Crustal S-wave velocity structure of the Yellowstone region using a seismic ambient noise method

The Yellowstone volcano is one of the largest active volcanoes in the world, and its potential hazards demand detailed seismological and geodetic studies. Previous studies with travel time tomography and receiver functions have revealed a low-velocity layer in the crust beneath the Yellowstone volcano, suggesting the presence of a magma chamber at depth. We use ambient seismic noise from regional seismic stations to retrieve short-period surface waves and then study the shallow shear velocity structure of the Yellowstone region by surface wave dispersion analysis. We first obtained a crustal model of the area outside of the Yellowstone volcano and then constructed an absolute shear wave velocity structure in combination with receiver function results for the crust beneath the Yellowstone volcano. The velocity model shows a low-velocity layer with shear velocity at around 1.3 km/s, suggesting that a large-scale magma chamber exists at shallow levels within the crust of the Yellowstone volcanic region.

运用26s定点持续脉动源的同步洲际地震台网

地震学的定量研究需要精确的仪器时钟。最近的研究进展表明,可利用背景噪声来检测存在软件/硬件问题的海底地震仪(OBS)或陆上地震仪的台站时钟漂移情况。在稀疏的全球地震台网尺度下,从背景噪声中提取的短周期(<20s)瑞利波信号相对较弱,应用时受到限制。位于几内亚湾的持续稳定的26s固定脉动源,辐射出较强的噪声信号,可以被全球台站记录到,因而可以利用它同步加大距离台站间的时钟漂移情况。本文基于噪声互相关方法,我们尝试运用该26s的脉动信号检测非洲、北美和欧洲等地区地震台站的时钟精度。结果发现TAM,OBN台站的时钟在2002~2009年间相对稳定;CCM台站的时钟在2006~2009年间出现了约1s偏差,并且时钟的漂移量不稳定;KOWA台站的时钟漂移从2012年10月的约150s最大上升至2013年1月的约500s。本文将得到的结果与Stehly等(2007)利用背景噪声方法得到的结果、以及远震P波初至到时残差进行了对比分析。利用本文提出的方法,通过与经精确校正过的陆地台站同步,可校正北大西洋海底地震仪的时钟。

Involvement of XZFP36L1,an RNA-binding protein,in Xenopus neural development

Xenopus ZFP36L1(zinc finger protein 36,C3H type-like 1)belongs to the ZFP36 family of RNA-binding proteins,which contains two characteristic tandem CCCH-type zinc-finger domains.The ZFP36 proteins can bind AU-rich elements in 3'untranslated regions of target mRNAs and promote their turnover.However,the expression and role of ZFP36 genes during neural development in Xenopus embryos remains largely unknown.The present study showed that Xenopus ZFP36L1 was expressed at the dorsal part of the forebrain,forebrain-midbrain boundary,and midbrain-hindbrain boundary from late neurula stages to tadpole stages of embryonic development.Overexpression of XZFP36L1 in Xenopus embryos inhibited neural induction and differentiation,leading to severe neural tube defects.The function of XZP36L1 requires both its zinc finger and C terminal domains,which also affect its subcellular localization.These results suggest that XZFP36L1 is likely involved in neural development in Xenopus and might play an important role in post-transcriptional regulation.

Interacting with α7 nAChR is a new mechanism for AChE to enhance the inflammatory response in macrophages

Acetylcholine(ACh)regulates inflammation viaα7 nicotinic acetylcholine receptor(α7 nAChR).Acetylcholinesterase(AChE),an enzyme hydrolyzing ACh,is expressed in immune cells suggesting non-classical function in inflammatory responses.Here,the expression of PRiMA-linked G4 AChE was identified on the surface of macrophages.In lipopolysaccharide-induced inflammatory processes,AChE was upregulated by the binding of NF-κB onto the ACHE promotor.Conversely,the overexpression of G4 AChE inhibited ACh-suppressed cytokine release and cell migration,which was in contrast to that of applied AChE inhibitors.AChEmt,a DNA construct without enzymatic activity,was adopted to identify the protein role of AChE in immune system.Overexpression of G4 AChEmt induced cell migration and inhibited ACh-suppressed cell migration.The co-localization ofα7 nAChR and AChE was found in macrophases,suggesting the potential interaction ofα7 nAChR and AChE.Besides,immunoprecipitation showed a close association ofα7 nAChR and AChE protein in cell membrane.Hence,the novel function of AChE in macrophage by interacting withα7 nAChR was determined.Together with hydrolysis of ACh,AChE plays a direct role in the regulation of inflammatory response.As such,AChE could serve as a novel target to treat age-related diseases by antiinflammatory responses.

