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University of Ioannina

EducationIoannina, Greece
About: University of Ioannina is a education organization based out in Ioannina, Greece. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 7654 authors who have published 20594 publications receiving 671560 citations. The organization is also known as: Panepistimio Ioanninon.


Papers
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Journal ArticleDOI
TL;DR: In this article, a unified approach to improved L p Hardy inequalities in R N was presented, where Hardy potentials that involve either the distance from a point, or distance from the boundary, or even the intermediate case where the distance is taken from a surface of codimension 1 < k < N were considered.
Abstract: We present a unified approach to improved L p Hardy inequalities in R N . We consider Hardy potentials that involve either the distance from a point, or the distance from the boundary, or even the intermediate case where the distance is taken from a surface of codimension 1 < k < N. In our main result, we add to the right hand side of the classical Hardy inequality a weighted L p norm with optimal weight and best constant. We also prove nonhomogeneous improved Hardy inequalities, where the right hand side involves weighted L q norms, q ¬= p.

253 citations

Journal ArticleDOI
Valérie Turcot1, Yingchang Lu2, Yingchang Lu3, Heather M. Highland4  +486 moreInstitutions (129)
TL;DR: Exome-wide analysis identifies rare and low-frequency coding variants associated with body mass index that confirm enrichment of neuronal genes and provide new evidence for adipocyte and energy expenditure biology, widening the potential of genetically supported therapeutic targets in obesity.
Abstract: Genome-wide association studies (GWAS) have identified >250 loci for body mass index (BMI), implicating pathways related to neuronal biology. Most GWAS loci represent clusters of common, noncoding variants from which pinpointing causal genes remains challenging. Here we combined data from 718,734 individuals to discover rare and low-frequency (minor allele frequency (MAF) < 5%) coding variants associated with BMI. We identified 14 coding variants in 13 genes, of which 8 variants were in genes (ZBTB7B, ACHE, RAPGEF3, RAB21, ZFHX3, ENTPD6, ZFR2 and ZNF169) newly implicated in human obesity, 2 variants were in genes (MC4R and KSR2) previously observed to be mutated in extreme obesity and 2 variants were in GIPR. The effect sizes of rare variants are ~10 times larger than those of common variants, with the largest effect observed in carriers of an MC4R mutation introducing a stop codon (p.Tyr35Ter, MAF = 0.01%), who weighed ~7 kg more than non-carriers. Pathway analyses based on the variants associated with BMI confirm enrichment of neuronal genes and provide new evidence for adipocyte and energy expenditure biology, widening the potential of genetically supported therapeutic targets in obesity.

252 citations

Journal ArticleDOI
TL;DR: Chronic psychosocial stress, in the presence of physical inactivity, is likely to contribute to the epidemic of cardiometabolic and emotional disease of the current society and the way to prevent and combat this burden is by regular exercise.
Abstract: The human body, when under threat, elicits a set of neuroendocrine responses, including an increased secretion of glucocorticoids (GCs) and catecholamines from the adrenal gland and the activation of the sympathetic nervous system. These hormonal secretions allow a "fight or flight" response by mobilizing endogenous substrate and inducing a state of insulin resistance in the liver and skeletal muscles. Although the stress response was essential in ancient times to survive physical aggression, this threat has disappeared in our industrialized societies. However, in today's environment, the same stress responses can be elicited by emotional stimuli or professional and social stress. Such psychological stress may be protracted and unrelated to an increased metabolic demand. Thus, the energy mobilized is not used but is stored in visceral fat depots by the combined action of hypercortisolism and hyperinsulinemia. In addition, chronic activation of the stress system causes suppression of the gonadal, growth hormone (GH), and thyroid axes. These metabolic disturbances, in concert, lead to the clinical expression of a number of comorbidities including central obesity, hypertension, dyslipidemia, and endothelial dysfunction, all components of the metabolic syndrome and cardiometabolic risk factors. Moreover, chronic stress has deleterious effects on the brain and, in particular, affects hippocampal structure and function leading to cognitive and mood disturbances. Importantly, this stress-induced clinical phenotype is likely to be exaggerated in the presence of physical inactivity, resulting in a "stress-induced/exercise deficient" phenotype. Assuming that the stress response is a neuroendocrine mechanism that occurs in anticipation of physical action, then physical activity should be the natural means to prevent the consequences of stress. Indeed, accumulating evidence documents the beneficial effects of regular exercise in preventing or ameliorating the metabolic and psychological comorbidities induced by chronic stress. These benefits are thought to derive from a central effect of exercise to reduce the sensitivity to stress and also peripheral actions influencing metabolic functions and, in particular, insulin sensitivity and the partitioning of fuels toward oxidation rather than storage. It is concluded that chronic psychosocial stress, in the presence of physical inactivity, is likely to contribute to the epidemic of cardiometabolic and emotional disease of our current society. The way to prevent and combat this burden is by regular exercise.

