Publications by authors named "Goichiro Yoshida"

Article Synopsis
  • - The study examined poor sleep quality among Japanese student-athletes during the COVID-19 pandemic in 2020 and a year later in 2021, involving surveys from six universities with a total of 1,672 participants.
  • - Results showed that poor sleep quality was reported by 33.6% in 2020 and 36.6% in 2021, with different associated lifestyle habits and psychological factors influencing sleep issues each year.
  • - In both years, psychological distress was a common risk factor, but the factors contributing to poor sleep were more pandemic-specific in 2020 while resembling pre-pandemic habits in 2021.
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Background: Due to various factors, water balance may vary across seasons. These effects may be particularly prominent in athletes and dependent upon energy expenditure during training.

Methods: Japanese male kendo college athletes participated in this study during their training sessions.

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Article Synopsis
  • This study aimed to identify risk factors for sleep disorders among student athletes, focusing on lifestyle habits, competition activities, and psychological distress.
  • Conducted with 906 student athletes from various Japanese universities, the research used surveys to assess factors like sleep quality, daily habits, and stress levels.
  • Findings highlighted that poor sleep was associated with late bedtimes, early rises, smartphone use at night, job stress, and competition-related pressures, indicating a need for better management of these issues.
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Physical fitness is an indicator of systemic well-being in humans. Little is known about the role of physical fitness for maintaining systemic health in the elderly. Here, we study elderly subjects to determine the relationships between physical fitness and CD56 and CD16 surface NK cell markers on peripheral blood lymphocytes, as well as to analyze the relationship between the surface markers and incidence of death.

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The food habit is involved in the onset and development of lifestyle-related diseases. In this review I would like to describe a historical case of vitamin B1 deficiency, as well as our case study of fatty acid metabolism abnormality due to carnitine deficiency. In history, the army and navy personnel in Japan at the end of the 19th century received food rations based on a high-carbohydrate diet including white rice, resulting in the onset of beriberi.

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Carnitine-deficient juvenile visceral steatosis (JVS) mice, suffering from fatty acid metabolism abnormalities, have reduced locomotor activity after fasting. We examined whether JVS mice exhibit specific defect in the feeding response to fasting, a key process of anti-famine homeostatic mechanism. Carnitine-deficient JVS mice showed grossly defective feeding response to 24 h-fasting, with almost no food intake in the first 4 h, in marked contrast to control animals.

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Carnitine is an essential cofactor for the oxidation of fatty acid in the mitochondria and an efficient therapeutics for primary carnitine deficiency. We herein analyzed the prolonged effects of carnitine on the reduced locomotor activity and energy metabolism of fasted carnitine-deficient juvenile visceral steatosis (jvs(-/-)) mice. We found that a single carnitine administration to 24-h fasted jvs(-/-) mice in the morning increased both the locomotor activity and oxygen consumption at night not only on the same day, but also on the next day, when the carnitine levels in the blood and tissues were already as low as at the original carnitine-deficient state.

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We found reduced locomotor activity (LA) under fasting in systemic carnitine-deficient juvenile visceral steatosis (jvs(-/-)) mice. When food was withdrawn at 8:00 a.m.

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Juvenile visceral steatosis (JVS) mouse is an animal model of human primary carnitine deficiency caused by a mutation of the gene encoding carnitine transporter, and suffers from various symptoms, such as fatty liver, growth retardation, hyperammonemia, hypoglycemia, and cardiac hypertrophy. We have shown that hyperammonemia during the weaning period (15-26 days of age) is caused by suppression of urea cycle enzyme gene expression. The suppression resulted from activation of a transcription factor, AP-1.

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