Cath-KP,a novel peptide derived from frog skin,prevents oxidative stress damage in a Parkinson’s disease model

Parkinson’s disease(PD)is a neurodegenerative condition that results in dyskinesia,with oxidative stress playing a pivotal role in its progression.Antioxidant peptides may thus present therapeutic potential for PD.In this study,a novel cathelicidin peptide(Cath-KP;GCSGRFCNLF NNRRPGRLTLIHRPGGDKRTSTGLIYV)was identified from the skin of the Asiatic painted frog(Kaloula pulchra).Structural analysis using circular dichroism and homology modeling revealed a uniqueαββconformation for Cath-KP.In vitro experiments,including free radical scavenging and ferric-reducing antioxidant analyses,confirmed its antioxidant properties.Using the 1-methyl-4-phenylpyridinium ion(MPP^(+))-induced dopamine cell line and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced PD mice,Cath-KP was found to penetrate cells and reach deep brain tissues,resulting in improved MPP^(+)-induced cell viability and reduced oxidative stress-induced damage by promoting antioxidant enzyme expression and alleviating mitochondrial and intracellular reactive oxygen species accumulation through Sirtuin-1(Sirt1)/Nuclear factor erythroid 2-related factor 2(Nrf2)pathway activation.Both focal adhesion kinase(FAK)and p38 were also identified as regulatory elements.In the MPTP-induced PD mice,Cath-KP administration increased the number of tyrosine hydroxylase(TH)-positive neurons,restored TH content,and ameliorated dyskinesia.To the best of our knowledge,this study is the first to report on a cathelicidin peptide demonstrating potent antioxidant and neuroprotective properties in a PD model by targeting oxidative stress.These findings expand the known functions of cathelicidins,and hold promise for the development of therapeutic agents for PD.

基于断裂力学的腐蚀钢丝疲劳S-N曲线研究

高强冷拔钢丝因其优异的力学性能被广泛应用于缆索承重结构,服役过程中钢丝腐蚀与断裂威胁着结构安全。钢丝腐蚀后表面的蚀坑因应力集中效应易产生疲劳裂纹,因此腐蚀钢丝剩余疲劳寿命主要取决于裂纹的扩展阶段,且裂纹扩展受到腐蚀程度(初始损伤)的显著影响。精确表征腐蚀程度并准确评估服役期钢丝腐蚀后的剩余寿命,仍是亟待解决的维修难题。首先采用蚀坑最大深度表征钢丝腐蚀程度,以应力强度因子幅作为裂纹扩展驱动力指标,基于断裂力学的Paris公式建立受拉钢丝裂纹扩展理论模型,进而推导腐蚀钢丝的疲劳S-N曲线。大量既有的腐蚀钢丝疲劳试验结果与理论预测值的比较验证了所提理论模型及疲劳S-N曲线的合理性和有效性。含多个蚀坑的钢丝裂纹扩展有限元模拟表明,等效单裂纹适用于多腐蚀坑钢丝疲劳寿命的简化分析。参数分析表明,蚀坑深度和腐蚀环境是腐蚀钢丝疲劳强度的关键影响因素,而应力比和疲劳加载频率影响较小,所提出的S-N曲线在钢丝常规服役条件下适用于评估其剩余寿命,可得到合理的预测结果。基于断裂力学所提的理论方法和疲劳S-N曲线可为腐蚀钢丝的疲劳强度和寿命评估提供参考。

A novel binary effective medium model to describe the prepeak stressstrain relationship of combined bodies of rock-like material and rock

Combined bodies of rock-like material and rock are widely encountered in geotechnical engineering,such as tunnels and mines.The existing theoretical models describing the stress-strain relationship of a combined body lack a binary feature.Based on effective medium theory,this paper presents the governing equation of the“elastic modulus”for combined and single bodies under triaxial compressive tests.A binary effective medium model is then established.Based on the compressive experiment of concretegranite combined bodies,the feasibility of determining the stress threshold based on crack axial strain is discussed,and the model is verified.The model is further extended to coal-rock combined bodies of more diverse types,and the variation laws of the compressive mechanical parameters are then discussed.The results show that the fitting accuracy of the model with the experimental curves of the concretegranite combined bodies and various types of coal-rock combined bodies are over 95%.The crack axial strain method can replace the crack volumetric strain method,which clarifies the physical meanings of the model parameters.The variation laws of matrix parameters and crack parameters are discussed in depth and are expected to be more widely used in geotechnical engineering.

