Seismic Response of Bridges Accounting for Soil-Structure Interaction effects and the Non-Synchronous Ground Motion due to 1D and 2D site analysis.

This work focuses on the effects of soil-structure interaction and the spatial variability of seismic motion due to site effects on the seismic response of a multi-span viaduct on pile foundations. In particular, site effects induced in a soft clay deposit by an inclined bedrock layout are evaluated through different models, characterised by an increasing level of accuracy, which allows determining the free-field motion that is adopted to perform soilstructure interaction analyses in the frame of the substructure approach. The seismic input is represented at the outcropping bedrock by a set of suitably selected and scaled real accelerograms. After a brief presentation of the adopted numerical procedure, analyses results are presented focusing on both site and structural response. Amplifications effects obtained from simplified linear equivalent 1D and nonlinear 2D site response models are compared, discussing the applicability of the simplified approach. Structural responses, obtained by considering the non-synchronous motion resulting from the local stratigraphic conditions, in conjunction with soil-structure interaction effects, are shown in terms of piers displacement and ductility demands. Furthermore, the role of soil structure interaction is clarified comparing results with those obtained from fixed base bridge models, proving that its contribution is more significant if the simplified model for site response is adopted

Effects of Exercise on the Airways

In the last ten years, the effects of exercise on bronchial epithelial cells and inflammatory cells in the airways have been studied in detail, and such new information has been combined with previous knowledge on bronchial reactivity and asthma evoked by exercise in asthmatic patients and athletes. The resulting picture is very complex, and the potential clinical consequences are often contradictory, suggesting the opportunity to define different phenotypes of exercise-associated airway changes (Lee & Anderson, 1985; Haahtela et al., 2008; Moreira et al., 2011a). Studies in asthmatic athletes in the 90\u2019 had began to explore the possibility that airway inflammation might be involved in exercise-associated respiratory symptoms. However, studies in non-asthmatic athletes also found increased number of inflammatory cells not only at rest, but also after strenuous endurance exercise (Bonsignore et al., 2001). It was therefore hypothesized that endurance exercise may physiologically cause influx of inflammatory cells into the airways, associated with low or absent inflammatory activation (Bonsignore et al., 2003a). Subsequent studies in athletes and animal models have extended these finding, but the mechanisms of inflammatory cell recruitment into the airways and the tight control of inflammatory activation physiologically associated with exercise remain poorly understood. Exercise is a known cause of bronchoconstriction in asthmatic patients (Cabral et al., 1999) and athletes (Parsons & Mastronarde, 2005). A large number of asthmatic elite athletes participate to international top-level competitions, and guidelines regarding management of asthmatic athletes (Fitch et al., 2008) and rules on the use of anti-asthmatic drugs have been issued (World Anti-Doping Agency, WADA, Oct. 18 2010 report). However, exercise is a powerful physiologic stimulus for bronchodilatation, and some reports underlined that exercise training may actually downmodulate bronchial reactivity in normal subjects (Scichilone et al., 2005, 2010), asthmatic children (Bonsignore et al., 2008) and animal models of asthma (Hewitt et al., 2010). This chapter will summarize the changes induced by acute exercise and training in bronchial reactivity and airway cells in both humans and animal models. It will also discuss the changing paradigm regarding the impact of physical activity in patients with bronchial asthma, and the new perspectives of exercise-based rehabilitation in patients with respiratory diseases such as chronic obstructive pulmonary disease (COPD)

Endurance training: Is it bad for you?

Endurance exercise training exerts many positive effects on health, including improved metabolism, reduction of cardiovascular risk, and reduced all-cause and cardiovascular mortality. Intense endurance exercise causes mild epithelial injury and inflammation in the airways, but does not appear to exert detrimental effects on respiratory health or bronchial reactivity in recreational/ non-elite athletes. Conversely, elite athletes of both summer and winter sports show increased susceptibility to development of asthma, possibly related to environmental exposures to allergens or poor conditioning of inspired air, so that a distinct phenotype of “sports asthma” has been proposed to characterise such athletes, who more often practise aquatic and winter sports. Overall, endurance training is good for health but may become deleterious when performed at high intensity or volume

Bronchial epithelial damage after a half-marathon in nonasthmatic amateur runners

