Force-displacement characteristics of simply supported beam laminated with shape memory alloys

As a preliminary step in the nonlinear design of shape memory alloy（SMA） composite structures,the force-displacement characteristics of the SMA layer are studied.The bilinear hysteretic model is adopted to describe the constitutive relationship of SMA material.Under the assumption that there is no point of SMA layer finishing martensitic phase transformation during the loading and unloading process,the generalized restoring force generated by SMA layer is deduced for the case that the simply supported beam vibrates in its first mode.The generalized force is expressed as piecewise-nonlinear hysteretic function of the beam transverse displacement.Furthermore the energy dissipated by SMA layer during one period is obtained by integration,then its dependencies are discussed on the vibration amplitude and the SMA＇s strain（Ms-Strain） value at the beginning of martensitic phase transformation.It is shown that SMA＇s energy dissipating capacity is proportional to the stiffness difference of bilinear model and nonlinearly dependent on Ms-Strain.The increasing rate of the dissipating capacity gradually reduces with the amplitude increasing.The condition corresponding to the maximum dissipating capacity is deduced for given value of the vibration amplitude.The obtained results are helpful for designing beams laminated with shape memory alloys.

Effect of Panax notoginseng saponins on the expression of beta-amyloid protein in the cortex of the parietal lobe and hippocampus, and spatial learning and memory in a mouse model of senile dementia

BACKGROUND： The pharmacological actions of Panax notoginseng saponins （PNS） lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheimer＇s disease. OBJECTIVE： Using the Morris water maze, immunohistochemistry, real-time PCR and RT-PCR, this study aimed to measure improvement in spatial learning, memory, expression of amyloid precursor protein （App） and β -amyloid （A β ）, to investigate the mechanism of action of PNS in the treatment of AD in the senescence accelerated mouse-prone 8 （SAMP8） and compare the effects with huperzine A. DESIGN, TIME AND SETTING： A completely randomized grouping design, controlled animal experiment was performed in the Center for Research ＆ Development of New Drugs, Guangxi Traditional Chinese Medical University from July 2005 to April 2007. MATERIALS： Sixty male SAMP8 mice, aged 3 months, purchased from Tianjin Chinese Traditional Medical University of China, were divided into four groups： PNS high-dosage group, PNS low-dosage group, huperzine A group and control group. PNS was provided by Weihe Pharmaceutical Co., Ltd. （batch No.： Z53021485, Yuxi, Yunan Province, China）. Huperzine A was provided by Zhenyuan Pharmaceutical Co., Ltd. （batch No.： 20040801, Zhejiang, China）. METHODS： The high-dosage group and low-dosage group were treated with 93.50 and 23.38 mg/kg PNS respectively per day and the huperzine A group was treated with 0.038 6 mg/kg huperzine A per day, all by intragastric administration, for 8 consecutive weeks. The same volume of double distilled water was given to the control group. MAIN OUTCOME MEASURES： After drug administration, learning and memory abilities were assessed by place navigation and spatial probe tests. The recording indices consisted of escape latency （time-to-platform）, and the percentage of swimming time spent in each quadrant. The number of A β 1-40, A β 1-42 and App immunopositive neurons in the brains of SAMP8 mice was analyzed by immunohistochemistry. The mRNA content ofApp, tau, acetylcholinesterase, and synaptophysin （Syp） was tested by real time PCR and RT-PCR. RESULTS： The PCR results show that PNS can downregulate the expression of the App gene and upregulate the expression of the Syp gene in the parietal cortex and hippocampus of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than those of the PNS low-dosage group and the huperzine A group （P 〈 0.05）. The results of the Morris water maze and immunohistochemistry indicated that PNS can improve the capacity for spatial learning and memory in SAMP8 mice, and reduce the content of A β 1-40, A β 1-42 and expression of App in the brains of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than that of the PNS low-dosage group and the huperzine A group （P 〈 0.05）. CONCLUSION： These results support the hypothesis that PNS plays a therapeutic and protective role on the pathological lesions and learning dysfunction of Alzheimer＇s disease. The therapeutic effects of PNS for Alzheimer＇s disease are possibly achieved through downregulating the expression of the App gene and upregulating the expression of the Syp gene. The therapeutic effects of PNS are dose-dependent and are greater than the effect of huperzine A.

