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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >SLEEP ELECTROENCEPHALOGRAM DELTA-FREQUENCY AMPLITUDE, NIGHT PLASMA LEVELS OF TUMOR NECROSIS FACTOR ALPHA, AND HUMAN IMMUNODEFICIENCY VIRUS INFECTION
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SLEEP ELECTROENCEPHALOGRAM DELTA-FREQUENCY AMPLITUDE, NIGHT PLASMA LEVELS OF TUMOR NECROSIS FACTOR ALPHA, AND HUMAN IMMUNODEFICIENCY VIRUS INFECTION

机译：睡眠电生理学三角波幅值，肿瘤坏死因子α的夜间血浆水平和人免疫缺陷病毒感染

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摘要

We tested the hypothesis that increases in tumor necrosis factor alpha (TNF-alpha) induced by human immunodeficiency virus (HIV) are associated with the increases in slow-wave sleep seen in early HIV infection and the decrease with sleep fragmentation seen in advanced HIV infection, Nocturnal sleep disturbances and associated fatigue contribute to the disability of MV infection, TNF-alpha causes fatigue in clinical use and promotes slow-wave sleep in animal models, With slow progress toward a vaccine and weak effects from current therapies, efforts are directed toward extending productive life of HIV-infected individuals and shortening the duration of disability in terminal illness, We describe previously unrecognized nocturnal cyclic variations in plasma levels of TNF-alpha in all subjects, In 6 of 10 subjects (1 control subject, 3 HIV-seropositive patients with CD4(+) cell number > 400 cells per mu l, and 2 HIV-positive patients with CD4(+) cell number < 400 cells per mu l), these fluctuations in TNF-alpha were coupled to the known rhythm of electroencephalogram delta amplitude (square root of power) during sleep. This coupling was not present in 3 HIV-positive subjects with CD4(+) cell number < 400 cells per pi and 1 control subject, In 5 HIV subjects with abnormally low CD4(+) cell counts (< 400 cells per mu l), the number of days since seroconversion correlated significantly with low correlation between TNF-alpha and delta amplitude, We conclude that a previously unrecognized normal, physiological coupling exists between TNF-alpha and delta amplitude during sleep and that the lessened likelihood of this coupling in progressive HIV infection may be important in understanding fatigue-related symptoms and disabilities.
机译：我们测试了以下假设：人类免疫缺陷病毒（HIV）诱导的肿瘤坏死因子α（TNF-alpha）的增加与早期HIV感染中慢波睡眠的增加以及晚期HIV感染中睡眠破碎的减少有关，夜间睡眠障碍和相关的疲劳导致MV感染的丧失，TNF-α在临床使用中引起疲劳并促进动物模型中的慢波睡眠。随着疫苗进展缓慢以及当前疗法的不良影响，人们将努力转向延长了HIV感染者的生产寿命并缩短了绝症中的残障持续时间，我们描述了所有受试者中TNF-α血浆水平先前无法识别的夜间循环变化，在10名受试者中有6名（1名对照受试者，3名HIV血清阳性） CD4（+）细胞数> 400细胞/μl的患者和2例CD4（+）细胞数<400细胞/μl的HIV阳性患者） TNF-α的变化与睡眠过程中脑电图增量幅度（功率平方根）的已知节律有关。在3名HIV阳性受试者中，每个pi的CD4（+）细胞数少于400个细胞，而1名对照受试者中不存在这种偶联。在5名CD4（+）细胞计数异常低（每亩<400个细胞）的HIV受试者中，血清转化以来的天数与TNF-α和δ幅度之间的低相关性显着相关，我们得出结论，睡眠期间TNF-α和δ幅度之间存在以前无法识别的正常生理耦合，并且这种进行性HIV耦合的可能性降低感染对于理解疲劳相关症状和残疾可能很重要。

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