Background: Taurine (2-aminoethanesulfonic acid) is a semi-essential amino acid found in mammalian tissues that is not involved in protein synthesis. The function of taurine is not completely understood. Some studies have demonstrated that taurine supplementation reduces death rate in rabbits with heart failure (HF) and diminishes HF severity in human models of congestive HF. In this study we have evaluated the effect of taurine supplementation on exercise capacity of patients with HF.
Methods: A randomized single-blind placebo-controlled clinical trial was conducted on 29 patients with HF with left ventricular ejection fraction (LVEF) less than 50% who were in functional class II or III according to New York Heart Association classification. A total of 15 patients received taurine supplementation 500 mg three times a day while the remaining 14 patients received placebo for 2 weeks. All patients performed exercise tolerance test before and after taurine and placebo supplementation.
Results: The mean age of patients was 60.57 ± 6.54 years, they were mostly male (26 of 29), and had mean LVEF of 29.27 ± 6.97%. There were no significant differences in terms of LVEF, body mass index, and also exercise time, metabolic equivalents (METS) and exercise distance before supplementation. Exercise time, METS, and exercise distance increased significantly in patients who received taurine supplement for 2 weeks (p-value<0.0001 for all), but did not increase significantly in patients who received placebo (p-values 0.379, 0.244, and 0.577 respectively).
Conclusion: Taurine supplementation in patients with HF who are taking standard medical treatment can increase their exercise capacity.
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http://dx.doi.org/10.1016/j.jjcc.2011.01.007 | DOI Listing |
Mitochondrial tRNA (mt-tRNA) modifications play pivotal roles in decoding and sustaining tRNA stability, thereby enabling synthesis of essential respiratory complex proteins in mitochondria. Consequently, loss of human mt-tRNA modifications caused by mutations in the mitochondrial or nuclear genome can cause life-threatening mitochondrial diseases such as encephalopathy and cardiomyopathy. In this article, we first provide a comprehensive overview of the functions of mt-tRNA modifications, the responsible modification enzymes, and the diseases caused by loss of mt-tRNA modifications.
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State Key Laboratory of Food Science and Resources, Jiangnan University, Wuxi, Jiangsu, China.
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Psychology, Santa Barbara City College, Santa Barbara, CA 93109, USA.
Autism spectrum disorder (ASD) is a neurodevelopmental disability that presents significant challenges in communication and behavior. ASD prevalence exceeds 2% among eight-year-old children and is at similar levels globally. We propose that critical periods during fetal development and early postnatal years establish the conditions for either neurotypical development or the emergence of autism through mechanisms that influence immune function or delay neuronal development.
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State Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
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Male infertility is a complex and multifactorial clinical condition affecting a large population attributed to several factors, including perturbation in oxidative stress and the level of essential trace elements. Oxidative stress exerts multiple issues related to reproductive health, including male infertility, decreased sperm motility, sperm DNA damage, and an increased susceptibility to genetic disorders. Besides chemical toxins and food allergens in junk food items, many drugs can also lead to male infertility.
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