Optogenetics-induced activation of glutamate receptors improves memory function in mice with Alzheimer’s disease

Optogenetics is a combination of optics and genetics technology that can be used to activate or inhibit specific cells in tissues. It has been used to treat Parkinson’s disease, epilepsy and neurological diseases, but rarely Alzheimer’s disease. Adeno-associated virus carrying the CaMK promoter driving the optogenetic channelrhodopsin-2 (CHR2) gene (or without the CHR2 gene, as control) was injected into the bilateral dentate gyri, followed by repeated intrahippocampal injections of soluble low-molecular-weight amyloid-β1–42 peptide (Aβ1–42). Subsequently, the region was stimulated with a 473 nm laser (1–3 ms, 10 Hz, 5 minutes). The novel object recognition test was conducted to test memory function in mice. Immunohistochemical staining was performed to analyze the numbers of NeuN and synapsin Ia/b-positive cells in the hippocampus. Western blot assay was carried out to analyze the expression levels of glial fibrillary acidic protein, NeuN, synapsin Ia/b, metabotropic glutamate receptor-1a (mGluR-1a), mGluR-5, N-methyl-D-aspartate receptor subunit NR1, glutamate receptor 2, interleukin-1β, interleukin-6 and interleukin-10. Optogenetic stimulation improved working and short-term memory in mice with Alzheimer’s disease. This neuroprotective effect was associated with increased expression of NR1, glutamate receptor 2 and mGluR-5 in the hippocampus, and decreased expression of glial fibrillary acidic protein and interleukin-6. Our results show that optogenetics can be used to regulate the neuronal-glial network to ameliorate memory functions in mice with Alzheimer’s disease. The study was approved by the Animal Resources Committee of Jinan University, China (approval No. LL-KT-2011134) on February 28, 2011.

Imperatorin alleviates Aβ-induced spatial learning memory impairment and neuroinflam⁃mation in model mice of Alzheimer disease

OBJECTIVE To investigate the effects of imperatorin on the spatial learning memory impairment and neuroinflammation in model mice of Alzheimer disease(AD)induced by intracerebroventricular injection of Aβ1-42.METHODS Mouse model of AD was established by injection of Aβ1-42 into the lateral ventricles.Im⁃peratorin(2.5 and 5.0 mg·kg-1,daily)was inject⁃ed by intraperitoneally 1 h after intracerebroven⁃tricular injection for 13 d.The effect of imperato⁃rin on the spatial learning and memory impair⁃ment was assessed by eight arm maze tests.The levels of cytokines TNF-α,IL-1β,IL-6,IL-18 and chemokines MCP-1 in mouse cortex and hip⁃pocampus were detected by ELISA.The protein expression of NF-κB P65,TLR4,MyD88,p-P38,p-ERK,and p-JNK were detected by Western blotting.RESULTS As compared with the AD model group,imperatorin treatment significantly attenuated Aβ1-42-induced spatial learning and memory impairment assessed by eight arm maze tests.In addition,imperatorin significantly reduced the levels of cytokines TNF-α,IL-1β,IL-6,IL-18 and chemokines MCP-1 in the cerebral cortex and hippocampus.Meanwhile,Western blotting results showed that imperatorin treat⁃ment significantly down-regulated the protein expression of NF-κB P65,TLR4,MyD88,p-P38,p-ERK,and p-JNK.CONCLUSION Imperatorin has neuroprotective effects in the Aβ1-42 induced AD model mice and its mechanism may be partially associated with the inhibition of inflam⁃matory response in the cortex and hippocampus.

Adolescent Exposure of JWH-018 “Spice” Produces Subtle Effects on Learning and Memory Performance in Adulthood

