13 research outputs found

    Effects of a 10-week musical instrument training on cognitive function in healthy older adults: implications for desirable tests and period of training

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    IntroductionPrevious studies have shown that musical instrument training programs of 16 or more weeks improve verbal memory (Logical Memory Test delayed recall), processing speed (Digit Symbol Coding Test), and executive function (Trail Making Test Part B) of musically untrained healthy older adults. However, it is unclear whether shorter-period instrument training can yield similar effects. We sought to (1) verify those results and (2) clarify if intervention effects could be detected using other measures such as reaction time.MethodsHealthy older adults (mean age = 73.28 years) were pseudo-randomly assigned to an untrained control group (n = 30) or an intervention group (n = 30) that received a weekly 10-session musical instrument training program (using melodica). We conducted neuropsychological tests on which intervention effects or association with musical training were reported in previous studies. We newly included two reaction time tasks to assess verbal working memory (Sternberg task) and rhythm entrainment (timing task). Intervention effects were determined using a “group × time” analysis of variance (ANOVA).ResultsThe intervention effects were detected on the reaction time in Sternberg task and phonological verbal fluency. Although intervention effects had been reported on Logical Memory test, Digit Symbol Coding Test and Trail Making Test in previous studies with longer training periods, the present study did not show such effects. Instead, the test-retest practice effect, indicated by significant improvement in the control group, was significant on these tests.DiscussionThe present results indicated the usefulness of working memory assessments (Verbal Fluency Test and Sternberg task) in detecting the effects of short-term melodica training in healthy older adults. The practice effect detected on those three tasks may be due to the shorter interval between pre- and post-intervention assessments and may have obscured intervention effects. Additionally, the findings suggested the requirement for an extended interval between pre- and post-tests to capture rigorous intervention effects, although this should be justified by a manipulation of training period

    Toxic AGE (TAGE) Theory for the Pathophysiology of the Onset/Progression of NAFLD and ALD

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    Non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) are among the most common causes of chronic liver diseases in the westernized world. NAFLD and ALD are frequently accompanied by extrahepatic complications, including hepatocellular carcinoma and cardiovascular diseases, which have a negative impact on patient survival. The chronic ingestion of an excessive daily diet containing sugar/high-fructose corn syrup increases the level of the fructose/glucose metabolite, glyceraldehyde (GA), while the chronic consumption of an excessive number of alcoholic beverages increases the level of the alcohol metabolite, acetaldehyde (AA) in the liver. GA and AA are known to react non-enzymatically with the ε- or α-amino groups of proteins, thereby generating advanced glycation end-products (AGEs, GA-AGEs, and AA-AGEs, respectively) in vivo. The interaction between GA-AGEs and the receptor for AGEs (RAGE) alters intracellular signaling, gene expression, and the release of pro-inflammatory molecules and also elicits the production of reactive oxygen species by human hepatocytes and hepatic stellate cells, all of which may contribute to the pathological changes associated with chronic liver diseases. We herein discuss the pathophysiological roles of GA-AGEs and AA-AGEs (toxic AGEs, TAGE) and a related novel theory for preventing the onset/progression of NAFLD and ALD

    Sleep disordered breathing and metabolic comorbidities across gender and menopausal status in East Asians; the Nagahama Study

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    生活習慣病に睡眠時無呼吸症候群がひそむことを解明 --アジア最大資料数のながはまコホートより--. 京都大学プレスリリース. 2020-05-19.It is well known that the prevalence of sleep disordered breathing (SDB) is increased in patients with obesity or metabolic comorbidities. However, the way in which the prevalence of SDB increases in relation to comorbidities according to the severity of obesity remains unclear. This cross-sectional study evaluated 7713 community participants with nocturnal oximetry ≥2 nights. SDB was assessed by the 3% oxygen desaturation index corrected for sleep duration obtained by wrist actigraphy (Acti-ODI3%). SDB severity was defined by Acti-ODI3%. Obesity was defined as body mass index ≥25 kg·/m−2. The prevalence of SDB was 41.0% (95% CI 39.9–42.1), 46.9% (45.8–48.0), 10.1% (9.5–10.8), and 2.0% (1.7–2.3) in normal, mild, moderate, and severe SDB, respectively, with notable sex differences evident (men >post-menopausal women >pre-menopausal women). Comorbidities such as hypertension, diabetes, and metabolic syndrome were independently associated with the prevalence of moderate-to-severe SDB, and coincidence of any one of these with obesity was associated with a higher probability of moderate-to-severe SDB (OR 8.2, 95% CI 6.6–10.2; 7.8, 5.6–10.9; 6.7, 5.2–8.6, respectively). Dyslipidemia in addition to obesity was not additively associated with the prevalence of moderate to-severe SDB. The number of antihypertensive drugs was associated with SDB (p for trend <0.001). Proportion of a high cumulative percentage of sleep time with SpO2 <90% increased even among moderate-to-severe SDB with increases in obesity. Metabolic comorbidities contribute to SDB regardless of the degree of obesity. We should recognise the extremely high prevalence of moderate-to-severe SDB in patients with obesity and metabolic comorbidities
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