睡眠的体液调节机制

目前对睡眠的测定尚无理想的直接方法,通常由一些生理指标如脑电图,肌电图,脑内温度变化,眼球运动来推测。根据睡眠过程中所记录的这些生理指标,可将睡眠分为两个主要时相,即快动眼期（ＲＥＭＳ）和非快动眼期（ＮＲＥＭＳ）。一次睡眠是由清醒、ＲＥＭＳ和ＮＲＥＭ...     

大鼠慢波睡眠和睡眠过渡期脑电信号的小波变换分析

EEG信号经常包含许多快速的时变信息 ,将较长时间段的EEG信号近似看作平稳信号 ,进行FFT谱估计 ,存在其局限性。应用多分辨率小波变换方法 ,在频域和时域上可以同时定位分析大鼠慢波睡眠和睡眠过渡期脑电的动态变化特性。采用慢性埋植电极记录自由活动大鼠的皮层脑电 ,将信号用小波变换分解成δ、θ、α和 β四个分量 ,求各分量的功率和功率百分比的时间变化曲线 ,并与FFT功率谱分析结果进行比较。结果表明 :慢波睡眠期EEG中有 2 6 .2 %± 7.7%的时间段上δ分量功率小于总功率的 5 0 % ,且δ分量较大时 ,其他分量较小 ;δ分量较小时 ,其他分量较大 ,差别显著。此结果揭示了δ节律与θ和α节律之间的一种互补关系。而传统的FFT功率谱分析方法只能显示δ分量为主 (占总功率 70 .6 %± 6 .4 % )的功率谱 ,不能提供时变信息。对于睡眠过渡期的非稳态EEG信号 ,利用小波变换分解得到的θ和α分量可以鉴别出睡眠纺锤波 ,计算睡眠纺锤波的平均持续时间 ,并比较纺锤波和非纺锤波时期各个频谱分量的变化情况。由此可见 ,小波变换可用于计算新的EEG时频定量分析指标用于分析生理、病理和药理作用引起的睡眠EEG的变化过程 ,以弥补传统FFT功率谱分析的不足之处     

婴儿夜间睡眠脑电纺锤波的观察

婴儿夜间睡眠脑电纺锤波的观察张慧秀,朱国庆,张景行,孔秀（安徽医科大学睡眠障碍研究室,安徽医科大学附属医院合肥２３００３２）婴儿睡眠纺锤波是作为慢波睡眠（ＳＷＳ）的一个标志,也可作为中枢神经系统机能正常与否的一个指标。为了解婴儿睡眠纺锤波发育情况并明...     

激素调节与心脏损害

激素调节与心脏损害＠胡家会＠陈玉红激素调节与心脏损害胡家会陈玉红俗话说，人生自古谁无死，生老病死是人类的自然规律。有的人为保卫祖国边疆战死在沙场上，重于泰山；有的人为个人某私利而死，轻于鸿毛；有的人死于自然灾害，命里注定；更多的人死于疾病与衰老，不可避免；...     

睡眠研究的科学前沿

关于睡眠机制的研究是一门历史悠久的学科.在过去的几十年中,运用细胞电生理学来研究睡眠取得了可喜的成果.由于种种技术上的困难,近年来该领域的研究多集中于临床和医学范围,例如嗜睡症、抑郁症等.虽说睡眠的节律性较易理解,但作为其本质———睡眠的基因和分子水平的自动平衡调节仍是一个谜.细胞因子(IL-1和TNFα)对睡眠的诱导作用已显示从分子水平上了解睡眠的可能性.到目前为止,关于睡眠的功能已有不少理论和假说,但人类对睡眠的生化机制的认识尚处于起步阶段.     

对血糖激素调节的商榷

在《生物学通报》2006年第2期的目次Ⅱ页刊登了徐国恒老师对“胰岛素有抑制胰高血糖素分泌的作用,为何胰高血糖素的产生却能促进胰岛素的产生呢?”问题的解答,我认为徐老师的解答不够清楚,不便于学生的理解。在此与大家进行探讨。     

水,电解质平衡的激素调节

本文综述心钠素、抗利尿激素和肾素-血管紧张素-醛固酮系统对水、电解质的调节作用及其相互作用。机体内存在排钠、排水和保钠、保水两大类激素,两类激素的平衡,对水、电解质平衡的调节具有重要意义。     

昆虫保幼激素生物合成的调节与测定

<正> 保幼激素(JH)是由昆虫的咽侧体(CA)产生。它调节着发育和生殖。从昆虫中已分离出3种具有JH活性的化合物,分别称为JH1、JH2、JH3。它们的生理活性大不相同。JH3是大部分成虫的主要激素,可促进卵巢的发育,所以是一种促性腺激素。JH1和JH2主要在鳞翅目幼虫和蜚蠊若虫内,它们在变态开始就参与这一过程的调节作用,称为变态激素。     