The active components associated with the bio-designer drugs known variously as “Spice” or “K2” have rapidly gained in popularity among recreational users, forcing the United States Drug Enforcement Administration to classify these compounds as Schedule I drugs in the Spring of 2011. However, although there is some information about many of the synthetic cannabinoids used in Spice products, little is known about the consequences of the main constituent, (1-pentyl-3-(1-naphthoyl)indole;JWH-018), on neuropsychological development or behavior. In the present experiment, adolescent rats were given repeated injections of either saline or 100 μg/kg of JWH-018. Once the animals were 75 days of age, they were trained using tasks with spatial components of various levels of difficulty and a spatial learning set task. On early trials with water maze tasks of varying difficulty, the JWH-018 treated rats were impaired relative to controls. However, by the end of each phase of testing, drug and control animals were comparable, although on probe trials the drug-treated animals spent significantly less time in the target quadrant. In addition, the performance of the drug-treated rats was inferior to that of the control animals on a learning set task, suggesting some difficulty in adapting their responses to changing task demands. The results suggest that chronic exposure to this potent cannabinoid CB1 receptor agonist during adolescence is capable of producing a variety of subtle changes affecting spatial learning and memory performance in adulthood, well after the drug exposure period.

NP-14 Effects of Osthole on the Improvement of Learning and Memory Impairment in A Mouse Model Injected with Aβ25-35

Objective:We aimed to investigate the effects of osthole on learning and memory impairment of AD mice induced by injection of Aβ25-35 and the content of Ca2+、GLU、Ab1-42 in the brain tissue and peripheral blood.Methods:Mice were randomly assigned to sham operation,Aβ25-35,Aβ25-35+Ost-L,Aβ25-35+Ost-M,and Aβ25-35+Ost-H group.Water maze test was performed to assessing spatial learning ability of mice.It is determined that the MDA level and the activity of SOD in the brain tissue of mice in each group by colorimetry.The GLU kit and Ca2+kit were used to detect the GLU,Ca2+in tissue and serum.Elisa was used to detect the expression of Aβ1-42 in the hippocampus and serum of mice.HE staining and silver staining were used to detect neuron apoptosis and pathological changes in brain slices.Results:①Effects of osthole on learning and memory:With the increase of training day,the escape latencies continuously reduced in each experimental group,the escape latencies of the model group was longer on the 1st,2nd,3rd,and 5th days than the normal group,the difference was statistically significant(day 3,4:P<0.05,day 5:P<0.01);compared with the model group,the escaping latency on the fifth day of the OST low-medium high-dose group was significantly shortened,which was statistically significant(P<0.05).②Effects on oxidative stresspathway:the SOD activity of AD mice in the hippocampus model group was lower than that in the normal group,which was statistically significant(P<0.05);The SOD activity in the OST group was higher than that in the model group,which was statistically significant(P<0.05).The MDA content in the model group was significantly higher than that in the normal group(P<0.05).The MDA content in the OST high-dose group was lower than that in the model group,which was statistically significant(P<0.05).③Effects of GLU levels on neurotransmitters:the results of the detection of GLU in cortical area and GLU in serum of AD mice in OST dose groups showed that serum GLU levels in the model group were significantly lower than those in the sham group,which was statistically significant(P<0.05).GLU levels in the cortical area were also significantly higher than those in the sham group,which was statistically significant(P<0.05).Compared with the model group,GLU levels in the OST administration group were significantly downregulated.Among the serum,the effect of medium dose group was obvious.Although there was a trend of down-regulation in the cortical administration group,there was no statistical significance.④Changes in Ca2+concentration in the brain;Detection of intracellular Ca ion concentration in AD mice by OST doses showed that,compared with the sham group,the model group was significantly upregulated in cortical Ca2+levels.There was no statistical difference in the administration group.Compared with the model group,the concentration of Ca2+in the OST-H group significantly decreased.⑤Effect on levels of Ab1-42 in hippocampus and serum:model group had significantly higher Ab1-42 levels in hippocampus than in sham operation group,which was statistically significant(P<0.05).Ab1-42 in serum was also significantly upregulated compared to the sham group,which was statistically significant(P<0.05).Compared with the model group,the levels of Aβ1-42 in the OST administration group were significantly down-regulated,with the lower and middle doses in the hippocampus being more significant,while the serum was more pronounced at lower doses.⑥Silver staining to detect the tangles of hippocampal neurons:Neuron tangles in the hippocampal CA1 region showed a dark brown-yellow granule distribution in the nuclei of the model group(positive expression).Nerve cell body and dendrites,axons are black or black red,background light yellow.Compared with the model group,the administration group has improved significantly.Conclusion:OST improves spatial learning and memory of dementia model mice injected with Ab25-35 in both hippocampus.Experimental studies have shown that OST has different degrees of regulation on neuronal apoptosis,Ca2+/GLU/oxidative stress and other pathways,and it plays a role in improving multiple AD pathological changes and delaying the pathogenesis of neurodegenerative diseases.

