50 research outputs found

    Promotion of Seeded Berry Setting on the Clusters of 'Pione' Grapes by Cane Pruning and B9 Spray on Prebloom Clusters

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    1.短梢せん定方式で栽培した‘ピオーネ’では,多くの無核果が着粒するが,これらは有核果に比べて著しく小粒になる. 有核果の着粒を増加させることを目的として,開花前の花穂に対するB9散布と,長梢せん定方式への切換えを行ってみた. 2.B9散布により,有核果及び無核果の両方の着粒率が増加したが,長梢せん定にすると結実した果粒の有核果率が高まり,ともに果房あたりの有核果粒数が増加した. 3.開花期前の胚珠及び胚のうの初期発育は,短梢せん定樹でB9を散布しない花穂のほうが早く進行したが,開花期においては,B9散布区及び長梢せん定区のほうが,完成した胚のうを持つ正常胚珠の比率が高かった. 4.花粉管の胎座下部への伸長及び珠孔から胚のう内への到達は,区による差がなかった. 5.山梨県内で‘ピオーネ’を連年長梢せん定し,B9散布も行っている経済栽培園では,さらに多数の有核果粒が着生していた. この場合も,開花日における正常胚珠の比率が高かったが,花粉管の生長には差がなかった

    Field-induced quantum phase in a frustrated zigzag-square lattice

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    This study presents the experimental realization of a spin-1/2 zigzag-square lattice in a verdazyl-based complex, namely (mm-Py-V-2,6-F2_2)[[Cu(hfac)2]_2]. Molecular orbital calculations suggest the presence of five types of frustrated exchange couplings. Our observations reveal an incremental increase in the magnetization curve beyond a critical field, signifying a phase transition from the antiferromagnetic ordered state to a quantum state characterized by a 1/2 plateau. This intriguing behavior arises from the effective stabilization of a zigzag chain by the external fields. These results provide evidence for field-induced dimensional reduction in a zigzag-square lattice attributed to the effects of frustration.Comment: 5 pages, 4 figure

    Integrated genetic and epigenetic analysis defines novel molecular subgroups in rhabdomyosarcoma.

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    横紋筋肉腫におけるゲノム・エピゲノム異常の全体図を解明 -横紋筋肉腫を4群に分類-. 京都大学プレスリリース. 2015-07-03.Rhabdomyosarcoma (RMS) is the most common soft-tissue sarcoma in childhood. Here we studied 60 RMSs using whole-exome/-transcriptome sequencing, copy number (CN) and DNA methylome analyses to unravel the genetic/epigenetic basis of RMS. On the basis of methylation patterns, RMS is clustered into four distinct subtypes, which exhibits remarkable correlation with mutation/CN profiles, histological phenotypes and clinical behaviours. A1 and A2 subtypes, especially A1, largely correspond to alveolar histology with frequent PAX3/7 fusions and alterations in cell cycle regulators. In contrast, mostly showing embryonal histology, both E1 and E2 subtypes are characterized by high frequency of CN alterations and/or allelic imbalances, FGFR4/RAS/AKT pathway mutations and PTEN mutations/methylation and in E2, also by p53 inactivation. Despite the better prognosis of embryonal RMS, patients in the E2 are likely to have a poor prognosis. Our results highlight the close relationships of the methylation status and gene mutations with the biological behaviour in RMS

    Does External Exposure of Glycidol-Related Chemicals Influence the Forming of the Hemoglobin Adduct, N-(2,3-dihydroxypropyl)valine, as a Biomarker of Internal Exposure to Glycidol?

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    Glycidyl fatty acid esters (GE) are constituents of edible oils and fats, and are converted into glycidol, a genotoxic substance, in vivo. N-(2,3-dihydroxypropyl)valine (diHOPrVal), a hemoglobin adduct of glycidol, is used as a biomarker of glycidol and GE exposure. However, high background levels of diHOPrVal are not explained by daily dietary exposure to glycidol and GE. In the present study, several glycidol-related chemicals (glycidol, (±)-3-chloro-1,2-propanediol, glycidyl oleate, epichlorohydrin, propylene oxide, 1-bromopropane, allyl alcohol, fructose, and glyceraldehyde) that might be precursors of diHOPrVal, were administered to mice, and diHOPrVal formation from each substance was examined with LC-MS/MS. DiHOPrVal was detected in animals treated with glycidol and glycidyl oleate but not in mice treated with other chemicals (3-MCPD, epichlorohydrin, propylene oxide, 1-bromopropane, allyl alcohol, fructose, and glyceraldehyde). The amount of diHOPrVal per administered dose produced from other chemicals was negligible compared to the amounts associated with dietary glycidol and GE. The present study provides important knowledge for exploring other sources for internal exposure to glycidol

