAs and AA in diabetic rats were measured by the gas chromatography and mass spectrometry (GC/MS) method. The ratio of peak area of TAAs to AA with selected ion of 79 was estimated by a group t-test. Thrombospondin-1 (TSP-1) in the rat retinas and BRECs extracts were examined by Western blotting. The phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) protein was examined by Western blotting in BRECs incubated with high glucose.The TAAs to AA ratio (TAAs/AA) was significantly increased in the serum at 8, 12 and 16 weeks after STZ injection (P0.05), with no noticeable change found at 2 or 4 weeks (P0.05). Expression of TSP-1 in the retina of diabetic rats was progressively elevated according to the duration of diabetes. TSP-1 expression was increased in BRECs incubated with high glucose at 48 hours. Moreover, high glucose also increased ERK1/2 expression, which peaked at 30 minutes and then decreased in the following 48 hours.An elevation of TAAs/AA is associated with high glucose-induced nitrative stress, which probably involves upregulation of TSP-1 through activating ERK1/2.