电针对PTSD样大鼠学习记忆及海马CA1区Bcl-2/Bax表达的影响

目的探讨电针对创伤后应激障碍(PTSD)样大鼠学习记忆及海马CA1区Bcl-2/Bax表达的影响。方法将48只健康清洁级雄性SD大鼠随机均分为4组:正常对照组、模型组、电针组和电针对照组,采用国际认定的单次延长应激(SPS)方法制作大鼠PTSD模型,在造模6 h后给予电针组和电针对照组针刺治疗,通过旷场实验和Morris水迷宫实验测试大鼠的情绪唤醒水平和学习记忆能力,采用HE染色观察大鼠海马组织CA1区组织形态变化,Western blot实验检测大鼠海马组织CA1区Bcl-2/Bax蛋白的表达。结果与模型组大鼠比较,正常对照组和电针组大鼠站立与跨格次数均增多,平均上台潜伏期和穿台潜伏期缩短,穿台次数增加,差异均有统计学意义(P<0.05);HE染色结果表明,与正常对照组比较,模型组大鼠海马组织CA1区海马经元排列紊乱,结构异常,电针组CA1区海马神经元排列较整齐,结构趋于正常;与正常对照组比较,模型组大鼠海马组织CA1区Bcl-2/Bax蛋白表达升高,与模型组比较,电针组大鼠海马组织CA1区Bcl-2/Bax蛋白表达降低,差异有统计学意义(P<0.05)。结论电针治疗可改善PTSD样大鼠的学习记忆能力,可能与下调海马组织CA1区Bcl-2/Bax蛋白表达有关。

MPEG-2编码器中一种新型的DCT/IDCT结构

针对DCT变换编码是MPEG 2标准中运算量较大的部分 ,采用行列分解法设计的 8× 8二维DCT/IDCT结构 ,仅用一个 1维DCT核完成MPEG 2编码的二维DCT/IDCT变换 ,1维DCT核的流水数据宽度为两像素宽 ,较同类结构[1,2 ] 有更好的利用率。该设计是在完成MPEG 2编码器结构实现时提出的 ,整体结构规整 ,适合VLSI实现 。

基于Bi-LSTM的非等时距路基工后沉降滚动预测

为了实现路基工后沉降的早期、精准预测,提出基于双向长短期记忆网络(Bi-LSTM)的路基沉降预测技术.采用Akima法将观测数据内插为适应时序分析法的等时距序列,提取“填土高度-时间-地基沉降”曲线中的6个影响因素作为变量训练Bi-LSTM模型,结合滚动迭代方法实现沉降预测的后延更新.研究表明,利用深度学习技术可以有效地利用路基施工期信息,增加训练样本量,提升沉降早期预测的可靠性.Bi-LSTM模型对观测信息进行双向特征提取,同等样本量下的预测效果更精确.依托6个中等压缩性土地基和1个复合地基监测断面信息,仅利用路堤填筑期及工后3个月数据,沉降预测的均方根误差(RMSE)和平均绝对百分误差(MAPE)平均值可以控制为1.19 mm、1.04%.

后摩尔时代的3D封装技术--高端通信网络芯片对3D封装技术的应用驱动

认为通过封装技术的发展创新延续摩尔定律,满足未来通信芯片及消费性电子的需求已成为业界新的热点。介绍了3D封装技术发展现状与优势,提出"高带宽、高性能、大容量、高密度"通信网络芯片对3D封装技术有迫切的应用需求,并深入分析了堆叠封装技术如何解决400G网络处理器(NP)所面临的瓶颈问题。建议中国芯片产业链应协同合作,从整体上推动IC产业的发展。

