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【目的】生活史を活用した高齢者理解を深める授業教材として，研究者が試作した視聴覚教材の有用性を検討することを目的とした．【方法】研究には協力の同意が得られた施設入所中のAさんの生活史と現在の生活に関する半構成的インタビューから作成した11の話題からなる12 分の試作教材DVD（以下DVD試作版とする）を用いた．看護学部1年次生16名に，DVD試作版視聴後に自記式質問紙調査を実施した．DVDの時間や内容の適切さに関する回答は統計的解析を行い，高齢者理解と重要と思う高齢者ケアに関する記述は内容分析を行った．【結果】対象者の87.5％がDVD試作版を高齢者へ関心をもてる内容と評価したが，高齢者を理解するためにわかりやすい内容と回答した者は50.0％で，祖父母との同居経験や身近な高齢者と接する機会の有無とは有意な関連を認めなかった．高齢者理解と重要と思う高齢者ケアに関する記述にはDVD試作版の10の話題からAさんの言動が引用されていた．また，対象者は，Aさんのこれまでの生き方だけでなく，現在のAさんの理解にも生活史を活用していた．対象者の高齢者理解には，Aさんの言動を解釈して理解しようとするものと自分の考えや生活状況を基準に理解しようとするものがみられていた．一方ではAさんの語りが理解できないという捉えもみられていた．【考察】半構成的インタビューによるDVD試作版は，限られた生活史情報から高齢者を理解する実践的な能力を育成する事例教材として有用であり，DVD試作版視聴による個人学習後，授業でAさんの語りの捉えなおしを行う取組において有用に活用できる可能性が示唆された．

せん妄に関する看護研究は約半世紀に亘り取り組まれてきた．2008年までの文献検討の結果では，発症要因を探索する研究と，予防や発症時のケアに関する研究に大別された．しかし未だにせん妄患者の看護は確立されておらず，看護上の課題が指摘されている． そこで2009年～2014年までの研究成果の特徴を再度確認し，今後のせん妄に関する研究の示唆を得たいと考え，文献検討に取り組んだ． 文献は，「急性期（急性）」「せん妄」「看護」をKey word として検索した．検索範囲は，医学中央雑誌WEB 版Ver.5 及びCiNii（Citation Information by NII, NII 学術情報ナビゲータ）である．その結果，医中誌WEB にて120件，CiNii36件の計156件を抽出した．その中から「原著論文」のみを再度検索し，13文献を選定した． 分析は，これまでの文献検討が研究者の主観で行われ，その客観性が問われてきた．そのため今回は，質的データを量的（多変量解析）に分析する，計量テキスト分析を用いた．その結果，これまでと同様の因子探索を目的とした【せん妄発症を誘発する個人要因】【せん妄発症要因とせん妄発症によるリスク】【せん妄と脳梗塞の関連】【看護師のアセスメント視点とせん妄ケア】【看護師によるせん妄の経験的予測と判断】【せん妄予防と治療の効果】であった．そのため疾患や治療の異なる事例を対象として，同一のアセスメント視点や介入，せん妄の判断基準に基づく評価を行う，共通の看護過程に応じた一貫性のあるプログラムを導入し，事例研究の蓄積を通して検証する必要性が示唆された．

Previous reports revealed that interleukin-1 (IL-1) was involved in the process of premature labor in the cases with intrauterine infection. However, the roles of the cytokine in normal spontaneous labor remain uncertain. The present studies aimed at determining the involvement of the cytokine in prostaglandin (PG)E2 production during labor by the third trimester decidual cells. The cells were obtained at the time of normal spontaneous delivery (NVD) and elective cesarean section (ECS). The NVD cells produced significantly more amount of PGE2 than the ECS cells and the both cells responded to the addition of IL-1 beta to increase PGE2 production. A specific inhibitor of cyclooxygenase-2 (COX-2), NS398, decreased basal PGE2 production and inhibited the stimulatory effect of IL-1 beta in a dose dependent manner in NVD cells. The NVD cells secreted more amount of IL-1 beta than the ECS cells and contained more amount of preprocessed 31kD IL-1 beta inside the cells. The addition of recombinant soluble human IL-1 receptor (type I) not only blocked the effect of IL-1 beta on PG secretion, but significantly reduced the basal production of PGE2 by NVD cells. These results indicate that decidual PG production depends upon COX-2 after the onset of labor. Besides it seems likely that endogenously produced IL-1 beta may be involved in autocrine or paracrine fashion in inducing COX-2 after the onset of labor.

