Assessment of Ecosystems Damages Caused by Russian War against Ukraine

The question of the impact of war on ecosystems still remains secondary in the internal and external policy of states, society and the agenda of international organizations. From the point of view of losses in monetary terms, the values of ecosystem damages obtained in the work, which are a consequence of the impact of hostilities on the environment, correspond to the annual budgets of the largest countries in the world or exceed them. The presented calculations significantly exceed the known normative methods, the use of which in the conditions of war is limited in space and time. Objective difficulties associated with the uncertainty of many processes of the development of ecological systems and their reaction to the multifactorial impact of war are also significant limitations. Therefore, as part of the study, a method of assessing the impact of war on the environment is proposed, which is based on the patterns of energy flows in ecosystems from the moment it is binding by producers. This made it possible to take into account in the calculations the principle of functional integrity of the ecological system, according to which the destruction or damage of the components of a functionally whole environment will necessarily cause negative phenomena in the development of ecological systems. The results are presented in the form of real values of ecological losses in energy and monetary equivalents, as consequences of the loss of ecosystem services. As the results of the research show, the minimum amount of damage to ecosystems from Russian tanks is 43,500 USD per day. Environmental damage from Russian fighter jets has been estimated at $1.5 billion per week since the start of the war. Noise from military operations causes losses of at least 2.3 billion US dollars per year. The obtained results create prerequisites for improving the system of ensuring environmental safety at the local, state, and international levels and transferring the obtained solutions into safety-shaping practice.

Overexpression of fibroblast growth factor 13 ameliorates amyloid-β-induced neuronal damage

Previous studies have shown that fibroblast growth factor 13 is downregulated in the brain of both Alzheimer’s disease mouse models and patients,and that it plays a vital role in the learning and memory.However,the underlying mechanisms of fibroblast growth factor 13 in Alzheimer’s disease remain unclear.In this study,we established rat models of Alzheimer’s disease by stereotaxic injection of amyloid-β(Aβ_(1-42))-induced into bilateral hippocampus.We also injected lentivirus containing fibroblast growth factor 13 into bilateral hippocampus to overexpress fibroblast growth factor 13.The expression of fibroblast growth factor 13 was downregulated in the brain of the Alzheimer’s disease model rats.After overexpression of fibroblast growth factor 13,learning and memory abilities of the Alzheimer’s disease model rats were remarkably improved.Fibroblast growth factor 13 overexpression increased brain expression levels of oxidative stress-related markers glutathione,superoxide dismutase,phosphatidylinositol-3-kinase,AKT and glycogen synthase kinase 3β,and anti-apoptotic factor BCL.Furthermore,fibroblast growth factor 13 overexpression decreased the number of apoptotic cells,expression of pro-apoptotic factor BAX,cleaved-caspase 3 and amyloid-βexpression,and levels of tau phosphorylation,malondialdehyde,reactive oxygen species and acetylcholinesterase in the brain of Alzheimer’s disease model rats.The changes were reversed by the phosphatidylinositol-3-kinase inhibitor LY294002.These findings suggest that overexpression of fibroblast growth factor 13 improved neuronal damage in a rat model of Alzheimer’s disease through activation of the phosphatidylinositol-3-kinase/AKT/glycogen synthase kinase 3βsignaling pathway.

Lamotrigine protects against cognitive deficits,synapse and nerve cell damage,and hallmark neuropathologies in a mouse model of Alzheimer’s disease