Plasma Post Oxidation of Plasma Nitrocarburized SKD 61 Steel

Plasma nitrocarburizing and plasma oxidizing treatments were performed to improve the wear and corrosion resistance of SKD 61 steel.Plasma nitrocarburizing was conducted for 12 h at 540℃in the nitrogen, hydrogen and methane atmosphere to produce theε-Fe-（2-3）（N,C） phase.The compound layer produced by plasma nitrocarburising was predominantly composed ofε-phase,with a small proportion ofγ′-Fe-4 （N,C） phase. The thickness of the compound layer and the diffusion layer are about 10μm and about 200μm,respectively. Plasma post oxidation was performed on the nitrocarburized samples with various oxygen/hydrogen ratio at constant temperature of 500℃for 1 h.The very thin magnetite （Fe-3O-4） layer of 1-2μm in thickness on top of the compound layer was obtained.Anodic polarization test revealed that plasma nitrocarburizing process contributed a significant improvement of corrosion resistance of SKD 61 steel.However,the corrosion characteristics of the nitrocarburized compound layer was deteriorated by oxidation treatment.

Nb对NiTi微激光焊缝组织M-A相变温度的影响

为了获得0.2 mm板厚的NiTi形状记忆合金(NiTi-SMA)焊缝金属与母材相变温度差异不大的焊接接头,以满足实际应用需要。采用添加焊丝的方式在焊缝中引入Nb元素,焊后时效处理焊接接头,以实现调控焊缝金属相变温度,使其达到与母材相变温度相近的水平。结果表明,添加Nb丝的NiTi-SMA接头焊缝主要由B2、B19′、NbTi、Nb及(NiTi,Nb)组成;600℃时效处理后焊缝金属析出Ni4Ti3;通过“Nb元素调控+600℃时效处理”,使母材和焊缝的M-A相变温度趋于一致。

Comparison between N_2 and O_2 anneals on the integrity of an Al_2O_3/Si_3N_4/SiO_2/Si memory gate stack

In this paper the endurance characteristics and trap generation are investigated to study the effects of different postdeposition anneals （PDAs） on the integrity of an Al2O3/Si3N4/SiOz/Si memory gate stack. The flat-band voltage （Vfb） turnarounds are observed in both the programmed and erased states of the N2-PDA device. In contrast, this turnaround is observed only in the erased state of the O2-PDA device. The Vfb in the programmed state of the O2-PDA device keeps increasing with increasing program/erase （P/E） cycles. Through the analyses of endurance characteristics and the low voltage round-trip current transients, it is concluded that in both kinds of device there are an unknown type of pre-existing characteristic deep traps and P/E stress-induced positive oxide charges. In the O2-PDA device two extra types of trap are also found： the pre-existing border traps and the P/E stress-induced negative traps. Based on these four types of defects we can explain the endurance characteristics of two kinds of device. The switching property of pre-existing characteristic deep traps is also discussed.

Osthole prevents cognitive impairment through modulating neuron cells in Aβ25-35-injected mice

