2,181 research outputs found

    Numerical Sensitivity Tests of Volatile Organic Compounds Emission to PM2.5 Formation during Heat Wave Period in 2018 in Two Southeast Korean Cities

    Get PDF
    A record-breaking severe heat wave was recorded in southeast Korea from 11 July to 15 August 2018, and the numerical sensitivity simulations of volatile organic compound (VOC) to secondarily generated particulate matter with diameter of less than 2.5 mu m (PM2.5) concentrations were studied in the Busan and Ulsan metropolitan areas in southeast Korea. A weather research and forecasting (WRF) model coupled with chemistry (WRF-Chem) was employed, and we carried out VOC emission sensitivity simulations to investigate variations in PM2.5 concentrations during the heat wave period that occurred from 11 July to 15 August 2018. In our study, when anthropogenic VOC emissions from the Comprehensive Regional Emissions Inventory for Atmospheric Transport Experiment-2015 (CREATE-2015) inventory were increased by approximately a factor of five in southeast Korea, a better agreement with observations of PM2.5 mass concentrations was simulated, implying an underestimation of anthropogenic VOC emissions over southeast Korea. The simulated secondary organic aerosol (SOA) fraction, in particular, showed greater dominance during high temperature periods such as 19-21 July, 2018, with the SOA fractions of 42.3% (in Busan) and 34.3% (in Ulsan) among a sub-total of seven inorganic and organic components. This is considerably higher than observed annual mean organic carbon (OC) fraction (28.4 +/- 4%) among seven components, indicating the enhancement of secondary organic aerosols induced by photochemical reactions during the heat wave period in both metropolitan areas. The PM2.5 to PM10 ratios were 0.69 and 0.74, on average, during the study period in the two cities. These were also significantly higher than the typical range in those cities, which was 0.5-0.6 in 2018. Our simulations implied that extremely high temperatures with no precipitation are significantly important to the secondary generation of PM2.5 with higher secondary organic aerosol fraction via photochemical reactions in southeastern Korean cities. Other possible relationships between anthropogenic VOC emissions and temperature during the heat wave episode are also discussed in this study

    Grape seed proanthocyanidin extract inhibits glutamate-induced cell death through inhibition of calcium signals and nitric oxide formation in cultured rat hippocampal neurons

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>Proanthocyanidin is a polyphenolic bioflavonoid with known antioxidant activity. Some flavonoids have a modulatory effect on [Ca<sup>2+</sup>]<sub>i</sub>. Although proanthocyanidin extract from blueberries reportedly affects Ca<sup>2+ </sup>buffering capacity, there are no reports on the effects of proanthocyanidin on glutamate-induced [Ca<sup>2+</sup>]<sub>i </sub>or cell death. In the present study, the effects of grape seed proanthocyanidin extract (GSPE) on glutamate-induced excitotoxicity was investigated through calcium signals and nitric oxide (NO) in cultured rat hippocampal neurons.</p> <p>Results</p> <p>Pretreatment with GSPE (0.3-10 μg/ml) for 5 min inhibited the [Ca<sup>2+</sup>]<sub>i </sub>increase normally induced by treatment with glutamate (100 μM) for 1 min, in a concentration-dependent manner. Pretreatment with GSPE (6 μg/ml) for 5 min significantly decreased the [Ca<sup>2+</sup>]<sub>i </sub>increase normally induced by two ionotropic glutamate receptor agonists, N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). GSPE further decreased AMPA-induced response in the presence of 1 μM nimodipine. However, GSPE did not affect the 50 mM K<sup>+</sup>-induced increase in [Ca<sup>2+</sup>]<sub>i</sub>. GSPE significantly decreased the metabotropic glutamate receptor agonist (<it>RS</it>)-3,5-Dihydroxyphenylglycine-induced increase in [Ca<sup>2+</sup>]<sub>i</sub>, but it did not affect caffeine-induced response. GSPE (0.3-6 μg/ml) significantly inhibited synaptically induced [Ca<sup>2+</sup>]<sub>i </sub>spikes by 0.1 mM [Mg<sup>2+</sup>]<sub>o</sub>. In addition, pretreatment with GSPE (6 μg/ml) for 5 min inhibited 0.1 mM [Mg<sup>2+</sup>]<sub>o</sub>- and glutamate-induced formation of NO. Treatment with GSPE (6 μg/ml) significantly inhibited 0.1 mM [Mg<sup>2+</sup>]<sub>o</sub>- and oxygen glucose deprivation-induced neuronal cell death.</p> <p>Conclusions</p> <p>All these data suggest that GSPE inhibits 0.1 mM [Mg<sup>2+</sup>]<sub>o</sub>- and oxygen glucose deprivation-induced neurotoxicity through inhibition of calcium signals and NO formation in cultured rat hippocampal neurons.</p

    Tachykinin acts upstream of autocrine Hedgehog signaling during nociceptive sensitization in Drosophila

    Get PDF
    Pain signaling in vertebrates is modulated by neuropeptides like Substance P (SP). To determine whether such modulation is conserved and potentially uncover novel interactions between nociceptive signaling pathways we examined SP/Tachykinin signaling in a Drosophila model of tissue damage-induced nociceptive hypersensitivity. Tissue-specific knockdowns and genetic mutant analyses revealed that both Tachykinin and Tachykinin-like receptor (DTKR99D) are required for damage-induced thermal nociceptive sensitization. Electrophysiological recording showed that DTKR99D is required in nociceptive sensory neurons for temperature-dependent increases in firing frequency upon tissue damage. DTKR overexpression caused both behavioral and electrophysiological thermal nociceptive hypersensitivity. Hedgehog, another key regulator of nociceptive sensitization, was produced by nociceptive sensory neurons following tissue damage. Surprisingly, genetic epistasis analysis revealed that DTKR function was upstream of Hedgehog-dependent sensitization in nociceptive sensory neurons. Our results highlight a conserved role for Tachykinin signaling in regulating nociception and the power of Drosophila for genetic dissection of nociception