前列腺素D2与睡眠调节

前列腺素D2（PGD2）是目前已知最有潜力的内源性促睡眠物质之一。鼠脑脊液（CSF）中PGD2浓度与睡眠－觉醒周期一致,呈现节律性改变,并且随睡眠剥夺期间嗜睡倾向增加而增加,催化PGH2转变为PGD2的特生酶有两种：Lipocalin型前列腺素D合成酶（L－PGDS）和脾型PGDS。L－PGDS主要在大脑蛛网膜和脉络丛产生,并分泌入CSF。L－PGDS和PGD2在脑室系统、蛛网膜下腔及细胞外间隙中循环,循环中的PGD2可与前脑头端基底腹内侧面的化学感受器中的前列腺素D2受体（DPR）相互作用,通过活化具有腺苷A2a受体的元以产生促进睡眠的信号。PGD2敏感区内DPR的活化可导致腹侧视前区（VLPO）内神经元的活化,其可通过抑制结节乳头核（TMN）而促进睡眠。相反,PGE2在维持大脑清醒状态下起主要作用。PGD2和PGE2的平衡对正常睡眠－觉醒周期的维持十分关键。     

大鼠发育期睡眠/觉醒周期的神经调节

幼年期大鼠的睡眠/觉醒周期和成年期的有显著差异,最为显著的特点是快眼动(REM) 睡眠在24 小时内的百分比远多于其他任何年龄阶段,随着脑发育成熟而逐渐减少.与此同时,非快眼动(NREM) 睡眠和觉醒的百分比逐渐增加.后者与参与NREM睡眠和觉醒调节的神经元在发育早期的成熟程度较为一致.鉴于大鼠发育早期REM睡眠每日的百分比由最高开始逐渐降低,而触发和促进REM睡眠的胆碱能神经元各生化成分的活性则是由最低开始逐渐升高,此期的REM睡眠应该还有胆碱能以外的动力驱动.新近的资料表明,促肾上腺皮质激素释放因子(CRF)可能是幼年期REM睡眠的另一主要驱动力量.     

Real-Time Monitoring of Slow-Wave Sleep by Electroencephalogram Variance

Based on statistical variance as an index of electroencephalogram (EEG) parameters, we monitored slow-wave sleep in both humans and rats in real time and on-line with a widely used personal computer. This EEG variance method may be a useful tool to carry out biological rhythm research, including sleep studies.     

Regulation of insulin sensitivity by adipose tissue-derived hormones and inflammatory cytokines

PURPOSE OF REVIEW: The aim of this review is to assess the role of adipose tissue-derived hormones and inflammatory cytokines in the pathogenesis of obesity-linked type II diabetes, with a special focus on articles published between December 2002 and December 2003. RECENT FINDINGS: Insulin resistance is widely recognized as a fundamental defect seen in obesity and type II diabetes. Although the molecular mechanisms triggering the development of insulin resistance remain elusive, recent studies have suggested that adipose tissue and adipose tissue-derived hormones and inflammatory cytokines play essential roles in the overall insulin sensitivity in vivo. Dysfunctions of adipose tissue can lead to systemic insulin resistance. SUMMARY: Understanding the regulation of the metabolic and secretory functions of adipose tissue, as well as its subsequent impact on overall insulin sensitivity, is becoming increasingly important given the therapeutic potential of targeting the root causes of insulin resistance in the treatment of type 2 diabetes and its associated complications, such as cardiovascular and cerebrovascular diseases.     

Anti-inflammatory effects and changes in prostaglandin patterns induced by 7beta-hydroxy-epiandrosterone in rats with colitis

High dose levels of dehydroepiandrosterone and its 7-hydroxylated derivatives have been shown to reduce oxidative stress and inflammatory responses in dextran sodium sulfate (DSS)-induced colitis in rats. Another endogenous steroid, 7beta-hydroxy-epiandrosterone (7beta-hydroxy-EpiA) has been shown to exert neuroprotective effects at much smaller doses. Our aims were to evaluate whether 7beta-hydroxy-EpiA pre-treatment prevents DSS-induced colitis and to determine whether the effects involve changes in anti-inflammatory prostaglandin (PG) D(2) and 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)) levels. Rats were administered 0.01, 0.1 and 1mg/kg 7beta-hydroxy-EpiA i.p. once a day for 7 days. Thereafter, colitis was induced by administration of 5% DSS in drinking water for 7 days. Levels of the PGs and the expression of cyclooxygenase (COX-2) and PG synthases were assessed during the course of the experiment. Administration of 7beta-hydroxy-EpiA caused a transient increase in COX-2 and PGE synthase expression within 6-15h and augmented colonic tissue levels of 15d-PGJ(2) levels starting at day 2. Treatment with DSS resulted in shortened colon length, depleted mucus in goblet cells and induced oxidative stress. COX-2 and mPGES-1 synthase expression were enhanced and accompanied by increased PGE(2), D(2) and 15d-PGJ(2) production. Although all dose levels of 7beta-hydroxy-EpiA reduced PGE(2) production, only the lowest dose (0.01mg/kg) of the steroid completely prevented colitis damage and tissue inflammation. 7beta-Hydroxy-EpiA pre-treatment prevents the occurrence of DSS-induced colitis through a shift from PGE(2) to PGD(2) production, associated with an early but transient increase in COX-2 expression and a sustained increase in the production of the anti-inflammatory prostaglandin 15d-PGJ(2).     

