干湿循环对风化砂改良膨胀土无荷膨胀率的影响

对掺砂改良后的膨胀土进行了干湿循环作用下的无荷膨胀率试验,研究了试样的无荷膨胀率（绝对膨胀率）、相对膨胀率以及终止吸水量随干湿循环次数的变化规律,深入分析了不同干湿循环次数后,改良膨胀土的膨胀量随浸水时间的增长特征.试验表明：1）无荷膨胀率以及终止吸水量随干湿次数的增长变化规律基本一致,在相同的风化砂掺量下,无荷膨胀率呈3次函数形式降低,且无荷膨胀率在第2-3次干湿循环后,降低幅度较大,之后降低幅度逐渐减小,最后基本趋于稳定;2）掺风化砂对抑制无荷膨胀的发生效果不大,当风化砂由0增至50%时,无荷膨胀率降低幅度较小,且这一降低幅度随着干湿循环次数的增大为逐渐减小;3）无荷膨胀量在浸水1h内的增长速度较快,之后逐渐变缓,在相同的风化砂掺量下,无荷膨胀量达到稳定时的时间随着干湿循环次数的增加而逐渐缩短.

Aniracetam attenuates H_2O_2-induced deficiency of neuron viability, mi-tochondria potential and hippocampal long-term potentiation of mice in vitro

Objective It is known that free radicals are involved in neurodegeneration and cognitive dysfunction, as seen in Alzheimer＇s disease （AD） and aging. The present study examines the protective effects of aniracetam against H2O2- induced toxicity to neuron viability, mitochondria potential and hippocampal long-term potentiation （LTP）. Methods Tetrazolium salt 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide （MTT） was used to detect neuronal viability. MitoTracker Red （CMX Ros）, a fluorescent stain for mitochondria, was used to measure mitochondria potential. Electrophysiological technique was carried out to record hippocampual LTE Results H2O2 exposure impaired the viability of neurons, reduced mitochondria potential, and decreased LTP in the CA region of hippocampus. These deficient effects were significantly rescued by pre-treatment with aniracetam （10 ～100μmol/L）. Conclusion These results indicate that aniracetam has a strong neuroprotective effect against H2O2-induced toxicity, which could partly explain the mechanism of its clinical application in neurodegenerative diseases.

Role of Specific Synaptic Plasticity Interfering Peptides in the Expression of Morphine Induced Conditioned Place Preference in Mice

Learned association between context and drug abuse is essential for the drug conditioned place preference （CPP）, which is an animal model widely used to measure drug reward. Synaptic plasticity, in the form of long-term potentiation （LTP） and depression （LTD）, is regarded as a proposed cellular substrate of learning and memory. However, the exact role of LTP/LTD in addiction is not known yet. Therefore, by bioinformatics we designed peptides aiming to interfere with LTP and LTD respectively, to study their individual role in the expression of morphine CPP. We found that the interfering peptide Pep-A2 can specifically block hippocampal LTP in CA1 region, whereas Pep-A3 can block LTD in this region. Treatment of either of their cell penetrating forms （Tat-A2 or Tat-A3） before test can block the expression of Morphine CPP in mice. These results suggested that both LTP and LTD are required in the drug-associated learning and memory.

A novel derivative of xanomeline improved memory function in aged mice

Objective To characterize the function of a new xanomeline-derived M 1 agonist, 3-[3-（3-florophenyl-2-propyn- 1- ylthio）-1,2,5-thiadiazol-4-yl]-1,2,5,6- tetrahydro-1-methylpyridine Oxalate （EUK1001）, the acute toxicity and the effects on synaptic plasticity and cognition of EUK1001 were evaluated. Methods To examine the median lethal dose （LD50） of EUK1001, a wide dose range of EUK1001 was administered by p.o. and i.p. in aged mice. Furthermore, novel object recognition task and in vitro electrophysiological technique were utilized to investigate the effects of EUK1001 on recognition memory and hippocampal synaptic plasticity in aged mice. Results EUK1001 exhibited lower toxicity than xanomeline, and improved the performance of aged mice in the novel object recognition test. In addition, bath application of 1 μmol/L EUK1001 directly induced long-term potentiation in the hippocampus slices. Conclusion We conclude that EUK1001 can improve the agerelated cognitive deficits.