Bushen Yizhi Formula regulates the IRE1αpathway to alleviate endoplasmic reticulum stress in an Alzheimer’s disease rat model

While the Bushen Yizhi Formula can treat Alzheimer’s disease(AD),the yet to be ascertained specific mechanism of action was explored in this work.Methods:Different concentrations of the Bushen Yizhi Formula and amyloid-beta peptide(Aβ)were used to treat rat pheochromocytoma cells(P12)and human neuroblastoma cells(SH-SY5Y).Cell morphological changes were observed to determine the in vitro cell damage.Cell Counting Kit(CCK)-8 assay and flow cytometry were employed to identify cell viability and apoptosis/cell cycle,respectively.Western blotting and immunohistochemistry were employed to measure the expressions of endoplasmic reticulum stress(ERS)-related proteins(GRP78 and CHOP),p-IRE1α,IRE1α,ASK1,p-JNK,JNK,Bax,Bcl-2,XBP-1,and Bim.Fura 2-acetoxymethyl ester(Fura-2/AM)was used to determine the intracellular calcium(Ca^(2+))concentration.Also,an AD model was constructed by injecting Aβinto the CA1 area of the hippocampus in Sprague Dawley rats.AD model rats were gavaged with different concentrations of Bushen Yizhi Formula for 14 consecutive days.The Morris water maze experiment was conducted to test the learning and memory of rats.Hematoxylin&Eosin(H&E)and Terminal-deoxynucleotidyl Transferase(TdT)-mediated dUTP Nick-End Labeling(TUNEL)staining were done to determine histopathological changes in the brain.Results:Bushen Yizhi Formula relieved the Aβ-induced effects including cell injury,decreased viability,increased apoptosis,G0/G1 phase cell cycle arrest,upregulation of GRP78,CHOP,p-IRE1α,p-JNK,Bax,XBP-1 and Bim,as well as down-regulation of Bcl-2.These results were also seen with IRE1αsilencing.While Aβsuppressed the learning and memory abilities of rats,the Bushen Yizhi Formula alleviated these effects of Aβ.Brain nerve cell injury induced by Aβcould also be treated with Bushen Yizhi Formula.Conclusion:Bushen Yizhi Formula could influence ERS through the IRE1αsignaling pathway to achieve its therapeutic effects on AD.

Neuroprotective effects of curculigoside against Alzheimer’s disease via regulation oxidative stress mediated mitochondrial dysfunction in L-Glu-exposed HT22 cells and APP/PS1 mice

Curculigoside(CCG)is a phenolic glycoside compound extracted from the root of a natural plant called Curculigo orchioides Gaertn.In this study,the neuroprotective effect of CCG through oxidative stress mediated mitochondrial dysfunction on L-glutamate(L-Glu)-damaged hippocampal neuron cell line(HT22)and APPswe/PSEN1dE9 transgenic(APP/PS1)mice were investigated.Observably,CCG in L-Glu-damaged HT22 cells suppressed apoptosis,reduced the accumulation of reactive oxygen species,balanced the mitochondrial membrane potential and prevented the over-influx of calcium.In APP/PS1 mice,4-week CCG administration significantly improved their memory and behavioral impairments,enhanced the function of cholinergic system,reduced the deposition of Aβand neurofibrillary fiber tangles caused by tau phosphorylation,and suppressed the development and progression of oxidative stress in brains of APP/PS1 mice.Based on the screening of proteomic analysis on hippocampus,CCG were confirmed that it could regulate the expression levels of proteins related to mitochondrial dysfunction,mainly through activating on AMPK/Nrf2 signaling,in APP/PS1 mice and L-Glu-exposed HT22 cells.CCG has a prominent neuroprotective effect on regulate the AMPK/Nrf2-mediated mitochondrial dysfunction in cells APP/PS1 mice support CCG is a potentially potent drug for AD treatment and merits further investigation.

