997 resultados para A9-11D
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利用东北地区172个气象台站30a(1961年~1990年)的整编温度资料和东北地区500m×500mDEM数据,建立了东北地区温度要素的空间分布模型。结果表明,温度要素的宏观本底值的模拟以三维二次幂级数展开法效果较好,其误差气温多在02℃~04℃,≥10℃初日、终日为11d~20d,≥10℃初终间隔日数为22d~29d,≥10℃积温为56℃·d~89℃·d。3省各温度要素的小地形影响程度不同,文中对小地形影响显著的要素进行了模型修正。利用建立的温度要素空间分布模型,构建了东北地区各温度要素的网格数字专题
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本论文在解析了南黄海生态环境的基础上,首次研究揭示了浮游植物固碳强度的年际变化及生态反馈机制,获得了东中国近海浮游植物固碳强度及对海域源/汇格局的影响程度;同时,用室内模拟实验探讨了重金属和有机污染物胁迫下海水无机碳体系和源汇格局的变化过程,获得了一些新的认识。主要结论如下: 1. 南黄海浮游植物固碳强度具有明显的时空变化特征,与海域光照、流系和水团变化、海水磷的浓度等因素密切相关,并在一定程度上决定海区碳源/汇的性质。2005年秋季浮游植物日固碳量达9.5万吨,1983-2005年间,南黄海浮游植物固碳强度有降低的趋势,与海水关键营养盐-磷的限制有关。东中国近海浮游植物年总固碳量约为2.2亿吨,约占全球近海浮游植物的年固碳量的2.0%。 在综合分析秋季南黄海水文、化学、生物背景的基础上,系统阐明了海域浮游植物固碳体系的生物地球化学机制。结果表明,2005年秋季南黄海浮游植物固碳强度,即初级生产力变化在 97−701 mgC m-2 d-1之间,平均为307 mg C m-2 d-1;与其关系比较密切的环境因子为海水透明度、盐度、pH、氨氮 (NH4-N)、磷酸盐 (PO4-P) 以及Chl a。在这些因素中,PO4-P对初级生产力的影响最大,显然11月份南黄海的磷是浮游植物生长的限制因子,次之的影响因素是Chl a和NH4-N。 对南黄海源汇格局的研究发现,如果除去涌升流较为活跃的站位(A9、B7、B8、B9、C8、C9、 D9和A1),2005年秋季表层海水pCO2与浮游植物固碳强度明显负相关(r=-0.8,n=23, p<0.001)。在南黄海东部浮游植物固碳强度较高,pCO2值较低;而在西部海区浮游植物固碳强度较低的区域,其pCO2值较高。碳源/汇转折点浮游植物固碳强度为230 mgC m-2 d-1,即小于此值,海区为大气二氧化碳的源,反之为汇,并且CO2汇区浮游植物固碳强度平均值约是CO2源区的2倍多;浮游植物固碳作用,在某一时间和空间尺度内,基本决定了海区的源汇格局。估算结果显示,东中国近海浮游植物固碳量约为222×106t a-1,约为东中国近海通过海-气界面总表观碳汇强度每年1369万吨的16.2倍,仅就浮游植物的年固碳量而言,东中国近海约占全球近海浮游植物的年固碳量的2.0%。 研究揭示了近年来南黄海浮游植物固碳强度具有区域与年际变化明显这一显著特点。一般,近岸区(由黄海沿岸水和表层水控制)内,光照是浮游植物固碳的主要限制因子;从2001年后的大多数年份中,中央区(黄海冷水团控制)的浮游植物固碳强度均与磷酸盐浓度显著正相关,但与氮浓度的相关性不大,说明南黄海生态系统普遍存在着磷限制而非氮限制;混合区终年受黄、东海混合水控制,受到光照条件和营养盐浓度同时影响。根据本次观测所获数据,结合以前研究者的调查资料,我们发现从1983年到2005年,南黄海浮游植物优势种由Bacillariophyta变为Pyrrophyta,浮游植物细胞丰度和Chl a明显下降,浮游植物固碳强度几乎下降了二分之一 (由569.50 mgC m-2 d-1下降至306.83 mgC m-2 d-1),说明南黄海在世界边缘海固碳过程中的作用在降低。经过相关水质参数及生态环境变化的分析,以上现象是对关键营养盐磷的限制以及光限制响应的缘故。此外,研究还发现,由于南黄海初级生产者产量下降所引起的一些生态反馈信息,如浮游动物固碳量的下降和鱼类产量的锐减。 2. 室内模拟实验显示,重金属(铅、铜、镉和锌)及有机污染物(乙醇、丙酮、尿素和多灭磷)对水体生物固碳体系有重要影响,较低浓度时可提高水体的固碳能力,相应水体中的DIC、HCO3-和 Pco2 与对照组相比都明显下降 (P<0.01);当污染物达到一定浓度后,水体生物的固碳能力明显下降,其有机碳可降解转化为无机碳。当污染物小于转折浓度水体为大气二氧化碳的汇,反之为源。 水体固碳体系对于不同种类、不同浓度的污染物质所表现的受胁迫情况不同,低浓度各污染物(包括重金属和有机污染物)添加组中(对于重金属为0.1和1µmol•L-1,醇和酮分别为<0.5 mol L-1和<0.75 mol L-1),藻干重及固碳量均要大于初始值,说明适量的外源污染可能会促进藻类生长,提高水体的固碳能力,相应水体中的DIC、HCO3- 和PCO2与对照组相比都明显下降 (P<0.01)。当污染物达到一定浓度后,由于其毒害作用,使得水体内生物的固碳能力下降,甚至分解并转化为无机碳,从会引起DIC、HCO3- 和PCO2含量的升高,其含量上升幅度会因固碳体系对不同种类污染物耐受程度的差异而不同。对于尿素和多灭磷,二者浓度分别达到80和20mgL-1时,水体中二氧化碳各参数仍呈现下降趋势,说明在该浓度范围内,大型藻类(如石莼)仍可利用添加物中的氮和磷,将其做为氮源或磷源,促进水体总固碳量的增加。 污染物胁迫对水体碳源汇能力及格局可起到一定的调控作用,与污染物的浓度密切相关,污染物存在着一转折浓度,分别为5µmol L-1(铜)、20µmol L-1(镉) 0.75mol L-1(酮),当污染物添加小于转折浓度并排除其他影响因素时,水体表现为大气CO2的汇,并且适量的增加污染物浓度会使海洋碳汇能力有所增强;而当污染物超出转折浓度时,水体成为CO2的源,其CO2的释放量是随着污染物浓度的增加而增大。对与研究中其他种类的污染物,在实验室设计范围内,水体始终表现为大气CO2的汇。