Progressive familial cholestasis (PFIC) 2 and benign recurrent intrahepatic cholestasis (BRIC) 2 are caused by mutations in the bile salt export pump (BSEP, ABCB11) gene; however, their prognosis differs. PFIC2 progresses to cirrhosis and requires liver transplantation, whereas BRIC2 is clinically benign. To identify the molecular mechanism(s) responsible for the phenotypic differences, eight PFIC2 and two BRIC2 mutations were introduced in rat Bsep, which was transfected in MDCK II cells. Taurocholate transport activity, protein expression, and subcellular distribution of these mutant proteins were studied in a polarized MDCK II monolayer. The taurocholate transport activity was approximately half of the wild-type (WT) in BRIC2 mutants (A570T and R1050C), was substantially less in two PFIC2 mutants (D482G and E297G), and was almost abolished in six other PFIC2 mutants (K461E, G982R, R1153C, R1268Q, 3767–3768insC, and R1057X). Bsep protein expression levels correlated closely with transport activity, except for R1057X. The half-life of the D482G mutant was shorter than that of the WT (1.35 h vs. 3.49 h in the mature form). BRIC2 mutants and three PFIC mutants (D482G, E297G, and R1057X) were predominantly distributed in the apical membrane. The other PFIC2 mutants remained intracellular. The R1057X mutant protein was stably expressed and trafficked to the apical membrane, suggesting that the COOH-terminal tail is required for transport activity but not for correct targeting. In conclusion, taurocholate transport function was impaired in proportion to rapid degradation of Bsep protein in the mutants, which were aligned in the following order: A570T and R1050C > D482G > E297G > K461E, G982R, R1153C, R1268Q, 3767–3768insC, and R1057X. These results may explain the phenotypic difference between BRIC2 and PFIC2.

The aim of this study was to determine the role of N-linked glycosylation in protein stability, intracellular trafficking, and bile acid transport activity of the bile salt export pump [Bsep (ATP-binding cassette B11)]. Rat Bsep was fused with yellow fluorescent protein, and the following mutants, in which Asn residues of putative glycosylation sites (Asn109, Asn116, Asn122, and Asn125) were sequentially replaced with Gln, were constructed by site-directed mutagenesis: single N109Q, double N109Q + N116Q, triple N109Q + N116Q + N122Q, and quadruple N109Q + N116Q + N122Q + N125Q. Immunoblot and glycosidase cleavage analysis demonstrated that each site was glycosylated. Removal of glycans decreased taurocholate transport activity as determined in polarized MDCK II cells. This decrease resulted from rapid decay of the mutant Bsep protein; biochemical half-lives were 3.76, 3.65, 3.24, 1.35, and 0.52 h in wild-type, single-mutant, double-mutant, triple-mutant, and quadruple-mutant cells, respectively. Wild-type and single- and double-mutant proteins were distributed exclusively along the apical membranes, whereas triple- and quadruple-mutant proteins remained intracellular. MG-132 but not bafilomycin A1extended the half-life, suggesting a role for the proteasome in Bsep degradation. To determine whether a specific glycosylation site or the number of glycans was critical for protein stability, we studied the protein expression of combinations of N-glycan-deficient mutants and observed that Bsep with one glycan was considerably unstable compared with Bsep harboring two or more glycans. In conclusion, at least two N-linked glycans are required for Bsep protein stability, intracellular trafficking, and function in the apical membrane.

Allogeneic cultured dermal substitute (CDS) was prepared by culturing fibroblasts on a two-layered spongy matrix of hyaluronic acid (HA) and atelo-collagen (Col). Allogeneic CDS can be cryopreserved and transported to other hospitals in a frozen state. Vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), hepatocyte growth factor (HGF), platelet derived growth factor (PDGF)-AA, transforming growth factor (TGF)-beta1, keratinocytes growth factor (KGF), interleukin (IL)-6 and IL-8 were contained in the culture medium which was used in preparing CDS over a cultivation period of one week (fresh CDS culture medium sample). After thawing a cryopreserved CDS, the CDS was recultured in a culture medium for one week. VEGF, bFGF, HGF, TGF-beta1 and IL-8 were contained in the culture medium which was used in reculturing CDS for one week (cryopreserved CDS culture medium sample), although some cytokines were detected at a lower level than those before freezing. This finding suggests that the cryopreserved CDS retains its ability to release these cytokines. Clinical research on allogeneic CDS, which was newly developed at the R & D Center for Artificial Skin of Kitasato University, has been carried out in medical centers across Japan with the support of the Millennium Project of the Ministry of Health, Labor and Welfare. It was demonstrated that the allogeneic CDS functions as an excellent cell therapy for intractable skin ulcers as well as burn injuries. The spongy matrix itself, as well as the cytokines released from the allogeneic CDS, seemed to be beneficial for the treatment of intractable skin defect.

The intrauterine tissues including decidua have been investigated as the sites of prostaglandin (PG) production in connection with its involvement in the onset or progress of labor (1–4). The recent papers suggested that the intrauterine infection was responsible for the pathophysiology of preterm labor through the set of events from the generation of various types of cytokines such as interleukin-1 (IL-1), the induction of cyclooxygenase (COX) to the PG synthesis in these tissues (5–7). On the other hand, IL-1 has been reported to induce COX-2, an inducible type of COX in cultured decidual cells (8). Therefore, COX-2 induction in decidua by IL-1 would play a role in the initiation of spontaneous labor as well as preterm labor. Though the physiological role of IL-1 secreted in decidual cells remains still uncertain (9), this study was aimed to reveal endogenous role of IL-1 synthesized and secreted by decidual cells in the formation of PGE2. In addition, we investigated the selective role of COX-2 in decidual cells for the initiation or maintenance of labor by using a specific inhibitor for the enzyme, NS-398.

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