97 research outputs found
Some Inequalities for Normal Operators in Hilbert Spaces
No full textSome inequalities for normal operators in Hilbert spaces are given. For this purpose, some results for vectors in inner product spaces due to Buzano, Dunkl-Williams, Hile, Goldstein-Ryff-Clarke, Dragomir-S´andor and the author are employed
The Perturbed Median Principle for Integral Inequalities with Applications
No full textIn this paper a perturbed version of the Median Principle introduced
by the author in 'The median principle for inequalities and applications' is developed. Applications for various Riemann-
Stieltjes integral and Lebesgue integral inequalities are also provided
New Reverse Inequalities for Normal Operators in Hilbert Spaces
No full textIn this paper, more reverse inequalities for the class of normal
operators, are established. Some of the obtained results are based on recent
reverse results for the Schwarz inequality in Hilbert spaces due to the author
Upper Bounds for the Euclidean Operator Radius and Applications
No full textThe main aim of the present paper is to establish various sharp
upper bounds for the Euclidean operator radius of an n−tuple of bounded
linear operators on a Hilbert space. The tools used are provided by several
generalisations of Bessel inequality due to Boas-Bellman, Bombieri and the
author. Natural applications for the norm and the numerical radius of bounded
linear operators on Hilbert spaces are also given
Inequalities for some Functionals Associated with Bounded Linear Operators in Hilbert Spaces
No full textSome inequalities between the operator norm, numerical radius
and functional are established. New upper bounds for the nonnegative
quantity that complement some recent results of the author are given as well
On the Hermite-Hadamard Inequality and Other Integral Inequalities Involving Two Functions
No full textWe establish some new Hermite-Hadamard-type inequalities involving product of two functions. Other integral inequalities for two functions are obtained as well. The analysis used in the proofs is fairly elementary and based on the use of the Minkowski, Hölder, and Young inequalities
Između ambicija i iluzija : nuklearna politika Jugoslavije : 1945-1990: nuklearna politika Jugoslavije : 1945-1990
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Iterative Refinements of the Hermite-Hadamard Inequality, Applications to the Standard Means
No full text Two adjacent recursive processes converging to the mean value of a real-valued convex function are given. Refinements of the Hermite-Hadamard inequality are obtained. Some applications to the special means are discussed. A brief extension for convex mappings with variables in a linear space is also provided.</p
On Hadamard-Type Inequalities Involving Several Kinds of Convexity
No full text We do not only give the extensions of the results given by Gill et al. (1997) for log-convex functions but also obtain some new Hadamard-type inequalities for log-convex -convex, and -convex functions.</p
Mechanisms mediating macrophage activation during acetaminophen-induced hepatotoxicity: role of high mobility group box-1 and galectin-3
No full textClassically and alternatively activated macrophages and inflammatory mediators they release play a key role in the pathogenesis of acetaminophen (APAP)-induced hepatotoxicity. In the present studies, we investigated the role of the DNA-binding protein, high mobility group box-1 (HMGB1), and the β-galactoside binding lectin, galectin-3 (Gal-3), in regulating the phenotype of activated macrophages in the liver following APAP intoxication. Culture medium collected from hepatocytes treated for 24 h with 5 mM APAP (CM-AA) stimulated macrophage production of reactive oxygen species and upregulated expression of the antioxidant enzymes catalase and heme oxygenase-1 (HO-1). CM-AA also upregulated expression of the proinflammatory chemokines MIP-1α (CCL3) and MIP-2 (CXCL2), and the eicosanoid biosynthetic enzymes, COX-2 and 12/15-LOX, effects dependent on the p44/42 MAP kinase. Treatment of hepatocytes with ethyl pyruvate (EP) prior to APAP blunted the effects of CM-AA on macrophage ROS production, expression of antioxidant proteins, and COX-2, suggesting that part of the activity in CM-AA was HMGB1. Further studies demonstrated that APAP-induced hepatotoxicity was associated with upregulation of Gal-3 mRNA and protein expression. Loss of Gal-3 resulted in reduced hepatotoxicity in response to APAP. This correlated with decreases in APAP-induced expression of the inflammatory proteins lipocalin 2 (24p3), inducible nitric oxide synthase (iNOS), interleukin-12 (IL-12), tumor necrosis factor- (TNF-), macrophage inflammatory protein-3 (MIP-3α), CD98, the macrophage Gal-3 receptor, and TNF-α receptor 1 (TNFR1). In contrast, APAP-induced expression of the alternative activation markers Ym1 and Fizz-1, as well as tissue repair, was increased in Gal-3-/- mice. These results suggest that Gal-3 contributes to inflammatory mediator production and hepatotoxicity after APAP. We next investigated the role of Gal-3 in regulating macrophage proinflammatory phenotype. Following APAP intoxication, increased numbers of proinflammatory CD11b+/Ly6Chi macrophages accumulated in necrotic regions of the liver. These cells were distinct from resident Kupffer cells and expressed Gal-3. Loss of Gal-3 resulted in reduced accumulation of CD11b+/Ly6Chi macrophages in response to APAP and increased accumulation of anti-inflammatory CD11b+/Ly6Clo macrophages. These results suggest that Gal-3 promotes a proinflammatory, classically activated macrophage phenotype in the liver during APAP-induced hepatotoxicity. Taken together, these studies indicate that multiple mechanisms contribute to proinflammatory macrophage activation following APAP intoxication.Ph. D.Includes bibliographical referencesIncludes vitaby Ana-Cristina Dragomi
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