断层相互作用产生同震库仑应力改变分布图像

讨论了同震库仑应力改变的基本含义,以及基于静应力位错理论求解同震库仑应力改变的边界元方法,对与发震断层相互平行和相互垂直两种典型构造模式下,断层相互作用产生的同震库仑应力改变进行了数值模拟研究,分别获取了相应条件下的同震库仑应力改变空间分布图像.结果表明:不同构造模式的断层相互作用,其产生的同震库仑应力改变分布图像存在较大差异,在分析和评价断层相互作用产生的同震库仑应力改变,及其对活动断层地震危险性的影响时,应该充分考虑待评价断层与发震断层之间的空间几何关系、断层的性质和产状等特定的构造条件.     

Role of the prolyl isomerase Pin1 in protecting against age-dependent neurodegeneration

The neuropathological hallmarks of Alzheimer's disease and other tauopathies include senile plaques and/or neurofibrillary tangles. Although mouse models have been created by overexpressing specific proteins including beta-amyloid precursor protein, presenilin and tau, no model has been generated by gene knockout. Phosphorylation of tau and other proteins on serine or threonine residues preceding proline seems to precede tangle formation and neurodegeneration in Alzheimer's disease. Notably, these phospho(Ser/Thr)-Pro motifs exist in two distinct conformations, whose conversion in some proteins is catalysed by the Pin1 prolyl isomerase. Pin1 activity can directly restore the conformation and function of phosphorylated tau or it can do so indirectly by promoting its dephosphorylation, which suggests that Pin1 is involved in neurodegeneration; however, genetic evidence is lacking. Here we show that Pin1 expression is inversely correlated with predicted neuronal vulnerability and actual neurofibrillary degeneration in Alzheimer's disease. Pin1 knockout in mice causes progressive age-dependent neuropathy characterized by motor and behavioural deficits, tau hyperphosphorylation, tau filament formation and neuronal degeneration. Thus, Pin1 is pivotal in protecting against age-dependent neurodegeneration, providing insight into the pathogenesis and treatment of Alzheimer's disease and other tauopathies.     

ASYMPTOTIC NORMALITY OF SOME ESTIMATORS IN A FIXED-DESIGN SEMIPARAMETRIC REGRESSION MODEL WITH LINEAR TIME SERIES ERRORS

Consider a semiparametric regression model with linear time series errors Yk = x'kβ g(tk) εk, 1 < k < n, where Yk's are responses, xk = (xk1,xk2,..... ,xkp)' and tk ∈T ∪R are fixed design points, β= (β1, β2, ....., βp)' is an unknown parameter vector, g(.) is an unknown bounded real-valued function defined on a compact subset T of the real line R, and εk is a linear process given by εk = ∑j=0∞j(?)ek-j,(?)= 1, where , are i.i.d. random variables. In this paper we establish the asymptotic normality of the least squares estimator of β, a smooth estimator of g(.), and estimators of the autocovariance and autocorrelation functions of the linear process εk.     

克里雅河流域水资源利用及其生态环境响应研究

克里雅河是和田地区于田县最大的河流,也是历史上曾经注入塔里木河、横穿塔克拉玛干大沙漠的绿色走廊之一。克里雅河流域人口与经济发展而带来的水土资源开发利用程度的增加,对流域生态环境产生了重大的影响。由于中上游水土资源开发面积急剧增加,导致下游输水逐年减少、年内分配趋于集中,导致下游河段断流,生态环境恶化等现象。克里雅河流域水土资源开发引起的环境响应有积极建设性的一面,也有消极的破坏原有生态环境的一面。前者主要表现在：①绿洲内部水资源利用量逐年增长,绿洲环境逐步改善,②提高了绿洲土地生产能力,③已形成引、蓄、输、排为一体的网络,提高了抗旱能力和水资源的利用效益。后者主要表现在：地表水流程缩短,下游生态环境恶化；土壤次生盐渍化严重,影响了土地生产力；绿洲外围小气候的恶化、生态环境的破坏威胁着绿洲的稳定性。在流域水土资源开发的同时重视生态环境建设与调控具有重要意义。图2,表3,参7。     

二向性归一化植被指数:概念及应用

最近发布的星载法国地表反射的极化与方向性观测仪(POILDER)与美国中分辨率成像光谱仪(MODIS)的地表二向性反射(BRDF)数据产品,其输入数据的大气纠正未能满足定量遥感的需求.提出了二向性归一化植被指数(BiNDVI)的概念,以同时考虑地表反射的二向性与大气程辐射的影响,并用于定义卫星多角度遥感观测值的大气质量指数.用该指数加权迭代反演,能明显改进MODIS-BRDF的数据产品质量.     

Anthropogenic ocean acidification over the twenty-first century and its impact on calcifying organisms

Today's surface ocean is saturated with respect to calcium carbonate, but increasing atmospheric carbon dioxide concentrations are reducing ocean pH and carbonate ion concentrations, and thus the level of calcium carbonate saturation. Experimental evidence suggests that if these trends continue, key marine organisms--such as corals and some plankton--will have difficulty maintaining their external calcium carbonate skeletons. Here we use 13 models of the ocean-carbon cycle to assess calcium carbonate saturation under the IS92a 'business-as-usual' scenario for future emissions of anthropogenic carbon dioxide. In our projections, Southern Ocean surface waters will begin to become undersaturated with respect to aragonite, a metastable form of calcium carbonate, by the year 2050. By 2100, this undersaturation could extend throughout the entire Southern Ocean and into the subarctic Pacific Ocean. When live pteropods were exposed to our predicted level of undersaturation during a two-day shipboard experiment, their aragonite shells showed notable dissolution. Our findings indicate that conditions detrimental to high-latitude ecosystems could develop within decades, not centuries as suggested previously.     

