Language：English   Publisher：シュプリンガー・ジャパン(株)  

急性心不全(AHF)患者における抗精神病薬使用と嚥下機能および身体機能との関連を明らかにするため、入院患者を対象とした前向きコホート研究を実施した。対象は325例(平均81.5歳、女性53.2%)で、このうち34例(10.5%)が抗精神病薬を定期内服していた。多変量解析の結果、抗精神病薬使用は退院時の嚥下障害と有意に関連しており、オッズ比は7.724(95%CI 2.585～23.081、p<0.001)であった。また、入院中の嚥下障害発生リスクも有意に高かった。退院時Barthel Indexとの関連は認められなかった。以上より、AHF患者における抗精神病薬の定期的な使用は身体機能との関連は認められなかった一方で、退院時の嚥下障害および入院中の嚥下障害発生リスクの増加と強く関連していることが示された。

Language：Japanese   Publisher：(株)羊土社  

＜Point＞・摂食嚥下障害の原因は様々であり,障害のされ方も異なるため,適切な評価と対応が重要である・複数の評価法を組合わせた総合的アセスメントを行うことがより適切な対応につながる・多職種連携による包括的アプローチが不可欠である(著者抄録)

Language：Japanese   Publisher：(株)メディカ出版  

Language：Japanese   Publisher：日総研出版  

Language：Japanese   Publisher：Japanese Society for Parenteral and Enteral Nutrition Therapy  

DOI： 10.11244/ejspen.6.1_51

CiNii Research

Language：Japanese

This chapter explores the molecular mechanisms underlying sarcopenia, an age-related disorder characterized by the progressive loss of skeletal muscle mass, strength, and function. The decline in muscle function is attributed to complex and interrelated factors, including reduced protein synthesis, mitochondrial dysfunction, impaired autophagy, and changes in regulatory pathways such as the PI3-K/Akt/mTOR signaling cascade. Although the ubiquitin-proteasome system (UPS) is known to regulate muscle atrophy, its activation in sarcopenia remains inconclusive. Additionally, deficits in autophagy have been implicated in the accumulation of dysfunctional proteins and organelles, further exacerbating muscle degeneration. In this chapter, the role of myostatin and growth differentiation factor 11 (GDF11) in muscle aging is examined, revealing contradictory findings regarding their impact on muscle atrophy. Furthermore, the chapter discusses the influence of chronic low-grade inflammation in sarcopenia, although its effects appear distinct from those observed in cachexia. Potential therapeutic approaches, including endurance training and caloric restriction, are highlighted as interventions that may mitigate sarcopenic progression by modulating autophagy and muscle preservation pathways. Overall, this chapter underscores the need for further research into the molecular determinants of sarcopenia to develop effective countermeasures against age-related muscle deterioration.

DOI： 10.1201/9781003190875-14

Scopus

Language：Japanese

Skeletal muscle provides a fundamental basis for human function, enabling locomotion and respiration. Autophagy occurs in all eukaryotic cells and is evolutionarily conserved from yeast to human beings. The autophagy machinery is a critical pathway for cell homeostasis, but it has been insufficiently studied in skeletal muscle. Particular emphasis has been given on the role played by autophagic defects in disease pathogenesis, its involvement in atrophy, and the possible effects of exercise as a countermeasure. Recent studies indicated that the age-related defects of autophagy signaling in normal skeletal muscle, whereas denervation, unloading, and cachexia, frequently involved with aging, modulate the autophagy-dependent system. The autophagic defect in sarcopenia may be influenced by new candidates [glycogen synthase kinase (GSK)-3a, mitofusin 2, and Rubicon]. Endurance training and calorie restriction have positive effects on sarcopenia and several forms of muscle wasting by activating the autophagy system. This review describes recent research advances regarding autophagy-dependent signaling in sarcopenia.

DOI： 10.1016/B978-0-12-822146-4.00001-6

Scopus

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese