735 research outputs found

    Quick Models for Saccade Amplitude Prediction

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    This paper presents a new saccade amplitude prediction model. The model is based on a Kalman filter and regression analysis. The aim of the model is to predict a saccade’s am-plitude extremely quickly, i.e., within two eye position samples at the onset of a saccade. Specifically, the paper explores saccade amplitude prediction considering one or two sam-ples at the onset of a saccade. The models’ prediction performance was tested with 35 subjects. The amplitude accuracy results yielded approximately 5.26° prediction error, while the error for direction prediction was 5.3% for the first sample model and 1.5% for the two samples model. The practical use of the proposed model lays in the area of real-time gaze-contingent compression and extreme eye-gaze aware interaction applications. The paper provides theoretical evaluation of the benefits of saccade amplitude prediction to the gaze-contingent multimedia compression, estimating a 21% improvement in com-pression for short network delays

    VEGFR2 but not VEGFR3 governs integrity and remodeling of thyroid angiofollicular unit in normal state and during goitrogenesis

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    Thyroid gland vasculature has a distinguishable characteristic of endothelial fenestrae, a critical component for proper molecular transport. However, the signaling pathway that critically governs the maintenance of thyroid vascular integrity, including endothelial fenestrae, is poorly understood. Here, we found profound and distinct expression of follicular epithelial VEGF-A and vascular VEGFR2 that were precisely regulated by circulating thyrotropin, while there were no meaningful expression of angiopoietin-Tie2 system in the thyroid gland. Our genetic depletion experiments revealed that VEGFR2, but not VEGFR3, is indispensable for maintenance of thyroid vascular integrity. Notably, blockade of VEGF-A or VEGFR2 not only abrogated vascular remodeling but also inhibited follicular hypertrophy, which led to the reduction of thyroid weights during goitrogenesis. Importantly, VEGFR2 blockade alone was sufficient to cause a reduction of endothelial fenestrae with decreases in thyrotropin-responsive genes in goitrogen-fed thyroids. Collectively, these findings establish follicular VEGF-Avascular VEGFR2 axis as a main regulator for thyrotropindependent thyroid angiofollicular remodeling and goitrogenesis.Peer reviewe

    Acute Effects of Asian Dust Events on Respiratory Symptoms and Peak Expiratory Flow in Children with Mild Asthma

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    The aim of this study was to investigate the possible adverse effects of Asian dust events on respiratory health in asthmatic children. Fifty-two children with mild asthma were studied for eight consecutive weeks in the spring of 2004 (March 8 to May 2). During the study period, five Asian dust days were identified; we included a lag period of two days following each of the events. Subjects recorded their respiratory symptom diaries and peak expiratory flow (PEF) twice daily during the study period; and they underwent methacholine bronchial challenge tests. The subjects reported a significantly higher frequency of respiratory symptoms during the Asian dust days than during the control days. They showed significantly more reduced morning and evening PEF values, and more increased PEF variability (10.1%±3.5% vs. 5.5%±2.2%) during the Asian dust days than during the control days. Methacholine PC20 was not significantly different between before and after the study period (geometric mean: 2.82 mg/mL vs. 3.16 mg/mL). These results suggest that the short-term Asian dust events might be associated with increased acute respiratory symptoms and changes in PEF outcomes. However, there might be little long-term influence on airway hyperresponsiveness in children with mild asthma

    Induction of IL-10-producing CD4(+)CD25(+ )T cells in animal model of collagen-induced arthritis by oral administration of type II collagen

