48 research outputs found

    Theory of the Giant Magnetostriction in Fe_2TiO_4(Physics)

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    The anomalous properties of Fe_2TiO_4, i.e. (i) the giant magnetostriction ((c-a)/a=7.5×10^ at 77 K), (ii) the anomalously small elastic constant (c_-c_), and (iii) the positive magnetic anisotropy constant, are explained by taking into account both the Jahn-Teller effect of Fe^ ions in the A-sites of the spinel structure and the spin-lattice coupling of Fe^ ions in the B-sites. It is shown that when the direction of the Jahn-Teller distortion is determined so as to lower the energy of the coupling between the spins in the B-sites and local distortions due to the Jahn-Teller effect, the Jahn-Teller distortion itself behaves as if it were a giant magnetostriction. The temperature dependences of the distortion, elastic constants and the specific heat are calculated. It is found that (c_-c_) has a minimum and the excess specific heat due to the Jahn-Teller ions has a maximum below the Neel temperature. Discussions on the magnetic anisotropy constant are also given

    Regulation of functional KCNQ1OT1 lncRNA by β-catenin.

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    Long noncoding RNAs (lncRNAs) have been implicated in many biological processes through epigenetic mechanisms. We previously reported that KCNQ1OT1, an imprinted antisense lncRNA in the human KCNQ1 locus on chromosome 11p15.5, is involved in cis-limited silencing within an imprinted KCNQ1 cluster. Furthermore, aberration of KCNQ1OT1 transcription was observed with a high frequency in colorectal cancers. However, the molecular mechanism of the transcriptional regulation and the functional role of KCNQ1OT1 in colorectal cancer remain unclear. Here, we show that the KCNQ1OT1 transcriptional level was significantly increased in human colorectal cancer cells in which β-catenin was excessively accumulated in the nucleus. Additionally, overexpression of β-catenin resulted in an increase in KCNQ1OT1 lncRNA-coated territory. On the other hand, knockdown of β-catenin resulted in significant decrease of KCNQ1OT1 lncRNA-coated territory and an increase in the mRNA expression of the SLC22A18 and PHLDA2 genes that are regulated by KCNQ1OT1. We showed that β-catenin can promote KCNQ1OT1 transcription through direct binding to the KCNQ1OT1 promoter. Our evidence indicates that β-catenin signaling may contribute to development of colorectal cancer by functioning as a novel lncRNA regulatory factor via direct targeting of KCNQ1OT1

    Evolution of Anemone AR NOAA 10798 and the Related Geo-Effective Flares and CMEs

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    We present a detailed examination of the features of the Active Region (AR) NOAA 10798. This AR generated coronal mass ejections (CMEs) that caused a large geomagnetic storm on 24 August 2005 with the minimum Dst index of -216 nT. We examined the evolution of the AR and the features on/near the solar surface and in the interplanetary space. The AR emerged in the middle of a small coronal hole, and formed a {\it sea anemone} like configuration. Hα\alpha filaments were formed in the AR, which have southward axial field. Three M-class flares were generated, and the first two that occurred on 22 August 2005 were followed by Halo-type CMEs. The speeds of the CMEs were fast, and recorded about 1200 and 2400 km s1^{-1}, respectively. The second CME was especially fast, and caught up and interacted with the first (slower) CME during their travelings toward Earth. These acted synergically to generate an interplanetary disturbance with strong southward magnetic field of about -50 nT, which was followed by the large geomagnetic storm.Comment: 32 pages, 9 figures, JGR accepte

    Allele-Specific Expression Analysis of PEG1/MEST in Head and Neck Squamous Cell Carcinomas

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    Genomic imprinting is an epigenetic feature that plays a significant role in carcinogenesis. In this study, we examined the expression status of an imprinted gene, paternally expressed gene 1/mesoderm-specific transcript PEG1/MEST, in 38 cases of head and neck squamous cell carcinomas (HNSCCs) and in 17 oral squamous cancer cell lines. Loss of imprinting (LOI) of PEG1/MEST was found in 8 of 10 (80%) in tumor specimens, and 6 of 10 (60%) informative cases even in the extracted normal tissue specimens. As for the oral squamous cancer cell lines, LOI was detected in 5 of 8 (62.5%) informative cases in PEG1/MEST. Thus, these data showed that abnormal expression of PEG1/MEST was found at a high frequency in the tumor, the extracted normal tissue specimens and the oral squamous cancer cell lines. PEG1/MEST LOI in extracted normal tissue specimens may have a potential individual cancer risk for HNSCC

    ショクヒンンチュウ ビリョウ ゲンソ ノ キョウチンホウ オ オウヨウシタ タゲンソ ドウジ ブンセキホウ オヨビ ショクヒンチュウ ノ リンサン ジョキョ ニヨル エイキョウ