Inhibition of the MAPK/ERK cascade: a potential transcription-depen-dent mechanism for the amnesic effect of anesthetic propofol

Intravenous anesthetics are known to cause amnesia, but the underlying molecular mechanisms remain elusive. To identify a possible molecular mechanism, we recently turned our attention to a key intracellular signaling pathway organized by a family of mitogen-activated protein kinases （MAPKs）. As a prominent synapse-to-nucleus superhighway, MAPKs couple surface glutamate receptors to nuclear transcriptional events essential for the development and/or maintenance of different forms of synaptic plasticity （long-term potentiation and long-term depression） and memory formation. To define the role of MAPK-dependent transcription in the amnesic property of anesthetics, we conducted a series of studies to examine the effect of a prototype intravenous anesthetic propofol on the MAPK response to N-methyl-D-aspartate receptor （NMDAR） stimulation in hippocampal neurons. Our results suggest that propofol possesses the ability to inhibit NMDAR-mediated activation of a classic subclass of MAPKs, extracellular signal-regulated protein kinase 1/2 （ERK1/2）. Concurrent inhibition of transcriptional activity also occurs as a result of inhibited responses of ERK1/2 to NMDA. These findings provide first evidence for an inhibitory modulation of the NMDAR-MAPK pathway by an intravenous anesthetic and introduce a new avenue to elucidate a transcription-dependent mechanism processing the amnesic effect of anesthetics.

A software reliability growth model for component-based software incorporating debugging delay and imperfect debugging

In view of the problems and the weaknesses of component-based software （ CBS ） reliability modeling and analysis, and a lack of consideration for real debugging circumstance of integration tes- ting, a CBS reliability process analysis model is proposed incorporating debugging time delay, im- perfect debugging and limited debugging resources. CBS integration testing is formulated as a multi- queue muhichannel and finite server queuing model （MMFSQM） to illustrate fault detection process （FDP） and fault correction process （FCP）. A unified FCP is sketched, given debugging delay, the diversities of faults processing and the limitations of debugging resources. Furthermore, the impacts of imperfect debugging on fault detection and correction are explicitly elaborated, and the expres- sions of the cumulative number of fault detected and corrected are illustrated. Finally, the results of numerical experiments verify the effectiveness and rationality of the proposed model. By comparison, the proposed model is superior to the other models. The proposed model is closer to real CBS testing process and facilitates software engineer＇ s quantitatively analyzing, measuring and predicting CBS reliability. K

干湿循环效应对风化砂改良膨胀土膨胀力影响的研究

本文将0、10％、20％、30％、40％、50％的风化砂掺入膨胀土中，分别进行0、1、2、3、4、5次干湿循环，对干湿循环之后的试样进行膨胀力测试；研究了不同掺量风化砂改良膨胀土膨胀力的大小及增长时程随着干湿循环次数的变化规律，分析了干湿循环作用一定次数后，风化砂掺量对试样表面的剥落程度及裂隙发育的影响。实验结果表明：干湿循环效应对风化砂改良膨胀土的膨胀力影响较为显著，且膨胀力与干湿循环次数间的关系可以用三次方函数很好地进行描述；在风化砂掺量一定时，经过2～3次干湿循环时膨胀力降低幅度最大，且随着风化砂掺量的增加，这一降低幅度在逐渐减少，干湿循环4～5后膨胀力趋于稳定；当风化砂掺量相同时，随着干湿循环次数的增加，膨胀力达到稳定所需要的时间逐渐减少，而膨胀力的增长速度先增大后减小；干湿循环5次后，试样表面的裂隙发育已基本达到稳定，裂隙数量随着风化砂掺量的增加而逐渐减少；当风化砂掺量为30％时，试样周边基本上不存在剥落现象。

Effects of synaptic plasticity regulated by 17β-estradiol on learning and memory in rats with Alzheimer's disease

Objective To investigate whether estrogen modulates learning and memory and long-term potentiation （LTP） in the hippocampus of rats with Alzheimer＇s disease （AD）. Methods The rats were divided into ovariectomy （OVX） and estrogen replacement therapy （ERT） groups. Rats in the ERT group received OVX, followed by ERT, while rats in the OVX group received only OVX. The rat model of AD was established by injection of 1 μL （10 μg/μL） amyloid-beta peptide 1-40（Aβ1-40） into the hippocampus. The learning and memory ability and LTP were determined by Morris water maze and electrophysiological method, respectively. Results The escape latency in Morris water maze significantly decreased in ERT group compared with that in OVX group （P 〈 0.05）. Besides, rats in ERT group exhibited a significant enhancement of the magnitude of LTP at 30 min after high-frequency stimulation （HFS）, compared with that in OVX group （P 〈 0.01）. Conclusion ERT can attenuate the cognitive deficits in the rat model of AD, and estrogen can regulate LTP and synaptic remodeling in AD rats.

