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Selenium is an essential trace element. In cattle, selenium deficiency causes dysfunction of various organs, including skeletal and cardiac muscles. In humans as well, lack of selenium is associated with many disorders, but despite accumulation of clinical reports, muscle diseases are not generally considered on the list. The goal of this review is to establish the connection between clinical observations and the most recent advances obtained in selenium biology. Recent results about a possible role of selenium-containing proteins in muscle formation and repair have been collected. Selenoprotein N is the first selenoprotein linked to genetic disorders consisting of different forms of congenital muscular dystrophies. Understanding the muscle disorders associated with selenium deficiency or selenoprotein N dysfunction is an essential step in defining the causes of the disease and obtaining a better comprehension of the mechanisms involved in muscle formation and maintenance. Received 13 July 2005; received after revision 9 September 2005; accepted 4 October 2005  相似文献   
3.
植物钙营养与贮存关系的研究   总被引:1,自引:0,他引:1  
多年多点试验表明:钙在4种石灰性土壤以及一些植物体内的运输缓慢;在生殖生长为主期间,根外喷施0.4%CaCl2溶液,可改变果实表皮细胞形状,有效地延长果品贮存期,t检验处理均高于对照,差异均达极显著。  相似文献   
4.
Periodic circadian (24-h) cycles play an important role in daily hormonal and behavioural rhythms. Usually our sleep/wake cycle, temperature and melatonin rhythms are internally synchronized with a stable phase relationship. When there is a desynchrony between the sleep/wake cycle and circadian rhythm, sleep disorders such as advanced and delayed sleep phase syndrome can arise as well as transient chronobiologic disturbances, for example from jet lag and shift work. Appropriately timed bright light is effective in re-timing the circadian rhythm and sleep pattern to a more desired time, ameliorating these disturbances. Other less potent retiming effects may also be obtained from the judicious use of melatonin and exercise.  相似文献   
5.
Summary In the realm of human circadian rhythms, the masking effect is defined as the change in the course of deep body temperature induced by changes in the degree of physical activity, or by the alteration between sleep and wake. This effect is particularly obvious during internal desynchronization where the rhythms of deep body temperature, and the sleep-wake sleep-wake sleep cycle — i.e. one of the masking factors — run with different periods.Every sleep onset is accompanied by a rapid drop, and wake onset by a rapid rise in deep body temperature, each one with an overshoot of about 50% of the steady state variations. When rhythms are calculated, with the dominant temperature period as the screening period, exclusively from data obtained during sleep episodes, on the one hand, and from those obtained exclusively during wake, on the other, two average cycles emerge: the sleep temperature curve and the wake temperature curve. Both run in parallel but are separated by the masking effcct. As derived from many experiments, the mean masking effect amounts to 0.28±0.06°C. The masking effect also depends to some extent on the phase of the temperature rhtthm; it is larger than average around the temperature maximum and during the descending phase of the temperature cycle, where the alertness commonly is highest and the probability to sleep, in general, and the REM sleep propensity, in particular, are smaller than average. This also can be interpreted to indicate that the sleep temperature curve is phase advanced relative to the wake temperature curve; this, on the average, by 0.9±0.3 h.If the individually determined amount of masking is added to the temperature data obtained during sleep, or substracted from the temperature data obtained during wake, a temperature curve emerges that can be though of as being purified of the masking effect. Analyses of this artificial curve allow estimation of that part of the internal interactions uninfluenced by the masking effect. On the average, about half of the amount of interaction between the rhythm of sleep-wake and that of deep body temperature is explained by the masking effect, whereas the other half is oscillatory interaction. Both types of interaction are inherent and inseparable parts of the circadian clock mechanism, as can be deduced from model considerations.  相似文献   
6.
介绍了基于网络的睡眠监护与分析系统的软硬件设计方案.对系统设计中需要解决的网络数据传输.图形实时显示.以及数据库管理等一些关键性的问题.提出了解决方法.基于这些方法进行了初步的系统实验.取得了较为满意的效果.本系统可望成为未来数字化家庭的重要医疗单元和今后进一步开展远程医疗研究的基础.  相似文献   
7.
为了减轻传统接触式睡眠生理监测系统对人体造成的负担,设计了一种基于微波技术的非接触式睡眠生理信号采集与分析系统,提出一种基于体动射频信号的睡眠分期识别算法.通过小波变换对射频运动传感器(RFMS)采集的体动信号进行预处理,再计算出体动信号的能量值,最后通过判别式处理和阈值法实现了睡眠分期:醒觉期、浅睡期、中睡期、深睡期.实验采集分析了8个实验者为期46天的睡眠生理信号,同时同步采集视频信息、TANITA水床睡眠信息、接触式呼吸脉搏信号.与视频结果比较发现醒觉期正确率达到90%;与TANITA水床睡眠结果相比,本系统的结果与其吻合程度达到70%;与不同睡眠状态下呼吸率、心率的变化相比,本系统的结果吻合度达到80%.  相似文献   
8.
阻塞性睡眠呼吸暂停综合症的观察及护理   总被引:5,自引:0,他引:5  
通过对55例阻塞性睡眠呼吸暂停综合症患者术前、术后的护理及观察,总结了护理体会,着重对术前、术后健康教育及心理、术后伤口出血情况,气管切开护理,咽部水肿,饮食及口腔清洁,并发症观察护理进行了总结,并通过术前,术后血氧饱和度、呼吸、心率的监测,总结了阻塞性睡眠呼吸暂停综合症患者的手术疗效。  相似文献   
9.
Recent findings concerning human slow wave sleep (hSWS-stages 3+4; delta EEG activity) are critically reviewed. Areas covered include the significance of the first hSWS cycle; hSWS in extended sleep; relationship between hSWS, prior wakefulness and sleep loss; hSWS influence on sleep length; problems with hSWS deprivation; influence of the circadian rhythm; individual differences in hSWS, especially, age, gender and constitutional variables such as physical fitness and body composition. Transient increases in hSWS can be produced by increasing both the quality and quantity of prior wakefulness, with an underlying mechanism perhaps relating to the waking level of brain metabolism. Whilst there may also be thermoregulatory influences on hSWS, hypotheses that energy conservation and brain cooling are major roles for hSWS are debatable. hSWS seems to offer some form of cerebral recovery, with the prefrontal cortex being particularly implicated. The hSWS characteristics of certain forms of major psychiatric disorders may well endorse this prefrontal link.  相似文献   
10.
Comparison of the growing number of disorders known to be associated with triplet repeat expansions reveals both common features and a diversity of molecular pathways. Despite significant progress towards the characterization of proteins coded by the mutant genes, the complex nature of these disorders requires identification of all molecular components of the triplet repeat pathways. In this brief review we will discuss recent progress in determining the molecular mechanisms of disorders with unstable trinucleotide mutations. Received 13 January 1999; received after revision 8 March 1999; accepted 9 March 1999  相似文献   
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