    Glycidol Fatty Acid Ester and 3-Monochloropropane-1,2-Diol Fatty Acid Ester in Commercially Prepared Foods

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    Glycidyl fatty acid esters (GEs), which are the main pollutant in processed oils, are potential mutagens or carcinogens. 3-Monochloropropane-1,2-diol fatty acid esters (3-MCPDEs) are also well-known food processing contaminants. 3-MCPDEs are believed to be a precursor to GEs in foodstuffs. In vivo, lipase breaks down the phosphate ester of GEs and 3-MCPDEs to produce glycidol and 3-MCPD, respectively, which are genotoxic carcinogens. Thus, it is important to determine human exposure to GEs and 3-MCPDEs through foodstuffs. There are only reports on the amount of GE and 3-MCPDE in cooking oils and cooked foods. The content in multiple types of foods that are actually on the market was not clarified. In this study, 48 commercially prepared foods were analyzed to identify other sources of exposure to GE and 3-MCPDE. All of them contained relatively high amounts of GEs and 3-MCPDEs. The correlation between GEs and 3-MCPDEs in individual foods was examined. There was a correlation between the amounts of GEs and 3-MCPDEs in the food products (r = 0.422, p < 0.005). This is the first report on the content in multiple types of commercially prepared foods that are actually on the market was clarified

    The effect of foliar application of ferrous iron to eggplant (Solanum melongena) on iron and calcium contents in leaves

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    Effect of Polyphenols on Inflammation Induced by Membrane Vesicles from <i>Staphylococcus aureus</i>

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    Staphylococcus aureus, a bacterium found on human skin, produces toxins and various virulence factors that can lead to skin infections such as atopic dermatitis. These toxins and virulence factors are carried in membrane vesicles (MVs), composed of the bacterium’s own cell membranes, and are expected to reach host target cells in a concentrated form, inducing inflammation. This study investigated the effects of two polyphenols, (–)-epigallocatechin gallate (EGCG) and nobiletin (NOL), on the expression of S. aureus virulence factors and the inflammation induced by MVs. The study found that EGCG alone decreased the production of Staphylococcal Enterotoxin A (SEA), while both EGCG and NOL reduced biofilm formation and the expression of virulence factor-related genes. When S. aureus was cultured in a broth supplemented with these polyphenols, the resulting MVs showed a reduction in SEA content and several cargo proteins. These MVs also exhibited decreased levels of inflammation-related gene expression in immortalized human keratinocytes. These results suggest that EGCG and NOL are expected to inhibit inflammation in the skin by altering the properties of MVs derived from S. aureus

    A comparison of the exposure system of glycidol-related chemicals on the formation of glycidol-hemoglobin adducts

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    Glycidol fatty acid esters that are present in foods are degraded in vivo to the animal carcinogen glycidol, which binds to the N-terminal valine of hemoglobin (Hb) to form N-(2,3-dihydroxypropyl)valine (diHOPrVal) adducts. The existence of other chemicals that are converted to glycidol is unknown. To determine the effect of different exposure conditions on the formation of diHOPrVal adducts, several glycidol-related chemicals (3-monochloropropane-1,2-diol; 3-MCPD, epichlorohydrin, glyceraldehyde, acrylic acid, and 1,2-propanediol) were evaluated using in vitro and in vivo (single/repeated dose) methods. In vitro, the reaction of 3-MCPD or epichlorohydrin with human Hb produced 17% and 0.7% of diHOPrVal, as compared to equimolar glycidol, respectively. Following a single administration of glycidol-related compounds to ICR mice, diHOPrVal formation was observed only in the epichlorohydrin-treated group after day 5 of exposure. After 14 days of repeated dosing, the amounts of diHOPrVal produced by epichlorohydrin and 3-MCPD in vivo were &lt;1% of diHOPrVal produced by an equal molar concentration of glycidol. Furthermore, glyceraldehyde group produced 0.2% of diHOPrVal at the same molar concentration of glycidol equivalents, in which diHOPrVal formation could not be confirmed by the in vitro assay. The results indicate the usefulness of diHOPrVal as an exposure marker for glycidol; however, the contribution of its formation in vivo by exposure to various chemicals will be necessary to validate and interpret the results
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