Activation of extracellular signal-regulated kinase in the anterior cingulate cortex contributes to the induction of long-term potentiation in rats

Objective To explore the role of the extracellular signal-regulated kinase （ERK）/cAMP response element binding protein （CREB） pathway in the induction of long-term potentiation （LTP） in the anterior cingulate cortex （ACC） that may be implicated in pain-related negative emotion. Methods LTP of field potential was recorded in ACC slice and the expressions of phospho-ERK （pERK） and phospho-CREB （pCREB） were examined using immunohistochemistry method. Results LTP could be induced stably in ACC slice by high frequency stimulation （2-train, 100 Hz, 1 s）, while APv （an antagonist of NMDA receptor） could block the induction of LTP in the ACC, indicating that LTP in this experiment was NMDA receptor-dependent. Bath application of PD98059 （50 μmol/L）, a selective MEK inhibitor, at 30 min before tetanic stimulation could completely block the induction of LTP. Moreover, the protein level of pERK in the ACC was transiently increased after LTP induction, starting at 5 rain and returning to basal at 1 h after tetanic stimulation. The protein level of pCREB was also increased after LTP induction. The up-regulation in pERK and pCREB expressions could be blocked by pretreatment of PD98059. Double immunostaining showed that after LTP induction, most pERK was co-localized with pCREB. Conclusion NMDA receptor and ERK-CREB pathway are necessary for the induction of LTP in rat ACC and may play important roles in pain emotion.

Neural circuits and temporal plasticity in hindlimb representation of rat primary somatosensory cortex:revisited by multi-electrode array on brain slices

Objective The well-established planar multi-electrode array recording technique was used to investigate neural circuits and temporal plasticity in the hindlimb representation of the rat primary somatosensory cortex （S1 area） . Methods Freshly dissociated acute brain slices of rats were subject to constant perfusion with oxygenated artificial cerebrospinal fluid （95% O2 and 5% CO2） , and were mounted on a Med64 probe （64 electrodes, 8×8 array） for simultaneous multi-site electrophysiological recordings. Current sources and sinks across all the 64 electrodes were transformed into two-dimensional current source density images by bilinear interpolation at each point of the 64 electrodes. Results The local intracortical connection, which is involved in mediation of downward information flow across layers II-VI, was identified by electrical stimulation （ES） at layers II-III. The thalamocortical connection, which is mainly involved in mediation of upward information flow across layers II-IV, was also characterized by ES at layer IV. The thalamocortical afferent projections were likely to make more synaptic contacts with S1 neurons than the intracortical connections did. Moreover, the S1 area was shown to be more easily activated and more intensively innervated by the thalamocortical afferent projections than by the intracortical connections. Finally, bursting conditioning stimulus （CS） applied within layer IV of the S1 area could success-fully induce long-term potentiation （LTP） in 5 of the 6 slices （83.3%） , while the same CS application at layers II-III induced no LTP in any of the 6 tested slices. Conclusion The rat hindlimb representation of S1 area is likely to have at least 2 patterns of neural circuits on brain slices： one is the intracortical circuit （ICC） formed by interlaminar connections from layers II-III, and the other is the thalamocortical circuit （TCC） mediated by afferent connections from layer IV. Besides, ICC of the S1 area is spatially limited, with less plasticity, while TCC is spatially extensive and exhibits a better plasticity in response to somatosensory afferent stimulation. The present data provide a useful experimental model for further studying microcircuit properties in S1 cortex at the network level in vitro.

Differential effects of long and short train theta burst stimulation on LTP induction in rat anterior cingulate cortex slices:Multi-electrode array recordings

Objective There is substantial evidence supporting the notion that the anterior cingulate cortex （ACC） is an important limbic structure involved in multiple brain functions such as sensory perception, motor conflict monitoring, memory, emotion and cognition. It has been shown that long term potentiation （LTP） is an important synaptic model of neural plasticity in the ACC, however, little is known about the spatiotemporal properties of ACC at network level. The present study was designed to see the LTP induction effects across different layers of the ACC by using different conditioning stimuli （CS） protocols. Methods A unique multi-electrode array recording technique was used in the acutely-dissociated ACC slices of rats. Long and short train theta burst stimulation （TBS） paradigms were applied in layer V-VI as the CS and the LTP induction effects were compared across different layers of the ACC. Briefly, both long and short train TBS are composed of bursts （4 pulses at 100 Hz） with a 200 ms interval, however, the former （TBS1） was with 10 trains and the latter （TBS2） was with 5 trains. After test stimulation at layer V-VI in the ACC, network field potentials （FPs） could be simultaneously recorded across all layers of the ACC. Results The waveforms of FPs were different across different layers. Namely, positive-going waveforms were recorded in layer I and negative-going waveforms were recorded in layers V-VI, in contrast, complex waveforms were localized mainly in layers II-III. Following application of two CS protocols, the induction rate of LTP was significantly different between TBS 1 and TBS2 regardless of the spatial properties. TBS1 had more than 60% success, while TBS2 was less than 25% in induction of LTP. Moreover, both the 2 CS protocols could induce LTP in layers II-III and layers V-VI without layer-related difference. However, no LTP was inducible in layer I. Conclusion The present findings indicate that stimulation protocols may, at least in part, account for a large portion of variations among previous LTP studies, and hence highlight the importance of selecting the best LTP induction protocol when designing such experiments. Moreover, the present results demonstrate the prominent superiority of multi-electrode array recording in revealing the network properties of synaptic activities in the ACC, especially in comparing the spatiotemporal characteristics between different layers of this structure.