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We consider a stochastic process driven by a linear ordinary differential equation whose right-hand side switches at exponential times between a collection of different matrices. We construct planar examples that switch between two matrices where the individual matrices and the average of the two matrices are all Hurwitz (all eigenvalues have strictly negative real part), but nonetheless the process goes to infinity at large time for certain values of the switching rate. We further construct examples in higher dimensions where again the two individual matrices and their averages are all Hurwitz, but the process has arbitrarily many transitions between going to zero and going to infinity at large time as the switching rate varies. In order to construct these examples, we first prove in general that if each of the individual matrices is Hurwitz, then the process goes to zero at large time for sufficiently slow switching rate and if the average matrix is Hurwitz, then the process goes to zero at large time for sufficiently fast switching rate. We also give simple conditions that ensure the process goes to zero at large time for all switching rates. © 2014 International Press.
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Haemopoietic stem/progenitor cell (HSPC) development is regulated by extrinsic and intrinsic stimuli. Extrinsic modulators include growth factors and cell adhesion molecules, whereas intrinsic regulation is achieved with many transcription factor families, of which the HOX gene products are known to be important in haemopoiesis. Umbilical cord blood CD133(+) HSPC proliferation potential was tested in liquid culture with 'TPOFLK' (thrombopoietin, flt-3 ligand and c-kit ligand, promoting HSPC survival and self-renewal), in comparison to 'K36EG' (c-kit-ligand, interleukins-3 and -6, erythropoietin and granulocyte colony-stimulating factor, inducing haemopoietic differentiation). TPOFLK induced a higher CD133(+) HSPC proliferation (up to 60-fold more, at week 8) and maintained a higher frequency of the primitive colony-forming cells than K36EG. Quantitative polymerase chain reaction analysis revealed opposite expression patterns for specific HOX genes in expanding cord blood CD133(+) HSPC. After 8 weeks in liquid culture, TPOFLK increased the expression of HOX B3, B4 and A9 (associated with uncommitted HSPC) and reduced the expression of HOX B8 and A10 (expressed in committed myeloid cells) when compared to K36EG. These results suggest that TPOFLK induces CD133(+) HSPC proliferation, self-renewal and maintenance, up-regulation of HOX B3, B4 and A9 and down-regulation of HOX B8 and A10 gene expression.