Lamotrigine(LTG)is a widely used drug for the treatment of epilepsy.Emerging clinical evidence suggests that LTG may improve cognitive function in patients with Alzheimer’s disease.However,the underlying molecular mechanisms remain unclear.In this study,amyloid precursor protein/presenilin 1(APP/PS1)double transgenic mice were used as a model of Alzheimer’s disease.Five-month-old APP/PS1 mice were intragastrically administered 30 mg/kg LTG or vehicle once per day for 3 successive months.The cognitive functions of animals were assessed using Morris water maze.Hyperphosphorylated tau and markers of synapse and glial cells were detected by western blot assay.The cell damage in the brain was investigated using hematoxylin and eosin staining.The levels of amyloid-βand the concentrations of interleukin-1β,interleukin-6 and tumor necrosis factor-αin the brain were measured using enzyme-linked immunosorbent assay.Differentially expressed genes in the brain after LTG treatment were analyzed by high-throughput RNA sequencing and real-time polymerase chain reaction.We found that LTG substantially improved spatial cognitive deficits of APP/PS1 mice;alleviated damage to synapses and nerve cells in the brain;and reduced amyloid-βlevels,tau protein hyperphosphorylation,and inflammatory responses.High-throughput RNA sequencing revealed that the beneficial effects of LTG on Alzheimer’s disease-related neuropathologies may have been mediated by the regulation of Ptgds,Cd74,Map3k1,Fosb,and Spp1 expression in the brain.These findings revealed potential molecular mechanisms by which LTG treatment improved Alzheimer’s disease.Furthermore,these data indicate that LTG may be a promising therapeutic drug for Alzheimer’s disease.

Study regarding typical liquefaction damage during the 2021 Maduo M_(s)7.4 earthquake in China

The most important method of understanding liquefaction-induced engineering failures comes from the investigation and analysis of earthquake damage.In May 2021,the Maduo M_(s)7.4 earthquake occurred on the Tibetan Plateau of China.The most representative engineering disaster caused by this earthquake was bridge damage on liquefied sites.In this study,the mutual relationships between the anti-liquefaction pre-design situation,the ground motion intensity,the site liquefaction severity,and the bridge damage state for this earthquake were systematically analyzed for typical bridge damage on the liquefied sites.Using field survey data and the current Chinese industry code,simulations of the liquefaction scenarios at typical bridge sites were performed for the pre-design seismic ground motion before the earthquake and the seismic ground motion during the earthquake.By combining these results with post-earthquake investigation results,the reason for the serious bridge damage resulting from this earthquake is revealed,and the necessary conditions for avoiding serious seismic damage to bridges built in liquefiable sites is presented.

Real-time prediction of earthquake potential damage:A case study for the January 8,2022 M_(S) 6.9 Menyuan earthquake in Qinghai,China

It is critical to determine whether a site has potential damage in real-time after an earthquake occurs,which is a challenge in earthquake disaster reduction.Here,we propose a real-time Earthquake Potential Damage predictor(EPDor)based on predicting peak ground velocities(PGVs)of sites.The EPDor is composed of three parts:(1)predicting the magnitude of an earthquake and PGVs of triggered stations based on the machine learning prediction models;(2)predicting the PGVs at distant sites based on the empirical ground motion prediction equation;(3)generating the PGV map through predicting the PGV of each grid point based on an interpolation process of weighted average based on the predicted values in(1)and(2).We apply the EPDor to the 2022 M_(S) 6.9 Menyuan earthquake in Qinghai Province,China to predict its potential damage.Within the initial few seconds after the first station is triggered,the EPDor can determine directly whether there is potential damage for some sites to a certain degree.Hence,we infer that the EPDor has potential application for future earthquakes.Meanwhile,it also has potential in Chinese earthquake early warning system.

甘肃积石山 M_(s)6.2级地震的震害特征与启示

2023年12月18日,甘肃省临夏回族自治州积石山保安族东乡族撒拉族自治县(35.70°N,102.79°E)发生了6.2级地震,震中烈度为VIII度。地震发生后,通过实地烈度评估与科学考察,对震区VI~VIII度区不同建(构)筑物与生命线工程的震害特点进行了统计分析;从抗震设计与施工管理、场地放大效应与地震次生灾害对建筑结构抗震性能的影响等角度,提出了此次地震的震害启示。结果表明:1)严重破坏和毁坏的建筑结构主要集中在老旧的土木结构、砖木结构和无设防或设防不规范的砖混结构。2)造成建筑结构破坏的主要原因是少量自建房抗震设计和施工的不规范、场地放大效应和地震次生灾害。3)优化和改良生土砌筑材料,改进纵横墙间的拉结措施,强化结构整体性是提高土木结构抗震的有效方法;普及“上下圈梁与构造柱”等基本抗震设防措施,规范水泥砂浆强度,提升农村工匠的施工水平,可有效提高砌体结构的整体性,避免房屋出现整体性垮塌;室内洗手间的墙体应该与房顶、纵横墙间建立有效联接,提高结构的抗震性能。4)孤突斜坡、河流高阶地与岸边为抗震不利地带。当建造用地极为匮乏,不得不选址在这些场地之上时,应该综合考虑场地的地形地貌特征、岩土体物理力学特性、水文地质条件、抗震设防目标、建筑结构类型等影响因素,做好地震灾害风险评估,根据评估结果进行科学设防。灾后重建过程中,应由政府统一规划选址、统一设计,规范施工。

