The Amino Acid Sequence of the Insoluble Tryptic Peptide,βT10,11,12 from theβ-Polypeptide Chain in Macaca mulatta Monkey Hemoglobin

Globin prepared from macaca mulatta monkey hemoglobin was separated into α and β-polypeptide chains by countercurrent distribution method. The β-polypeptide chain was digested with trypsin. The insoluble tryptic peptide (so-called β-core), the precipitate of the digest at pH 6.4, was obtained by centrifugation. This insoluble tryptic peptide after oxidized with performic acid was digested with pepsin or redigested with trypsin, and the amino acid composition was examined. Next, the amino acid sequence of the β-core containing 38 amino acid residues was determined by the DNP method, the PTC method, and the carboxypeptidase method. The result was compared with the known sequence of the β-core of human hemoglobin. Between these two hemoglobins, two amino acid substitutions were found; that is, the 5th and 22nd residues from the N-terminus are threonine and arginine in case of human hemoglobin, but glutamine and lysine, respectively in case of macaca mulatta monkey hemoglobin

The systematic investigations of high-pressure polymorphs in shocked L type ordinary chondrites

第6回極域科学シンポジウム[OA] 南極隕石11月16日（月）　国立国語研究所 2階 講

Electron emission from conduction band of diamond with negative electron affinity

Experimental evidence explaining the extremely low-threshold electron emission from diamond reported in 1996 has been obtained for the first time. Direct observation using combined ultraviolet photoelectron spectroscopy/field emission spectroscopy (UPS/FES) proved that the origin of field-induced electron emission from heavily nitrogen (N)-doped chemical vapour deposited (CVD) diamond was at conduction band minimum (CBM) utilising negative electron affinity (NEA). The significance of the result is that not only does it prove the utilisation of NEA as the dominant factor for the extremely low-threshold electron emission from heavily N-doped CVD diamond, but also strongly implies that such low-threshold emission is possible from other types of diamond, and even other materials having NEA surface. The low-threshold voltage, along with the stable intensity and remarkably narrow energy width, suggests that this type of electron emission can be applied to develop a next generation vacuum nano-electronic devices with long lifetime and high energy resolution.Comment: 17 pages, 4 figures, Phys. Rev. B in pres

Kチヤネル遺伝子変異によるQT延長症候群の臨床的特徴とチヤネル機構の解明

金沢大学附属病院研究課題/領域番号:16790415, 研究期間(年度):2004出典：「Kチヤネル遺伝子変異によるQT延長症候群の臨床的特徴とチヤネル機構の解明」研究成果報告書　課題番号16790415（KAKEN：科学研究費助成事業データベース（国立情報学研究所））（https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-16790415/)を加工して作

QT延長症候群における新しいKCNQ1遺伝子異常(F193L)の臨床的,電気生理学的特徴

取得学位 : 博士（医学）, 学位授与番号 : 医博乙第1580号, 学位授与年月日 : 平成15年7月16日, 学位授与大学 : 金沢大

Meridional changes of zooplankton community and copepods population along 110°E transect in the Indian sector of the Southern Ocean during austral summer

The Tenth Symposium on Polar Science/Ordinary sessions : [OB] Polar Biology, Wed. 4 Dec. / Entrance Hall (1st floor) , National Institute of Polar Researc

COVID-19患者との接触が精神科病院職員に与えた影響

博士（医学）・乙第1515号・令和3年12月21日© 2020 The Authors Psychiatry and Clinical Neurosciences.© 2020 Japanese Society of Psychiatry and Neurology.This is the peer reviewed version of the following article: [https://onlinelibrary.wiley.com/doi/10.1111/pcn.13179], which has been published in final form at [https://doi.org/10.1111/pcn.13179]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited

Par6 regulates skeletogenesis and gut differentiation in sea urchin larvae

Partitioning-defective (par) genes were originally identified as genes that are essential for the asymmetric division of the Caenorhabditis elegans zygote. Studies have since revealed that the gene products are part of an evolutionarily conserved PAR-atypical protein kinase C system involved in cell polarity in various biological contexts. In this study, we analyzed the function of par6 during sea urchin morphogenesis by morpholino-mediated knockdown and by manipulation swapping of the primary mesenchyme cells (PMCs). Loss of Par6 resulted in defects in skeletogenesis and gut differentiation in larvae. Phenotypic analyses of chimeras constructed by PMC swapping showed that Par6 in non-PMCs is required for differentiation of archenteron into functional gut. In contrast, Par6 in both PMCs and ectodermal cells cooperatively regulates skeletogenesis. We suggest that Par6 in PMCs plays an immediate role in the deposition of biomineral in the syncytial cable, whereas Par6 in ectoderm may stabilize skeletal rods via an unknown signal(s). © 2012 Springer-Verlag

Embryonic Lethality, Liver Degeneration, and Impaired NF-κB Activation in IKK-β-Deficient Mice

AbstractIκB kinase-α and -β (IKK-α and IKK-β), the catalytic subunits of the IKK complex, phosphorylate IκB proteins on specific serine residues, thus targeting IκB for degradation and activating the transcription factor NF-κB. To elucidate the in vivo function of IKK-β, we generated IKK-β-deficient mice. The homozygous mouse embryo dies at ∼14.5 days of gestation due to liver degeneration and apoptosis. IKK-β-deficient embryonic fibroblasts have both reduced basal NF-κB activity and impaired cytokine-induced NF-κB activation. Similarly, basal and cytokine-inducible kinase activities of the IKK complex are greatly reduced in IKK-β-deficient cells. These results indicate that IKK-β is crucial for liver development and regulation of NF-κB activity and that IKK-α can only partially compensate for the loss of IKK-β