252 citations

Journal ArticleDOI
TL;DR: Inhibition of the aromatase system, in particular with third-generation aromatases inhibitors and inactivators, appears to be associated with statistically significant improved survival of patients with advanced breast cancer compared with standard hormonal treatments.
Abstract: Background: Aromatase inhibitors and inactivators have been extensively tested in patients with advanced breast cancer, but it is unclear whether they offer any survival benefi ts compared with standard hormonal treatment with tamoxifen or progestagens. We performed a meta-analysis of randomized controlled trials that compared several generations of aromatase inhibitors and inactivators with standard hormonal treatment in patients with advanced breast cancer. Methods: The endpoint that we assessed was survival. Trials were located through searches of PubMed and Cochrane Library (last update March 2006). Relative hazards (RHs) were summarized across trials through fi xed- and randomeffects analyses, and heterogeneity was assessed with the Q and I 2 statistics. All statistical tests were two-sided. Results: Twenty-fi ve different comparisons, with a total of 8504 patients, were included in the meta-analysis. We found statistically signifi cant survival benefi ts with third-generation aromatase inhibitors and inactivators (vorozole, letrozole, examestane, and anastrazole) (RH = 0.87, 95% confi dence interval [CI] = 0.82 to 0.93; P <.001) but not with fi rst-generation (aminoglutethimide) or second-generation (formestane and fadrozole) agents. The difference in the summary effects between these two groups of trials was statistically signifi cant ( P = .04). The survival benefi t with third-generation agents in fi rst-line trials, in which these agents were compared with tamoxifen (11% RH reduction, 95% CI = 1% to 19%; P = .03), was identical to their benefi t in second- and subsequentline trials in which these agents were compared with other treatments (14% RH reduction, 95% CI = 6% to 21%; P <.001). Conclusions: Inhibition of the aromatase system, in particular with third-generation aromatase inhibitors and inactivators, appears to be associated with statistically signifi cant improved survival of patients with advanced breast cancer compared with standard hormonal treatments. [J Natl Cancer Inst 2006;98: 1285 – 91 ]

252 citations

Journal ArticleDOI
TL;DR: Two watermarking approaches that are robust to geometric distortions are presented, one based on image normalization, and the other based on a watermark resynchronization scheme aimed to alleviate the effects of random bending attacks.
Abstract: In this paper, we present two watermarking approaches that are robust to geometric distortions. The first approach is based on image normalization, in which both watermark embedding and extraction are carried out with respect to an image normalized to meet a set of predefined moment criteria. We propose a new normalization procedure, which is invariant to affine transform attacks. The resulting watermarking scheme is suitable for public watermarking applications, where the original image is not available for watermark extraction. The second approach is based on a watermark resynchronization scheme aimed to alleviate the effects of random bending attacks. In this scheme, a deformable mesh is used to correct the distortion caused by the attack. The watermark is then extracted from the corrected image. In contrast to the first scheme, the latter is suitable for private watermarking applications, where the original image is necessary for watermark detection. In both schemes, we employ a direct-sequence code division multiple access approach to embed a multibit watermark in the discrete cosine transform domain of the image. Numerical experiments demonstrate that the proposed watermarking schemes are robust to a wide range of geometric attacks.

252 citations


Authors

Showing all 7724 results

NameH-indexPapersCitations
John P. A. Ioannidis1851311193612
Kay-Tee Khaw1741389138782
Elio Riboli1581136110499
Mercouri G. Kanatzidis1521854113022
Dimitrios Trichopoulos13581884992
Gyorgy Vesztergombi133144494821
Niki Saoulidou132106581154
Apostolos Panagiotou132137088647
Ioannis Evangelou131122582178
Ioannis Papadopoulos129120185576
Nikolaos Manthos129125681865
Panagiotis Kokkas128123481051
Costas Foudas128111283048
Zoltan Szillasi128121484392
Matthias Schröder126142182990
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202335
2022131
20211,222
20201,203
20191,125
20181,003