OBJECTIVE To investigate the effects of osthole on learning and memory impairment of AD mice induced by injection of Aβ25-35 and the content of Ca2+, GLU and Aβ1-42 in the brain tissue and peripheral blood. METHODS Mice were randomly assigned to sham operation, Aβ25-35, Aβ25-35+Ost-L,Aβ25-35+Ost-M, and Aβ25-35+Ost-H group. Water maze test was performed to assessing spatial learning ability of mice. It is determined that the MDA level and the activity of SOD in the brain tissue of mice in each group by colorimetry. The GLU kit and Ca2 +kit were used to detect the GLU, Ca2 +in tissue and serum. ELISA was used to detect the expression of Aβ1-42 in the hippocampus and serum of mice. HE staining and silver staining were used to detect neuron apoptosis and pathological changes in brain slices and so on. RESULTS(1) Effects of osthole on learning and memory: With the increase of training day,the escape latencies continuously reduced in each experimental group, the escape latencies of the model group was longer on the 1 st, 2 nd, 3 rd, and 5 thdays than the normal group, the difference was statistically significant(day 3 and 4: P<0.05, day 5: P<0.01);compared with the model group, the escaping latency on the 5 thday of the OST low-medium high-dose group was significantly shortened, which was statistically significant(P<0.05).(2) Effects on oxidative stresspathway: the SOD activity of AD mice in the hippocampus model group was lower than that in the normal group, which was statistically significant(P<0.05);The SOD activity in the OST group was higher than that in the model group, which was statistically significant(P<0.05). The MDA content in the model group was significantly higher than that in the normal group(P<0.05). The MDA content in the OST high-dose group was lower than that in the model group, which was statistically significant(P<0.05).(3) Effects of GLU levels on neurotransmitters:the results of the detection of GLU in cortical area and GLU in serum of AD mice in OST dose groups showed that serum GLU levels in the model group were significantly lower than those in the sham group, which was statistically significant(P<0.05). GLU levels in the cortical area were also significantly higher than those in the sham group, which was statistically significant(P<0.05). Compared with the model group, GLU levels in the OST administration group were significantly down-regulated. Among the serum, the effect of medium dose group was obvious. Although there was a trend of down-regulation in the cortical administration group, there was no statistical significance.(4) Changes in Ca2+concentration in the brain. Detection of intracellular Ca2 +concentration in AD mice by OST doses showed that,compared with the sham group, the model group was significantly upregulated in cortical Ca2 +levels.There was no statistical difference in the administration group. Compared with the model group, the concentration of Ca2+in the OST-H group significantly decreased.(5) Effect on levels of Aβ1-42 in hippocampus and serum: model group had significantly higher Aβ1-42 levels in hippocampus than in sham operation group, which was statistically significant(P<0.05). Aβ1-42 in serum was also significantly upregulated compared to the sham group, which was statistically significant(P<0.05). Compared with the model group, the levels of Aβ1-42 in the OST administration group were significantly down-regulated,with the lower and middle doses in the hippocampus being more significant, while the serum was more pronounced at lower doses.(6) Silver staining to detect the tangles of hippocampal neurons: Neuron tangles in the hippocampal CA1 region showed a dark brown-yellow granule distribution in the nuclei of the model group(positive expression). Nerve cell body and dendrites, axons are black or black red,background light yellow. Compared with the model group, the administration group has improved significantly. CONCLUSION OST improves spatial learning and memory of dementia model mice injected with Aβ25-35 in both hippocampus. Experimental studies have shown that OST has different degrees of regulation on neuronal apoptosis, Ca2 +/GLU/oxidative stress and other pathways, and it plays a role in improving multiple AD pathological changes and delaying the pathogenesis of neurodegenerative diseases.

STUDY ON THE THERAPEUTIC EFFECTS OF GINSENOSIDE Rg-1 AND GASTRODINE ON AD MODEL RATS INDUCED BY β-AMYLOID PEPTIDE (25-35)

Objective To study the therapeutic effects of Ginsenoside Rg-1 and Gastrodine on rats model of Alzheimer's disease(AD). Methods Aggregated β-Amyloid peptide (25-35) was injected into the lateral ventricle of rats to establish AD models. Ginsenoside Rg-1, Gastrodine and Ginsenoside Rg-1+Gastrodine were intraperitoneally injected into rats of each test group(Ginsenoside Rg-1∶10mg/kg·day; Gastrodine 100mg/kg·day) for 4 weeks, the rats of control group received equal volume of saline. Passive avoidance task and Morris maze test were done to assess the ability of learning and memory. The content of superoxide dismutase (SOD), malondiadehyde (MDA), total-antioxidative capability (T-AOC), Choline acetyltransferase (ChAT) and acetylcholinesterase (AchE) in brain tissue were measured. Results Ginsenoside Rg-1 and Gastrodine significantly improved learning and memory deficits in the rats with AD induced by β-Amyloid peptide (25-35) (P<0.05). Ginsenoside Rg-1+Gastrodine group were better than Ginsenoside Rg-1 group and Gastrodine group (P<0.05). Ginsenoside Rg-1 reduced the increase of SOD, MDA, but inhibited the decrease of T-AOC, AchE and ChAT; Gastrodine reduced the increase of SOD, MDA, while inhibited the decrease of T-AOC. Gastrodine could also prevent the activity of ChAT and AchE decline in AD rats. Conclusion Both Ginsenoside Rg-1 and Gastrodine have therapeutic effects on rats with AD; Ginsenoside Rg-1 and Gastrodine injection at the same time were better than only using one of them. Their mechanisms might different. Ginsenoside Rg-1 can not only inhibit peroxidation but also increase the activity of AchE and ChAT in brain tissue, while Gastrodine can inhibit peroxidation only, but it can't prevent the decline of ChAT and AchE activity in AD rats.