前列腺素E2对免疫细胞及炎症相关疾病的调控作用

前列腺素E2(prostaglandin E2,PGE2)是一种极其重要的脂质代谢产物,在受到生理或病理的各种刺激,尤其是有害刺激时被释放,在发热、炎症和血压调节中均发挥着重要作用.PGE2通过4种功能相互拮抗的的受体(E-prostanoid receptors,EP1、EP2、EP3和EP4)而广泛参与机体及细胞代谢过程.一直以来,人们都认为前列腺素在免疫过程中发挥的作用相当有限,部分原因是因为抑制类前列腺素合成的非甾体类抗炎药在机体免疫过程中没有发挥明显作用.但近来的研究表明,PGE2很可能在免疫细胞的发育分化及免疫应答过程中也起重要作用.本文主要对前列腺素与免疫系统的关系进行分析和总结,并重点讨论相关研究的新近进展.     

Serum levels of appetite-regulating hormones and pro-inflammatory cytokines are ameliorated by a CLA diet and endurance exercise in rats fed a high-fat diet

[Purpose]

This study examined whether conjugated linoleic acid (CLA) supplementation and endurance exercise affect appetite-regulating hormones and pro-inflammatory cytokines in rats.

[Methods]

Seven-week-old male Sprague-Dawley rats were divided randomly into the high-fat diet sedentary group (HS, n=8), the 1.0% CLA supplemented high-fat diet sedentary group (CS, n=8), and the 1.0% CLA supplemented high-fat diet exercise group (CE, n=8). Rats in the CE group swam 60 min/day, 5 days/week for 4 weeks.

[Results]

Leptin and insulin levels in the CS and CE groups were significantly lower than those in the HS group (p<0.001), whereas leptin (p<0.01) and insulin (p<0.05) levels decreased significantly in the CE compared to those in the CS group. Interleukin (IL)-1β (p<0.001) and IL-6 (p<0.01) levels in the CS and CE groups decreased significantly compared to those in the HS group. Leptin (IL-1β: r=0.835, p<0.001), IL-6 (r=0.607, p<0.05), insulin (IL-1β: r=0.797, p<0.01), and IL-6 (r=0.827, p<0.01) levels were positively related with pro-inflammatory cytokine levels.

[Conclusion]

Endurance exercise may play an important role during CLA supplementation of rats on a high-fat diet.     

睡眠2期脑电信号产生的生理机制模型仿真研究

目前慢波睡眠生理机制研究已有的理论及动物实验结果显示,慢波睡眠中,皮层-丘脑系统神经元存在三种不同节律的振荡:慢振荡(<1 HZ)、δ振荡(1-4Hz)和纺锤振荡(7-14Hz)。这些神经元电活动在皮层水平广泛同步化,产生慢波睡眠脑电。提出了能分别产生这三种节律的三种神经元环路模型,并将之组合简化成一个七细胞环路模型。由这样的大量环路组成的网络模型在合适的突触连接参数范围内,能在皮层处产生人类慢波睡眠脑电2期的完整波形。这一结果说明了如何将动物实验观察到的睡眠生理机制的结果与人自然睡眠活动的脑电结果联系起来,并提示脑信息处理中由微观神经元群放电特征整合为脑的宏观功能状态的主要环节。     

Sleep-enhancing effects of far-infrared radiation in rats

Unrestrained male rats continuously exposed to far-infrared radiation exhibited a significant increase in slow wave sleep (SWS) during the light period but not in the dark period. The change was largely due to the elevated occurrence of SWS episodes but not to the prolongation of their duration. Paradoxical sleep was not affected throughout the observation period except for a significant decrease at the end of the dark period. Thus the far-infrared radiation exerted a sleep modulatory effect closely related to the circadian activity-rest cycle.     

Regulation of gene activity by hormones

Summary Regulation of gene expression, i.e. the reading of the genetic message, is of great importance for many vital processes. According to Jacob and Monod, genes are regulated by a repressor (a protein) which may interact with an inducer (a small molecule). In higher organisms, hormones often function as inducers. Evidence stems from (i) the induction of puffs in giant chromosomes by the insect hormone ecdysone, (ii) the stimulation of nucleic acid synthesis by hormones in vivo and in vitro, (iii) the induction of enzymes by hormones, e.g. cortisol, and (iv) the action of hormones on isolated nuclei where the activity of the DNA-dependent RNA polymerase is stimulated. This is most probably due to an increased template activity of the chromatin. — The implication of these findings for developmental processes are discussed.     

Regulation of apoptosis by steroid hormones

Steroid hormones play major roles in regulation of growth, development, homeostasis, and cell death. Together with other hormones and growth factors, steroids regulate both the function and cellular composition of organs throughout the body. In this article we will discuss the mechanisms of steroid hormone regulated apoptosis. Emphasis will be placed on the effect of glucocorticoids on lymphoid cells.