Apparent stress as an indicator of stress meta-instability:The 2021 M_(S)6.4 Yangbi earthquake in Yunnan,China

Investigating spatiotemporal changes in crustal stress associated with major earthquakes has implications for understanding seismogenic processes.However,in individual earthquake cases,the characteristics of the stress after it reaches its maximum value are rarely discussed.In this study,we use the 2021 M_S6.4 Yangbi earthquake in Yunnan,China and events of magnitudes M_L≥3.0 occurred in the surrounding area in the previous 11 years to investigate the spatiotemporal evolution of apparent stress.The results indicate that apparent stress began to increase in January 2015 and reached a maximum in January 2020.Apparent stress then remained at a high level until October 2020,after which it declined considerable.We suggest that the stress was in the accumulation stage from January 2015 to January 2020,and entered the meta-instability stage after October 2020.During the meta-instability stage,the zone of decreasing stress expanded continuously and the apparent stress increased around the Yangbi earthquake source region.These features are generally consistent with the results of laboratory rock stress experiments.We propose that apparent stress can be a good indicator for determining whether the stress at a specific location has entered the meta-instability stage and may become the epicenter of an impending strong earthquake.

Chloride Resistance of Concrete under Complex Stress and Environment

The presence of stress is shown to have a significant impact on chloride ions in concrete. Reinforced concrete is usually durable and cost-effective which has resulted in its widespread use for construction, however, the concrete subjected to environment and load has become increasingly apparently that attacked by aggressive agents such as chloride ion. In this study, the coupling influences are stress effects and environmental problems on the coastline concrete durability have been investigated. A series of cyclic of a wet-dry cycle and submersion tests were performed onto the stressed concrete to obtain an understanding of the physical mechanisms causing the accumulation of chlorides in the interior pores of concrete under different stress types and exposure environments, based on the same duration. Specimens were prepared and subjected to NaCl solution in a wet-dry cycle and submersion, the chloride in the tension zone is gradual with increasing the stress level, as well as the chloride ion in the wet-dry cycle, is increasing the number of cycles. The apparent diffusion coefficient of each specimen was calculated respectively, the profile of concentration at a different section of tension and compression zones were presented in influence factors of the number of cycles, the length of drying phase, and periodic wetting cycles with sodium solution was discussed. After employed Fick’s second law, the results suggested Da in a wet-dry cycle is much higher than the Da in submersion zones.

CO_(2)分压对S135钢在CO_(2)/H_(2)S共存体系中腐蚀行为的影响

为了给井下油气管材的选择和腐蚀预测模型的建立提供理论依据,利用高温高压反应釜进行S135钢在CO_(2)/H_(2)S共存体系中的腐蚀模拟试验,采用失重法、恒载荷法、X射线衍射(XRD)、扫描电镜(SEM)、能谱(EDS)、三维轮廓扫描仪等手段研究了CO_(2)分压对S135钢在温度100℃、CO_(2)/H_(2)S共存体系中腐蚀行为的影响及规律。结果表明,随CO_(2)分压升高,S135钢的腐蚀速率增大,屈服强度损伤加剧,CO_(2)分压为5,10,15,20 MPa时,其屈服强度(σs)损伤率分别为1.4%、3.6%、4.5%和15.9%;抗拉强度(σb)损伤率分别为1.2%、3.4%、5.2%和15.4%。S135钢在低CO_(2)分压下发生全面腐蚀,随CO_(2)分压增大发展为以全面腐蚀为主,辅以局部腐蚀。应力腐蚀裂纹在萌生阶段以局部阳极溶解作用(点蚀)为主,随CO_(2)分压增大应力腐蚀裂纹更易生长,应力腐蚀敏感性增加,加剧了基体的腐蚀进程。

Polyoxidovanadates a new therapeutic alternative for neurodegenerative and aging diseases

