In this Editorial,we highlight the possible role that metabolism dysfunction-associated steatotic liver disease(MASLD)may play in the future,regarding liver disease in patients with transfusion-dependent β-thalassemi...In this Editorial,we highlight the possible role that metabolism dysfunction-associated steatotic liver disease(MASLD)may play in the future,regarding liver disease in patients with transfusion-dependent β-thalassemia(TDBT).MASLD is characterized by excessive accumulation of fat in the liver(hepatic steatosis),in the presence of cardiometabolic factors.There is a strong correlation between the occurrence of MASLD and insulin resistance,while its increased prevalence parallels the global epidemic of diabetes mellitus(DM)and obesity.Patients with TDBT need regular transfusions for life to ensure their survival.Through these transfusions,a large amount of iron is accumulated,which causes saturation of transferrin and leads to the circulation of free iron molecules,which cause damage to vital organs(primarily the liver and myocardium).Over the past,the main mechanisms for the development of liver disease in these patients have been the toxic effect of iron on the liver and chronic hepatitis C,for which modern and effective treatments have been found,resulting in successful treatment.Additional advances in the treatment and monitoring of these patients have led to a reduction in deaths,and an increase in their life expectancy.This increased survival makes them vulnerable to the onset of diseases,which until recently were mainly related to the non-thalassemic general population,such as obesity and DM.There is insufficient data in the literature regarding the prevalence of MASLD in this population or on the risk factors for its occurrence.However,it was recently shown by a study of 45 heavily transfused patients with beta-thalassemia(Padeniya et al,BJH),that the presence of steatosis is a factor influencing the value of liver elastography and thus liver fibrosis.These findings suggest that future research in the field of liver disease in patients with TDBT should be focused on the occurrence,the risk factors,and the effect of MASLD on these patients.展开更多
背景:目前运动疗法是非药物治疗腰痛的有效方法,运动疗法可通过骨骼和肌肉之间的机械-化学偶联维持腰椎的稳定,但目前尚无关于运动疗法通过机械-化学偶联缓解慢性非特异性下背痛之间研究进展及最佳治疗方案的明确阐述。目的:综述运动疗...背景:目前运动疗法是非药物治疗腰痛的有效方法,运动疗法可通过骨骼和肌肉之间的机械-化学偶联维持腰椎的稳定,但目前尚无关于运动疗法通过机械-化学偶联缓解慢性非特异性下背痛之间研究进展及最佳治疗方案的明确阐述。目的:综述运动疗法时椎旁肌通过机械-化学偶联影响腰椎稳定性进而缓解慢性非特异性下背痛的相关研究进展,以及目前运动疗法治疗慢性非特异性下背痛的最佳方案。方法:在万方数据库、中国知网、维普、Web of Science和PubMed数据库进行文献检索,以“慢性非特异性下背痛,腰椎稳定,椎旁肌,运动疗法”为中文检索词,以“chronic nonspecific low back pain,lumbar stabilization,paravertebral muscle,exercise therapy”为英文检索词,检索各数据库建库至2024年1月发表的相关文献,最终纳入93篇文献进行归纳总结。结果与结论:运动疗法可以通过适当的机械刺激作用于椎旁肌和骨骼并使其产生相应的变化。运动疗法主要通过机械-化学偶联方式来提高椎旁肌的质量,进而维持腰椎稳定,从而更好地缓解慢性非特异性下背痛,是慢性非特异性下背痛的重要干预措施。但是,对于运动疗法通过腰椎稳定来治疗慢性非特异性下背痛的确切有效方案尚无明确报道。个体化运动方案的制定对于慢性非特异性下背痛的治疗和预后尤为重要。同一个体的肌肉质量与骨骼质量是密切相关的,影像学评估椎旁肌的质量和体积对于疾病的发现和干预具有重要意义。展开更多
背景:阿尔茨海默病患者存在严重的脑能量障碍,近年来基于酮体干预的脑能量拯救策略在阿尔茨海默病的治疗中越来越受到重视。目的:探讨β-羟基丁酸能否改善β淀粉样蛋白1-42(β-amyloid protein 1-42,Aβ_(1-42))诱导的小鼠海马神经元HT2...背景:阿尔茨海默病患者存在严重的脑能量障碍,近年来基于酮体干预的脑能量拯救策略在阿尔茨海默病的治疗中越来越受到重视。目的:探讨β-羟基丁酸能否改善β淀粉样蛋白1-42(β-amyloid protein 1-42,Aβ_(1-42))诱导的小鼠海马神经元HT22细胞能量障碍。方法:将HT22细胞分为4组,分别为对照组、β-羟基丁酸组、Aβ_(1-42)组、Aβ_(1-42)+β-羟基丁酸组。使用相应试剂盒检测HT22细胞的存活率、ATP水平、α-酮戊二酸脱氢酶活性、Na^(+)K^(+)-ATP酶活性、线粒体膜电位及活性氧水平。结果与结论:与对照组相比,Aβ_(1-42)组HT22细胞的存活率、ATP水平、α-酮戊二酸脱氢酶活性、Na^(+)K^(+)-ATP酶活性、线粒体膜电位均显著降低(P<0.05),活性氧水平显著升高(P<0.05)。与Aβ_(1-42)组相比,Aβ_(1-42)+β-羟基丁酸组HT22细胞的存活率、ATP水平、α-酮戊二酸脱氢酶活性、Na^(+)K^(+)-ATP酶活性、线粒体膜电位均显著升高(P<0.05),活性氧水平显著降低(P<0.05)。结果表明:β-羟基丁酸提高了线粒体生物能量功能和细胞存活率,最终改善了Aβ_(1-42)诱导的HT22细胞能量障碍。展开更多
