422 research outputs found
Commutativity, comonotonicity, and Choquet integration of self-adjoint operators
In this work, we propose a definition of comonotonicity for elements of [Formula: see text], i.e. bounded self-adjoint operators defined over a complex Hilbert space [Formula: see text]. We show that this notion of comonotonicity coincides with a form of commutativity. Intuitively, comonotonicity is to commutativity as monotonicity is to bounded variation. We also define a notion of Choquet expectation for elements of [Formula: see text] that generalizes quantum expectations. We characterize Choquet expectations as the real-valued functionals over [Formula: see text] which are comonotonic additive, [Formula: see text]-monotone, and normalized
pH and acid phosphatase determinations after growth of Aspergillus nidulans on solid medium
pH and acid phosphatase determinations after growth of Aspergillus nidulans on solid mediu
The levels of mRNA expressed by gene palF of A. nidulans do not appear to be pH regulated
Although pal genes are putative members of a signaling cascade involved in ambient pH sensing and in the consecutive activation of PacC protein, recent findings show that most of them (palA, B, C, H and I) do not respond to ambient pH at the transcriptional level. Here, we show that mRNA levels of the remainding palF gene are also constant at various growth pH values
PATIENTS WITH MIXED CRYOGLOBULINEMIA AND HCV INFECTION, IN PRESENCE OR ABSENCE OF AUTOIMMUNE THYROIDITIS, HAVE HIGH SERUM LEVELS OF (CXC MOTIF) LIGAND (CXCL)9 AND CXCL11 CHEMOKINES
No data are present in the literature regarding chemokine (CXC motif) ligand (CXCL)9 and CXCL11 circulating levels in cryoglobulinemia associated with hepatitis C (MC+HCV), in presence/absence of autoimmune thyroiditis (AT). Serum CXCL9 and CXCL11 have been measured in 38 MC+HCV patients without AT (MCo), 38 MC+HCV patients with AT (MC+AT), and in matched controls without (control 1) or with thyroiditis (control 2). Serum CXCL9 and CXCL11 were significantly higher: in control 2 than control 1 (p<0.05); in MCo than control 1 and control 2 (p<0.001, for both); in MC+AT than control 1 and control 2 (p<0.0001, for both), and than MCo (p=0.01, for both). Our study demonstrates markedly high serum levels of CXCL9 and CXCL11 in patients with MC+HCV compared to healthy controls; in MC+HCV patients increased CXCL9 and CXCL11 levels were significantly associated with the presence of AT. Moreover, a strong relation between circulating CXCL9 and CXCL11 in MC+HCV has been shown
Strong laws of large numbers for sub-linear expectations
We investigate three kinds of strong laws of large numbers for capacities
with a new notion of independently and identically distributed (IID) random
variables for sub-linear expectations initiated by Peng. It turns out that
these theorems are natural and fairly neat extensions of the classical
Kolmogorov's strong law of large numbers to the case where probability measures
are no longer additive. An important feature of these strong laws of large
numbers is to provide a frequentist perspective on capacities.Comment: 10 page
Properties of a constitutive alkaline phosphatase from strain 74A of the mold Neurospora crassa
Elicitation of Preferences under Ambiguity
This paper is about behaviour under ambiguity ‒ that is, a situation in which probabilities either do not exist or are not known. Our objective is to find the most empirically valid of the increasingly large number of theories attempting to explain such behaviour. We use experimentally-generated data to compare and contrast the theories. The incentivised experimental task we employed was that of allocation: in a series of problems we gave the subjects an amount of money and asked them to allocate the money over three accounts, the payoffs to them being contingent on a ‘state of the world’ with the occurrence of the states being ambiguous. We reproduced ambiguity in the laboratory using a Bingo Blower. We fitted the most popular and apparently empirically valid preference functionals [Subjective Expected Utility (SEU), MaxMin Expected Utility (MEU) and α-MEU], as well as Mean-Variance (MV) and a heuristic rule, Safety First (SF). We found that SEU fits better than MV and SF and only slightly worse than MEU and α-MEU
Genetic variation and recombination of RdRp and HSP 70h genes of Citrus tristeza virus isolates from orange trees showing symptoms of citrus sudden death disease
<p>Abstract</p> <p>Background</p> <p>Citrus sudden death (CSD), a disease that rapidly kills orange trees, is an emerging threat to the Brazilian citrus industry. Although the causal agent of CSD has not been definitively determined, based on the disease's distribution and symptomatology it is suspected that the agent may be a new strain of <it>Citrus tristeza virus </it>(CTV). CTV genetic variation was therefore assessed in two Brazilian orange trees displaying CSD symptoms and a third with more conventional CTV symptoms.</p> <p>Results</p> <p>A total of 286 RNA-dependent-RNA polymerase (RdRp) and 284 heat shock protein 70 homolog (HSP70h) gene fragments were determined for CTV variants infecting the three trees. It was discovered that, despite differences in symptomatology, the trees were all apparently coinfected with similar populations of divergent CTV variants. While mixed CTV infections are common, the genetic distance between the most divergent population members observed (24.1% for RdRp and 11.0% for HSP70h) was far greater than that in previously described mixed infections. Recombinants of five distinct RdRp lineages and three distinct HSP70h lineages were easily detectable but respectively accounted for only 5.9 and 11.9% of the RdRp and HSP70h gene fragments analysed and there was no evidence of an association between particular recombinant mosaics and CSD. Also, comparisons of CTV population structures indicated that the two most similar CTV populations were those of one of the trees with CSD and the tree without CSD.</p> <p>Conclusion</p> <p>We suggest that if CTV is the causal agent of CSD, it is most likely a subtle feature of population structures within mixed infections and not merely the presence (or absence) of a single CTV variant within these populations that triggers the disease.</p
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