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.     

黄河干流白银市水川段水面线计算方法对比分析

为克服能量方程逐段试算方法在河道水面线计算上存在的不足与局限,本文以黄河干流白银市水川段为例,采用二维水动力数值计算模型,对4种洪水频率工况下黄河干流白银市段的水面线高程进行计算,并将二维数值计算结果与能量方程计算结果进行复核和评价。经计算可知两种计算方法在计算结果上存在偏差,能量方程在河道水面线计算上是一种近似成果,而二维数值计算能够更加真实反映河道的实际情况,因此在水面线计算时推荐二维数值计算方法。     

基于关键闸坝优选的区域水网水量调控

为实现区域水网水量的高效调控,从水量、水生态、水质和闸坝管理等4个方面构建包含10个指标的闸坝优选评价指标体系,以廊坊市凤河-永定河区域水网为研究对象,计算区域内32座闸坝的综合关键指数并给出影响程度排序,采用水动力数学模型验证关键闸坝选取的合理性。结果表明：优选出的永丰闸和东张务闸是区域水网的关键闸坝,通过调节这两座闸坝的开度即可满足区域水网的生态需水和防洪排涝调度目标,保持区域水网较优的水力连通能力,提高区域水网水量调控效率。     

妫水河入官厅水库水污染成因及减排措施评估

为保障妫水河入官厅水库入流水质达标,分析水质成因,分步制订水质改善措施。采用MIKE21耦合植物作用的Ecolab生态水质模型,对妫水河下游入官厅水库断面至东大桥断面、支流三里河水域进行模拟。通过对丰水期和枯水期监测数据及模拟结果进行分析,流域上游来流水量及水质、区间污染源及河流湿地等自净作用是影响官厅水库入流水质的主要原因,其中:妫水河入流污染负荷对水库入流水质贡献率最大,丰枯水期氨氮、总磷和总氮的贡献率分别为18.32%～45.76%、9.31%～31.17%和29.34%～67.56%;区间入河污染源氨氮、总磷和总氮削减率分别为19.41%、31.31%和24.94%;丰枯水期河道自净对氨氮、总磷和总氮削减率分别为44.85%～61.29%、51.40%～77.92%和8.40%～23.06%。为改善官厅水库入流水质,在流经城市区的妫水河下游及三里河修建了河流湿地公园,对区域污染源进行截污,使得入库水质可达到Ⅲ类水。为长远确保官厅水库的水质,控制来流水质和加强流域治理是关键,同时营造岸带湿地,对水质改善有积极的作用。研究结果及方法可为水库污染防治及负荷量削减提供理论依据。     

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.