新疆罗布泊周边胀果甘草内生芽孢杆菌BLG-542产碱性纤维素酶最佳条件的研究

文章以罗布泊胀果甘草中分离出的78个菌株中初步筛选出7株产碱性纤维素酶的菌株为研究对象,进行产碱性纤维素酶最佳优化条件的研究.碱性的胀果甘草内生芽孢杆菌菌株接种于CMC-Na为碳源,复合蛋白胨为氮源的培养基中,分析研究菌株产碱性纤维素酶的最佳条件优化.通过从78株本实验室于2006年保藏的罗布泊胀果甘草内生菌中筛选出能产生胞外碱性纤维素酶的7株菌,其中酶活力最高的菌株为BLG-542.本研究主要以酶活力最高的菌株BLG-542为出发菌株进行研究.经过对产酶条件优化,获得了胀果甘草内生菌产碱性纤维素酶最佳配方培养基:D-木糖10g/L,复合蛋白胨10g/L,可溶性淀粉10g/L,酵母粉5g/L,K2 HPO4 1g/L,MgSO4 0.2g/L,NaCl 20g/L,Na2CO3 10g/L;实验产酶最佳接种量为6％,最佳培养温度为37℃,最佳培养时间为48h,产酶最佳PH为9.0;菌种生长最佳PH为7.6,经过优化产酶条件纤维素酶活力从优化前的3.8U/mL提高到6.26 U/mL,是优化之前的1.8倍;该研究表明特殊生态环境的植物内生菌与次生代谢产物、活性物质、酶类有密切的关系,环境除对内生菌酶的产生极其活性影响外,还影响着内生菌的次生代谢.该地区植物内生菌均有潜在的应用价值.     

一类非线性反应扩散方程的数值解法

对一类非线性反应扩散方程的初边值问题采用有限差分方法,在离散过程中针对非线性项的特性进行线性化处理,提出了一种新的差分格式,并在差分格式稳定性分析时,采用能量方法给出了差分格式的稳定性条件。经数值计算表明,与以往构造的差分格式相比,所构造的差分格式具有计算简单、精度较高、稳定性条件较好的特点。     

Angiotensin-converting enzyme 2 is an essential regulator of heart function

Cardiovascular diseases are predicted to be the most common cause of death worldwide by 2020. Here we show that angiotensin-converting enzyme 2 (ace2) maps to a defined quantitative trait locus (QTL) on the X chromosome in three different rat models of hypertension. In all hypertensive rat strains, ACE2 messenger RNA and protein expression were markedly reduced, suggesting that ace2 is a candidate gene for this QTL. Targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart. Genetic ablation of ACE on an ACE2 mutant background completely rescues the cardiac phenotype. But disruption of ACER, a Drosophila ACE2 homologue, results in a severe defect of heart morphogenesis. These genetic data for ACE2 show that it is an essential regulator of heart function in vivo.     

Prion-like behaviour and tau-dependent cytotoxicity of pyroglutamylated amyloid-β

Extracellular plaques of amyloid-β and intraneuronal neurofibrillary tangles made from tau are the histopathological signatures of Alzheimer's disease. Plaques comprise amyloid-β fibrils that assemble from monomeric and oligomeric intermediates, and are prognostic indicators of Alzheimer's disease. Despite the importance of plaques to Alzheimer's disease, oligomers are considered to be the principal toxic forms of amyloid-β. Interestingly, many adverse responses to amyloid-β, such as cytotoxicity, microtubule loss, impaired memory and learning, and neuritic degeneration, are greatly amplified by tau expression. Amino-terminally truncated, pyroglutamylated (pE) forms of amyloid-β are strongly associated with Alzheimer's disease, are more toxic than amyloid-β, residues 1-42 (Aβ(1-42)) and Aβ(1-40), and have been proposed as initiators of Alzheimer's disease pathogenesis. Here we report a mechanism by which pE-Aβ may trigger Alzheimer's disease. Aβ(3(pE)-42) co-oligomerizes with excess Aβ(1-42) to form metastable low-n oligomers (LNOs) that are structurally distinct and far more cytotoxic to cultured neurons than comparable LNOs made from Aβ(1-42) alone. Tau is required for cytotoxicity, and LNOs comprising 5% Aβ(3(pE)-42) plus 95% Aβ(1-42) (5% pE-Aβ) seed new cytotoxic LNOs through multiple serial dilutions into Aβ(1-42) monomers in the absence of additional Aβ(3(pE)-42). LNOs isolated from human Alzheimer's disease brain contained Aβ(3(pE)-42), and enhanced Aβ(3(pE)-42) formation in mice triggered neuron loss and gliosis at 3 months, but not in a tau-null background. We conclude that Aβ(3(pE)-42) confers tau-dependent neuronal death and causes template-induced misfolding of Aβ(1-42) into structurally distinct LNOs that propagate by a prion-like mechanism. Our results raise the possibility that Aβ(3(pE)-42) acts similarly at a primary step in Alzheimer's disease pathogenesis.