431 research outputs found
Feedback-based active reset of a spin qubit in silicon
Feedback control of qubits is a highly demanded technique for advanced
quantum information protocols such as quantum error correction. Here we
demonstrate active reset of a silicon spin qubit using feedback control. The
active reset is based on quantum non-demolition readout of the qubit and
feedback according to the readout results, which is enabled by hardware data
processing and sequencing. We incorporate a cumulative readout technique to the
active reset protocol, enhancing initialization fidelity above a limitation
imposed by accuracy of the single QND measurement fidelity. Based on an
analysis of the reset protocol, we suggest a way to achieve the initialization
fidelity sufficient for the fault-tolerant quantum computation
末端肥大症の成因における遺伝子的研究
金沢大学附属病院腫瘍の発生にはいくつかの遺伝子異常が関与し、成長ホルモン産生下垂体腺腫の一部にG蛋白の遺伝子異常が報告されている。成長ホルモン過剰は成人において末端肥大症を引き起こし高血圧、糖尿病をはじめとする代謝異常より心血管病を引き起こすだけでなく悪性新生物の合併頻度も高く、この疾患における平均寿命も健康人に比して短い。われわれはこれまで成長ホルモン産生下垂体腺腫に対してはG蛋白遺伝子などの解析を行ったが、これらの異常は見いだせなかった。そこで、DNAマイクロアレイ法による機能解析より成長ホルモン産生下垂体腺腫の成因を検討することとした。平成13年度のDNAマイクロアレイ法を用いた検討よりヒト非ホルモン産生下垂体腺腫と成長ホルモン産生細胞腺腫組織間で、いくつかの細胞内情報伝達系に関わる遺伝子の発現量に差を認めた。ヒト非ホルモン産生下垂体腺腫に比べ成長ホルモン産生細胞腺腫で発現の増加を認めた遺伝子はDLG-3,NOTCH1,RFC37,CTC85,RAD52,GRM1,NACHRA6,bystin, LCFであり、逆に低下していた遺伝子はCDKN2,CETP, IRF1,VLA4,DLK, WNT2,WNT10Bであった。平成14年度は、これらの遺伝子ひとつひとつについてmRNAの発現をノーザンブロット法でも検討した。マイクロアレイ法と同様、成長ホルモン産生細胞腺腫ではDLG-3,NOTCH1,RFC37,CTC85,RAD52,GRM1,NACHRA6,bystin, LCFのmRNAの発現増加が認められた。発現の低下していた遺伝子のひとつであるCDKN2のプロモーター領域のメチル化が他の下垂体腺腫においてみられることより、成長ホルモン産生細胞腺腫についてもCDKN2のプロモーター領域のメチル化の有無を検討したが認められなかった。研究課題/領域番号:13770630, 研究期間(年度):2001-2002出典:「末端肥大症の成因における遺伝子的研究」研究成果報告書 課題番号13770630(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-13770630/ )を加工して作
ストレプトゾトシン糖尿病ラットの血管障害に果たすエンドセリンの役割に関する研究
取得学位 : 博士(医学), 学位授与番号 : 医博甲第1107号, 学位授与年月日:平成6年3月25日,学位授与年:199
Cell type-dependent gene regulation by Staufen2 in conjunction with Upf1
<p>Abstract</p> <p>Background</p> <p>Staufen2 (Stau2), a double-stranded RNA-binding protein, is a component of neuronal RNA granules, which are dendritic mRNA transport machines. Although Stau2 is thought to be involved in the dendritic targeting of several mRNAs in neurons, the mechanism whereby Stau2 regulates these mRNAs is unknown. To elucidate the functions of Stau2, we screened for novel binding partners by affinity purification of GST-tagged Stau2 from 293F cells.</p> <p>Results</p> <p>Three RNA helicases, RNA helicase A, Upf1 and Mov10, were identified in Stau2-containing complexes. We focused our studies on Upf1, a key player in nonsense-mediated mRNA decay. Stau2 was found to bind directly to Upf1 in an RNA-independent manner <it>in vitro</it>. Tethering Stau2 to the 3'-untranslated region (UTR) of a reporter gene had little effect on its expression in HeLa cells. In contrast, when the same tethering assay was performed in 293F cells, we observed an increase in reporter protein levels. This upregulation of protein expression by Stau2 turned out to be dependent on Upf1. Moreover, we found that in 293F cells, Stau2 upregulates the reporter mRNA level in an Upf1-independent manner.</p> <p>Conclusions</p> <p>These results indicate that the recruitment of Stau2 alone or in combination with Upf1 differentially affects the fate of mRNAs. Moreover, the results suggest that Stau2-mediated fate determination could be executed in a cell type-specific manner.</p
Two mechanisms of oral malodor inhibition by zinc ions
Objectives The aim of this study was to reveal the mechanisms by which zinc ions inhibit oral malodor. Material and Methods The direct binding of zinc ions to gaseous hydrogen sulfide (H2S) was assessed in comparison with other metal ions. Nine metal chlorides and six metal acetates were examined. To understand the strength of H2S volatilization inhibition, the minimum concentration needed to inhibit H2S volatilization was determined using serial dilution methods. Subsequently, the inhibitory activities of zinc ions on the growth of six oral bacterial strains related to volatile sulfur compound (VSC) production and three strains not related to VSC production were evaluated. Results Aqueous solutions of ZnCl2, CdCl2, CuCl2, (CH3COO)2Zn, (CH3COO)2Cd, (CH3COO)2Cu, and CH3COOAg inhibited H2S volatilization almost entirely. The strengths of H2S volatilization inhibition were in the order Ag+ >; Cd2+ >; Cu2+ >; Zn2+. The effect of zinc ions on the growth of oral bacteria was strain-dependent. Fusobacterium nucleatum ATCC 25586 was the most sensitive, as it was suppressed by medium containing 0.001% zinc ions. Conclusions Zinc ions have an inhibitory effect on oral malodor involving the two mechanisms of direct binding with gaseous H2S and suppressing the growth of VSC-producing oral bacteria
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