Expression of miR-9-5p and RHOA in aluminum-induced rat cognitive dysfunction

Objective:To investigate the possible mechanism of microRNA-9-5p(miR-9-5p)and Ras homologous gene family A(RHOA)in aluminum-induced cognitive dysfunction in rats.Methods:According to the principle of randomization,48 Wistar rats were randomly divided into four groups(n=12)of blank control,low dose,medium dose and high dose.The blank control group was gavaged daily saline,and the other three dose groups were given daily gavage AlCl3 aqueous solution at three doses of 25 mg/kg,50 mg/kg,and 100 mg/kg to create a rat model of cognitive impairment for three months.The water maze(MWM)positioning navigation experiment was used to record the time t(s),namely,the incubation period,on the platform of rats,and the incubation period of each group was used to determine whether the rats in the infected group had learning and memory impairment.Hematoxylin-eosin(HE)and Nissl stains observed the pathological changes of nerve cells in the hippocampus of the four groups.Western blot detected the protein expression levels of RHOA and cranial neurotrophic factor(BDNF)in fresh rat hippocampal tissues.RT-qPCR detected the mRNA expression of miR-9-5p,RHOA,and BDNF in rat hippocampal tissues.Results:The results of Morris water maze positioning navigation test showed that the incubation period of each group was calculated on the 1st,3rd and 5th days of the experiment,and the motor incubation period of the infected group was higher than that of the control group.The results of HE staining showed that the rat nerve cells in the control group were morphologically intact,the staining was clear,the nucleus was clearly visible,and the edge of the cell membrane was sharp.The rat neurons in the infected group were damaged to varying degrees,the nucleus gradually dissolved,the cytoplasmic staining became deeper,the edges of the cell membrane were blurred and disordered,and the cells were deformed and arranged disordered.The results of Nissl staining showed that the well-stained Nissl body particles were visible in the nerve cells of rats in the control group,and the dissipation of Nissl bodies in the nerve cells of the infected group was reduced,and the staining was shallow.The results of RT-qPCR showed that compared with the control group,the mRNA expression of miR-9-5p and BDNF was decreased in the infected group,and the mRNA expression of RHOA was increased(P<0.05 or P<0.001).The Western blot results showed that compared with the control group,the relative expression of BDNF in the three infected groups was decreased,and the relative expression of RHOA increased(P<0.05).Conclusion:In aluminum-induced cognitive impairment,miR-9-5p is downregulated and RHOA is upregulatd.

卒中后失语工作记忆的事件相关电位及时频特征

目的 探索卒中后失语(PSA)工作记忆的任务态脑电特征。方法 2020年9月至2021年2月,于北京中医药大学东直门医院招募PSA患者(PSA组)和健康受试者(HC组)各8例,采集脑电图和记忆量表数据,通过工作记忆任务态的脑电数据分析时域事件相关电位(ERP)和时频的脑电频段指标特点,与记忆量表中的各项目进行相关性分析。结果 最终纳入10例,每组5例。ERP分析发现前额区诱发N1和P2成分,顶枕区诱发P300成分。与HC组相比,PSA组在出现条件下,中央前额区N1和P2激活增强,右侧顶枕区P300活动降低(|t|> 2.193, P <0.05)。与HC组相比,PSA组在未出现条件下右侧前额区、中央顶枕区θ频段能量降低,左侧顶枕区α1频段能量降低,左侧中央区γ频段能量增加(t> 2.398, P <0.05)。相关性分析显示,γ频段的能量与听觉词语学习测验中的即刻回忆(r=0.914, P=0.030)、正确再认(r=0.931, P=0.022)和数字广度测验中的倒背(r=0.924, P=0.025)、顺背(r=0.889, P=0.044)呈强正相关。结论 视觉工作记忆任务可调动PSA患者记忆相关脑区代偿活动,可作为PSA工作记忆相关研究的评价客观指征。语言损伤与工作记忆之间存在密切联系。

