Institution
University of Patras
Education•Pátrai, Greece•
About: University of Patras is a education organization based out in Pátrai, Greece. It is known for research contribution in the topics: Population & Catalysis. The organization has 13372 authors who have published 31263 publications receiving 677159 citations. The organization is also known as: Panepistímio Patrón.
Topics: Population, Catalysis, Finite element method, Nonlinear system, Graphene
Papers published on a yearly basis
Papers
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Technical University of Denmark1, Simon Fraser University2, University of Southern California3, National Renewable Energy Laboratory4, University of Denver5, University of Texas at Dallas6, University of North Texas7, University of Florida8, University of Pittsburgh9, Eindhoven University of Technology10, Linköping University11, Katholieke Universiteit Leuven12, IMEC13, École Polytechnique Fédérale de Lausanne14, University of Patras15, Ben-Gurion University of the Negev16, Alcan17
TL;DR: A round robin for the performance of roll-to-roll coated flexible large-area polymer solarcell modules involving 18 different laboratories in Northern America, Europe and Middle East is presented in this paper.
220 citations
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TL;DR: In this paper, a cross-comparative study of the societal and technical barriers of nZEB implementation in 7 Southern European countries is presented, and the authors provide recommendations for actions to shift the identified gaps into opportunities for future development of climate adaptive high performance buildings.
220 citations
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TL;DR: The findings indicate that in patients with AS, circulating bone formation-promoting factors functionally prevail, which can be at least partially attributed to decreased Dkk-1-mediated inhibition.
Abstract: Objective
Dkk-1 is an inhibitory molecule that regulates the Wnt pathway, which controls osteoblastogenesis. This study was undertaken to explore the potential role of Dkk-1 in ankylosing spondylitis (AS), a prototypical bone-forming disease.
Methods
Serum Dkk-1 levels were measured in 45 patients with AS, 45 patients with rheumatoid arthritis (RA), 15 patients with psoriatic arthritis (PsA), and 50 healthy subjects by sandwich enzyme-linked immunosorbent assay (ELISA). A functional ELISA was used to assess the binding of Dkk-1 to its receptor (low-density lipoprotein receptor–related protein 6). Furthermore, we studied the effect of sera from patients with AS and healthy subjects on the activity of the Wnt pathway in the Jurkat T cell model, with and without a neutralizing anti–Dkk-1 monoclonal antibody, by Western immunoblotting.
Results
Serum Dkk-1 levels were significantly increased in patients with AS (mean ± SEM 2,730 ± 135.1 pg/ml) as compared with normal subjects (P = 0.040), patients with RA (P = 0.020), and patients with PsA (P = 0.049). Patients with AS receiving anti–tumor necrosis factor α (anti-TNFα) treatment had significantly higher serum Dkk-1 levels than patients with AS not receiving such treatment (P = 0.007). Patients with AS studied serially prior to and following anti-TNFα administration exhibited a significant increase in serum Dkk-1 levels (P = 0.020), in contrast to patients with RA, who exhibited a dramatic decrease (P < 0.001). Jurkat cells treated with serum from AS patients exhibited increased Wnt signaling compared with cells treated with control serum. In that system, Dkk-1 blockade significantly enhanced Wnt signaling in control serum–treated, but not AS serum–treated, Jurkat T cells.
Conclusion
Our findings indicate that in patients with AS, circulating bone formation–promoting factors functionally prevail. This can be at least partially attributed to decreased Dkk-1–mediated inhibition.
219 citations
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University Hospital of Lausanne1, Harvard University2, University of Patras3, University of Colorado Boulder4, New York University5, University of California, San Francisco6, Technical University of Denmark7, Boston Children's Hospital8, Broad Institute9, Poznan University of Medical Sciences10, Helsinki University Central Hospital11, Newcastle University12, Sofia Medical University13, Brigham and Women's Hospital14, Centre Hospitalier Universitaire Sainte-Justine15, University of British Columbia16
TL;DR: It is hypothesized that mutations in genes encoding a broader range of modulators of the FGFR1 pathway might contribute to the genetics of CHH as causal or modifier mutations and validate the ability of a bioinformatics algorithm on the basis of protein-protein interactome data (interactome-based affiliation scoring [IBAS]) to identify high-quality candidate genes.
