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Purpose: Random noise-moving images (noises) can make glaucoma patients with no subjective symptoms aware of visual field abnormalities. To explore this concept, we developed a noise using computer graphics (CG) and investigated the difference in the subjective perception of visual field abnormalities between CG and conventional analog noises. Methods: We enrolled individuals with glaucoma (205 eyes), preperimetric glaucoma (PPG; 19 eyes), and normal eyes (35 eyes). For a CG noise, a series of still images was made by randomly selecting five monochromatic tones on 2-mm square dots, and these images were drawn at 60 frames per second (fps) to create a noise-moving image. The participants were asked to describe their perceived shadows on a paper. The results were categorized as follows based on the pattern deviation probability map of the Humphrey field analyzer (HFA): "agreement," "partial agreement," "disagreement," and "no response." The glaucoma stage was classified into four stages, from M1 to M4, based on the HFA's mean deviation. Result: The detection rates (agreement and partial agreement) were 80.5% and 65.4% for the CG and analog noises, respectively, with CG noise showing a significantly higher detection rate in all glaucoma eyes (P < 0.001). The detection rates tended to increase as the glaucoma stage progressed, and in Stage M3, these were 93.9% and 78.8% for the CG and analog noises, respectively. The PPG eyes did not exhibit subjective abnormalities for both noises. The specificity values were 97.1% and 100% for the CG and analog noises, respectively. Conclusion: The CG noise is more effective than the analog noise in evaluating the subjective perception of visual field abnormalities in patients with glaucoma. [ABSTRACT FROM AUTHOR]

The widespread use of tris(1,3‐dichloro‐2‐propyl) phosphate (TDCIPP) as a flame retardant has led to its release to the environment. Thus, the toxicological effects of TDCIPP on humans and animals are of importance. For better understanding of its potential toxicities, TDCIPP (250, 500, or 650 mg/kg/day) or vehicle control was administrated orally to adult male Wistar‐Imamichi rats for 7 days. After the final administration of compounds, organ weights, histopathology, blood biochemistry, and hematology were examined. Hepatic toxicity was observed at doses ≥ 500 mg/kg/day of TDCIPP, and renal toxicity was observed at 650 mg/kg/day. The anti‐androgenic activity of TDCIPP was previously confirmed in vitro and in vivo, but weights of epididymis, an androgen‐dependent organ, were not affected by TDCIPP treatment in adults. Serum alkaline phosphatase activity was significantly decreased in all TDCIPP‐treated rats independent of dose. Hemoglobin concentration, hematocrit, red blood cell count, and reticulocyte count were decreased in all TDCIPP‐treated rats, but mean corpuscular volume, total iron‐binding capacity, and serum iron were normal, suggesting that renal anemia was caused by TDCIPP. Together with previous reports on effects of anti‐androgenic substances on red blood cell indices, anemia caused by TDCIPP could be due to its anti‐androgenic activity. These considerations will contribute to further assessment of the toxicity of the compound. Tris(1,3‐dichloro‐2‐propyl) phosphate (TDCIPP) was administrated orally to adult male Wistar‐Imamichi rats for 7 days. Serum ALP activity was significantly decreased in all TDCIPP‐treated rats independent of dose. Hemoglobin concentration, hematocrit, red blood cell count, and reticulocyte count were decreased by TDCIPP, suggesting that renal anemia is possibly caused by its anti‐androgenic activity. These considerations will contribute to further assessment of the toxicity of the compound. [ABSTRACT FROM AUTHOR]

Abstract Background Although fungi have been implicated as initiating/deteriorating factors for allergic asthma, their contributing components have not been fully elucidated. We previously isolated soluble β-glucan from Candida albicans (CSBG) (Ohno et al., 2007). In the present study, the effects of CSBG exposure on airway immunopathology in the presence or absence of other immunogenic allergen was investigated in vivo, and their cellular mechanisms were analyzed both in vivo and in vitro. Methods In vivo, ICR mice were divided into 4 experimental groups: vehicle, CSBG (25 μg/animal), ovalbumin (OVA: 2 μg/animal), and CSBG + OVA were repeatedly administered intratracheally. The bronchoalveolar lavage cellular profile, lung histology, levels of cytokines and chemokines in the lung homogenates, the expression pattern of antigen-presenting cell (APC)-related molecules in the lung digests, and serum immunoglobulin values were studied. In vitro, the impacts of CSBG (0–12.5 μg/ml) on the phenotype and function of immune cells such as splenocytes and bone marrow-derived dendritic cells (BMDCs) were evaluated in terms of cell proliferation, the surface expression of APC-related molecules, and OVA-mediated T-cell proliferating activity. Results In vivo, repeated pulmonary exposure to CSBG induced neutrophilic airway inflammation in the absence of OVA, and markedly exacerbated OVA-related eosinophilic airway inflammation with mucus metaplasia in mice, which was concomitant with the amplified lung expression of Th2 cytokines and IL-17A and chemokines related to allergic response. Exposure to CSBG plus OVA increased the number of cells bearing MHC class II with or without CD80 in the lung compared to that of others. In vitro, CSBG significantly augmented splenocyte proliferation in the presence or absence of OVA. Further, CSBG increased the expression of APC-related molecules such as CD80, CD86, and DEC205 on BMDCs and amplified OVA-mediated T-cell proliferation through BMDCs. Conclusion CSBG potentiates allergic airway inflammation with maladaptive Th immunity, and this potentiation was associated with the enhanced activation of APCs including DC.

BACKGROUND: Hexabromocyclododecane (HBCD) is an additive flame retardant used in the textile industry and in polystyrene foam manufacturing. Because of its lipophilicity and persistency, HBCD accumulates in adipose tissue and thus has the potential of causing metabolic disorders through disruption of lipid and glucose homeostasis. However, the association between HBCD and obesity remains unclear. OBJECTIVES: We investigated whether exposure to HBCD contributes to initiation and progression of obesity and related metabolic dysfunction in mice fed a normal diet (ND) or a high-fat diet (HFD). METHODS: Male C57BL/6J mice were fed a HFD (62.2 kcal% fat) or a ND and treated orally with HBCD (0, 1.75, 35, or 700 µg/kg body weight) weekly from 6 to 20 weeks of age. We examined body weight, liver weight, blood biochemistry, histopathological changes, and gene expression profiles in the liver and adipose tissue. RESULTS: In HFD-fed mice, body and liver weight were markedly increased in mice treated with the high (700 µg/kg) and medium (35 µg/kg) doses of HBCD compared with vehicle. This effect was more prominent in the high-dose group. These increases were paralleled by increases in random blood glucose and insulin levels and enhancement of microvesicular steatosis and macrophage accumulation in adipose tissue. HBCD-treated HFD-fed mice also had increased mRNA levels of Pparg (peroxisome proliferator-activated receptor-γ) in the liver and decreased mRNA levels of Glut4 (glucose transporter 4) in adipose tissue compared with vehicle-treated HFD-fed mice. CONCLUSIONS: Our findings suggest that HBCD may contribute to enhancement of diet-induced body weight gain and metabolic dysfunction through disruption of lipid and glucose homeostasis, resulting in accelerated progression of obesity. 10.1289/ehp.1307421, Introduction Hexabromocyclododecane (HBCD) (for chemical structure, see Supplemental Material, Figure S1) is a brominated flame retardant (BFR) that is incorporated into plastics, electrical and electronic products, textiles, and other materials [...]