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采用蒙特卡罗法分析离散坐标法的假散射 总被引:1,自引:1,他引:0
采用蒙特卡罗法获得了离散坐标方程的不含任何假散射的高精度解,其基本思路是:当采用一个离散坐标格式来计算一个漫射表面的热辐射时,就意味着用有限个离散方向去“代表”2π立体空间上的无穷多个方向,因此,不妨假定存在着这样一个虚拟表现:该表面的确只沿着该离散坐标格式的离散方向上发射热辐射,并且在每个方向上的热流也完全遵循离散坐标方程,然后将蒙特卡罗法应用于此虚拟表现,由此所获得解即为此有面的高精度解,不言而喻它也等效于离散坐标方程的高精度解,在此基础上,分析了离散坐标法的假散射对计算结果的影响。 相似文献
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Multiplicative computation in a visual neuron sensitive to looming 总被引:12,自引:0,他引:12
Multiplicative operations are important in sensory processing, but their biophysical implementation remains largely unknown. We investigated an identified neuron (the lobula giant movement detector, LGMD, of locusts) whose output firing rate in response to looming visual stimuli has been described by two models, one of which involves a multiplication. In this model, the LGMD multiplies postsynaptically two inputs (one excitatory, one inhibitory) that converge onto its dendritic tree; in the other model, inhibition is presynaptic to the LGMD. By using selective activation and inactivation of pre- and postsynaptic inhibition, we show that postsynaptic inhibition has a predominant role, suggesting that multiplication is implemented within the neuron itself. Our pharmacological experiments and measurements of firing rate versus membrane potential also reveal that sodium channels act both to advance the response of the LGMD in time and to map membrane potential to firing rate in a nearly exponential manner. These results are consistent with an implementation of multiplication based on dendritic subtraction of two converging inputs encoded logarithmically, followed by exponentiation through active membrane conductances. 相似文献
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Postel-Vinay S Véron AS Tirode F Pierron G Reynaud S Kovar H Oberlin O Lapouble E Ballet S Lucchesi C Kontny U González-Neira A Picci P Alonso J Patino-Garcia A de Paillerets BB Laud K Dina C Froguel P Clavel-Chapelon F Doz F Michon J Chanock SJ Thomas G Cox DG Delattre O 《Nature genetics》2012,44(3):323-327
Ewing sarcoma, a pediatric tumor characterized by EWSR1-ETS fusions, is predominantly observed in populations of European ancestry. We performed a genome-wide association study (GWAS) of 401 French individuals with Ewing sarcoma, 684 unaffected French individuals and 3,668 unaffected individuals of European descent and living in the United States. We identified candidate risk loci at 1p36.22, 10q21 and 15q15. We replicated these loci in two independent sets of cases and controls. Joint analysis identified associations with rs9430161 (P = 1.4 × 10(-20); odds ratio (OR) = 2.2) located 25 kb upstream of TARDBP, rs224278 (P = 4.0 × 10(-17); OR = 1.7) located 5 kb upstream of EGR2 and, to a lesser extent, rs4924410 at 15q15 (P = 6.6 × 10(-9); OR = 1.5). The major risk haplotypes were less prevalent in Africans, suggesting that these loci could contribute to geographical differences in Ewing sarcoma incidence. TARDBP shares structural similarities with EWSR1 and FUS, which encode RNA binding proteins, and EGR2 is a target gene of EWSR1-ETS. Variants at these loci were associated with expression levels of TARDBP, ADO (encoding cysteamine dioxygenase) and EGR2. 相似文献
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Yara Bou Saada Vlada Zakharova Boris Chernyak Carla Dib Gilles Carnac Svetlana Dokudovskaya Yegor S. Vassetzky 《Cellular and molecular life sciences : CMLS》2017,74(19):3439-3449
Skeletal muscle is a highly oxygen-consuming tissue that ensures body support and movement, as well as nutrient and temperature regulation. DNA damage induced by reactive oxygen species is present in muscles and tends to accumulate with age. Here, we present a summary of data obtained on DNA damage and its implication in muscle homeostasis, myogenic differentiation and neuromuscular disorders. Controlled and transient DNA damage appears to be essential for muscular homeostasis and differentiation while uncontrolled and chronic DNA damage negatively affects muscle health. 相似文献
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Jérémie Gautheron Gilles Courtois 《Cellular and molecular life sciences : CMLS》2010,67(18):3101-3113
Ubiquitination has emerged over the years as the most sophisticated way to modify proteins to affect their fate and function.
In particular, it has been reported to be instrumental in regulating several steps of the NF-κB signalling pathway which controls
inflammation, immunity, adhesion and cell survival. Integrating ubiquitination into NF-κB activation requires the regulatory
subunit of IKK, NEMO, which not only displays affinity for polyubiquitin chains, but is also posttranslationally modified
by a complex set of reactions involving ubiquitin. Here, we examine how studies of the NEMO/ubiquitin relationship have provided
novel insights into the IKK activation process and have uncovered molecular mechanisms that should represent in the future
attractive targets for specifically modulating NF-κB function. 相似文献