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    Induction of oral tolerance has long been considered a promising approach to the treatment of chronic autoimmune diseases, including rheumatoid arthritis (RA). Oral administration of type II collagen (CII) has been proven to improve signs and symptoms in RA patients without troublesome toxicity. To investigate the mechanism of immune suppression mediated by orally administered antigen, we examined changes in serum IgG subtypes and T-cell proliferative responses to CII, and generation of IL-10-producing CD4(+)CD25(+ )T-cell subsets in an animal model of collagen-induced arthritis (CIA). We found that joint inflammation in CIA mice peaked at 5 weeks after primary immunization with CII, which was significantly less in mice tolerized by repeated oral feeding of CII before CIA induction. Mice that had been fed with CII also exhibited increased serum IgG(1 )and decreased serum IgG(2a )as compared with nontolerized CIA animals. The T-cell proliferative response to CII was suppressed in lymph nodes of tolerized mice also. Production of IL-10 and of transforming growth factor-β from mononuclear lymphocytes was increased in the tolerized animals, and CD4(+ )T cells isolated from tolerized mice did not respond with induction of IFN-γ when stimulated in vitro with CII. We also observed greater induction of IL-10-producing CD4(+)CD25(+ )subsets among CII-stimulated splenic T cells from tolerized mice. These data suggest that when these IL-10-producing CD4(+)CD25(+ )T cells encounter CII antigen in affected joints they become activated to exert an anti-inflammatory effect

    Methylation-dependent regulation of HIF-1 alpha stability restricts retinal and tumour angiogenesis

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    Hypoxia-inducible factor-1 alpha (HIF-1 alpha) mediates hypoxic responses and regulates gene expression involved in angiogenesis, invasion and metabolism. Among the various HIF-1 alpha posttranslational modifications, HIF-1 alpha methylation and its physiological role have not yet been elucidated. Here we show that HIF-1 alpha is methylated by SET7/9 methyltransferase, and that lysine-specific demethylase 1 reverses its methylation. The functional consequence of HIF-1 alpha methylation is the modulation of HIF-1 alpha stability primarily in the nucleus, independent of its proline hydroxylation, during long-term hypoxic and normoxic conditions. Knock-in mice bearing a methylation-defective Hif1a(KA/KA) allele exhibit enhanced retinal angiogenesis and tumour vascularization via HIF-1 alpha stabilization. Importantly, S28Y and R30Q mutations of HIF-1 alpha, found in human cancers, are involved in the altered HIF-1 alpha stability. Together, these results demonstrate a role for HIF-1 alpha methylation in regulating protein stability, thereby modulating biological output including retinal and tumour angiogenesis, with therapeutic implications in human cancer.1

    Distributions of Antibody Titers to Mycoplasma pneumoniae in Korean Children in 2000-2003

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    The aim of study was to describe Mycoplasma pneumoniae epidemics in a hospital-based population. Special attention was paid to the relationship between antibody titer to M. pneumoniae and sex, age, and atopy. During the eight 6-month periods between January 2000 and December 2003, serum samples were obtained from 1,319 Korean children who presented with respiratory symptoms, and were examined for antibodies to M. pneumoniae using the indirect particle agglutination test. Geometric mean antibody titers peaked in the second half of 2000 and then decreased gradually, a second peak occurred in the second half of 2003. Likewise, the frequency of high antibody titers (≥1:640) also peaked during these two periods. Antibody titers in children aged 0-3 yr were lower than in older children during both peak periods and for 2 yr after the first peak. Sex and atopy had no effect on antibody titers. During the years 2000-2003, geometric mean antibody titers and the frequencies of high antibody titers varied with time. These changes suggest a cyclic pattern of M. pneumoniae infection, with two epidemic peaks separated by 3 yr

    A Case of Tuberculous Arthritis Following the Use of Etanercept

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    Etanercept is a tumor necrosis factor (TNF) inhibitor that has been used for the treatment of chronic inflammatory diseases including rheumatoid arthritis, ankylosing spondylitis and psoriatic arthritis. Because of its immunosuppressive activity, opportunistic infections have been noted in treated patients, most notably caused by Mycobacterium tuberculosis. Tuberculosis may present in an extrapulmonary or disseminated form. Since TNF-α inhibitors have been used in Korea, a few cases of TNF-α inhibitor associated tuberculosis have been described. However, tuberculous arthritis has not been previously reported. We describe a case of tuberculous arthritis in a 57-year-old woman with rheumatoid arthritis who was treated with etanercept
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