Plasma post oxidation of nitrocarburized AISI 4140 steel

Plasma nitrocarburizing and plasma oxidizing treatments were performed to improve the wear and corrosion resistance of AISI 4140 steel. Plasma nitrocarburizing was conducted for 3 h at 570 ℃ in the nitrogen, hydrogen and methane atmosphere to produce the ε-Fe2-3(N,C) phase. It was found that the compound layer produced by plasma nitrocarburising was predominantly composed of ε-phase, with a small proportion of γ′-Fe4(N,C) phase. The thickness of the compound layer was about 10 μm and the diffusion layer was about 300 μm in thickness, respectively. Plasma post oxidation was performed on the nitrocarburized samples with various oxygen/hydrogen ratio at a constant temperature of 500 ℃ for 1 h. The very thin magnetite (Fe3O4) layer 1-2 μm in thickness on top of the compound layer was obtained by plasma post oxidation. It was confirmed that the corrosion characteristics of the nitrocarburized compound layer can be further improved by the application of the superficial magnetite layer.

S1-9 Involvement of TGR5 in Aβ-Induced Neurotoxicity in Vivo

TGR5(Takeda G-protein-coupled receptor 5)is a bile acid G protein-coupled receptor primarily expressed in liver,gallbladder,intestine,spleen,and brain and activated by bile acids.(AD).Herein,we evaluated the neuroprotective effects of TGR5 agonist,6α-ethyl-23(S)methylcholic acid(S-EMCA,INT-777),in the Aβ1-42-treated mouse model of acute neurotoxicity.Single intracerebroventricular(i.c.v.)injection of aggregated Aβ1-42(410 pmol/mouse;5μL)into the mouse brain induced cognitive impairment,neuroinflammation,apoptosis,and synaptic dysfunction.In contrast,INT-777(1.5 or 3.0μg/mouse,i.c.v.)significantly improved Aβ1-42-induced cognitive impairment,as reflected by better performance in memory tests.Importantly,INT-777 treatment reversed Aβ1-42-induced TGR5 down-regulation,suppressed the increase of nuclear NF-κB p65,and mitigated neuroinflammation,as evidenced by lower proinflammatory cytokines and less Iba1-positive cells in the hippocampus and frontal cortex.INT-777 treatment also pronouncedly suppressed apoptosis through the reduction of TUNEL-positive cells,decreased activation of caspase-3,increased the ratio of Bcl-2/Bax,and ameliorated synaptic dysfunction by promoting dendritic spine generation with the upregulation of postsynaptic(PSD95)and presynaptic proteins in Aβ1-42-treated mice.Our results indicate that INT-777 has potent neuroprotective effects against Aβ1-42-induced neurotoxicity.Taken together,these findings suggest that TGR5 might participate in the pathogenesis of Alzheimer’s disease.

S3A-3 Involvement of TGR5 in Aβ-Induced Neurotoxicity in Vivo

TGR5(Takeda G-protein-coupled receptor 5)is a bile acid G protein-coupled receptor primarily expressed in liver,gallbladder,intestine,spleen,and brain and activated by bile acids.(AD).Herein,we evaluated the neuroprotective effects of TGR5 agonist,6α-ethyl-23(S)-methylcholic acid(S-EMCA,INT-777),in the Aβ1-42-treated mouse model of acute neurotoxicity.Single intracerebroventricular(i.c.v.)injection of aggregated Aβ1-42(410 pmol/mouse;5μL)into the mouse brain induced cognitive impairment,neuroinflammation,apoptosis,and synaptic dysfunction.In contrast,INT-777(1.5 or 3.0μg/mouse,i.c.v.)significantly improved Aβ1-42-induced cognitive impairment,as reflected by better performance in memory tests.Importantly,INT-777 treatment reversed Aβ1-42-induced TGR5 down-regulation,suppressed the increase of nuclear NF-κB p65,and mitigated neuroinflammation,as evidenced by lower proinflammatory cytokines and less Iba1-positive cells in the hippocampus and frontal cortex.INT-777 treatment also pronouncedly suppressed apoptosis through the reduction of TUNEL-positive cells,decreased activation of caspase-3,increased the ratio of Bcl-2/Bax,and ameliorated synaptic dysfunction by promoting dendritic spine generation with the upregulation of postsynaptic(PSD95)and presynaptic(synaptophysin)proteins in Aβ1-42-treated mice.Our results indicate that INT-777 has potent neuroprotective effects against Aβ1-42-induced neurotoxicity.Taken together,these findings suggest that TGR5 might participate in the pathogenesis of Alzheimer’s disease.