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The Hox family are master transcriptional regulators of developmental processes, including hematopoiesis. The Hox regulators, caudal homeobox factors (Cdx1-4), and Meis1, along with several individual Hox proteins, are implicated in stem cell expansion during embryonic development, with gene dosage playing a significant role in the overall function of the integrated Hox network. To investigate the role of this network in normal and aberrant, early hematopoiesis, we employed an in vitro embryonic stem cell differentiation system, which recapitulates mouse developmental hematopoiesis. Expression profiles of Hox, Pbx1, and Meis1 genes were quantified at distinct stages during the hematopoietic differentiation process and compared with the effects of expressing the leukemic oncogene Tel/PDGFRß. During normal differentiation the Hoxa cluster, Pbx1 and Meis1 predominated, with a marked reduction in the majority of Hox genes (27/39) and Meis1 occurring during hematopoietic commitment. Only the posterior Hoxa cluster genes (a9, a10, a11, and a13) maintained or increased expression at the hematopoietic colony stage. Cdx4, Meis1, and a subset of Hox genes, including a7 and a9, were differentially expressed after short-term oncogenic (Tel/PDGFRß) induction. Whereas Hoxa4-10, b1, b2, b4, and b9 were upregulated during oncogenic driven myelomonocytic differentiation. Heterodimers between Hoxa7/Hoxa9, Meis1, and Pbx have previously been implicated in regulating target genes involved in hematopoietic stem cell (HSC) expansion and leukemic progression. These results provide direct evidence that transcriptional flux through the Hox network occurs at very early stages during hematopoietic differentiation and validates embryonic stem cell models for gaining insights into the genetic regulation of normal and malignant hematopoiesis.
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Performance evaluation of parallel software and architectural exploration of innovative hardware support face a common challenge with emerging manycore platforms: they are limited by the slow running time and the low accuracy of software simulators. Manycore FPGA prototypes are difficult to build, but they offer great rewards. Software running on such prototypes runs orders of magnitude faster than current simulators. Moreover, researchers gain significant architectural insight during the modeling process. We use the Formic FPGA prototyping board [1], which specifically targets scalable and cost-efficient multi-board prototyping, to build and test a 64-board model of a 512-core, MicroBlaze-based, non-coherent hardware prototype with a full network-on-chip in a 3D-mesh topology. We expand the hardware architecture to include the ARM Versatile Express platforms and build a 520-core heterogeneous prototype of 8 Cortex-A9 cores and 512 MicroBlaze cores. We then develop an MPI library for the prototype and evaluate it extensively using several bare-metal and MPI benchmarks. We find that our processor prototype is highly scalable, models faithfully single-chip multicore architectures, and is a very efficient platform for parallel programming research, being 50,000 times faster than software simulation.
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Objectives: The purpose of this investigation was to determine for dispensed multiples (1 through 4) of powder (P) and liquid (L) in hand-mixed dental cement whether: (1) the mean (P/L) ratio (m/m) and (2) the maximum difference in (P/L) ratio is dependent on the number of multiples dispensed. The Null hypotheses were: (a) mean (P/L) ratio is independent of the number of multiples dispensed and (b) maximum difference in (P/L) ratio is independent of the number of multiples dispensed.
Methods: The materials investigated are listed in the Table. The masses of dispensed aliquots of powder and liquid were measured by a single operator (n=10, for multiples 1 through 4) on a 4-place analytical balance. All measurements were made independently and all possible (P/L) ratios calculated for each sample. The effect of multiple dispensations on (P/L) ratios and maximum (P/L) differences was by one-way ANOVA and linear regression, respectively, with the Tukey post-hoc correction for multiple comparisons.MULTIPLE DISPENSEDDISPENSED MU(x1)(x2)(x3)(x4)Zinc phosphateHeraeus12.271(0.691)a13.051(1.269)b13.215(0.824)b13.118(1.149)bFuji IXGC4.209(0.373)a4.085(0.275)b4.095(0.226)b4.095(0.217)bIRMDentsply7.933(0.767)a7.430(0.451)b7.977(0.729)a8.186(0.929)aKetac-Cem3M Espe9.6206(0.613)a9.714(0.523)a9.298(0.314)b9.321(0.292)bMean (SD) powder/liquid ratio (m/m). Superscript letters represent significances (α = 0.05) within each material
Results: Mean (SD) (P/L) ratios are presented in the Table. Null hypothesis (a) is rejected: either (x1) or (x2) dispensation yields a different (P/L) ratio to (x3) or (x4) (p < 0.05). Null hypothesis (b) is rejected: a negative correlation is observed in max (P/L) ratio difference with dispensed multiple for Ketac Cem (p = 0.029).
Conclusion: For hand-mixed dental cements: (1) more consistent (P/L) ratios may be observed with multiple dispensations of powder & liquid; (2) maximum differences in (P/L) ratio may be negatively correlated with dispensation multiple in some materials.
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We present observations of the unusual optical transient SN 2010U, including spectra taken 1.03 days to 15.3 days after maximum light that identify it as a fast and luminous Fe II type nova. Our multi-band light curve traces the fast decline (t 2 = 3.5 ± 0.3 days) from maximum light (MV = -10.2 ± 0.1 mag), placing SN 2010U in the top 0.5% of the most luminous novae ever observed. We find typical ejecta velocities of ≈1100 km s-1 and that SN 2010U shares many spectral and photometric characteristics with two other fast and luminous Fe II type novae, including Nova LMC 1991 and M31N-2007-11d. For the extreme luminosity of this nova, the maximum magnitude versus rate of decline relationship indicates a massive white dwarf (WD) progenitor with a low pre-outburst accretion rate. However, this prediction is in conflict with emerging theories of nova populations, which predict that luminous novae from massive WDs should preferentially exhibit an alternate spectral type (He/N) near maximum light.
