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您的检索式：作者名="PENG Licai"
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| 1 | B, Sr, O and H Isotopic Compositions of Formation Waters from the Bachu Bulge in the Tarim Basin显示文摘以便阐明在 BachuBulge 的 basinal 盐水的起源和迁居, Tarim 盆,我们,在化学成分,和硼上执行了分析,和从 Paleozoicstrata 的粘土矿物的 XRD 的形成水的氢和氧同位素。水表演 Ca, B,李和 Sr 丰富和 SO_4 弄空在含碳并且奥陶纪和 K 丰富部分地相对海水的奥陶纪。在三角洲 D 和 delta^(18 ) 之间的关系 O 证明水的所有数据近与他们的交叉向全球 MeteoricWater 线衰退到今日的本地天落水,建议那现代天落水与蒸发的海水混合了。^(87 )Sr/^(86 ) Sr 比率范围 from0.7090 到 0.7011,比那些显著地高当代的海水。detla^(11 ) Hvalues 每千从 +19.7 到 +32.3,显示出有深度和 Bconcentrations 的减少。结果建议 isotopic 结盟不同 B, Sr 从外部来源被导出。然而,后来,伊利石的百分比被显示在学习区域在粘土矿物之中与深度增加,即,伊利石由于降水而非在更深的埋葬期间沥滤,它是不大可能的让伊利石作出贡献 B 的重要数量到水。因此,有 B 珍视的低 delta^(11 ) 的 B 被解释在寒武纪、更低的奥陶纪主要从热降级 ofkerogen 或暗岩被补充说。 | CAI Chunfang PENG Licai MEI Bowen XIAO Yingkai | 2006 | Acta Geologica Sinica(English Edition)2006，80，4： | 7 |
| 2 | Vagus nerve stimulation protects against cerebral injury after cardiopulmonary resuscitation by inhibiting inflammation through the TLR4/NF-κB and α7nAChR/JAK2 signaling pathways显示文摘BACKGROUND: Our previous research proved that vagus nerve stimulation(VNS) improved the neurological outcome after cardiopulmonary resuscitation(CPR) by activating α7 nicotinic acetylcholine receptor(α7nAChR) in a rat model, but the underlying mechanism of VNS in neuroprotection after CPR remains unclear.METHODS: In vivo, we established a mouse model of cardiac arrest(CA)/CPR to observe the survival rate, and the changes in inflammatory factors and brain tissue after VNS treatment. In vitro, we examined the effects of α7nAChR agonist on ischemia/reperfusion(I/R)-induced inflammation in BV2 cells under oxygen-glucose deprivation/reoxygenation(OGD/R) conditions. We observed the changes in cell survival rate, the levels of inflammatory factors, and the expressions of α7nAChR/Janus kinase 2(JAK2) and toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB).RESULTS: In vivo, VNS preconditioning enhanced functional recovery, improved the survival rate, and reduced hippocampal CA1 cell damage, and the levels of inflammatory mediators after CA/CPR. The application of α7nAChR agonists provided similar effects against cerebral injury after the return of spontaneous circulation(ROSC), while α7nAChR antagonists reversed these neuroprotective impacts. The in vitro results mostly matched the findings in vivo. OGD/R increased the expression of tumor necrosis factor-alpha(TNF-α), TLR4 and NF-κB p65. When nicotine was added to the OGD/R model, the expression of TLR4, NF-κB p65, and TNF-α decreased, while the phosphorylation of JAK2 increased, which was prevented by preconditioning with α7nAChR or JAK2 antagonists.CONCLUSION: The neuroprotective effect of VNS correlated with the activation of α7nAChR. VNS may alleviate cerebral IR injury by inhibiting TLR4/NF-κB and activating the α7nAChR/JAK2 signaling pathway. | Shuang Xu Lang Guo Weijing Shao Licai Liang Tingting Shu Yuhan Zhang He Huang Guangqi Guo Qing Zhang Peng Sun | 2023 | World Journal of Emergency Medicine2023，14，6： | 0 |
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