    Decreased Angiopoietin Expression in Underactive Bladder Induced by Long-term Bladder Outlet Obstruction

    Get PDF
    Purpose Ischemia of the bladder can occur if neovascular formation cannot keep pace with hypoxia induced by chronic bladder outlet obstruction (BOO). The aim of this study was to examine changes in angiogenesis growth factor expression generated by chronic BOO in a rat model of underactive bladder. Methods Twenty female Sprague-Dawley rats aged 6 weeks were assigned to 4 groups (5 rats per group). Group 1 was the control. Group 2 underwent sham surgery. The rats in groups 3 and 4 underwent BOO and were followed up for 1 week and 8 weeks. Cystometry was carried out together with bladder tissue analysis at 1 week and 8 weeks postoperatively. Real-time polymerase chain reaction (PCR) assays were conducted to determine the expression level of angiogenesis-related growth factors. A hypoxia signaling pathway PCR array was additionally carried out. Results The group that underwent BOO for 8 weeks showed abnormal bladder function, with a diminished intercontraction interval, decreased maximal voiding pressure, and higher volume of residual urine (P<0.05). Hypoxia-inducible factor-1 alpha expression was elevated in this group. The expression levels of vascular endothelial growth factor (VEGF) and VEGF receptor messenger RNA (mRNA) in the BOO group were comparable to those in the control group. However, angiotensin/tie receptor mRNA expression levels increased at 1 week after BOO, but decreased at 8 weeks after BOO. In animals that underwent BOO, fewer blood vessels exhibited positive immunofluorescent staining for von Willebrand factor. Alterations were also seen in the hypoxia signaling pathway PCR array. Conclusions In a rat model of underactive bladder caused by surgical BOO, reduced angiopoietin expression was demonstrated. This observation might underlie visceral ischemia and fibrosis associated with the procedure. The findings of this study might offer an improved understanding of the disease processes underlying BOO and facilitate selection of the appropriate time to repair the organ in this condition

    Genomic characterization of Nocardia seriolae strains isolated from diseased fish

    Get PDF
    Members of the genus Nocardia are widespread in diverse environments; a wide range of Nocardia species are known to cause nocardiosis in several animals, including cat, dog, fish, and humans. Of the pathogenic Nocardia species, N. seriolae is known to cause disease in cultured fish, resulting in major economic loss. We isolated two N. seriolae strains, CK‐14008 and EM15050, from diseased fish and sequenced their genomes using the PacBio sequencing platform. To identify their genomic features, we compared their genomes with those of other Nocardia species. Phylogenetic analysis showed that N. seriolae shares a common ancestor with a putative human pathogenic Nocardia species. Moreover, N. seriolae strains were phylogenetically divided into four clusters according to host fish families. Through genome comparison, we observed that the putative pathogenic Nocardia strains had additional genes for iron acquisition. Dozens of antibiotic resistance genes were detected in the genomes of N. seriolae strains; most of the antibiotics were involved in the inhibition of the biosynthesis of proteins or cell walls. Our results demonstrated the virulence features and antibiotic resistance of fish pathogenic N. seriolae strains at the genomic level. These results may be useful to develop strategies for the prevention of fish nocardiosis.

    Changes in activity and isozyme patterns of peroxidase and chitinase in kiwifruit pollen

    Get PDF
    In this study, changes in activity and isozyme patterns of peroxidase (POD) and chitinase in kiwifruit (Actinidia chinensis) pollen were investigated under different storage conditions. Although residual activity was detected in heat-treated pollen, changes in POD activity were observed due to difference in storage conditions as revealed by preliminary studies in which pollen germination varied with different storage conditions. POD activity of kiwifruit pollen increased as proportions of viable pollen increased, indicating a positive correlation (R2=0.993) between pollen viability and POD activity. There was a detectable difference in the relative activity of POD enzyme between heat-treated and viable pollen. Decoloration of Congo Red was observed in germination medium which fresh pollen was cultured. The activity of individual chitinase isozymes present in kiwifruit pollen differed depending on storage conditions, which had a direct impact on pollen vigor. Although direct evidence showing that chitinase isozymes are implicated in pollen vigor is still uncertain, distinction of isozymes may facilitate more precise identification of viable pollen which possesses germination potential from non-viable pollen. Taken together, these results suggest that monitoring the activity of POD and chitinase can be an attractive alternative to evaluate pollen vigor in kiwifruit

    Down-regulation of phospholipase D during differentiation of mouse F9 teratocarcinoma cells

    Get PDF
    AbstractPhospholipase D has been recognized as playing an important role in signal transduction in many types of cells. We investigated the expression of phospholipase D during the differentiation of F9 embryonal teratocarcinoma cells. The ADP ribosylation factor-dependent phospholipase D activity, as measured by an in vitro assay, and H2O2-induced phospholipase D activity and phospholipase D protein content in whole cells were decreased during the differentiation of F9 cells induced by a combination of dibutyryl cyclic AMP and all-trans retinoic acid. In contrast, these changes were not observed when cells were induced by retinoic acid. These results suggest that down-regulation of phospholipase D protein is associated with differentiation of F9 cells to a parietal endoderm lineage
    corecore