In situ temperature-compensated ultraviolet spectrophotometry to estimate nitrate and chloride concentrations in estuarine seawater with different salinity and composition.

Various methods have been proposed for in situ measurement of nitrate concentrations from the ultraviolet (UV) absorbance spectrum of seawater with stable salinity and constituents. However, salinity and temperature affect the UV absorption spectrum of seawater. In sea areas with large variability in salinity and water temperature, accurate nitrate ion concentration measurements remain challenging. We performed in situ measurements of nitrate, chloride, and bromide in estuarine seawater with different salinity compositions and applied water temperature compensation. First, the impact of water temperature on the UV absorbance of chloride, bromide, and nitrate was experimentally investigated and represented in a mathematical model. Next, chloride, bromide, and nitrate concentrations were estimated by suppressing the impact of residual components from the UV absorbance spectra of seawater using principal component regression (PCR). Hence, the chloride, bromide, and nitrate concentrations were determined by measuring the UV absorbance spectrum of seawater alone, without measuring water temperature and electrical conductivity. The proposed method was more accurate (±1.39 µM below 100 µM and ±0.90 µM below 20 µM) than the conventional method (±2.35 µM below 100 µM and ±1.88 µM below 20 µM) and PCR without water temperature compensation (±3.67 µM). In a field study, an in situ UV spectrophotometer with water temperature compensation was used to measure depth profiles of nitrate concentrations in estuarine seawater. We successfully measured the depth profiles of low chloride and high nitrate concentrations in the surface layer as well as high chloride and low nitrate concentrations in the lower layer. The proposed method enables in situ measurements of nitrate concentrations in waters with either stable or highly variable salinity and composition. Unlike conventional chemical analysis, our method can describe detailed spatiotemporal variations in nitrate concentrations.

Role of oncostatin M in the pathogenesis of vernal keratoconjunctivitis: focus on tissue remodeling.

PURPOSE: Vernal keratoconjunctivitis (VKC) is a severe and recurrent allergic conjunctivitis, the mechanism of which is not well understood. In this study, we investigated the role of oncostatin M (OSM) in the pathogenesis of VKC, with a focus on tissue remodeling. STUDY DESIGN: Clinical and experimental. PATIENTS AND METHODS: The OSM concentrations in tear fluid samples obtained from VKC patients and healthy controls were measured using ELISA, and the expression of OSM mRNA and protein in giant papillae resected from VKC patients was investigated using RT-PCR and immunohistochemistry, respectively. In cultured human conjunctival epithelial cells (HconEpiCs), expression of OSM receptor ß (OSMRß) was detected using immunocytochemical and FACS analyses. Finally, we investigated whether recombinant OSM activated STAT1 and STAT3 to induce the expression of various genes related to tissue remodeling in HconEpiCs, by using Western blot analysis, microarray analysis, and RT-PCR. RESULTS: The OSM concentration was higher in the tear fluid of VKC patients than in that of the healthy controls, and strong expression of OSM mRNA was found in the giant papillae. We also detected T cells expressing OSM in the giant papillae. In addition, HconEpiCs showed surface expression of OSMRß. Recombinant human OSM strongly activated both STAT1 and STAT3 in HconEpiCs and induced various tissue remodeling-related genes, including MMP-1, MMP-3, IL-24, IL-20, serpinB3, S100A7, tenascin C, and SOCS3. CONCLUSION: Our results suggest that OSM is one of the key molecules involved in remodeling of giant papillae in VKC.

Effects of maternal bisphenol A diglycidyl ether exposure during gestation and lactation on behavior and brain development of the offspring.

Bisphenol A diglycidyl ether (BADGE) is an epoxy resin used for the inner coating of canned food and beverages. BADGE can easily migrate from the containers and become a contaminant. In this study, we examined the effects of BADGE exposure to the dams on the behavioral, structural, and developmental abnormalities in the offspring. Female pregnant mice were fed with a diet containing BADGE (0.15 or 1.5 mg/kg/day) during gestation and lactation periods. In an open field test, the time spent in the corner area significantly increases in male mice of high-dose BADGE group at 5 weeks old. The histological analysis using offspring brain at postnatal day 1 delivered from BADGE (1.5 mg/kg/day)-treated dams demonstrates that positive signals of Forkhead box P2- and COUP-TF interacting protein 2 are restricted in each cortical layer, but not in the control brain. In addition, the maternal BADGE exposure reduces nestin-positive fibers of the radial glia and T-box transcription factor 2-positive intermediate progenitors in the inner subventricular zone. Furthermore, a direct BADGE exposure promotes neurite outgrowth and neuronal connection in the primary cultured cortical neurons. These data suggest that maternal BADGE exposure can accelerate neuronal differentiation in fetuses and induce anxiety-like behavior in juvenile mice.

