55 research outputs found

    Survival Strategy of the Cutlery Centers : A Case Study of Sheffield and Solingen

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    世界には有名な刃物産地がいくつかある。その中で、イギリスのシェフィールド、ドイツのゾーリンゲン、そして日本の岐阜県・関は世界三大刃物産地と呼ばれている。なぜ、これらの地域が世界的な刃物産地となりえたのか。本稿ではその理由を明らかにするために、地理的、歴史的要因を中心に論じる。例えばゾーリンゲンは13世紀にはすでに刃物の産地となっている。ゾーリンゲンが刃物産地となった大きな理由の一つがライン川の存在である。ライン川を通じて、貿易都市ケルンに繋がり、多くの製品が世界各国に輸出された。また、支流も含めて水力を利用することができ、そこに鍛冶屋や研磨工などの職人が集まった。シェフィールドもドン川の水力を利用して刃物の産地となっている。これらの地域では、徹底した分業と同業組合などの独自の仕組みにより品質維持が図られている。また刃物に加えて、はさみや食器、調理器具などの新製品に多角化するという企業家精神により産地は発展してきた。There are several famous cutlery producing areas in the world, namely Sheffield in England, Solingen in Germany, and Seki in Japan. Why could these areas become global cutlery centers? In this paper, we focus on geographical and historical factors to clarify the reasons. Solingen, for example, was already a cutlery production center in the 13th century, the existence of the Rhine being one of the major reasons behind this — the river connected it to the trading city of Cologne, and many products were exported to countries worldwide; Solingen also had access to hydraulic power, including tributaries, where craftsmen such as blacksmiths and polishers gathered. Sheffield too used hydraulic power, of the Don river, to produce cutlery. In all these areas, quality is maintained through the division of labor and unique mechanisms such as a trade association. In addition to cutlery, they have diversified into new products such as scissors, tableware, and cooking tools. In other words, they have developed through such entrepreneurship.本稿は平成30年度~令和3年度 科学研究費・基盤研究(C)「技能系老舗同族企業における事業・技能継承に関する研究」(課題番号18K01760) (代表者 : 曽根秀一、分担者 : 上野恭裕)の研究助成の成果の一部である

    Functional expansion of a TCA cycle operon mRNA by a 3′ end-derived small RNA

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    Global RNA profiling studies in bacteria have predicted the existence of many of small noncoding RNAs (sRNAs) that are processed off mRNA 3′ ends to regulate other mRNAs via the RNA chaperones Hfq and ProQ. Here, we present targets of SdhX (RybD), an Hfq-dependent sRNA that is generated by RNase E mediated 3′ processing of the ∼10 000-nt mRNA of the TCA cycle operon sdhCDAB-sucABCD in enteric bacteria. An in silico search predicted ackA mRNA, which encodes acetate kinase, as a conserved primary target of SdhX. Through base pairing, SdhX represses AckA synthesis during growth of Salmonella on acetate. Repression can be achieved by a naturally occurring 38-nucleotide SdhX variant, revealing the shortest functional Hfq-associated sRNA yet. Salmonella SdhX also targets the mRNAs of fumB (anaerobic fumarase) and yfbV, a gene of unknown function adjacent to ackA. Instead, through a slightly different seed sequence, SdhX can repress other targets in Escherichia coli, namely katG (catalase) and fdoG (aerobic formate dehydrogenase). This study illustrates how a key operon from central metabolism is functionally connected to other metabolic pathways through a 3′ appended sRNA, and supports the notion that mRNA 3′UTRs are a playground for the evolution of regulatory RNA networks in bacteria

    Omentin Prevents Myocardial Ischemic Injury Through AMP-Activated Protein Kinase- and Akt-Dependent Mechanisms

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    ObjectivesThis study examined the impact of omentin on myocardial injury in a mouse model of ischemia/reperfusion (I/R) and explored its underlying mechanisms.BackgroundObesity is a major risk factor for ischemic heart disease. Omentin is a circulating adipokine that is down-regulated by obesity.MethodsIn patients who underwent successful reperfusion treatment after acute myocardial infarction, cardiac function and perfusion defect were assessed by using scintigraphic images. Mice were subjected to myocardial ischemia followed by reperfusion.ResultsThis study found that high levels of plasma omentin were associated with improvement of heart damage and function after reperfusion therapy in patients with acute myocardial infarction. Systemic administration of human omentin to mice led to a reduction in myocardial infarct size and apoptosis after I/R, which was accompanied by enhanced phosphorylation of AMP-activated protein kinase (AMPK) and Akt in the ischemic heart. Fat-specific overexpression of human omentin also resulted in reduction of infarct size after I/R. Blockade of AMPK or Akt activity reversed omentin-induced inhibition of myocardial ischemic damage and apoptosis in mice. In cultured cardiomyocytes, omentin suppressed hypoxia/reoxygenation-induced apoptosis, which was blocked by inactivation of AMPK or Akt.ConclusionsOur data indicate that omentin functions as an adipokine that ameliorates acute ischemic injury in the heart by suppressing myocyte apoptosis through both AMPK- and Akt-dependent mechanisms

    STUDY ON LONG-TERM OCCUPANCY RECORDS OF PUBLIC RENTAL HOUSING

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