Potentiation of NMDA receptor currents by arachidonic acid.

Arachidonic acid is released by phospholipase A2 when activation of N-methyl-D-aspartate (NMDA) receptors by neurotransmitter glutamate raises the calcium concentration in neurons, for example during the initiation of long-term potentiation and during brain anoxia. Here we investigate the effect of arachidonic acid on glutamate-gated ion channels by whole-cell clamping isolated cerebellar granule cells. Arachidonic acid potentiates, and makes more transient, the current through NMDA receptor channels, and slightly reduces the current through non-NMDA receptor channels. Potentiation of the NMDA receptor current results from an increase in channel open probability, with no change in open channel current. We observe potentiation even with saturating levels of agonist at the glutamate- and glycine-binding sites on these channels; it does not result from conversion of arachidonic acid to lipoxygenase or cyclooxygenase derivatives, or from activation of protein kinase C. Arachidonic acid may act by binding to a site on the NMDA receptor, or by modifying the receptor's lipid environment. Our results suggest that arachidonic acid released by activation of NMDA (or other) receptors will potentiate NMDA receptor currents, and thus amplify increases in intracellular calcium concentration caused by glutamate. This may explain why inhibition of phospholipase A2 blocks the induction of long-term potentiation.     

高位钻孔瓦斯抽采参数优化设计

基于采空区覆岩裂隙分布规律、覆岩裂隙瓦斯流动规律和高位钻孔抽采技术研究现状,从覆岩竖三带、O形圈和U型通风条件下采动裂隙瓦斯流动规律出发,找出高位钻孔的理论合理布置区域,指出工作面后方50m范围内覆岩裂隙发育状况是高位钻孔层位设计的关键,针对祁南煤矿32煤层的特点,结合现场采用数值模拟方法模拟不同开采速度条件下覆岩裂隙发育规律,优化设计高位钻孔的抽采参数,在34下2工作面和3410工作面的现场试验中,高位钻孔抽采浓度和抽采率得到大大提高,取得了较好的抽采效果,验证了研究的正确性。     

水溶液中Co-Sb薄膜的电化学沉积

采用电化学循环伏安法分析了柠檬酸水溶液中Co2+、SbO+的沉积电位,利用恒电位沉积的方法,在不锈钢基片上,从柠檬酸水溶液中沉积出Co-Sb薄膜.运用X射线衍射和扫描电子显微镜对薄膜的结构、组成以及形貌进行了分析.结果表明,在柠檬酸水溶液中,Co2+和SbO+可同时沉积到不锈钢基片上,形成Co-Sb薄膜,在不同的沉积电位下,薄膜形成不同的物相.薄膜的形貌呈现颗粒状,分布比较均匀.薄膜在充满Ar的管式炉中热处理2h,热处理温度为400℃,结果发现薄膜物相组成发生了很大变化,转变为主要由晶体CoSb3组成,还有少量的CoSb形成.     

Restoration of grasp following paralysis through brain-controlled stimulation of muscles

Patients with spinal cord injury lack the connections between brain and spinal cord circuits that are essential for voluntary movement. Clinical systems that achieve muscle contraction through functional electrical stimulation (FES) have proven to be effective in allowing patients with tetraplegia to regain control of hand movements and to achieve a greater measure of independence in daily activities. In existing clinical systems, the patient uses residual proximal limb movements to trigger pre-programmed stimulation that causes the paralysed muscles to contract, allowing use of one or two basic grasps. Instead, we have developed an FES system in primates that is controlled by recordings made from microelectrodes permanently implanted in the brain. We simulated some of the effects of the paralysis caused by C5 or C6 spinal cord injury by injecting rhesus monkeys with a local anaesthetic to block the median and ulnar nerves at the elbow. Then, using recordings from approximately 100 neurons in the motor cortex, we predicted the intended activity of several of the paralysed muscles, and used these predictions to control the intensity of stimulation of the same muscles. This process essentially bypassed the spinal cord, restoring to the monkeys voluntary control of their paralysed muscles. This achievement is a major advance towards similar restoration of hand function in human patients through brain-controlled FES. We anticipate that in human patients, this neuroprosthesis would allow much more flexible and dexterous use of the hand than is possible with existing FES systems.     

