日本語版攻撃的行動に対する態度尺度（J-ATAS）の信頼性と妥当性：日本の認知症ケアにおける適用可能性の検討

　本研究では、ヨーロッパ5 カ国4 言語で信頼性と妥当性が検証されたthe Attitudes Towards Aggression Scale（ATAS）の日本語版（J-ATAS）を作成し、その信頼性と妥当性を検討し、本邦の認知症ケアにおける適用可能性について考察した。主成分分析の結果、J-ATAS は英語版の5 因子構造とはならず、3 因子構造を示した。また、内的整合性の評価では、第1 因子においては概ね良好な値が得られたが、 第2 因子では十分とは言えず、第3 因子に関しては低い結果しか得られなかった。さらに3 つの因子の相関パターンは、‘否定的態度’と‘肯定的態度’の2 つに分かれる可能性が示唆された。以上のことから、現段階におけるJ-ATAS は、ATAS の日本語版として本邦で活用するには、十分な信頼性・妥当性を有しているとは言えない結果となった。認知症の人の攻撃的行動に対する我が国のスタッフの態度を測定するには、J-ATAS およびその開発プロセスの課題を踏まえた新たな尺度を開発する必要がある

認知症高齢者グループホーム職員の看取り体験の思い

This study explored caregiver perceptions related to experiences of end-of-life (EOL) care at group homes (GH) for elderly people with dementia. A self-administered questionnaire was designed to elicit GH staff perceptions by asking what they feel about their EOL care experiences at GH. Eighty one participants shared their perspectives. Results were classified into seven categories, “Anxiety and tension related to EOL care,” “Regret and condolence,” “Response of care provided,” “Respect for deceased people,” “Pride in providing EOL care,” “Creative view of life and death,” and “Familial sense of loss,”. Although staff members who experienced EOL care felt imperfect, they were satisfied with the care they provided. Moreover, they had positive views in terms of EOL care experiences, which seemed to engender their personal growth. The study also revealed a distinctive view of EOL care in GH, where caregivers felt as if they had lost a family member when they confronted a resident’s death

Challenges of drug resistance in the management of pancreatic cancer

The current treatment of choice for metastatic pancreatic cancer involves single agent gemcitabine or combination of gemcitabine with capecitabine and erlotinib (tyrosine kinase inhibitor). Only 25-30% of patients respond to this treatment and patients who do respond initially ultimately exhibit disease progression. Median survival for pancreatic cancer patients has reached a plateau due to inherent and acquired resistance to these agents. Key molecular factors implicated in this resistance include: deficiencies in drug uptake, alteration of drug targets, activations of DNA repair pathways, resistance to apoptosis, and the contribution of the tumor microenvironment. Moreover, for newer agents including tyrosine kinase inhibitors, over expression of signaling proteins, mutations in kinase domains, activation of alternative pathways, mutations of genes downstream of the target, and/or amplification of the target represent key challenges for treatment efficacy. Here we will review the contribution of known mechanisms and markers of resistance to key pancreatic cancer drug treatments

Manganese Superoxide Dismutase: Guardian of the Powerhouse

The mitochondrion is vital for many metabolic pathways in the cell, contributing all or important constituent enzymes for diverse functions such as β-oxidation of fatty acids, the urea cycle, the citric acid cycle, and ATP synthesis. The mitochondrion is also a major site of reactive oxygen species (ROS) production in the cell. Aberrant production of mitochondrial ROS can have dramatic effects on cellular function, in part, due to oxidative modification of key metabolic proteins localized in the mitochondrion. The cell is equipped with myriad antioxidant enzyme systems to combat deleterious ROS production in mitochondria, with the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) acting as the chief ROS scavenging enzyme in the cell. Factors that affect the expression and/or the activity of MnSOD, resulting in diminished antioxidant capacity of the cell, can have extraordinary consequences on the overall health of the cell by altering mitochondrial metabolic function, leading to the development and progression of numerous diseases. A better understanding of the mechanisms by which MnSOD protects cells from the harmful effects of overproduction of ROS, in particular, the effects of ROS on mitochondrial metabolic enzymes, may contribute to the development of novel treatments for various diseases in which ROS are an important component

Mitochondria in Cell Senescence: Is Mitophagy the Weakest Link?

Cell senescence is increasingly recognized as a major contributor to the loss of health and fitness associated with aging. Senescent cells accumulate dysfunctional mitochondria; oxidative phosphorylation efficiency is decreased and reactive oxygen species production is increased. In this review we will discuss how the turnover of mitochondria (a term referred to as mitophagy) is perturbed in senescence contributing to mitochondrial accumulation and Senescence-Associated Mitochondrial Dysfunction (SAMD). We will further explore the subsequent cellular consequences; in particular SAMD appears to be necessary for at least part of the specific Senescence-Associated Secretory Phenotype (SASP) and may be responsible for tissue-level metabolic dysfunction that is associated with aging and obesity. Understanding the complex interplay between these major senescence-associated phenotypes will help to select and improve interventions that prolong healthy life in humans. Search strategy and selection criteria: Data for this review were identified by searches of MEDLINE, PubMed, and references from relevant articles using the search terms “mitochondria AND senescence”, “(autophagy OR mitophagy) AND senescence”, “mitophagy AND aging” and related terms. Additionally, searches were performed based on investigator names. Abstracts and reports from meetings were excluded. Articles published in English between 1995 and 2017 were included. Articles were selected according to their relevance to the topic as perceived by the authors