基于哨兵函数和S变换的风力机叶片材料损伤特性研究

利用声发射检测技术研究玻璃纤维增强环氧树脂复合材料的损伤特性,在此过程中,采用哨兵函数来表征该材料的损伤程度,并通过S变换和模糊C均值(FCM)聚类来分析声发射信号,从而获得材料的损伤特征。三点弯曲实验结束后对试件断口进行扫描电子显微镜(SEM)拍照来验证,可得:通过对SEM照片的分析得到基体开裂、纤维脱粘、分层破坏、纤维断裂4种损伤模式;对整个声发射事件进行哨兵函数分析,观察到试件在弯曲过程中哨兵函数曲线呈明显下降趋势;对依据哨兵函数划分的不同阶段的信号进行VMD降噪处理,然后采用S变换进行时频分析得到不同损伤的特征频率,最后采用FCM聚类进行验证。结果表明:哨兵函数值的突变可作为材料断裂的预警信号,材料损伤类型的识别可依据S变换的频率分布结果进行确定。

Theoretical derivation of risk-ratios for assessing wind damage in a coastal forest

Based on the discussion of relationships between thinning and wind damage, and published information, a method for estimating risk ratios of wind damage was developed. Estimations of risk-ratio for Pinus thunbergii trees and stands were de-duced from stem bending theory and coefficients characterizing wind profile, distribution of branches and optical stratification po-rosity. The results showed that if the value of constant b in the branch distribution-model equals the attenuation coefficient s in the wind profile model for a single tree crown, then the parameter H/D1.33 (height over stem diameter cubed) can be used to compare and evaluate the risk-ratio of wind damage for individual trees. The same method can be applied to stands using the coefficient of wind profile in a stand, i.e. attenuation coefficient , the coefficient from distributions of optical stratification porosity, i.e. extinction coefficient , and the parameter D1.33. The application of parameter H/D1.33 and the process of determining risk ra-tios of wind damage for stands were also given in the paper.

Targeting tau in Alzheimer's disease:from mechanisms to clinical therapy

Alzheimer’s disease is the most prevalent neurodegenerative disease affecting older adults.Primary features of Alzheimer’s disease include extra cellular aggregation of amyloid-βplaques and the accumulation of neurofibrillary tangles,fo rmed by tau protein,in the cells.While there are amyloid-β-ta rgeting therapies for the treatment of Alzheimer’s disease,these therapies are costly and exhibit potential negative side effects.Mounting evidence suggests significant involvement of tau protein in Alzheimer’s disease-related neurodegeneration.As an important microtubule-associated protein,tau plays an important role in maintaining the stability of neuronal microtubules and promoting axonal growth.In fact,clinical studies have shown that abnormal phosphorylation of tau protein occurs before accumulation of amyloid-βin the brain.Various therapeutic strategies targeting tau protein have begun to emerge,and are considered possible methods to prevent and treat Alzheimer’s disease.Specifically,abnormalities in post-translational modifications of the tau protein,including aberrant phosphorylation,ubiquitination,small ubiquitin-like modifier(SUMO)ylation,acetylation,and truncation,contribute to its microtubule dissociation,misfolding,and subcellular missorting.This causes mitochondrial damage,synaptic impairments,gliosis,and neuroinflammation,eventually leading to neurodegeneration and cognitive deficits.This review summarizes the recent findings on the underlying mechanisms of tau protein in the onset and progression of Alzheimer’s disease and discusses tau-targeted treatment of Alzheimer’s disease.