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    In order to carry out multielement determiation method of ten trace elements (Pb, Cd, Sn, Sb, Bi, Be,As, Se, Cr and Ge) in total diet samples by the polarized Zeeman atomic absorption spectrometry, the mostsuitable condition of ashing temprature, atomization temperature was dicided and effects of phosphoruselimination from total diet samples on copreecipitation were studied. The most suitable condition of ashing and atomization temperature was 500℃, 600℃, for Pb and Cd;600℃, 2200℃ for Sn, Sb and Bi ; 400℃, 2700℃ for Be, As and Se ; 800℃, 2800℃ for Cr and Ge,respetively. The most effective preconcentration of each element was the coprecipitation method with addinghydroxide zirconium as 10mg of zirconium at pH 9.5. The effects of the phosphorus elimination from total diet samples on recovery rates of trace elementswere compared among three preconcentration methods, which were non phosphoras elimination, hydroxidezirconium and ammonium molybdenic acid coprecipitation method. Recovery rates of Pb, Cd, Bi and Bewere no effects of phosphorus relimination. Recovery rates of Cr and Ge in hydrooxide zirconiumcoprecipitation method, and those of Sn, Sb, As, Se and Cr in ammonium molybdenic acid coprecipitationmethod clearly increased

    Physical and functional interaction between DDB and XPA in nucleotide excision repair

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    Damaged DNA-binding protein (DDB), consisting of DDB1 and DDB2 subunits recognizes a wide spectrum of DNA lesions. DDB is dispensable for in vitro nucleotide excision repair (NER) reaction, but stimulates this reaction especially for cyclobutane pyrimidine dimer (CPD). Here we show that DDB directly interacts with XPA, one of core NER factors, mainly through DDB2 subunit and the amino-acid residues between 185 and 226 in XPA are important for the interaction. Interestingly, the point mutation causing the substitution from Arg-207 to Gly, which was previously identified in a XP-A revertant cell-line XP129, diminished the interaction with DDB in vitro and in vivo. In a defined system containing R207G mutant XPA and other core NER factors, DDB failed to stimulate the excision of CPD, although the mutant XPA was competent for the basal NER reaction. Moreover, in vivo experiments revealed that the mutant XPA is recruited to damaged DNA sites with much less efficiency compared with wild-type XPA and fails to support the enhancement of CPD repair by ectopic expression of DDB2 in SV40-transformed human cells. These results suggest that the physical interaction between DDB and XPA plays an important role in the DDB-mediated NER reaction

    シロ ネズミ ニオケル ショクモツ センイ オヨビ ストロンチウム セッシュリョウ ト ハイベン トノ カンケイ

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    The rats were fed on the each feed contained 0, 1%, 3%, 5%, 10% dietary fiber and 10 ~300mg strontium. These researches were studied that the taking of dietary fiber wereaffected the gastrointestinal transit time, the percentage of water content in feces, thequantity of short chain fatty acids in serum. The increasing weights of air dried feces wereaccompanied with increasing dietary fiber in diet. The quantity of short chain fatty acids inserum was increased in case of feed contained over 5% dietary fiber in diet

    ショクモツ センイ ノ イチョウ ツウカ ジカン フンベン ヘノ エイキョウ

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    The rats were fed for three weeks on the each feed contained 1%, 3% and 5% dietary fiber fromcellulose, Chinese cabbage, radish, Cortinellus shiitake, and Undaria pinnatifida. The effects of the dietary fibers intake by the quantities and the kinds on the gastrointestinal transit time,percentage of water content in stools, the faecal weight of 100 pieces, the using rate of air dried feed wereevaluated. The shortening of gastrointestinal transit times were affected by the ratio of soluble andinsoluble dietary fiber, fermentation by intestinal microflora, increase of intestinal contents

    Roles of N-linked glycans in the recognition of microbial lipopeptides and lipoproteins by TLR2

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    Details of roles of carbohydrates attached to Toll-like receptors (TLRs) in the recognition of pathogen-associated molecular patterns and in the formation of the functional receptor complex still remain unknown. This study was designed to determine whether the glycans linked at Asn114, Asn199, Asn414 and Asn442 residues of TLR2 ectodomain were involved in the recognition of diacylated lipopeptide and lipoprotein. Single and multiple mutants were transfected into human embryonic kidney (HEK) 293 cells together with a NF-κB luciferase reporter plasmid. All of these mutants were expressed on the surface. SDS-PAGE of the transfectants demonstrated that these mutants migrated lower than wild-type TLR2 and their molecular masses decreased as the number of mutated Asn residues increased. TLR2N114A, TLR2N199A and TLR2N414A as well as wild-type TLR2 induced NF-κB activation when stimulated with these ligands, whereas TLR2N442A failed to induce NF-κB activation. All of triple and quadruple mutants failed to induce NF-κB activation, but were associated with both wild-type TLR2 and TLR6 in the transfectants. TLR2N114A,N199A, TLR2N114A,N414A and, to a lesser extent, TLR2N114A,N442A, in which two N-linked glycans are speculated to be exposed to the concave surface of TLR2 solenoid, not only induce NF-κB activation but also are associated with wild-type TLR2 and TLR6. These results suggest that the glycan at Asn442 and at least two N-linked glycans speculated to be exposed to the concave surface of TLR2 solenoid are involved in the recognition of ligands by TLR2 and/or in formation or maturation of a functional TLR2 receptor complex
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