981 resultados para kappa statistic
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Lennart Åqvist (1992) proposed a logical theory of legal evidence, based on the Bolding-Ekelöf of degrees of evidential strength. This paper reformulates Åqvist's model in terms of the probabilistic version of the kappa calculus. Proving its acceptability in the legal context is beyond the present scope, but the epistemological debate about Bayesian Law isclearly relevant. While the present model is a possible link to that lineof inquiry, we offer some considerations about the broader picture of thepotential of AI & Law in the evidentiary context. Whereas probabilisticreasoning is well-researched in AI, calculations about the threshold ofpersuasion in litigation, whatever their value, are just the tip of theiceberg. The bulk of the modeling desiderata is arguably elsewhere, if one isto ideally make the most of AI's distinctive contribution as envisaged forlegal evidence research.
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The crystal structure of [HgBr2(Pyp)(2)](n) (Pyp = pyrazine, C4H4N2) consists of almost linear HgBr2 molecules which are linked by pyrazine molecules to form double strands of a coordination polymer in the [010] direction. The Hg and Br atoms lie on mirror planes.
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Background: Hypercapnic acidosis exerts protective effects in acute lung injury but may also slow cellular repair. These effects may be mediated via inhibition of nuclear factor-kappa B (NF-kappa B), a pivotal transcriptional regulator in inflammation and repair.
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Tissue destruction characterizes infection with Mycobacterium tuberculosis (Mtb). Type I collagen provides the lung's tensile strength, is extremely resistant to degradation, but is cleaved by matrix metalloproteinase (MMP)-1. Fibroblasts potentially secrete quantitatively more MMP-1 than other lung cells. We investigated mechanisms regulating Mtb-induced collagenolytic activity in fibroblasts in vitro and in patients. Lung fibroblasts were stimulated with conditioned media from Mtb-infected monocytes (CoMTb). CoMTb induced sustained increased MMP-1 (74 versus 16 ng/ml) and decreased tissue inhibitor of metalloproteinase (TIMP)-1 (8.6 versus 22.3 ng/ml) protein secretion. CoMTb induced a 2.7-fold increase in MMP-1 promoter activation and a 2.5-fold reduction in TIMP-1 promoter activation at 24 hours (P = 0.01). Consistent with this, TIMP-1 did not co-localize with fibroblasts in patient granulomas. MMP-1 up-regulation and TIMP-1 down-regulation were p38 (but not extracellular signal–regulated kinase or c-Jun N-terminal kinase) mitogen-activated protein kinase–dependent. STAT3 phosphorylation was detected in fibroblasts in vitro and in tuberculous granulomas.STAT3 inhibition reduced fibroblast MMP-1 secretion by 60% (P = 0.046). Deletion of the MMP-1 promoter NF-B–binding site abrogated promoter induction in response to CoMTb. TNF-, IL-1ß, or Oncostatin M inhibition in CoMTb decreased MMP-1 secretion by 65, 63, and 25%, respectively. This cytokine cocktail activated the same signaling pathways in fibroblasts and induced MMP-1 secretion similar to that induced by CoMTb. This study demonstrates in a cellular model and in patients with tuberculosis that in addition to p38 and NF-B, STAT3 has a key role in driving fibroblast-dependent unopposed MMP-1 production that may be key in tissue destruction in patients.
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Background: The evaluation of the complexity of an observed object is an old but outstanding problem. In this paper we are tying on this problem introducing a measure called statistic complexity.
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Pretty vacant: The excellent oxygen storage capacity (OSC) of ?-Ce2Zr2O8 (see picture; Ce gray, Zr green, O red) is shown to be a result of its unique structural features; after removing oxygen atoms, the structural relaxation is local (vacancy shown in brown), and both the localized structural relaxation and the number of localized structural relaxations are maximized.
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A recent paper [L.-N. Hau and W.-Z. Fu, Phys. Plasmas 14, 110702 (2007)] deals with certain mathematical and physical properties of the kappa distribution. We comment on the authors' use of a form of distribution function that is different from the "standard" form of the kappa distribution, and hence their results, inter alia for an expansion of the distribution function and for the associated number density in an electrostatic potential, do not fully reflect the dependence on kappa that would be associated with the conventional kappa distribution. We note that their definition of the kappa distribution function is also different from a modified distribution based on the notion of nonextensive entropy.
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Dust ion acoustic solitons in an unmagnetized dusty plasma comprising cold dust particles, adiabatic fluid ions, and electrons satisfying a kappa distribution are investigated using both small amplitude and arbitrary amplitude techniques. Their existence domain is discussed in the parameter space of Mach number M and electron density fraction f over a wide range of values of kappa. For all kappa > 3/2, including the Maxwellian distribution, negative dust supports solitons of both polarities over a range in f. In that region of parameter space solitary structures of finite amplitude can be obtained even at the lowest Mach number, the acoustic speed, for all kappa. These cannot be found from small amplitude theories. This surprising behavior is investigated, and it is shown that f(c), the value of f at which the KdV coefficient A vanishes, plays a critical role. In the presence of positive dust, only positive potential solitons are found. (C) 2010 American Institute of Physics. [doi: 10.1063/1.3400229]
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Persistent activation of NF-B is central to the pathogenesis of many inflammatory lung disorders including Cystic Fibrosis, Asthma and Chronic Obstructive Pulmonary Disease. A20 is an endogenous negative regulator of NF-B signalling which has been widely described in autoimmune and inflammatory disorders including Diabetes and Crohn’s disease, but which has received little attention in terms of chronic lung disorders. This review examines the existing body of research on A20 regulation of NF-B signalling and details the mechanism and regulation of A20 action focusing, where possible, on pulmonary inflammation. A20 and its associated signalling molecules are highlighted as being of potential therapeutic interest for the treatment of inflammatory disorders and a proposed model of A20 activity in inflammatory lung disease is provided.