Institution
Marche Polytechnic University
Education•Ancona, Italy•
About: Marche Polytechnic University is a education organization based out in Ancona, Italy. It is known for research contribution in the topics: Population & Cancer. The organization has 5905 authors who have published 15769 publications receiving 382286 citations. The organization is also known as: Universitá Politecnica delle Marche & Universita Politecnica delle Marche.
Topics: Population, Cancer, Medicine, Context (language use), Prostate cancer
Papers published on a yearly basis
Papers
More filters
••
TL;DR: In this paper, the experimental assessment of the yearly thermal performance of a green roof compared to other passive cooling technologies under temperate climate was carried out, where all roofs were installed on highly insulated slabs.
100 citations
••
Radboud University Nijmegen1, Lund University2, Autonomous University of Madrid3, Seconda Università degli Studi di Napoli4, University of Milan5, University of Brescia6, Istanbul University7, University of Copenhagen8, Rambam Health Care Campus9, University of Paris10, University of Pécs11, Sapienza University of Rome12, University of L'Aquila13, Marche Polytechnic University14, Humboldt University of Berlin15, University of Florence16, University of Cologne17
TL;DR: A simple prognostic model using three disease factors to predict 5-year survival at diagnosis in SSc showed reasonable performance upon validation in a European multicentre study.
Abstract: Objective Systemic sclerosis (SSc) is associated with a significant reduction in life expectancy. A simple prognostic model to predict 5-year survival in SSc was developed in 1999 in 280 patients, but it has not been validated in other patients. The predictions of a prognostic model are usually less accurate in other patients, especially from other centres or countries. A study was undertaken to validate the prognostic model to predict 5-year survival in SSc in other centres throughout Europe. Methods A European multicentre cohort of patients with SSc diagnosed before 2002 was established. Patients with SSc according to the preliminary American College of Rheumatology classification criteria were eligible for the study when they were followed for at least 5 years or shorter if they died. The primary outcome was 5-year survival after diagnosis of SSc. The predefined prognostic model uses the following baseline variables: age, gender, presence of urine protein, erythrocyte sedimentation rate (ESR) and carbon monoxide diffusing capacity (DLCO). Results Data were available for 1049 patients, 119 (11%) of whom died within 5 years after diagnosis. Of the patients, 85% were female, the mean (SD) age at diagnosis was 50 (14) years and 30% were classified as having diffuse cutaneous SSc. The prognostic model with age (OR 1.03), male gender (OR 1.93), urine protein (OR 2.29), elevated ESR (1.89) and low DLCO (OR 1.94) had an area under the receiver operating characteristic curve of 0.78. Death occurred in 12 (2.2%) of 509 patients with no risk factors, 45 (13%) of 349 patients with one risk factor, 55 (33%) of 168 patients with two risk factors and 7 (30%) of 23 patients with three risk factors. Conclusion A simple prognostic model using three disease factors to predict 5-year survival at diagnosis in SSc showed reasonable performance upon validation in a European multicentre study.
100 citations
••
07 Oct 2014TL;DR: Age-related increase in plasma miR-126-3p found in CTRs was paralleled by a 5/6-fold increase in intra/extracellular miR+3p in in vitro-cultured HUVECs undergoing senescence, likely a senescENCE-associated compensatory mechanism that is blunted when endothelial cells are exposed to high glucose levels, a phenomenon that probably occurs in vivo in T2DM patients.
Abstract: Circulating miR-126-3p levels were determined in 136 healthy subjects (CTRs) aged 20-90 years and 193 patients with type-2 diabetes mellitus (T2DMs) aged 40-80 years, to explore the combined effect of age and glycemic state on miR-126-3p expression. Moreover, intra/extracellular miR-126-3p levels were measured in human endothelial cells (HUVECs) undergoing senescence under normo/hyper-glycemic conditions.
Plasma miR-126-3p was significantly higher in the oldest compared with the youngest CTRs ( 75 years; relative expression: 0.27±0.29 vs. 0.48±0.39, p=0.047). Age-based comparison between CTRs and T2DM demonstrated significantly different miR-126-3p levels only in the oldest (0.48±0.39 vs. 0.22±0.23, p<0.005). After multiple adjustments, miR-126-3p levels were seen to be lower in patients with poor glycemic control, compared with age-matched CTRs.
