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7篇 您的检索式:作者名="BAO SHIYAO"
    题名 作者 年代 出处 被引量
1Distribution characteristics and indicator significance of Dechloranes in multi-matrices at Ny-lesund in the Arctic显示文摘In recent years, Dechloranes have been widely detected in the environment around the world.However, understanding and knowledge of Dechloranes in remote regions, such as the Arctic,remain lacking. Therefore, the concentrations of 5 Dechloranes in surface seawater, sediment,soil, moss, and dung collected from Ny-lesund in the Arctic were measured with the concentrations 93 pg/L, 342, 325, 1.4, and 258 pg/g, respectively, which were much lower than those in Asian and European regions. The mean ratios of anti-Dechlorane Plus(DP) to total DP(fanti) in seawater, sediment, soil, moss, dung, and atmospheric samples were 0.36, 0.21, 0.18,0.27, 0.66, and 0.43, respectively. Results suggested that the main source of DP in seawater,sediment, soil, and moss was long-range atmospheric transport. However, the ratio identified in dung was different, for which the migration behavior of the organism is probably the main source of DP.Guangshui Na Wei Wei Shiyao Zhou Hui Gao Xindong Ma Lina Qiu Linke Ge Chenguang Bao Ziwei Yao 2015Journal of Environmental Sciences2015,27,2:3
2The effection of β-amyloid protein on amino acid of extracellular fluid in rat's hippocampus and frontal lobe 显示文摘LIU CHUNFENG DAI YONGPING BAO SHIYAO 2000Chinese Neurology Journal2000,33,1:1
3Robust normal estimation for point clouds with sharp features显示文摘Bao Li Ruwen Schnabel Reinhard Klein Zhiquan Cheng Gang Dang Shiyao Jin 2010Computers & Graphics2010,,2:1
4Effect of agonist on gamma-aminobutyric acid B receptor subunit expression in the hippocampus of epileptic rats显示文摘BACKGROUND:An amino acid imbalance has been considered to be responsible for epilepsy pathogenesis.Gamma-aminobutyric acid-B receptor(GABA_BR) inhibits voltage-sensitive calcium ion channels and GABA or glutamic acid(Glu) neurotransmitter release,which promotes or inhibits onset and development of epilepsy. OBJECTIVE:To explore the effect of baclofen on GBR1a and GBR2 mRNA expression in the hippocampus of epileptic rats following kainic acid(KA) induction,and to study the adaptability of GABA_BR subunits. DESIGN,TIME AND SETTING:A randomized,controlled,animal experiment based on molecular biology was performed at the Laboratory Research Center of Second Hospital Affiliated to Soochow University from November 2005 to March 2006. MATERIALS:KA was provided by Sigma,USA.In situ hybridization detection kit of GBR1a and GBR2 was provided by Wuhan Boster Biological Technology,China.GABA_BR agonist(baclofen) was provided by Sigma,USA. METHODS:Forty-four epileptic rats were randomly allocated to epileptic(n=28) and drug intervention(n=16) groups.The epileptic group was further divided into post-epileptic subgroups at different time points:6,12 hours,1,3,7,15,and 30 days(n=4).The drug intervention group was further divided into intervention controls subgroups at various time points:6 hours,1 day,and 3 days (n=4).Four additional rats were considered the normal control group and not modeled,but were injected with saline in the hippocampal CA3 region. MAIN OUTCOME MEASURES:GBR1a and GBR mRNA expression was detected in the right hippocampal CA1,CA3,and dentate gyrus(DG) areas of the control,epileptic,and interference groups at various time intervals according to in situ hybridization results. RESULTS:(1) During the early stage of epilepsy(6 and 12 hours),GBR1a and GBR2 mRNA expression was decreased,and expression was less than the control group at one day after KA induction(P<0.05).mRNA expression was increased in the DG,but was greater than the control group at day 3(P<0.05).Expression in the hippocampal CA1 and CA3 regions remained low(P<0.05),but gradually recovered to control levels.(2) The time points when subunit expression was decreased were prolonged following baclofen intervention,and expression was significantly greater than the epileptic group(P<0.05). CONCLUSION:Both mRNA expressions of GABA_BR subunits were up-regulated following decreased expression in the epileptic group,suggesting that the temporal lobe exhibited endogenous antiepileptic mechanisms during the early stages of epilepsy onset.Baclofen promoted mRNA expression of GBR1a and GBR2.Jihong Tang Shiyao Bao Siming Hu Zhilin Zhang 2009Neural Regeneration Research2009,4,8:1
5A model of experi mental symptomatic cerebralvasospasm following subarachnoid hemorrhage in rabbit显示文摘SHAO GUOFU BAO SHIYAO CHU BING 2000J Clin Neurol2000,13,:1
6THE RESEARCH ON MECHANISMS OF AMYLOID- β PROTEIN INDUCING ALZHEIMER'S DISEASE IN RAT AND EFFECTS OF NIMODIPINE TREATMENT显示文摘0bjective In order to clarify the mechanism of the neurotoxics of Aβ, we studied the effects on the rCBF, extra-cellular amino acid (EAA), apoptosis and Bcl-2 protein expression, and their relationship with learning and memory deficiency. Methods Aβ was injected into NBM in rats to establish the AD model, learning and memory abilities were observed by Y-maze. The rCBF was measured by hydrogen clearance method. The EAA was detected by microdialysis in vivo with HPLC. The apoptosis and Bc1-2 protein expression was examined by flow cytometry. The male SD rats were divided into three groups: the model group was injected Aβ (10 μ g) into NBM of the rat. The control group was injected NaC1 (0.9%) in the same way. The treatment group was made with intraperitoneal injections of Nimodipine for 2 weeks after A β injections. Results The administration of Aβ into rat′s NBM could lead to the loss of learning and memory abilities. It was found that in frontal cortex and hippocampus, the rCBF decrease, however, with no trend of progressive decline. On the other hand, the levels of EAA increased, especially glutamate. Furthermore, A β significantly induced neurons apoptosis of frontal cortex and hippocampi cell, and upregulated the expression of the bcl-2. The Nimodipine might entirely improve rCBF of AD rats nearly to normal level, lessen the release of EAA and augment restrain neurotransmission. It might reduce the apoptosis partly, but it couldn't improve the learning and memory disorders completely. Conclusion The results implied that the neurotoxic effect of Aβ exists multi-mechanism.Chunfeng Liu Shiyao Bao Yongping Dai 2000中国临床神经科学2000,8,z1:0
7Reduced glutathione alleviates the toxic effect of 6-hydroxydopamine on bone marrow stromal cells显示文摘We studied the effect of reduced glutathione on bone marrow stromal cells (BMSCs) treated with 6-hydroxydopamine (6-OHDA), which shows a toxic effect on dopaminergic neurons. The proliferation of BMSCs treated with 6-OHDA decreased, while that of BMSCs treated with reduced glutathione increased. The proliferation of BMSCs treated with both 6-OHDA and reduced glutathione was significantly higher compared with that treated with 6-OHDA alone. These findings indicate that reduced glutathione alleviates the toxic effect of 6-OHDA on BMSCs.Henghui Wang Weifeng Luo Xiaoxia wang Xiaoling Qin Shiyao Bao 2011Neural Regeneration Research2011,6,22:0
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