白格堰塞湖抢险处置应急管理与经验启示

基于2018年金沙江白格堰塞湖应急处置工作,全面总结了部际联合会商、央地协同联动等应急抢险工作机制,深入分析了金沙江中游梯级水库群联合调度削峰对防灾减灾所发挥的重要作用。研究表明,若无梨园水库拦蓄,将可能新增淹没面积约160 km²,必对沿江两岸造成更大的损失。据此认识到,迅速获取堰塞湖信息是抢险处置的前提,快速研判堰塞湖风险是重要支撑,精准分析溃决洪水是核心技术,协同联动工作机制是基本保证,动态抢险工程管理是科学方法,完善的高坝水库群是应对洪灾的根本手段。进而提出加强乏信息条件下堰塞湖多源信息快速获取与处理技术、乏信息条件下风险快速研判技术能力、抢险处置专用装备研发、抢险工程统筹管理和协同联动体系完善、高坝水库群开发建设和风险防控与应急调度体系建设等建议,为堰塞湖应急管理水平提升和流域综合防灾减灾提供借鉴。     

Population effect of a large‐scale stream restoration effort on Chinook salmon in the Pahsimeroi River,Idaho

Stream habitat restoration is an important tool for fisheries management in impaired lotic systems. Although small‐scale benefits of stream habitat restoration are commonly investigated, it is difficult to demonstrate population effects. The Pahsimeroi River Chinook salmon Oncorhynchus tshawytscha population was previously restricted to the lower portion of the river by multiple irrigation structures. To address fish passage issues, a combination of restoration projects was initiated including barrier removals, instream flow enhancements and installation of fish screens on diversions. The largest barrier was removed in 2009, more than doubling the amount of accessible linear habitat. We hypothesized restoration efforts would expand the distribution of spawning salmon in the Pahsimeroi River watershed, leading to a broader distribution of juveniles. We also hypothesized a broader juvenile distribution would have population effects by reducing the prevalence of density‐dependent growth and survival. Redds were documented in newly accessible habitat immediately following barrier removal and accounted for a median of 42% of all redds in the Pahsimeroi River watershed during 2009–2015. Snorkel surveys also documented juvenile rearing in newly accessible habitat. Juvenile productivity increased from a median of 64 smolts/female spawner for brood years 2002–2008 to 99 smolts/female spawner for brood years 2009–2014. Overall, results suggested increased habitat accessibility in the Pahsimeroi River broadened the distribution of spawning adult and rearing juvenile salmon and reduced the effects of density‐dependent survival. Large‐scale stream restoration efforts can have a population effect. Despite the large‐scale effort and response, habitat restoration alone is likely not sufficient to restore this population.     

某抽水蓄能电站上水库防渗帷幕深度优选研究

针对某抽水蓄能电站上水库地质条件较为复杂、库区存在两条由库内延伸到库外的中等宽度断层、副坝区基岩弱风化层较厚的特点,以及设计防渗方案不合理的问题,根据上库工程坝址区的地质结构、地形地貌及防渗帷幕设计,建立了三维有限元渗流分析模型。首先通过参数及地下水位反演确定了库区基岩的渗透系数和水库特征点处的地下水位,然后在设计防渗方案的基础上计算分析了不同防渗帷幕深度对库区渗流场、渗透流量及各部位渗透坡降的影响,并根据分析结果对防渗帷幕深度进行了方案优选。结果表明：河床断层附近和库周断层及副坝附近的防渗帷幕深度可增大10 m,左、右坝肩帷幕深度可分别减少10 m并降低至3 Lu标准,库周非断层及副坝附近的防渗帷幕深度可减少10 m。研究结果可为类似工程防渗帷幕深度方案的优选提供参考。     

煤矿井下便携式电子设备电源设计要点

针对便携式电子设备的电源性能影响设备稳定运行的问题,探讨了便携式电子设备电源设计要点:介绍了电池类型的选择,指出选择锂电池作为后备电池较为理想;分析了电源安全栅的保护方式,指出先限流后截止的安全栅保护方式可有效提高电源的抗干扰能力;针对电池Boost升压电路中出现的振铃问题,给出了优化Boost变换器关键环路的解决方法,有效减小了电源纹波。     

栅栏覆盖最大化生存周期调度算法

栅栏覆盖是近年来无线传感器网络的研究热点之一,如何延长生存周期是无线传感器网络研究的一个重要问题。针对无线传感器网络的栅栏覆盖应用,设计了两种最大化网络生存周期的调度算法:集中式的Greedy调度算法和分布式的DBCS调度算法。仿真实验表明:两种算法显著地延长了网络的生存周期;在较稀疏的网络中,DBCS算法与Greedy算法性能接近,分布式的DBCS算法适合应用于大规模传感器网络。     

Chemical composition and bond structure of carbon-nitride films deposited by CH4/N2 dielectric barrier discharge

Carbon nitride films have been deposited by dielectric barrier discharge with a CH₄/N₂ gas mixture at different conditions. Fourier Transform Infrared (FTIR) spectroscopy, X-ray photo electron spectroscopy (XPS), Raman spectroscopy, Atomic force microscopy (AFM) and ellipsometry were used to systematically study chemical composition, bond structure and surface morphology of deposited films. Various bonds between carbon, nitrogen, hydrogen, and also oxygen were observed.     