The age-related increase in plasma miR-126-3p found in CTRs was paralleled by a 5/6-fold increase in intra/extracellular miR-126-3p in in vitro-cultured HUVECs undergoing senescence. Notably, significant down-regulation of SPRED-1 protein, a validated miR-126-3p target, was found in senescent HUVECs. Moreover, miR-126-3p expression was down-regulated in intermediate-age HUVECs grown in high-glucose medium until senescence.
Aging/senescence-associated miR-126-3p up-regulation is likely a senescence-associated compensatory mechanism that is blunted when endothelial cells are exposed to high glucose levels, a phenomenon that probably occurs in vivo in T2DM patients.
100 citations
••
TL;DR: The antioxidant activity of Cuban monofloral honeys appeared to be a result of the combined activity of a range of compounds including phenolics and other minor components, including three glycosylated derivatives.
Abstract: Five typical Cuban monofloral honeys were analyzed for their in vitro total antioxidant capacity (TAC), phenolic compounds, and ascorbic acid content. Identification and quantification of phenolics were carried out by HPLC-DAD-ESI/MS. Fourteen phenolic compounds could be identified (eight phenolic acids and six flavonoids), including three glycosylated derivatives. Similar contents of total phenolics were found in the different honeys, although they differed in their qualitative profiles. A significant (positive) correlation was found between the results of TAC obtained by parallel FIA-ABTS system and ORAC assay (r=0.9565, p<0.001). Similar correlations were also established between total phenolics and TAC, determined by either the ORAC (r=0.9633; p
100 citations
••
TL;DR: Evidence is obtained that defective glutamate clearance can account for most of the facilitation of CSD initiation in FHM2‐knockin mice, pointing to excessive glutamatergic transmission as a key mechanism underlying the vulnerability to CSD ignition in migraine.
Abstract: Migraine is a common disabling brain disorder. A subtype of migraine with aura (familial hemiplegic migraine type 2: FHM2) is caused by loss-of-function mutations in α2 Na(+),K(+) ATPase (α2 NKA), an isoform almost exclusively expressed in astrocytes in adult brain. Cortical spreading depression (CSD), the phenomenon that underlies migraine aura and activates migraine headache mechanisms, is facilitated in heterozygous FHM2-knockin mice with reduced expression of α2 NKA The mechanisms underlying an increased susceptibility to CSD in FHM2 are unknown. Here, we show reduced rates of glutamate and K(+) clearance by cortical astrocytes during neuronal activity and reduced density of GLT-1a glutamate transporters in cortical perisynaptic astrocytic processes in heterozygous FHM2-knockin mice, demonstrating key physiological roles of α2 NKA and supporting tight coupling with GLT-1a. Using ceftriaxone treatment of FHM2 mutants and partial inhibition of glutamate transporters in wild-type mice, we obtain evidence that defective glutamate clearance can account for most of the facilitation of CSD initiation in FHM2-knockin mice, pointing to excessive glutamatergic transmission as a key mechanism underlying the vulnerability to CSD ignition in migraine.
99 citations
Authors
Showing all 6013 results
Name | H-index | Papers | Citations |
---|---|---|---|
Jonathan I. Epstein | 138 | 1121 | 80975 |
Antoni Ribas | 132 | 660 | 99227 |
Francesco Fiori | 128 | 1032 | 76699 |
Claudio Franceschi | 120 | 856 | 59868 |
Robert E. Coleman | 103 | 724 | 49796 |
Carmine Zoccali | 99 | 813 | 36774 |
Massimo Falconi | 94 | 667 | 41966 |
Mario Plebani | 91 | 1329 | 43055 |
Roberto Danovaro | 84 | 415 | 23735 |
Rodolfo Montironi | 83 | 958 | 30957 |
Diego Centonze | 81 | 463 | 22857 |
Saverio Cinti | 78 | 256 | 32760 |
Michele Brignole | 76 | 399 | 26758 |
Jürgen P. Rabe | 76 | 391 | 20174 |
Jean-Jacques Body | 70 | 384 | 19608 |