Oxidative stress, mitochondrial damage and neurodegenerative diseases

Oxidative stress and mitochondrial damage have been implicated in the pathogenesis of several neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Oxidative stress is characterized by the overproduction of reactive oxygen species, which can induce mitochondrial DNA mutations, damage the mitochondrial respiratory chain, alter membrane permeability, and influence Ca2＋ homeostasis and mitochondrial defense systems. All these changes are implicated in the development of these neurodegenerative diseases, mediating or amplifying neuronal dysfunction and triggering neurodegeneration. This paper summarizes the contribution of oxidative stress and mitochondrial damage to the onset of neurodegenerative diseases and discusses strategies to modify mitochondrial dysfunction that may be attractive therapeutic interventions for the treatment of various neurodegenerative diseases.

Strength and damage of marble in ductile failure

To study the effects of loading paths and stress states on rock strength and deformation, marble specimens were axially compressed to various displacements under a confining pressure (CP) firstly, and then the damaged specimens were recompressed under another CP. The bearing capacity of a marble specimen depends merely on CP at the stage of ductile deformation, and it has no relation with the loading history when CP keeps constant or increases. However, the damaged specimen turns into brittle when it is recompressed uniaxially or at a lower CP, and the Young’s modulus and strength are lower than those of a dense specimen. The increasing ratio of triaxial strength to CP has a close relation with the areas of fissures in the damaged specimens but not the internal friction angle. Material strength and bearing capacity are two different conceptions for rocks. Material strength decreases continually as the plastic deformation increases; however, the bearing capacity is determined by both the stress state and the material strength.

A CUMULATIVE FATIGUE DAMAGE RULE UNDER THE ALTERNATIVE OF CORROSION OR CYCLIC LOADING

Fatigue damage increases with the applied loading cycles in a cumulative manner and the material deteriorates with the corrosion time. A cumulative fatigue damage rule under the alternative of corrosion or cyclic loading was proposed. The specimens of aluminum alloy LY12-CZ soaked in corrosive liquid for different times were tested under the constant amplitude cyclic loading to obtain S-N curves. The test was carried out to verify the proposed cumulative fatigue damage rule under the different combinations among corrosion time, loading level, and the cycle numbers. It was shown that the predicted residual fatigue lives showed a good agreement with the experimental results and the proposed rule was simple and can be easily adopted.

MICROMECHANICAL DAMAGE MODEL FOR ROCKS AND CONCRETES SUBJECTED TO COUPLED TENSILE AND SHEAR STRESSES

Based on the analysis of the deformation in an infinite isotropic elastic matrix with an embedded elliptic crack under far field coupled tensile and shear stresses, the energy release rate and a mixed fracture criterion are obtained using an energy balance approach. The additional compliance tensor induced by a single opening elliptic microcrack in a representative volume element is derived, and the effect of microcracks with random orientations is analyzed with the Taylor＇s scheme by introducing an appropriate probability density function. A micromechanical damage model for rocks and concretes is obtained and is verified with experimental results.

Protective effects of MCI-186 on oxidative damage in a cell model of Alzheimer's disease

Oxidative stress has an important role in the development of Alzheimer＇s disease （AD）. Beta amyloid protein 25-35 （Aβ25-35） can generate oxygen free radicals, and MCI-186 （3-methyl-l-phenyl-2-pyrazolin-5-one, edaravone） can specifically eliminate hydroxyl radicals. The present study introduced Aβ25-35 into PC12 cells to establish a cell model of AD, and investigated the neuroprotective effects of MCI-186 on AD. Results showed that MCI-186 had a positive effect on the prevention and treatment of AD by inhibiting protein oxidative products, advanced glycation end products, lipid oxidative end products and DNA oxidative damage in PC12 cells induced by Aβ25-35.