Aging is a natural phenomenon characterized by a progressive decline in physiological integrity,leading to a deterioration of cognitive function and increasing the risk of suffering from chronic-degenerative diseases,including cardiovascular diseases,osteoporosis,cancer,diabetes,and neurodegeneration.Aging is considered the major risk factor for Parkinson’s and Alzheimer’s disease develops.Likewise,diabetes and insulin resistance constitute additional risk factors for developing neurodegenerative disorders.Currently,no treatment can effectively reverse these neurodegenerative pathologies.However,some antidiabetic drugs have opened the possibility of being used against neurodegenerative processes.In the previous framework,Vanadium species have demonstrated a notable antidiabetic effect.Our research group evaluated polyoxidovanadates such as decavanadate and metforminium-decavanadate with preventive and corrective activity on neurodegeneration in brain-specific areas from rats with metabolic syndrome.The results suggest that these polyoxidovanadates induce neuronal and cognitive restoration mechanisms.This review aims to describe the therapeutic potential of polyoxidovanadates as insulin-enhancer agents in the brain,constituting a therapeutic alternative for aging and neurodegenerative diseases.

基于等效结构应力法的高强钢焊接结构低温主S-N曲线

现有的疲劳S-N曲线已不再适用于北极的低温环境,为了评估北极海洋工程设备材料的低温疲劳寿命,有必要建立金属结构尤其是焊接结构的低温疲劳S-N曲线。本文基于等效结构应力法,计算出Q690高强钢管环焊缝的主S-N曲线,并通过共振疲劳试验对该方法进行了验证。在此基础上,结合大量的高强钢焊接结构试验结果,将温度敏感因子c引入到低温疲劳主S-N曲线的推导中,首次建立了基于低温金属焊接结构的主S-N曲线,并对文献中的疲劳S-N试验数据和ASME中的修正方法进行了对比和验证。结果表明,等效结构应力法能够较准确地计算出焊缝疲劳S-N曲线,推导出的金属焊接结构低温主S-N曲线与试验曲线吻合较好,能够满足低温地区工程要求,可为高强钢焊接结构在北极地区低温环境中的广泛应用提供理论指导。该方法可以为金属焊接结构的低温疲劳研究节省大量的成本,减少非标准试验操作造成的不必要的误差。这对北极海洋工程设备的设计、安全运行和疲劳评估具有重要意义。

Interplay between microglia and environmental risk factors in Alzheimer's disease

Alzheimer s disease,among the most common neurodegenerative disorders,is chara cterized by progressive cognitive impairment.At present,the Alzheimer’s disease main risk remains genetic ris ks,but major environmental fa ctors are increasingly shown to impact Alzheimer’s disease development and progression.Microglia,the most important brain immune cells,play a central role in Alzheimer’s disease pathogenesis and are considered environmental and lifestyle"sensors."Factors like environmental pollution and modern lifestyles(e.g.,chronic stress,poor dietary habits,sleep,and circadian rhythm disorde rs)can cause neuroinflammato ry responses that lead to cognitive impairment via microglial functioning and phenotypic regulation.However,the specific mechanisms underlying interactions among these facto rs and microglia in Alzheimer’s disease are unclear.Herein,we:discuss the biological effects of air pollution,chronic stress,gut micro biota,sleep patterns,physical exercise,cigarette smoking,and caffeine consumption on microglia;consider how unhealthy lifestyle factors influence individual susceptibility to Alzheimer’s disease;and present the neuroprotective effects of a healthy lifestyle.Toward intervening and controlling these environmental risk fa ctors at an early Alzheimer’s disease stage,understanding the role of microglia in Alzheimer’s disease development,and to rgeting strategies to to rget microglia,co uld be essential to future Alzheimer’s disease treatments.

Deep tectonics and seismogenic mechanisms of the seismic source zone of the Jishishan M_(s)6.2 earthquake on December 18,2023,at the northeast margin of the Tibetan Plateau