文摘In this Editorial,we highlight the possible role that metabolism dysfunction-associated steatotic liver disease(MASLD)may play in the future,regarding liver disease in patients with transfusion-dependent β-thalassemia(TDBT).MASLD is characterized by excessive accumulation of fat in the liver(hepatic steatosis),in the presence of cardiometabolic factors.There is a strong correlation between the occurrence of MASLD and insulin resistance,while its increased prevalence parallels the global epidemic of diabetes mellitus(DM)and obesity.Patients with TDBT need regular transfusions for life to ensure their survival.Through these transfusions,a large amount of iron is accumulated,which causes saturation of transferrin and leads to the circulation of free iron molecules,which cause damage to vital organs(primarily the liver and myocardium).Over the past,the main mechanisms for the development of liver disease in these patients have been the toxic effect of iron on the liver and chronic hepatitis C,for which modern and effective treatments have been found,resulting in successful treatment.Additional advances in the treatment and monitoring of these patients have led to a reduction in deaths,and an increase in their life expectancy.This increased survival makes them vulnerable to the onset of diseases,which until recently were mainly related to the non-thalassemic general population,such as obesity and DM.There is insufficient data in the literature regarding the prevalence of MASLD in this population or on the risk factors for its occurrence.However,it was recently shown by a study of 45 heavily transfused patients with beta-thalassemia(Padeniya et al,BJH),that the presence of steatosis is a factor influencing the value of liver elastography and thus liver fibrosis.These findings suggest that future research in the field of liver disease in patients with TDBT should be focused on the occurrence,the risk factors,and the effect of MASLD on these patients.
文摘背景:目前运动疗法是非药物治疗腰痛的有效方法,运动疗法可通过骨骼和肌肉之间的机械-化学偶联维持腰椎的稳定,但目前尚无关于运动疗法通过机械-化学偶联缓解慢性非特异性下背痛之间研究进展及最佳治疗方案的明确阐述。目的:综述运动疗法时椎旁肌通过机械-化学偶联影响腰椎稳定性进而缓解慢性非特异性下背痛的相关研究进展,以及目前运动疗法治疗慢性非特异性下背痛的最佳方案。方法:在万方数据库、中国知网、维普、Web of Science和PubMed数据库进行文献检索,以“慢性非特异性下背痛,腰椎稳定,椎旁肌,运动疗法”为中文检索词,以“chronic nonspecific low back pain,lumbar stabilization,paravertebral muscle,exercise therapy”为英文检索词,检索各数据库建库至2024年1月发表的相关文献,最终纳入93篇文献进行归纳总结。结果与结论:运动疗法可以通过适当的机械刺激作用于椎旁肌和骨骼并使其产生相应的变化。运动疗法主要通过机械-化学偶联方式来提高椎旁肌的质量,进而维持腰椎稳定,从而更好地缓解慢性非特异性下背痛,是慢性非特异性下背痛的重要干预措施。但是,对于运动疗法通过腰椎稳定来治疗慢性非特异性下背痛的确切有效方案尚无明确报道。个体化运动方案的制定对于慢性非特异性下背痛的治疗和预后尤为重要。同一个体的肌肉质量与骨骼质量是密切相关的,影像学评估椎旁肌的质量和体积对于疾病的发现和干预具有重要意义。
文摘背景:阿尔茨海默病患者存在严重的脑能量障碍,近年来基于酮体干预的脑能量拯救策略在阿尔茨海默病的治疗中越来越受到重视。目的:探讨β-羟基丁酸能否改善β淀粉样蛋白1-42(β-amyloid protein 1-42,Aβ_(1-42))诱导的小鼠海马神经元HT22细胞能量障碍。方法:将HT22细胞分为4组,分别为对照组、β-羟基丁酸组、Aβ_(1-42)组、Aβ_(1-42)+β-羟基丁酸组。使用相应试剂盒检测HT22细胞的存活率、ATP水平、α-酮戊二酸脱氢酶活性、Na^(+)K^(+)-ATP酶活性、线粒体膜电位及活性氧水平。结果与结论:与对照组相比,Aβ_(1-42)组HT22细胞的存活率、ATP水平、α-酮戊二酸脱氢酶活性、Na^(+)K^(+)-ATP酶活性、线粒体膜电位均显著降低(P<0.05),活性氧水平显著升高(P<0.05)。与Aβ_(1-42)组相比,Aβ_(1-42)+β-羟基丁酸组HT22细胞的存活率、ATP水平、α-酮戊二酸脱氢酶活性、Na^(+)K^(+)-ATP酶活性、线粒体膜电位均显著升高(P<0.05),活性氧水平显著降低(P<0.05)。结果表明:β-羟基丁酸提高了线粒体生物能量功能和细胞存活率,最终改善了Aβ_(1-42)诱导的HT22细胞能量障碍。