Effects of Secreted Mast Cell Mediators on Retinal Pigment Epithelial Cells: Focus on Mast Cell Tryptase.

Numerous mast cells are present in the choroid, but the effects of mast cell mediators on retinal pigment epithelial (RPE) cells are not well understood. We investigated the influence of mast cell mediators on RPE cells in vitro, focusing on tryptase. Expression of receptors was examined by the reverse transcription polymerase chain reaction. We also assessed production of interleukin 8 and vascular endothelial growth factor (VEGF) after RPE cells were stimulated with mast cell mediators by using an antibody array and enzyme-linked immunosorbent assay. Furthermore, we investigated the influence of tryptase on RPE cell migration and integrity by the scratch assay and the transepithelial resistance. RPE cells expressed protease-activated receptor 2 (PAR2), histamine receptor 1, tumor necrosis factor-α (TNF-α) receptor 1, and CCR 1, 3, 4, 8, and 11. Tryptase, PAR2 agonists, histamine, and TNF-α all enhanced interleukin 8 production by RPE cells, while only tryptase enhanced VEGF production. Tryptase also enhanced expression of phosphorylated extracellular signal-regulated kinases 1/2, resulting in increased migration of RPE cells. However, tryptase did not alter epithelial integrity or the expression of zonula occludens-1 and junctional adhesion molecule-A by RPE cells. Mast cell mediators, especially tryptase, may influence RPE cell inflammation.

Two Cases of Conjunctival Amyloidosis Found as Ptosis.

Background: Amyloidosis is a spectrum of disorders characterized by the deposition of amyloid that causes severe damage to many organ systems. However, conjunctival amyloidosis is thought to be the manifestation of a local immunologic disorder and rarely affects the organ systems. We present two cases of conjunctival amyloidosis found as unilateral ptosis at initial visit. Case 1: 43-year-old-woman presented with unilateral ptosis and discomfort for the left eye. She had been treated with topical antihistamines and corticosteroids for allergic conjunctivitis. However, as symptoms persisted she was referred to us. At initial visit, unilateral ptosis, subconjunctival hemorrhage and waxy-yellow mass were found. Incisional biopsy was performed and histpathological examination revealed amyloid in the conjunctival stroma. Case 2: 31-year-old woman presented with unilateral ptosis and discomfort of palpebral superior conjunctiva in the left eye. At initial visit, the examination of the left superior palpebral conjunctiva showed waxy-yellow mass and hemorrhage. Incisional biopsy was performed and histopathological examination revealed amyloid in the conjunctival stroma. Conclusion: Unilateral ptosis may be an indication of conjunctival amyloidosis.

Photoreceptor inner and outer segment layer thickness in multiple evanescent white dot syndrome.

PURPOSE: To evaluate the photoreceptor inner and outer segment layer thickness in eyes with MEWDS. DESIGN: Prospective, non-comparative, observational case series. The follow-up duration was 4 months. METHODS: Four women were diagnosed with unilateral MEWDS. The ages of the patients were 25, 24, 35, and 40 years. The retinal microstructure was assessed by spectral-domain optical coherence tomography (SD-OCT). The thickness of the photoreceptor inner (IS) and outer (OS) segments and sum of them (IS + OS) at the fovea were analyzed. RESULTS: The visual acuity was reduced in three of four eyes at the acute phase. SD-OCT showed that the border of IS and OS (IS/OS) line and the cone outer segment tips (COST) line in the macula area were not detected in all four eyes. The IS + OS thickness was 50.3 ± 5.6 µm and that of the healthy fellow eyes was 73.5 ± 7.0 µm (n = 4 eyes). The thickness of the IS was 27.8 ± 2.6 µm and that of the OS was 45.8 ± 7.3 µm. In all eyes, there was a spontaneous improvement of the visual acuity. SD-OCT showed a recovery of only the IS/OS line in the macular area, but the COST line was not visible in three cases. The mean IS + OS thickness increased to 56.0 ± 7.9 µm (n = 4), IS = 26.0 ± 2.0 µm (n = 3), and OS = 30.1 ± 8.7 µm (n = 3) in the early recovery phase, and to 64.8 ± 9.3 µm (n = 4), IS = 28.5 ± 1.7 µm (n = 4), and OS = 36.3 ± 7.9 µm (n = 4) in the late recovery phase. The mean inner and outer segment thickness remained unchanged in the fellow eyes. CONCLUSION: Eyes with MEWDS have changes in the photoreceptor microstructures. The change in the IS + OS thickness during the natural recovery course might be due to an increase in the OS length.