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Journal Article
Epigenetic mechanisms of pulmonary hypertension
Gene H. Kim, John J. Ryan, Glenn Marsboom and Stephen L. Archer
Pulmonary Circulation
Vol. 1, No. 3 (July 2011), pp. 347-356
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DOI: 10.32.87300
Stable URL: http://www.jstor.org/stable/10.32.87300
Page Count: 10
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Epigenetics
Methylation
Gene expression
Acetylation
Right ventricular hypertrophy
Pulmonary hypertension
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AbstractEpigenetics refers to changes in phenotype and gene expression that occur without alterations in DNA sequence. Epigenetic modifications of the genome can be acquired de novo and are potentially heritable. This review focuses on the emerging recognition of a role for epigenetics in the development of pulmonary arterial hypertension (PAH). Lessons learned from the epigenetics in cancer and neurodevelopmental diseases, such as Prader-Willi syndrome, can be applied to PAH. These syndromes suggest that there is substantial genetic and epigenetic cross-talk such that a single phenotype can result from a genetic cause, an epigenetic cause, or a combined abnormality. There are three major mechanisms of epigenetic regulation, including methylation of CpG islands, mediated by DNA methyltransferases, modification of histone proteins, and microRNAs. There is substantial interaction between these epigenetic mechanisms. Recently, it was discovered that there may be an epigenetic component to PAH. In PAH there is downregulation of superoxide dismutase 2 (SOD2) and normoxic activation of hypoxia inducible factor (HIF-1α). This decrease in SOD2 results from methylation of CpG islands in SOD2 by lung DNA methyltransferases. The partial silencing of SOD2 alters redox signaling, activates HIF-1α) and leads to excessive cell proliferation. The same hyperproliferative epigenetic abnormality occurs in cancer. These epigenetic abnormalities can be therapeutically reversed. Epigenetic mechanisms may mediate gene-environment interactions in PAH and explain the great variability in susceptibility to stimuli such as anorexigens, virus, and shunts. Epigenetics may be relevant to the female predisposition to PAH and the incomplete penetrance of BMPR2 mutations in familial PAH.
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This item contains 76 references.
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运动训练与脑内一氧化氮关系的研究进展
动过程中NO对中枢神经系统影响的研究未见人体实验。建议从训练理论与运动实践紧密结合的实际原理出发,更多地以人体尤其是运动员为研究对象,探索运动过程中NO与中枢神经系统的关系,为中枢性疲劳机制和运动性适应的研究提供一定的理论依据。参考文献:
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hypothalamo-pituiary–adrenocorticalaxis[J].TrendsNeurosc,i~84.
ZONGSHUBAOGAO
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(上接第127页)2.4?有运动损伤史的不同气质类型的学生运动项目分布特征在调查的246名有运动损伤史的学生共7项运动项目中,每个项目都存在着不同人数的运动损伤,各种气质类型的学生都有。通过表4可知,田径项目上发生的损伤次数最多,总共79人,损伤学生气质类型主要分布在多血质、粘液质这两种气质类型上。在篮球项目上有50名学生发生损伤,主要集中在多血质、粘液质、胆汁质-多血质混合型的气质类型上,各为20人、5人、5人。其余项目如体操、足球、排球、武术、健美操中由于损伤人数较少,气质类型分布无明显的规律特征,但仍可看出,多血质、粘液质气质类型发生运动损伤的人数较多。
表4?有运动损伤史的不同气质类型的学生运动项目
分布特征统计(单位:人)
气质类型多血质粘液质胆汁质抑郁质多-粘粘-抑胆-多-粘胆-多胆-抑篮球田径体操足球排球武术健美操其他总计
类型上。这是因为,多血质气质类型的学生表现为注意力不稳
定且易分散,兴趣容易转移,情绪容易变换,求之过急,缺乏持久力。心理不健康时,神经过敏加剧,随之会出现缄默、忧虑、急躁、悲观、自信心丧失等症状。粘液质气质类型的学生不够灵活,常有学习上的心理障碍,身心机能很难即刻发动。与这两种气质类型相关的混合型的气质类型也具有这两种的特点。而体育教学、训练自身的特点决定,学生在进行专业技术技能学习和教学比赛时,身体和心理机能都应尽快适应当时的运动要求。如果不能达到这种要求,就会导致动作变形,出现运动损伤。可见,这些气质类型学生的性格特点决定了其是易损伤人群,教学中应采取相应措施加以防范。要有针对性地加强克服学生气质弱点的专门性训练。如,平时要加强多血质气质类型学生集中注意力的训练,粘液质气质类型学生的反映能力训练等等。在运动损伤学生的气质类型中,抑郁质气质类型最少,这可能是因为抑郁质气质类型的学生办事心细、谨小慎微、与世无争的特征决定的。参考文献:
[1]张文普,史海现,毛卫国.有运动损伤史的学生气质类型分布特征的调查研究[J].广州体育学院学报,):51-52.
[2]方敏.体育专业学生神经类型与急性损伤的关系[J].四川体育科学,,32.
[3]张文普.体育专业学生严重运动损伤的现状与分析[J].四川体育科学,):16-17.
[4]刘晓莉,张琴.体育专业在校生运动损伤情况调查与分析[J].中国体育科技,):46-47.
3?结果与分析
无论是运动损伤学生气质类型的总体分布特征、性别分布特征、损伤程度分布特征还是损伤项目分布特征,主要集中于多血质、粘液质、胆汁质、多血质-粘液质混合型这4类气质
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