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看護系大学統合カリキュラムを卒業した自治体に働く新任期保健師の経時的成長の特徴
Full text link本研究は、看護系大学統合カリキュラムを卒業した5年目未満の新任期保健師の成長体験の経時的変遷を明らかにすることを目的とした。
北海道の自治体に就職した新任期保健師7名を対象にフォーカスグループインタビューを1年目、3年目、5年目の3回実施した。逐語録から成長体験の語りを抽出し、コード化し意味内容が類似したものをまとめ、サブカテゴリ、カテゴリを生成した。それらを経験年数別に更に意味内容が類似したものをまとめ中位カテゴリとした。中位カテゴリは【実践力の向上の自覚】【職場環境と役割の広がり】【自信と自信の無さの共存】【専門性の発達】
であり、これら4つの視点で成長していた。新任期保健師は、1年目は保健師活動から程遠い日々を過ごし理想と現実とのギャップに悩みながらも批判を封じ込め、試行錯誤ながら実践をしていた。
3年目は自由裁量が拡大し苦い経験の積み重ねから支援を学び自信をつけ、生活に慣れ順調に仕事をこなしながらも他職種との連携の壁にぶつかっていた。
5年目は企画力が身につき、行政の組織環境を批判的に観察しながらとるべき保健師の役割を考え、不足している行政能力向上の目標を立てていた。さらに保健師の専門性や本質がみえてきたと感じていた。5年間を通して自信と自信の無さの共存があった。
現任教育では自信の無さを成長課題としてとらえ、新任期の前期には経験を重視し活動の意味づけをすること、後期には行政組織の中で専門職と行政職の二側面で教育していく必要性が示唆された
Ghrelin acts in the brain to block colonic hyperpermeability in response to lipopolysaccharide through the vagus nerve （グレリンは脳に作用して迷走神経を介してLPSで誘導される腸管透過性亢進を抑制する）
Full text linkBrain ghrelin plays a role in gastrointestinal functions. Among them, ghrelin acts centrally to stimulate gastrointestinal motility and induce visceral antinociception. Intestinal barrier function, one of important gastrointestinal functions, is also controlled by the central nervous system. Little is, however, known about a role of central ghrelin in regulation of intestinal permeability. The present study was performed to clarify whether brain ghrelin is also involved in regulation of intestinal barrier function and its mechanism. Colonic permeability was estimated in vivo by quantifying the absorbed Evans blue in colonic tissue in rats. Intracisternal injection of ghrelin dose-dependently abolished increased colonic permeability in response to LPS while intraperitoneal injection of ghrelin at the same dose or intracisternal injection of des-acyl-ghrelin failed to block it. Carbachol potently attenuated LPS-induced intestinal hyperpermeability, and atropine or bilateral subdiaphragmatic vagotomy prevented the improvement of intestinal hyperpermeability by central ghrelin. Intracisternal (D-Lys3)-GHRP-6, a selective ghrelin receptor antagonist, significantly blocked improvement of intestinal barrier function by intravenously administered 2-deoxy-d-glucose, central vagal stimulant. Intracisternal injection of orexin 1 receptor antagonist, SB-334867 blocked intracisternal ghrelin-induced improvement of colonic hyperpermeability. These results suggest that exogenously administered or endogenously released ghrelin acts centrally to improve a disturbed intestinal barrier function through orexinergic signaling and the vagal cholinergic pathway. Central ghrelin may be involved in the pathophysiology and be a novel therapeutic option in not only gastrointestinal diseases such as irritable bowel syndrome but also non-gastrointestinal diseases associated with the altered intestinal permeability.博士（医学）旭川医科大
A maternal high-fat diet induces fetal origins of NASH-HCC in mice （母体高脂肪食はマウスにおいて胎生期起源性脂肪性肝炎－肝癌を誘発する）
Full text linkMaternal overnutrition affects offspring susceptibility to nonalcoholic steatohepatitis (NASH). Male offspring from high-fat diet (HFD)-fed dams developed a severe form of NASH, leading to highly vascular tumor formation. The cancer/testis antigen HORMA domain containing protein 1 (HORMAD1), one of 146 upregulated differentially expressed genes in fetal livers from HFD-fed dams, was overexpressed with hypoxia-inducible factor 1 alpha (HIF-1alpha) in hepatoblasts and in NASH-based hepatocellular carcinoma (HCC) in offspring from HFD-fed dams at 15 weeks old. Hypoxia substantially increased Hormad1 expression in primary mouse hepatocytes. Despite the presence of three putative hypoxia response elements within the mouse Hormad1 gene, the Hif-1alpha siRNA only slightly decreased hypoxia-induced Hormad1 mRNA expression. In contrast, N-acetylcysteine, but not rotenone, inhibited hypoxia-induced Hormad1 expression, indicating its dependency on nonmitochondrial reactive oxygen species production. Synchrotron-based phase-contrast micro-CT of the fetuses from HFD-fed dams showed significant enlargement of the liver accompanied by a consistent size of the umbilical vein, which may cause hypoxia in the fetal liver. Based on these findings, a maternal HFD induces fetal origins of NASH/HCC via hypoxia, and HORMAD1 is a potential therapeutic target for NASH/HCC.博士（医学）旭川医科大