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A Diabetes Mellitus (DM) compreende um conjunto de desordens metabólicas comuns caracterizadas por hiperglicemia, que afeta diferentes órgãos do organismo. Ao longo do tempo, ocorrem danos microvasculares no glomérulo renal, retina e nervos periféricos, bem como doença macrovascular nas artérias. A composição da saliva também é afetada pela DM, com consequências na homeostasia oral. No entanto, o proteoma e o peptidoma salivar têm sido pouco explorados na DM tipo 1 e nas suas complicações crónicas. Tendo em conta o crescente interesse na saliva como fluido diagnóstico, o objetivo principal deste trabalho foi avaliar os eventos proteolíticos subjacentes à DM tipo 1 e às suas complicações microvasculares, bem como, caracterizar as alterações induzidas pela DM tipo 1 no proteoma e peptidoma salivar. A DM tipo 1 e particularmente as complicações microvasculares associadas modulam o perfil proteolítico dos fluidos biológicos, com diferenças significativas de atividade observadas na urina e saliva, atribuídas principalmente ao complexo Metaloproteinase da Matriz (MMP)-9/lipocalina associada à gelatinase de neutrófilos, aminopeptidase N, azurocidina e calicreína 1. O aumento da atividade proteolítica observado na saliva total dos diabéticos resultou no aumento da percentagem de péptidos, principalmente de um número acrescido de fragmentos de colagénio do tipo I, refletindo possivelmente um estado inflamatório crónico dos tecidos orais e periodontais. O peptidoma também corrobora uma maior suscetibilidade das proteínas salivares, especificamente, das proteínas ricas em prolina básicas (bPRP) 1, bPRP2 e proteínas ricas em prolina ácidas (aPRP) à proteólise, evidenciando a geração de fragmentos de proteínas associadas à ligação a bactérias. A análise do proteoma salivar baseada em iTRAQ mostrou uma sobre-expressão de L-plastina, fator do adenocarcinoma do pâncreas e das proteínas S100-A8 e S100-A9, enfatizando a importância do sistema imune inato na patogénese da DM tipo 1 e das complicações microvasculares associadas. A análise integrada de todas as proteínas expressas diferencialmente entre os pacientes diabéticos com ou sem complicações microvasculares e indivíduos saudáveis foi realizada com o STRING, onde se observam três conjuntos funcionalmente ligados, um compreende a interação entre o colagénio tipo I, colagénio tipo II e MMP-9, um segundo conjunto envolve a MMP-2 e o colagénio de tipo I e um terceiro conjunto composto por proteínas salivares e inflamatórias. Estes conjuntos estão associados com as vias Kegg de interação recetor-matriz extracelular, de adesão focal e migração transendotelial dos leucócitos. Por outro lado, a análise do proteoma e peptidoma salivar destacou potenciais biomarcadores para o diagnóstico e prognóstico da DM tipo 1 e das suas complicações.
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We assessed the blockade of the renin-angiotensin system (RAS) achieved with 2 angiotensin (Ang) antagonists given either alone at different doses or with an ACE inhibitor. First, 20 normotensive subjects were randomly assigned to 100 mg OD losartan (LOS) or 80 mg OD telmisartan (TEL) for 1 week; during another week, the same doses of LOS and TEL were combined with 20 mg OD lisinopril. Then, 10 subjects were randomly assigned to 200 mg OD LOS and 160 mg OD TEL for 1 week and 100 mg BID LOS and 80 mg BID TEL during the second week. Blockade of the RAS was evaluated with the inhibition of the pressor effect of exogenous Ang I, an ex vivo receptor assay, and the changes in plasma Ang II. Trough blood pressure response to Ang I was blocked by 35+/-16% (mean+/-SD) with 100 mg OD LOS and by 36+/-13% with 80 mg OD TEL. When combined with lisinopril, blockade was 76+/-7% with LOS and 79+/-9% with TEL. With 200 mg OD LOS, trough blockade was 54+/-14%, but with 100 mg BID it increased to 77+/-8% (P<0.01). Telmisartan (160 mg OD and 80 mg BID) produced a comparable effect. Thus, at their maximal recommended doses, neither LOS nor TEL blocks the RAS for 24 hours; hence, the addition of an ACE inhibitor provides an additional blockade. A 24-hour blockade can be achieved with an angiotensin antagonist alone, provided higher doses or a BID regimen is used.