On December 18,2023,an M_(s)6.2 earthquake occurred in Jishishan,Gansu Province,China.This earthquake happened in the eastern region of the Qilian Orogenic Belt,which is situated at the forefront of the NE margin of the Tibetan Plateau(i.e.,Qinghai-Tibet Plateau),encompassing a rhombic-shaped area that intersects the Qilian-Qaidam Basin,Alxa Block,Ordos Block,and South China Block.In this study,we analyzed the deep tectonic pattern of the Jishishan earthquake by incorporating data on the crustal thickness,velocity structure,global navigation satellite system(GNSS)strain field,and anisotropy.We discovered that the location of the earthquake was related to changes in the crustal structure.The results showed that the Jishishan M_(s)6.2 earthquake occurred in a unique position,with rapid changes in the crustal thickness,Vp/Vs,phase velocity,and S-wave velocity.The epicenter of the earthquake was situated at the transition zone between high and low velocities and was in proximity to a low-velocity region.Additionally,the source area is flanked by two high-velocity anomalies from the east and west.The principal compressive strain orientation near the Lajishan Fault is primarily in the NNE and NE directions,which align with the principal compressive stress direction in this region.In some areas of the Lajishan Fault,the principal compressive strain orientations show the NNW direction,consistent with the direction of the upper crustal fast-wave polarization from local earthquakes and the phase velocity azimuthal anisotropy.These features underscore the relationship between the occurrence of the Jishishan M_(s)6.2 earthquake and the deep inhomogeneous structure and deep tectonic characteristics.The NE margin of the Tibetan Plateau was thickened by crustal extension in the process of northeastward expansion,and the middle and lower crustal materials underwent structural deformation and may have been filled with salt-containing fluids during the extension process.The presence of this weak layer makes it easier for strong earthquakes to occur through the release of overlying rigid crustal stresses.However,it is unlikely that an earthquake of comparable or larger magnitude would occur in the short term(e.g.,in one year)at the Jishishan east margin fault.

A novel mechanism of PHB2-mediated mitophagy participating in the development of Parkinson's disease

Endoplasmic reticulum stress and mitochondrial dysfunction play important roles in Parkinson s disease,but the regulato ry mechanism remains elusive.Prohibitin-2(PHB2)is a newly discove red autophagy receptor in the mitochondrial inner membrane,and its role in Parkinson’s disease remains unclear.Protein kinase R(PKR)-like endoplasmic reticulum kinase(PERK)is a factor that regulates cell fate during endoplasmic reticulum stress.Parkin is regulated by PERK and is a target of the unfolded protein response.It is unclear whether PERK regulates PHB2-mediated mitophagy thro ugh Parkin.In this study,we established a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced mouse model of Parkinson’s disease.We used adeno-associated virus to knockdown PHB2 expression.Our res ults showed that loss of dopaminergic neurons and motor deficits were aggravated in the MPTP-induced mouse model of Parkinson’s disease.Ove rexpression of PHB2 inhibited these abnormalities.We also established a 1-methyl-4-phenylpyridine(MPP+)-induced SH-SY5Y cell model of Parkinson’s disease.We found that ove rexpression of Parkin increased co-localization of PHB2 and microtubule-associated protein 1 light chain 3,and promoted mitophagy.In addition,MPP+regulated Parkin involvement in PHB2-mediated mitophagy through phosphorylation of PERK.These findings suggest that PHB2 participates in the development of Parkinson’s disease by intera cting with endoplasmic reticulum stress and Parkin.

纳米C-S-H晶核对水泥浆体流变性能的影响

纳米C-S-H晶核由于对水泥早期水化的显著加速效果逐渐被广泛用作早强剂,通过流变仪测试掺纳米C-S-H晶核水泥浆体的塑性黏度、动态屈服应力、静态屈服应力和触变性,以研究纳米C-S-H晶核对水泥浆体流变性能的影响。结果表明:纳米C-S-H晶核掺入水泥浆体后,水泥浆体塑性黏度、动态屈服应力、静态屈服应力和触变性均随之增加,掺量越大,增加越多。水灰比对水泥浆体的流变性能也具有显著影响,水灰比越小,浆体的塑性黏度、动态屈服应力、静态屈服应力和触变性越大。

山新杨谷胱甘肽S-转移酶PdbGST基因的克隆与胁迫表达分析

在植物中,谷胱甘肽S-转移酶是一类多功能酶,能够在其响应非生物胁迫中发挥作用。为研究该基因在杨树中的功能,本研究克隆了山新杨谷胱甘肽S-转移酶基因Pdb GST及其启动子序列,对其进行生物信息学分析和表达特征分析。结果显示,Pdb GST基因的开放阅读框(ORF)全长666 bp,编码221个氨基酸,其形成的蛋白质相对分子质量为25.57 k Da,为稳定亲水性酸性蛋白,定位于细胞质中。系统进化分析表明,山新杨Pdb GST蛋白与山新杨中的XP_034926648蛋白的同源性最高。对克隆获取的2 000 bp启动子序列进行分析,结构显示该启动子序列中,含有多种响应非生物胁迫的顺式作用元件。荧光定量PCR分析显示Pdb GST基因在山新杨根部表达量最高,其次在山新杨叶部也有较高表达量,相反在山新杨顶芽中表达量最低。此外,对Pdb GST基因响应非生物胁迫分析显示,山新杨根部Pdb GST基因受诱导后即出现持续且大量的表达。