Abstract: Congenital hypogonadotropic hypogonadism (CHH) and its anosmia-associated form (Kallmann syndrome [KS]) are genetically heterogeneous. Among the >15 genes implicated in these conditions, mutations in FGF8 and FGFR1 account for ∼12% of cases; notably, KAL1 and HS6ST1 are also involved in FGFR1 signaling and can be mutated in CHH. We therefore hypothesized that mutations in genes encoding a broader range of modulators of the FGFR1 pathway might contribute to the genetics of CHH as causal or modifier mutations. Thus, we aimed to (1) investigate whether CHH individuals harbor mutations in members of the so-called "FGF8 synexpression" group and (2) validate the ability of a bioinformatics algorithm on the basis of protein-protein interactome data (interactome-based affiliation scoring [IBAS]) to identify high-quality candidate genes. On the basis of sequence homology, expression, and structural and functional data, seven genes were selected and sequenced in 386 unrelated CHH individuals and 155 controls. Except for FGF18 and SPRY2, all other genes were found to be mutated in CHH individuals: FGF17 (n = 3 individuals), IL17RD (n = 8), DUSP6 (n = 5), SPRY4 (n = 14), and FLRT3 (n = 3). Independently, IBAS predicted FGF17 and IL17RD as the two top candidates in the entire proteome on the basis of a statistical test of their protein-protein interaction patterns to proteins known to be altered in CHH. Most of the FGF17 and IL17RD mutations altered protein function in vitro. IL17RD mutations were found only in KS individuals and were strongly linked to hearing loss (6/8 individuals). Mutations in genes encoding components of the FGF pathway are associated with complex modes of CHH inheritance and act primarily as contributors to an oligogenic genetic architecture underlying CHH.
219 citations
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TL;DR: It is demonstrated that short-term exposure to cold, as well as β3-adrenergic stimulation, causes a significant induction of FGF21 mRNA levels in BAT, without a concomitant increase in FGF 21 plasma levels.
Abstract: Fibroblast growth factor-21 (FGF21) is a pleiotropic protein involved in glucose, lipid metabolism and energy homeostasis, with main tissues of expression being the liver and adipose tissue. Brown adipose tissue (BAT) is responsible for cold-induced thermogenesis in rodents. The role of FGF21 in BAT biology has not been investigated. In the present study, wild-type C57BL/6J mice as well as a brown adipocyte cell line were used to explore the potential role of cold exposure and β3-adrenergic stimulation in the expression of FGF21 in BAT. Our results demonstrate that short-term exposure to cold, as well as β3-adrenergic stimulation, causes a significant induction of FGF21 mRNA levels in BAT, without a concomitant increase in FGF21 plasma levels. This finding opens new routes for the potential use of pharmaceuticals that could induce FGF21 and, hence, activate BAT thermogenesis.
219 citations
Authors
Showing all 13529 results
Name | H-index | Papers | Citations |
---|---|---|---|
Thomas J. Meyer | 120 | 1078 | 68519 |
Thoralf M. Sundt | 112 | 755 | 55708 |
Chihaya Adachi | 112 | 908 | 61403 |
Eleftherios P. Diamandis | 110 | 1064 | 52654 |
Roland Siegwart | 105 | 1154 | 51473 |
T. Geralis | 99 | 808 | 52221 |
Spyros N. Pandis | 97 | 377 | 51660 |
Michael Tsapatsis | 77 | 375 | 20051 |
George K. Karagiannidis | 76 | 653 | 24066 |
Eleftherios Mylonakis | 75 | 448 | 21413 |
Matthias Mörgelin | 75 | 332 | 18711 |
Constantinos C. Stoumpos | 75 | 194 | 27991 |
Raymond Alexanian | 75 | 211 | 21923 |
Mark J. Ablowitz | 74 | 374 | 27715 |
John Lygeros | 73 | 667 | 21508 |