Independence of the circadian rhythm in alertness from the sleep/wake cycle

It is common knowledge that our feelings of alertness or drowsiness vary throughout the day. Indeed, this diurnal variation is so widely accepted that it has been used to validate the drowsy/alert component of activation obtained from mood adjective checklists. There is, however, some evidence from sleep deprivation and shiftwork studies that this variation is not simply a reflection of our sleep/wake cycle, as might be expected, but is at least partially dependent on an endogenous circadian (approximately 24 h) oscillator such as that proposed to account for the circadian rhythm in body temperature and other physiological variables. Here we have tested this suggestion by separating the body-temperature rhythm from the sleep/wake cycle by progressively shortening artificial time cues (zeitgebers). Our results indicate that the circadian rhythm in alertness can become independent of both the sleep/wake cycle and the rhythm in body temperature. Further, and contrary to our expectations, the results suggest that the sleep/wake cycle exerts less influence on the alertness rhythm than it does on that of temperature.     

Assignment of circadian function for the Neurospora clock gene frequency.

Circadian clocks consist of three elements: entrainment pathways (inputs), the mechanism generating the rhythmicity (oscillator), and the output pathways that control the circadian rhythms. It is difficult to assign molecular clock components to any one of these elements. Experiments show that inputs can be circadianly regulated and outputs can feed back on the oscillator. Mathematical simulations indicate that under- or overexpression of a gene product can result in arrhythmicity, whether the protein is part of the oscillator or substantially part of a rhythmically expressed input pathway. To distinguish between these two possibilities, we used traditional circadian entrainment protocols on a genetic model system, Neurospora crassa.     

以塑性功函数为硬化参数的土的弹塑性模型

为解决清华弹塑性模型参数多和参数确定困难的问题 ,以永定河砂试验资料为基础 ,提出了以塑性功 Wp 的函数为硬化参数的土的弹塑性模型。给出了模型参数用等向压缩试验和常规三轴试验确定的方法。模型可用于三维应力状态的分析。应用所建模型对中密永定河砂的应力应变关系预测曲线与试验曲线进行比较 ,结果表明它可以较好模拟砂土变形的剪胀、剪缩特性     

对周期函数及其和、差、积、商函数周期性的探讨

针对高等学校教材中的两点不当,探讨了周期函数与周期的定义、周期函数的周期的性质及最小正周期的定义.进一步讨论了周期函数的和、差、积、商函数的周期性,从而得出了周期函数的和、差、积、商函数的周期性定理,并说明了定理的应用.     

Creatine accelerates the circadian clock in a unicellular alga

The circadian clock is considered to be a universal feature of eucaryotic organisms, controlling the occurrence and rates of many different aspects of life, ranging from single enzymatic reactions and metabolism to complex behaviours such as activity and rest. Although the nature of the underlying cellular/biochemical oscillator is still unknown, many substances are known to influence either phase or period of circadian rhythms in different organisms. These include D2O, electrolytes and ion channel inhibitors, small organic molecules such as alcohols and aldehydes, inhibitors of protein synthesis and amino-acid analogues. Certain transmitter and neurochemical drugs also influence the circadian clock in higher animals. We report here that the period of free-running circadian rhythms in the unicellular marine alga Gonyaulax polyedra is shortened by extracts from mammalian cells. The effect is dose-dependent, accelerating the circadian clock by as much as 4 hours per day. The substance responsible for this effect has been isolated from bovine muscle and identified as creatine. Authentic creatine has identical biological effects at micromolar concentrations and is known in animal systems for its involvement in cellular energy metabolism. A period shortening substance with similar chemical properties is also present in extracts of Gonyaulax itself.     

Sliding distance of actin filament induced by a myosin crossbridge during one ATP hydrolysis cycle

Muscle contraction results from a sliding movement of actin filaments induced by myosin crossbridges on hydrolysis of ATP, and many non-muscle cells are thought to move using a similar mechanism. The molecular mechanism of muscle contraction, however, is not completely understood. One of the major problems is the mechanochemical coupling at high velocity under near-zero load. Here, we report measurements of the sliding distance of an actin filament induced by a myosin crossbridge during one ATP hydrolysis cycle in an unloaded condition. We used single sarcomeres from which the Z-lines, structures which anchor the thin filaments in the sarcomere, had been completely removed by calcium-activated neutral protease (CANP) and trypsin, and measured both the sliding velocity of single actin filaments along myosin filaments and the ATPase activity during sliding. Our results show that the average sliding distance of the actin filament is less than or equal to 600 A during one ATP cycle, much longer than the length of power stroke of myosin crossbridges deduced from mechanical studies of muscle, which is of the order of 80 A (for example, ref. 15).     