Cutting Edge of the Pathogenesis of Atopic Dermatitis: Sphingomyelin Deacylase,the Enzyme Involved in Its Ceramide Deficiency,Plays a Pivotal Role

Atopic dermatitis (AD) is characterized clinically by severe dry skin and functionally by both a cutaneous barrier disruption and an impaired water-holding capacity in the stratum corneum (SC) even in the nonlesional skin. The combination of the disrupted barrier and water-holding functions in nonlesional skin is closely linked to the disease severity of AD, which suggests that the barrier abnormality as well as the water deficiency are elicited as a result of the induced dermatitis and subsequently trigger the recurrence of dermatitis. These functional abnormalities of the SC are mainly attributable to significantly decreased levels of total ceramides and the altered ceramide profile in the SC. Clinical studies using a synthetic pseudo-ceramide (pCer) that can function as a natural ceramide have indicated the superior clinical efficacy of pCer and, more importantly, have shown that the ceramide deficiency rather than changes in the ceramide profile in the SC of AD patients plays a central role in the pathogenesis of AD. Clinical studies of infants with AD have shown that the barrier disruption due to the ceramide deficiency is not inherent and is essentially dependent on postinflammatory events in those infants. Consistently, the recovery of trans-epidermal water loss after tape-stripping occurs at a significantly slower rate only at 1 day post-tape-stripping in AD skin compared with healthy control (HC) skin. This resembles the recovery pattern observed in Niemann–Pick disease, which is caused by an acid sphingomyelinase (aSMase) deficiency. Further, comparison of ceramide levels in the SC between before and after tape-stripping revealed that whereas ceramide levels in HC skin are significantly upregulated at 4 days post-tape-stripping, their ceramide levels remain substantially unchanged at 4 days post-tape-stripping. Taken together, the sum of these findings strongly suggests that an impaired homeostasis of a ceramide-generating process may be associated with these abnormalities. We have discovered a novel enzyme, sphingomyelin (SM) deacylase, which cleaves the N-acyl linkage of SM and glucosylceramide (GCer). The activity of SM deacylase is significantly increased in AD lesional epidermis as well as in the involved and uninvolved SC of AD skin, but not in the skin of patients with contact dermatitis or chronic eczema, compared with HC skin. SM deacylase competes with aSMase and β-glucocerebrosidase (BGCase) to hydrolyze their common substrates, SM and GCer, to yield their lysoforms sphingosylphosphorylcholine (SPC) and glucosylsphingosine (GSP), respectively, instead of ceramide. Consistently, those reaction products (SPC and GSP) accumulate to a greater extent in the involved and uninvolved SC of AD skin compared with chronic eczema or contact dermatitis skin as well as HC skin. Successive chromatographies were used to purify SM deacylase to homogeneity with a single band of ≈43 kDa and with an enrichment of >14,000-fold. Analysis of a protein spot with SM deacylase activity separated by 2D-SDS-PAGE using MALDI-TOF MS/MS allowed its amino acid sequence to be determined and to identify it as the β-subunit of acid ceramidase (aCDase), an enzyme consisting of α- and β-subunits linked by amino-bonds and a single S-S bond. Western blotting of samples treated with 2-mercaptoethanol revealed that whereas recombinant human aCDase was recognized by antibodies to the α-subunit at ≈56 and ≈13 kDa and the β-subunit at ≈43 kDa, the purified SM deacylase was detectable only by the antibody to the β-subunit at ≈43 kDa. Breaking the S-S bond of recombinant human aCDase with dithiothreitol elicited the activity of SM deacylase with an apparent size of ≈40 kDa upon gel chromatography in contrast to aCDase activity with an apparent size of ≈50 kDa in untreated recombinant human aCDase. These results provide new insights into the essential role of SM deacylase as the β-subunit aCDase that causes the ceramide deficiency in AD skin.     

The Neurovascular Unit Dysfunction in Alzheimer’s Disease

Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide. Histopathologically, AD presents with two hallmarks: neurofibrillary tangles (NFTs), and aggregates of amyloid β peptide (Aβ) both in the brain parenchyma as neuritic plaques, and around blood vessels as cerebral amyloid angiopathy (CAA). According to the vascular hypothesis of AD, vascular risk factors can result in dysregulation of the neurovascular unit (NVU) and hypoxia. Hypoxia may reduce Aβ clearance from the brain and increase its production, leading to both parenchymal and vascular accumulation of Aβ. An increase in Aβ amplifies neuronal dysfunction, NFT formation, and accelerates neurodegeneration, resulting in dementia. In recent decades, therapeutic approaches have attempted to decrease the levels of abnormal Aβ or tau levels in the AD brain. However, several of these approaches have either been associated with an inappropriate immune response triggering inflammation, or have failed to improve cognition. Here, we review the pathogenesis and potential therapeutic targets associated with dysfunction of the NVU in AD.