2,3,7,8-Tetrachlorodibenzo-p-dioxin promotes migration ability of primary cultured rat astrocytes via aryl hydrocarbon receptor

Emerging evidence showed that 2,3,7,8-Tetrachlorodibenzo-p-dioxin(TCDD) could induce expression of certain reactivation-associated genes in astrocytes, however, the consequent cellular effects and molecular mechanisms are still unclear. During the process of astrocyte reactivation, migration is a critical cellular event. In the present study, we employed woundhealing assay and Transwell? motility assay to explore the effects of TCDD on cell migration in primary cultured rat cortical astrocytes. We found that upon TCDD treatments at relative low concentrations(10^(-10) and/or 10^(-9) mol/L), the ability of primary astrocytes to migrate horizontally and vertically was promoted. In line with this cellular effect, the mR NA expression of two promigratory genes, including cell division cycle 42(CDC42) and matrix metalloproteinase 2(MMP2)was induced by TCDD treatment. Dioxin exerts its toxic effects mainly through aryl hydrocarbon receptor(AhR) pathway. So the role of AhR pathway in the pro-migratory effects of TCDD was examined using an AhR antagonist, CH223191. We found that application of CH223191 significantly reversed the pro-migratory effects of TCDD. Interestingly, the basal ability of horizontal migration as well as basal levels of CDC42 and MMP2 expression were dramatically reduced suggesting a possible physiological role of AhR in maintaining the endogenous migration ability of the primary astrocytes. These findings support the notion that dioxin promotes astrocyte reactivation at molecular and cellular levels.

Identification of differentially expressed genes response to TCDD in rat brain after long-term low-dose exposure

Several cohort studies have reported that dioxin and dioxin-like polychlorinated biphenyls might impair the nervous system and lead to neurological or neurodegenerative diseases in the elder people, but there is limited research on the involved mechanism. By using microarray analysis, we figured out the differentially expressed genes between brain samples from SD rats after low-dose（0.1 μg/（kg？bw）） dioxin exposure for six months and controls. To investigate the function changes in the course of dioxin exposure, Gene Ontology（GO） annotation and Kyoto Encyclopedia of Genes and Genomes（KEGG） pathway analysis were performed on the differentially expressed genes. And the changes of several picked genes have been verified by real-time PCR. A total of 145 up-regulated and 64 down-regulated genes were identified. The metabolic processes, interleukin-1 secretion and production were significantly associated with the differentially expressed genes. And the genes regulated by dioxin also clustered to cholinergic synapse and long-term potentiation. Candidate biomarker genes such as egr1, gad2, gabrb3, abca1, ccr5 and pycard may be toxicological targets for dioxin. Furthermore, synaptic plasticity and neuro-immune system may be two principal affected areas by dioxin.

Influence of pore pressure on tensile fracture growth in rocks： a new explanation based on numerical testing

The diffusion of pore fluid pressures may create both spatial and temporal effective stress gradients that influence or control the development and evolution of fractures within rock masses. To better understand the controls on fracturing behavior, numerical simulations are performed using a progressive fracture modeling approach that shares many of the same natural kinematic features in rocks, such as fracture growth, nucleation, and termination. First, the pinch-off breaking test is numerically performed to investigate the tensile failure of a rock specimen in a uniform pore pressure field. In this numerical simulation, both mechanical and hydrological properties of a suite of rocks are measured under simulated laboratory conditions. The complete tensional failure process of the rock specimen under pore pressure was reproduced. Second, a double-notched specimen is numerically extended to investigate how the water flow direction or pore pressure gradient influences the fracture growth. An exhaustive sensitivity study is conducted that examines the effects of varying both hydrological and mechanical boundary conditions. The simulation results indicate that local fluid pressure gradients strongly influence the state of stress in the solids and, thereby, fracture growth. Fracture and strength behavior is influenced not only by the pore pressure magnitude on a local scale around the fracture tip, but also by the orientation and distribution of pore pressure gradients on a global scale. Increasing the fracture growth rate increases the local model permeability and decreases the sample strength. The results of this study may provide useful information concerning the degree of hydrological and mechanical coupling action under geologic conditions.

Dioxin induces expression of hsa-mi R-146b-5p in human neuroblastoma cells

Dioxin can cause a series of neural toxicological effects. Micro RNAs（mi Rs） play important roles in regulating nervous system function and mediating cellular responses to environmental pollutants, such as dioxin. Hsa-mi R-146 b-5 p appears to be involved in neurodegenerative diseases and brain tumors. However, little is known about effects of dioxin on the expression of hsa-mi R-146 b-5 p. We found that the hsa-mi R-146 b-5 p expression and its promoter activity were significantly increased in dioxin treated SK-N-SH cells, a human-derived neuroblastoma cell line. Potential roles of hsa-mi R-146 b-5 p in mediating neural toxicological effects of dioxin may be due to the regulation of certain target genes. We further confirmed that hsa-mi R-146 b-5 p significantly suppressed acetylcholinesterase（ACh E） activity and targeted the3′-untranslated region of the ACh E T subunit, which has been down-regulated in dioxin treated SK-N-SH cells. Functional bioinformatic analysis showed that the known and predicted target genes of hsa-mi R-146 b-5 p were involved in some brain functions or cyto-toxicities related to known dioxin effects, including synapse transmission, in which ACh E may serve as a responsive gene for mediating the effect.