Institution
University of Crete
Education•Rethymno, Greece•
About: University of Crete is a education organization based out in Rethymno, Greece. It is known for research contribution in the topics: Population & Galaxy. The organization has 8681 authors who have published 21684 publications receiving 709078 citations. The organization is also known as: Panepistimio Kritis.
Topics: Population, Galaxy, Cancer, Context (language use), Laser
Papers published on a yearly basis
Papers
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University of Southampton1, University of Paris2, Nestlé3, French Institute of Health and Medical Research4, The Coca-Cola Company5, University of Naples Federico II6, University of Düsseldorf7, Spanish National Research Council8, University of Crete9, Kraft Foods10, Sapienza University of Rome11, Maastricht University12, University of Helsinki13, University of Graz14
TL;DR: Potential mechanisms are described and research gaps, which limit the understanding of the interaction between diet and postprandial and chronic low-grade inflammation, are identified.
Abstract: Low-grade inflammation is a characteristic of the obese state, and adipose tissue releases many inflammatory mediators. The source of these mediators within adipose tissue is not clear, but infiltrating macrophages seem to be especially important, although adipocytes themselves play a role. Obese people have higher circulating concentrations of many inflammatory markers than lean people do, and these are believed to play a role in causing insulin resistance and other metabolic disturbances. Blood concentrations of inflammatory markers are lowered following weight loss. In the hours following the consumption of a meal, there is an elevation in the concentrations of inflammatory mediators in the bloodstream, which is exaggerated in obese subjects and in type 2 diabetics. Both high-glucose and high-fat meals may induce postprandial inflammation, and this is exaggerated by a high meal content of advanced glycation end products (AGE) and partly ablated by inclusion of certain antioxidants or antioxidant-containing foods within the meal. Healthy eating patterns are associated with lower circulating concentrations of inflammatory markers. Among the components of a healthy diet, whole grains, vegetables and fruits, and fish are all associated with lower inflammation. AGE are associated with enhanced oxidative stress and inflammation. SFA and trans-MUFA are pro-inflammatory, while PUFA, especially long-chain n-3 PUFA, are anti-inflammatory. Hyperglycaemia induces both postprandial and chronic low-grade inflammation. Vitamin C, vitamin E and carotenoids decrease the circulating concentrations of inflammatory markers. Potential mechanisms are described and research gaps, which limit our understanding of the interaction between diet and postprandial and chronic low-grade inflammation, are identified.
872 citations
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TL;DR: In this paper, the authors examined how bank's specific characteristics and the overall banking environment affect the profitability of commercial domestic and foreign banks operating in the 15 EU countries over the period 1995-2001.
860 citations
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University of Crete1, National and Kapodistrian University of Athens2, University of Paris3, Leiden University Medical Center4, Radboud University Nijmegen5, University of Barcelona6, Charité7, University of Padua8, RWTH Aachen University9, Cliniques Universitaires Saint-Luc10, Stanford University11, University College London12, University Medical Center Groningen13, Imperial College London14, Great Ormond Street Hospital15, University of Genoa16, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico17, Complutense University of Madrid18, University of Düsseldorf19, Charles University in Prague20, University of Porto21, Karolinska University Hospital22, Hannover Medical School23, University of Birmingham24
TL;DR: Recommendations for the management of lupus nephritis were developed using an evidence-based approach followed by expert consensus and there is no evidence to suggest that management of LN should differ in children versus adults.
Abstract: Objectives To develop recommendations for the management of adult and paediatric lupus nephritis (LN).
849 citations
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Max Planck Society1, United States Naval Research Laboratory2, University of California, San Diego3, German Aerospace Center4, Tel Aviv University5, University of Warsaw6, University of Crete7, Utrecht University8, Royal Netherlands Meteorological Institute9, National Oceanic and Atmospheric Administration10
TL;DR: The Mediterranean Intensive Oxidant Study, performed in the summer of 2001, uncovered air pollution layers from the surface to an altitude of 15 kilometers, causing air pollution standards to be exceeded throughout the region.
Abstract: The Mediterranean Intensive Oxidant Study, performed in the summer of 2001, uncovered air pollution layers from the surface to an altitude of 15 kilometers. In the boundary layer, air pollution standards are exceeded throughout the region, caused by West and East European pollution from the north. Aerosol particles also reduce solar radiation penetration to the surface, which can suppress precipitation. In the middle troposphere, Asian and to a lesser extent North American pollution is transported from the west. Additional Asian pollution from the east, transported from the monsoon in the upper troposphere, crosses the Mediterranean tropopause, which pollutes the lower stratosphere at middle latitudes.
844 citations
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TL;DR: Evidence that mitophagy is impaired in the hippocampus of AD patients, in induced pluripotent stem cell-derived human AD neurons, and in animal AD models is provided, suggesting that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis and thatMitophagy represents a potential therapeutic intervention.
Abstract: Accumulation of damaged mitochondria is a hallmark of aging and age-related neurodegeneration, including Alzheimer's disease (AD). The molecular mechanisms of impaired mitochondrial homeostasis in AD are being investigated. Here we provide evidence that mitophagy is impaired in the hippocampus of AD patients, in induced pluripotent stem cell-derived human AD neurons, and in animal AD models. In both amyloid-β (Aβ) and tau Caenorhabditis elegans models of AD, mitophagy stimulation (through NAD+ supplementation, urolithin A, and actinonin) reverses memory impairment through PINK-1 (PTEN-induced kinase-1)-, PDR-1 (Parkinson's disease-related-1; parkin)-, or DCT-1 (DAF-16/FOXO-controlled germline-tumor affecting-1)-dependent pathways. Mitophagy diminishes insoluble Aβ1-42 and Aβ1-40 and prevents cognitive impairment in an APP/PS1 mouse model through microglial phagocytosis of extracellular Aβ plaques and suppression of neuroinflammation. Mitophagy enhancement abolishes AD-related tau hyperphosphorylation in human neuronal cells and reverses memory impairment in transgenic tau nematodes and mice. Our findings suggest that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis and that mitophagy represents a potential therapeutic intervention.
842 citations
Authors
Showing all 8725 results
Name | H-index | Papers | Citations |
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Mercouri G. Kanatzidis | 152 | 1854 | 113022 |
T. J. Pearson | 150 | 895 | 126533 |
Stylianos E. Antonarakis | 138 | 746 | 93605 |
William Wijns | 127 | 752 | 95517 |
Andrea Comastri | 111 | 706 | 49119 |
Costas M. Soukoulis | 108 | 644 | 50208 |
Elias Anaissie | 107 | 372 | 42808 |
Jian Zhang | 107 | 3064 | 69715 |
Emmanouil T. Dermitzakis | 101 | 294 | 82496 |
Andreas Engel | 99 | 448 | 33494 |
Nikos C. Kyrpides | 96 | 711 | 62360 |
David J. Kerr | 95 | 544 | 39408 |
Manolis Kogevinas | 95 | 623 | 28521 |
Thomas Walz | 92 | 255 | 29981 |
Jean-Paul Latgé | 91 | 343 | 29152 |