31 research outputs found

    On the q=1/2 non-extensive maximum entropy distribution

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    A detailed mathematical analysis on the q=1/2 non-extensive maximum entropy distribution of Tsallis’ is undertaken. The analysis is based upon the splitting of such a distribution into two orthogonal components. One of the components corresponds to the minimum norm solution of the problem posed by the fulfillment of the a priori conditions on the given expectation values. The remaining component takes care of the normalization constraint and is the projection of a constant onto the null space of the “expectation-values transformation”

    A non-extensive maximum entropy based regularization method for bad conditioned inverse problems

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    A regularization method based on the non-extensive maximum entropy principle is devised. Special emphasis is given to the q=1/2 case. We show that, when the residual principle is considered as constraint, the q=1/2 generalized distribution of Tsallis yields a regularized solution for bad-conditioned problems. The so devised regularized distribution is endowed with a component which corresponds to the well known regularized solution of Tikhonov

    Frames:a maximum entropy statistical estimate of the inverse problem

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    A maximum entropy statistical treatment of an inverse problem concerning frame theory is presented. The problem arises from the fact that a frame is an overcomplete set of vectors that defines a mapping with no unique inverse. Although any vector in the concomitant space can be expressed as a linear combination of frame elements, the coefficients of the expansion are not unique. Frame theory guarantees the existence of a set of coefficients which is “optimal” in a minimum norm sense. We show here that these coefficients are also “optimal” from a maximum entropy viewpoint

    Recessive mutations in the INS gene result in neonatal diabetes through reduced insulin biosynthesis

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    Heterozygous coding mutations in the INS gene that encodes preproinsulin were recently shown to be an important cause of permanent neonatal diabetes. These dominantly acting mutations prevent normal folding of proinsulin, which leads to beta-cell death through endoplasmic reticulum stress and apoptosis. We now report 10 different recessive INS mutations in 15 probands with neonatal diabetes. Functional studies showed that recessive mutations resulted in diabetes because of decreased insulin biosynthesis through distinct mechanisms, including gene deletion, lack of the translation initiation signal, and altered mRNA stability because of the disruption of a polyadenylation signal. A subset of recessive mutations caused abnormal INS transcription, including the deletion of the C1 and E1 cis regulatory elements, or three different single base-pair substitutions in a CC dinucleotide sequence located between E1 and A1 elements. In keeping with an earlier and more severe beta-cell defect, patients with recessive INS mutations had a lower birth weight (-3.2 SD score vs. -2.0 SD score) and were diagnosed earlier (median 1 week vs. 10 weeks) compared to those with dominant INS mutations. Mutations in the insulin gene can therefore result in neonatal diabetes as a result of two contrasting pathogenic mechanisms. Moreover, the recessively inherited mutations provide a genetic demonstration of the essential role of multiple sequence elements that regulate the biosynthesis of insulin in man

    RICORS2040 : The need for collaborative research in chronic kidney disease

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    Chronic kidney disease (CKD) is a silent and poorly known killer. The current concept of CKD is relatively young and uptake by the public, physicians and health authorities is not widespread. Physicians still confuse CKD with chronic kidney insufficiency or failure. For the wider public and health authorities, CKD evokes kidney replacement therapy (KRT). In Spain, the prevalence of KRT is 0.13%. Thus health authorities may consider CKD a non-issue: very few persons eventually need KRT and, for those in whom kidneys fail, the problem is 'solved' by dialysis or kidney transplantation. However, KRT is the tip of the iceberg in the burden of CKD. The main burden of CKD is accelerated ageing and premature death. The cut-off points for kidney function and kidney damage indexes that define CKD also mark an increased risk for all-cause premature death. CKD is the most prevalent risk factor for lethal coronavirus disease 2019 (COVID-19) and the factor that most increases the risk of death in COVID-19, after old age. Men and women undergoing KRT still have an annual mortality that is 10- to 100-fold higher than similar-age peers, and life expectancy is shortened by ~40 years for young persons on dialysis and by 15 years for young persons with a functioning kidney graft. CKD is expected to become the fifth greatest global cause of death by 2040 and the second greatest cause of death in Spain before the end of the century, a time when one in four Spaniards will have CKD. However, by 2022, CKD will become the only top-15 global predicted cause of death that is not supported by a dedicated well-funded Centres for Biomedical Research (CIBER) network structure in Spain. Realizing the underestimation of the CKD burden of disease by health authorities, the Decade of the Kidney initiative for 2020-2030 was launched by the American Association of Kidney Patients and the European Kidney Health Alliance. Leading Spanish kidney researchers grouped in the kidney collaborative research network Red de Investigación Renal have now applied for the Redes de Investigación Cooperativa Orientadas a Resultados en Salud (RICORS) call for collaborative research in Spain with the support of the Spanish Society of Nephrology, Federación Nacional de Asociaciones para la Lucha Contra las Enfermedades del Riñón and ONT: RICORS2040 aims to prevent the dire predictions for the global 2040 burden of CKD from becoming true

    Nurses' perceptions of aids and obstacles to the provision of optimal end of life care in ICU

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    Contains fulltext : 172380.pdf (publisher's version ) (Open Access

    A non-extensive maximum entropy based regularization method for bad conditioned inverse problems

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    A regularization method based on the non-extensive maximum entropy principle is devised. Special emphasis is given to the q=1/2 case. We show that, when the residual principle is considered as constraint, the q=1/2 generalized distribution of Tsallis yields a regularized solution for bad-conditioned problems. The so devised regularized distribution is endowed with a component which corresponds to the well known regularized solution of Tikhonov.Peer Reviewe

    On the q = ½ Non-Extensive Maximum Entropy Distribution

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    A detailed mathematical analysis on the q = 1=2 non-extensive maximum entropy distribution of Tsallis' is undertaken. The analysis is based upon the splitting of sucha distribution into two orthogonal components. One of the components corresponds to the minimum norm solution of the problem posed by the fulfillment of the a priori conditions on the given expectation values. The remaining component takes care of the normalization constraint and is the projection of a constant onto the Null space of the "expectationvalues -transformation"
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