2022年6月1日四川芦山M_(S)6.1地震的发震构造与力学机制探讨

2022年6月1日17时00分08秒(北京时间)四川雅安市芦山县发生M_(S)6.1地震,此次地震是继2008年汶川M_(S)8.0、2013年芦山M_(S)7.0地震后发生在龙门山断裂带的又一显著地震,与后者在空间上仅相距9 km.为揭示此次地震的发震构造特征及其与2013年芦山M_(S)7.0地震的关系,进而理解龙门山断裂带强震孕育动力学过程与地震危险性,本文采用CAP全波形反演方法计算了芦山M_(S)6.1地震的震源机制解,利用多阶段定位法对2013年芦山M_(S)7.0地震以来余震区地震进行了精确定位,并基于库仑应力讨论两次地震的应力触发关系.结果显示,芦山M_(S)6.1地震的震源机制解为:节面Ⅰ的走向、倾角和滑动角分别为221°、40°和105°;节面Ⅱ的参数为22°、52°和78°,矩心深度14 km,震源机制断层面解呈现一组与龙门山断裂带性质接近的节面.反演给出的P轴方位角为120°,倾角为6°,反映了此次地震主要受NWW-SEE向水平挤压应力作用,与龙门山断裂带南段背景构造应力场一致.地震精定位结果显示芦山M_(S)6.1地震序列发生在2013年芦山M_(S)7.0地震发震断层北西侧的一条倾向南东的反冲断层上,据此可判断震源机制解的节面Ⅱ为发震断层面.在此基础上,通过指定发震与接收断层,计算获得2013年芦山M_(S)7.0地震对此次M_(S)6.1地震所在断层的最大库仑应力加载值可达1.5 MPa,说明前者对后者有显著的触发作用.

2015年12月7日塔吉克斯坦M_(S)7.4地震对远场小震活动的动态应力触发

采用离散波数法计算2015年12月7日塔吉克斯坦M_(S)7.4地震远场产生的库仑破裂应力变化,并结合β统计值检验方法,分析该地震对远场区域地震活动的应力触发作用。结果表明,①塔吉克斯坦M_(S)7.4地震在新疆库车、巴楚和喀什-乌恰地区的远场接收点产生动态应力变化为正,变化峰值分别为1.31 MPa、0.14 MPa和0.5 MPa,对库车和喀什-乌恰地区小震活动具有动态触发作用,与此相关,β统计值结果显示,塔吉克斯坦M_(S)7.4地震后库车地区地震活动性发生了较明显的改变,这与库车地区接收点库仑应力变化大小一致。②塔吉克斯坦M_(S)7.4地震在2016年11月25日阿克陶M_(S)6.7地震震中位置造成的最大动态库仑应力变化为1.0 MPa,表明阿克陶M_(S)6.7地震可能受到了塔吉克斯坦M_(S)7.4地震的应力触发作用,动态触发作用更为明显。

