93 research outputs found
Generalized Swiss-cheese cosmologies: Mass scales
We generalize the Swiss-cheese cosmologies so as to include nonzero linear
momenta of the associated boundary surfaces. The evolution of mass scales in
these generalized cosmologies is studied for a variety of models for the
background without having to specify any details within the local
inhomogeneities. We find that the final effective gravitational mass and size
of the evolving inhomogeneities depends on their linear momenta but these
properties are essentially unaffected by the details of the background model.Comment: 10 pages, 14 figures, 1 table, revtex4, Published form (with minor
corrections
Static charged perfect fluid spheres in general relativity
Interior perfect fluid solutions for the Reissner-Nordstrom metric are
studied on the basis of a new classification scheme. General formulas are found
in many cases. Explicit new global solutions are given as illustrations. Known
solutions are briefly reviewed.Comment: 23 pages, Revtex (galley), journal version, to appear in Phys.Rev.
Chemiluminescent Assay for Catecholamines by the Generation of Hydrogen Peroxide in Basic Solution and the Use of Isoluminol-Microperoxidase.
Idiopathic environmental intolerances (IEI): From molecular epidemiology to molecular medicine
625-635Inherited or acquired impairment of
xenobiotics metabolism is a postulated mechanism underlying
environment-associated pathologies such as multiple chemical sensitivity,
fibromyalgia, chronic fatigue syndrome, dental amalgam disease, and others,
also collectively named idiopathic environmental intolerances (IEI). In view of
the poor current knowledge of their etiology and pathogenesis, and the absence
of recognised genetic and metabolic markers of the diseases. They are often
considered “medically unexplained syndromes”,. These disabling conditions share
the features of poly-symptomatic multi-organ syndromes, considered by part of
the medical community to be aberrant responses triggered by exposure to
low-dose organic and inorganic chemicals and metals, in concentrations far below
average reference levels admitted for environmental toxicants. A genetic
predisposition to altered biotransformation of environmental chemicals, drugs,
and metals, and of endogenous low-molecular weight metabolites, caused by
polymorphisms of genes coding for xenobiotic metabolizing enzymes, their
receptors and transcription factors appears to be involved in the
susceptibility to these environment-associated pathologies, along with
epigenetic factors. Free radical/antioxidant homeostasis may also be heavily
implicated, indirectly by affecting the regulation of xenobiotic metabolizing
enzymes, and directly by causing increased levels of oxidative products,
implicated in the chronic damage of cells and tissues, which is in part
correlated with clinical symptoms. More systematic studies of molecular
epidemiology, toxico- and pharmaco-genomics, elucidating the mechanisms of
regulation, expression, induction, and activity of antioxidant/detoxifying
enzymes, and the possible role of inflammatory mediators, promise a better
understanding of this pathologically increased sensitivity to low-level
chemical stimuli, and a solid basis for effective individualized antioxidant-
and/or chelator-based treatments
Biochemical Characterization of the Multi-enzyme System Produced by Penicillium decumbens
Idiopathic environmental intolerances (IEI): From molecular epidemiology to molecular medicine
Inherited or acquired impairment of xenobiotics metabolism is a postulated mechanism underlying environment-associated pathologies such as multiple chemical sensitivity, fibromyalgia, chronic fatigue syndrome, dental amalgam disease, and others, also collectively named idiopathic environmental intolerances (IEI). In view of the poor current knowledge of their etiology and pathogenesis, and the absence of recognised genetic and metabolic markers of the diseases. They are often considered "medically unexplained syndromes",. These disabling conditions share the features of polysymptomatic multi-organ syndromes, considered by part of the medical community to be aberrant responses triggered by exposure to low-dose organic and inorganic chemicals and metals, in concentrations far below average reference levels admitted for environmental toxicants. A genetic predisposition to altered biotransformation of environmental chemicals, drugs, and metals, and of endogenous low-molecular weight metabolites, caused by polymorphisms of genes coding for xenobiotic metabolizing enzymes, their receptors and transcription factors appears to be involved in the susceptibility to these environment-associated pathologies, along with epigenetic factors. Free radical/antioxidant homeostasis may also be heavily implicated, indirectly by affecting the regulation of xenobiotic metabolizing enzymes, and directly by causing increased levels of oxidative products, implicated in the chronic damage of cells and tissues, which is in part correlated with clinical symptoms. More systematic studies of molecular epidemiology, toxico- and pharmaco-genomics, elucidating the mechanisms of regulation, expression, induction, and activity of antioxidant/detoxifying enzymes, and the possible role of inflammatory mediators, promise a better understanding of this pathologically increased sensitivity to low-level chemical stimuli, and a solid basis for effective individualized antioxidant- and/or chelator-based treatments
An endogenous Electron Spin Resonance (ESR) signal discriminates nevi from melanomas in human specimens: a step forward in its diagnostic application.
Given the specific melanin-associated paramagnetic features, the Electron Spin Resonance (ESR, called also Electron Paramagnetic Resonance, EPR) analysis has been proposed as a potential tool for non-invasive melanoma diagnosis. However, studies comparing human melanoma tissues to the most appropriate physiological counterpart (nevi) have not been performed, and ESR direct correlation with melanoma clinical features has never been investigated. ESR spectrum was obtained from melanoma and non-melanoma cell-cultures as well as mouse melanoma and non-melanoma tissues and an endogenous ESR signal (g = 2.005) was found in human melanoma cells and in primary melanoma tissues explanted from mice, while it was always absent in non-melanoma samples. These characteristics of the measured ESR signal strongly suggested its connection with melanin. Quantitative analyses were then performed on paraffin-embedded human melanoma and nevus sections, and validated on an independent larger validation set, for a total of 112 sections (52 melanomas, 60 nevi). The ESR signal was significantly higher in melanomas (p = 0.0002) and was significantly different between "Low Breslow's and "High Breslow's" depth melanomas (p<0.0001). A direct correlation between ESR signal and Breslow's depth, expressed in millimetres, was found (R = 0.57; p<0.0001). The eu/pheomelanin ratio was found to be significantly different in melanomas "Low Breslow's" vs melanomas "High Breslow's" depth and in nevi vs melanomas "High Breslow's depth". Finally, ROC analysis using ESR data discriminated melanomas sections from nevi sections with up to 90% accuracy and p<0.0002. In the present study we report for the first time that ESR signal in human paraffin-embedded nevi is significantly lower than signal in human melanomas suggesting that spectrum variations may be related to qualitative melanin differences specifically occurring in melanoma cells. We therefore conclude that this ESR signal may represent a reliable marker for melanoma diagnosis in human histological sections
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