线性分式函数的迭代公式与还原周期

文[1]得出了线性分式函数的迭代公式[1],文[2]、文[3]探讨了几次迭代还原函数的构造定理[2][3],而定理不具有普遍性。利用高等代数知识推导出线性分式函数的另一迭代公式,用特征根之比得出还原周期,由此构造了任意次迭代还原函数。     

Twisted gastrulation can function as a BMP antagonist

Bone morphogenetic proteins (BMPs), including the fly homologue Decapentaplegic (DPP), are important regulators of early vertebrate and invertebrate dorsal-ventral development. An evolutionarily conserved BMP regulatory mechanism operates from fly to fish, frog and mouse to control the dorsal-ventral axis determination. Several secreted factors, including the BMP antagonist chordin/Short gastrulation (SOG), modulate the activity of BMPs. In Drosophila, Twisted gastrulation (TSG) is also involved in dorsal-ventral patterning, yet the mechanism of its function is unclear. Here we report the characterization of the vertebrate Tsg homologues. We show that Tsg can block BMP function in Xenopus embryonic explants and inhibits several ventral markers in whole-frog embryos. Tsg binds directly to BMPs and forms a ternary complex with chordin and BMPs. Coexpression of Tsg with chordin leads to a more efficient inhibition of the BMP activity in ectodermal explants. Unlike other known BMP antagonists, however, Tsg also reduces several anterior markers at late developmental stages. Our data suggest that Tsg can function as a BMP inhibitor in Xenopus; furthermore, Tsg may have additional functions during frog embryogenesis.     

Stimulated activity mediates phase shifts in the hamster circadian clock induced by dark pulses or benzodiazepines

A number of environmental and pharmacological stimuli capable of inducing phase shifts and/or period changes in the circadian clock of mammals have now been identified. Agents that can alter circadian clocks provide a means for investigating the cellular and neural mechanisms responsible for their generation, regulation and entrainment. Two stimuli that have been used to probe the basis of circadian rhythmicity are pulses of darkness on a background of constant light and injections of short-acting benzodiazepines, such as triazolam. Surprisingly, these two very different stimuli have remarkably similar phase-shifting effects on the circadian clock of hamsters. The observation that a short-term increase in locomotor activity occurs when the circadian activity rhythm of hamsters is shifted by dark pulses or triazolam injections, coupled with the finding that activity bouts themselves are capable of shifting this rhythm, raises the possibility that dark pulses or triazolam alter the circadian clock by inducing acute hyperactivity. Here we demonstrate that the phase-advancing and phase-delaying effects of dark pulses or triazolam on the circadian activity rhythm can be totally suppressed by immobilization of the animals during treatment. These results indicate that behavioural events mediate the phase-shifting effects of both dark pulses and triazolam on the circadian activity rhythm and question present hypotheses regarding the pathways by which light-dark information and pharmacological agents influence circadian pacemakers.     

Basal body movements as a mechanism for mitochondrial genome segregation in the trypanosome cell cycle

The mitochondrial genome of Trypanosoma brucei is organized in the form of a complex catenated network of circular DNA molecules. This mass of DNA, known as the kinetoplast, is present at a unique site in the single mitochondrion, and is replicated in a discrete, periodic S phase of the cell cycle. The single-copy nature of the kinetoplast suggests that there is a mechanism ensuring segregation fidelity of replicated copies to each daughter cell. Historically, speculation regarding the nature of this mechanism has often attributed significance to the close association between the kinetoplast and the flagellum basal body. We provide here direct evidence that this mitochondrial DNA complex is indeed linked to the basal body, and segregation of the kinetoplast DNA is dependent on a microtubule-mediated separation of the new and old flagellar basal bodies during the cell cycle. This unique system may represent the remnants of an evolutionarily archaic mechanism for genome segregation.