人尿激肽原酶对SAMP8小鼠模型认知功能的影响及机制

目的研究人尿激肽原酶(human urinary kallidinogenase,HUK)对SAMP8小鼠模型认知功能的影响及机制。方法SAMP8鼠分为5组:SAMP8组、治疗组(分别给予8.75×10^(-3)、1.75×10^(-2)、3.5×10^(-2)、7.0×10^(-2)PNAU·kg^(-1) HUK),并以SAMR1溶媒组作为空白对照。各组行Morris水迷宫检测空间认知水平,选取认知改善最明显一组(HUK组)进行后续实验。免疫组化检测CA3区ChAT表达情况,以RT-PCR进一步验证。Western blot检测PSD95、SYN、BDNF、pCREB蛋白表达。测定MPO活性及IL-1β、IL-18含量。结果SAMP8组小鼠的平台穿梭次数较SAMR1组减少(P<0.05),给予不同剂量HUK后,平台穿梭次数较SAMP8组增多(P<0.05或P<0.01),目的象限探索时间短(P<0.05或P<0.01),我们以7.0×10^(-2)PNAU·kg^(-1)剂量组(HUK组)进行后续实验。SAMP8组CA3区ChAT阳性细胞较SAMR1组表达明显减少;HUK组阳性细胞表达明显增多;RtPCR显示ChAT在SAMP8组表达明显低于SAMR1组,给予HUK治疗后ChAT表达明显高于SAMP8组。与SAMR1组比较,SAMP8组CA3区中IL-1β、IL-18含量、MPO活性明显升高,PSD95、SYN、BNDF和pCREB蛋白表达降低。经HUK干预后,IL-1β、IL-18含量及MPO活性降低,PSD95、SYN、BNDF和pCREB蛋白表达均增加。结论HUK改善SAMP8小鼠的空间认知功能,其机制可能是通过促进CA3区ChAT表达、减轻氧化应激水平及增加突触相关蛋白表达来实现。

2021年漾濞M_(S)6.4地震序列前后震源参数

利用漾濞地区共22个固定和流动台站记录到的数字地震波形资料,在扣除地震波衰减与台站场地响应后,联合反演计算得到2021年漾濞M_(S)6.4地震序列前后共819次M L≥1.0地震的震源参数,并对M L2.9~3.8地震应力降的时空演化过程进行分析。结果显示:①漾濞地震序列的地震矩与震级相关性较好,与破裂尺度之间存在一定的正相关关系,与拐角频率之间呈现出负相关关系,对于M L≤2.8的地震,应力降随震级增大而增大,而对于M L>2.8的地震,其应力降随震级的变化趋势并不明显;②漾濞M_(S)6.4地震序列前后的应力降受漾濞区域复杂构造环境背景的控制表现明显的分段特征,在前震序列阶段,震源区中段应力降有逐渐增强的趋势,处于应力加速积累的过程,一系列高度丛集的中小地震活动所造成的应力扰动可能导致了震源区北段漾濞M_(S)6.4主震的发生;M_(S)6.4主震发生以后,其余震序列活动自北西段向南东向破裂了整个余震区,余震区北西段由于主震的发生,该区域应力背景快速调整,应力降的时空分布表现为高值-低值起伏的状态;余震区中段至最大前震震中附近区域可能由于前震活动频繁,应力释放较多,表现为应力降相对低值区域;余震区南段则余震活动丰富,为应力降高值分布区域。漾濞地震序列中震级较大的地震活动与应力降高值区域一致性较好。

2021年5月21日漾濞M_(S)6.4地震及周边的构造应力场特征和动力学意义

文中利用CAP方法计算了2021年5月21日漾濞地震序列M_(S)≥4.0地震的震源机制解,再结合收集到的周边历史地震的震源机制解,反演计算了漾濞地震及周边区域的构造应力场,并根据反演得到的应力张量模拟了漾濞地区的相对应力值大小和震源机制解分布情况。研究结果表明:1)研究区以走滑型地震为主,其次是正断型地震,地震集中分布于15km以浅的深度范围,主要发生在脆性上地壳。2)漾濞震源区的构造应力场属于典型的走滑应力结构,最大主应力方位为NNW-SSE向,与区域构造应力场基本一致。研究区的分区反演结果显示,最大主应力轴和最小主应力轴的方位从东北至西南呈现出顺时针旋转的趋势。区内川滇菱形块体、腾冲和保山等地块内部的应力方位分布一致性较好,块体边界带是应力发生偏转的部位,表现出一定的差异性,区域构造应力场受到不同块体间相互作用的影响。3)应力形因子R值的分布上大致表现为自西北向东南逐渐增大,说明物质运移所需的压应力相对变小,结合研究区的地质构造背景认为,地块(物质)的运动速度自西北向东南逐渐变缓。4)根据模拟计算的漾濞地震相对剪应力和相对正应力大小推测认为,漾濞地震是在区域构造应力场作用下沿着最优释放节面滑动破裂而发生的,更容易发生错动的NW向节面为此次地震的发震断层面。