One-step cell biomanufacturing platform:porous gelatin microcarrier beads promote human embryonic stem cell-derived midbrain dopaminergic progenitor cell differentiation in vitro and survival after transplantation in vivo

Numerous studies have shown that cell replacement therapy can replenish lost cells and rebuild neural circuitry in animal models of Parkinson’s disease.Transplantation of midbrain dopaminergic progenitor cells is a promising treatment for Parkinson’s disease.However,transplanted cells can be injured by mechanical damage during handling and by changes in the transplantation niche.Here,we developed a one-step biomanufacturing platform that uses small-aperture gelatin microcarriers to produce beads carrying midbrain dopaminergic progenitor cells.These beads allow midbrain dopaminergic progenitor cell differentiation and cryopreservation without digestion,effectively maintaining axonal integrity in vitro.Importantly,midbrain dopaminergic progenitor cell bead grafts showed increased survival and only mild immunoreactivity in vivo compared with suspended midbrain dopaminergic progenitor cell grafts.Overall,our findings show that these midbrain dopaminergic progenitor cell beads enhance the effectiveness of neuronal cell transplantation.

Cardiac damage in athlete's heart: When the “supernormal” heart fails!

Intense exercise may cause heart remodeling to compensate increases in blood pressure or volume by increasing muscle mass. Cardiac changes do not involve only the left ventricle, but all heart chambers. Physiological cardiac modeling in athletes is associated with normal or enhanced cardiac function, but recent studies have documented decrements in left ventricular function during intense exercise and the release of cardiac markers of necrosis in athlete's blood of uncertain significance. Furthermore, cardiac remodeling may predispose athletes to heart disease and result in electrical remodeling, responsible for arrhythmias. Athlete's heart is a physiological condition and does not require a specific treatment. In some conditions, it is important to differentiate the physiological adaptations from pathological conditions, such as hypertrophic cardiomyopathy, arrhythmogenic dysplasia of the right ventricle, and non-compaction myocardium, for the greater risk of sudden cardiac death of these conditions. Moreover, some drugs and performance-enhancing drugs can cause structural alterations and arrhythmias, therefore, their use should be excluded.

Damage detection on framed structures: modal curvature evaluation using Stockwell Transform under seismic excitation

The key parameters for damage detection and localization are eigenfrequencies, related equivalent viscous damping factors and mode shapes. The classical approach is based on the evaluation of these structural parameters before and after a seismic event, but by using a modern approach based on time-frequency transformations it is possible to quantify these parameters throughout the ground shaking phase. In particular with the use of the S-Transform, it is possible to follow the temporal evolution of the structural dynamics parameters before, during and after an earthquake. In this paper, a methodology for damage localization on framed structures subjected to strong motion earthquakes is proposed based on monitoring the modal curvature variation in the natural frequency of a structure. Two examples of application are described to illustrate the technique: Computer simulation of the nonlinear response of a model, and several laboratory(shaking table) tests performed at the University of Basilicata(Italy). Damage detected using the proposed approach and damage revealed via visual inspections in the tests are compared.

2022年云南红河县M_(S)5.0地震震害特征

2022年11月19日云南省红河县(23.37°N,102.26°E)发生M_(S)5.0地震,打破了红河哈尼族彝族自治州21世纪以来未发生5级以上地震的记录。本文结合地震现场灾害损失调查和灾情资料收集整理,详细阐述了灾区的建筑物震害、生命线工程震害、地震地质灾害特征及原因分析,并与云南相近震级历史地震震害特征进行对比,结果表明,本次地震灾区受灾规模小,余震少,灾害损失相对较轻。

Analysis of nonlinear vibration for symmetric angle-ply laminated viscoelastic plates with damage

The behavior of nonlinear vibration for symmetric angle-ply laminated plates including the material viscoelasticity and damage evolution is investigated. By employing the von Karman＇s nonlinear theory, strain energy equivalence principle and Boltzmann superposition principle, a set of governing equations of nonlinear integro-differential type are derived. By applying the finite difference method, Newmark method and iterative procedure, the governing equations are solved. The effects of loading amplitudes, exciting frequencies and different ply orientations on the critical time to failure initiation and nonlinear vibration amplitudes of the structures are discussed. Numerical results are presented for the different parameters and compared with the available data.

Galantamine protects against beta amyloid peptide-induced DNA damage in a model for Alzheimer's disease

Alzheimer’s disease（AD）is the most common type of dementia in elderly population.With a growing aging population not only in the United States but also in the worldwide,AD constitutes an emergent public health problem.