Different time courses of learning-related activity in the prefrontal cortex and striatum

To navigate our complex world, our brains have evolved a sophisticated ability to quickly learn arbitrary rules such as 'stop at red'. Studies in monkeys using a laboratory test of this capacity--conditional association learning--have revealed that frontal lobe structures (including the prefrontal cortex) as well as subcortical nuclei of the basal ganglia are involved in such learning. Neural correlates of associative learning have been observed in both brain regions, but whether or not these regions have unique functions is unclear, as they have typically been studied separately using different tasks. Here we show that during associative learning in monkeys, neural activity in these areas changes at different rates: the striatum (an input structure of the basal ganglia) showed rapid, almost bistable, changes compared with a slower trend in the prefrontal cortex that was more in accordance with slow improvements in behavioural performance. Also, pre-saccadic activity began progressively earlier in the striatum but not in the prefrontal cortex as learning took place. These results support the hypothesis that rewarded associations are first identified by the basal ganglia, the output of which 'trains' slower learning mechanisms in the frontal cortex.     

导出矩阵与基底的正交化

给出导出矩阵的概念并利用它将Ｒｎ中任意一组基底正交化     

美国学校数学课程演化的历史观(1900-2006)

通过对100多年来美国学校数学课程演化的分析与思考,旨在提供一种认识美国数学课程的历史观,并从中窥探美国数学课程演化的艰巨性、曲折性和发展性,以启示如何更有效地进行数学课程改革.     

Modulation of the two promoters of the galactose operon of Escherichia coli.

The gal operon of Escherichia coli is controlled by two independent promotors--one is activated and the other inhibited by cyclic AMP and cyclic AMP receptor protein. The two promotors are modulated, however, by the same operator locus and receptor protein.     

基于声学参量阵理论的超声波防录音屏蔽研究与实现

随着智能设备的快速发展,利用一些录音设备诸如智能手机、录音笔等窃取信息的手段显得更为方便和隐蔽,这对于个人、企业和政府都存在着不小的隐患.传统的对抗方式有背景噪声屏蔽和电磁波屏蔽,但都有其局限性.前者通过播放大音量噪声覆盖对话声音,但这会影响对话的正常进行;后者发射大功率电磁波屏蔽录音设备,但其屏蔽距离与效果都十分有限.针对上述问题,本文提出一种基于声学参量阵理论的超声波防录音屏的方案,可以对录音窃听进行有效屏蔽,同时不妨碍正常对话.根据声学参量阵理论,多个高频的超声波经过非线性系统,会因为非线性作用产生低频声音信号.根据这一原理,首先生成低频宽带噪声信号,然后进行BASK调制将其调制到高频载波上,进行功率放大后由换能器发射向目标录音设备.实验测试结果表明对iPhone6S、华为P10、P20、荣耀9等智能手机的录音功能都可以实现有效屏蔽,最大屏蔽距离1～3 m不等.由于屏蔽原理的普适性,本文的方案可以屏蔽目前大多数型号的智能手机、录音笔等带录音功能的终端.     

An unexpected cooling effect in Saturn's upper atmosphere

The upper atmospheres of the four Solar System giant planets exhibit high temperatures that cannot be explained by the absorption of sunlight. In the case of Saturn the temperatures predicted by models of solar heating are approximately 200 K, compared to temperatures of approximately 400 K observed independently in the polar regions and at 30 degrees latitude. This unexplained 'energy crisis' represents a major gap in our understanding of these planets' atmospheres. An important candidate for the source of the missing energy is the magnetosphere, which injects energy mostly in the polar regions of the planet. This polar energy input is believed to be sufficient to explain the observed temperatures, provided that it is efficiently redistributed globally by winds, a process that is not well understood. Here we show, using a numerical model, that the net effect of the winds driven by the polar energy inputs is not to heat but to cool the low-latitude thermosphere. This surprising result allows us to rule out known polar energy inputs as the solution to the energy crisis at Saturn. There is either an unknown--and large--source of polar energy, or, more probably, some other process heats low latitudes directly.