Am J Physiol Lung Cell Mol Physiol. 2010 Jun;298(6):L857-62. Epub 2010 Apr 2. Bronchial epithelial damage after a half-marathon in nonasthmatic amateur runners. Chimenti L, Morici G, Paternò A, Santagata R, Bonanno A, Profita M, Riccobono L, Bellia V, Bonsignore MR. SourceDept. Biomedico Di Medicina Interna & Specialistica, Section of Pneumology, Univ. of Palermo, Via Trabucco 180, 90146 Palermo, Italy. [email protected] Abstract High neutrophil counts in induced sputum have been found in nonasthmatic amateur runners at rest and after a marathon, but the pathogenesis of airway neutrophilia in athletes is still poorly understood. Bronchial epithelial damage may occur during intense exercise, as suggested by investigations conducted in endurance-trained mice and competitive human athletes studied under resting conditions. To gain further information on airway changes acutely induced by exercise, airway cell composition, apoptosis, IL-8 concentration in induced sputum, and serum CC-16 level were measured in 15 male amateur runners at rest (baseline) and shortly after a half-marathon. Different from results obtained after a marathon, neutrophil absolute counts were unchanged, whereas bronchial epithelial cell absolute counts and their apoptosis increased significantly (P < 0.01). IL-8 in induced sputum supernatants almost doubled postrace compared with baseline (P < 0.01) and correlated positively with bronchial epithelial cell absolute counts (R(2) = 0.373, P < 0.01). Serum CC-16 significantly increased after all races (P < 0.01). These data show mild bronchial epithelial cell injury acutely induced by intense endurance exercise in humans, extending to large airways the data obtained in peripheral airways of endurance-trained mice. Therefore, neutrophil influx into the airways of athletes may be secondary to bronchial epithelial damage associated with intense exercise. PMID:20363849[PubMed - indexed for MEDLINE

Lack of Dystrophin Affects Bronchial Epithelium in mdx Mice

Mild exercise training may positively affect the course of Duchenne Muscular Dystrophy (DMD). Training causes mild bronchial epithelial injury in both humans and mice, but no study assessed the effects of exercise in mdx mice, a well known model of DMD. The airway epithelium was examined in mdx (C57BL/10ScSn-Dmdmdx) mice, and in wild type (WT, C57BL/10ScSc) mice either under sedentary conditions (mdx-SD, WT-SD) or during mild exercise training (mdx-EX, WT-EX). At baseline, and after 30 and 45 days of training (5 d/wk for 6 weeks), epithelial morphology and markers of regeneration, apoptosis, and cellular stress were assessed. The number of goblet cells in bronchial epithelium was much lower in mdx than in WT mice under all conditions. At 30 days, epithelial regeneration (PCNA positive cells) was higher in EX than SD animals in both groups; however, at 45 days, epithelial regeneration decreased in mdx mice irrespective of training, and the percentage of apoptotic (TUNEL positive) cells was higher in mdx-EX than in WT-EX mice. Epithelial expression of HSP60 (marker of stress) progressively decreased, and inversely correlated with epithelial apoptosis (r=-0.66, P=0.01) only in mdx mice. Lack of dystrophin in mdx mice appears associated with defective epithelial differentiation, and transient epithelial regeneration during mild exercise training. Hence, lack of dystrophin might impair repair in bronchial epithelium, with potential clinical consequences in DMD patients

Exercise intolerance at high altitude (5050 m): critical power and W'

The relationship between work rate (WR) and its tolerable duration (t(LIM)) has not been investigated at high altitude (HA). At HA (5050 m) and at sea level (SL), six subjects therefore performed symptom-limited cycle-ergometry: an incremental test (IET) and three constant-WR tests (% of IET WR(max), HA and SL respectively: WR(1) 70±8%, 74±7%; WR(2) 86±14%, 88±10%; WR(3) 105±13%, 104±9%). The power asymptote (CP) and curvature constant (W') of the hyperbolic WR-t(LIM) relationship were reduced at HA compared to SL (CP: 81±21 vs. 123±38 W; W': 7.2±2.9 vs. 13.1±4.3 kJ). HA breathing reserve (estimated maximum voluntary ventilation minus end-exercise ventilation) was also compromised (WR(1): 25±25 vs. 50±18 l min(-1); WR(2): 4±23 vs. 38±23 l min(-1); WR(3): -3±18 vs. 32±24 l min(-1)) with near-maximal dyspnea levels (Borg) (WR(1): 7.2±1.2 vs. 4.8±1.3; WR(2): 8.8±0.8 vs. 5.3±1.2; WR(3): 9.3±1.0 vs. 5.3±1.5). The CP reduction is consistent with a reduced O(2) availability; that of W' with reduced muscle-venous O(2) storage, exacerbated by ventilatory limitation and dyspnea. Copyright © 2011 Elsevier B.V. All rights reserved

Reduction of mdx mouse muscle degeneration by low-intensity endurance exercise: a proteomic analysis in quadriceps muscle of exercised versus sedentary mdx mice

In our recent study was shown a significant recovery of damaged skeletal muscle of mice with x-linked muscular dystrophy (mdx) following low-intensity endurance exercise, probably by reducing the degeneration of dystrophic muscle. Consequently, in the present work we aimed to identify proteins involved in the observed reduction of degenerating fibers. To this end, we used proteomic analysis to evaluate changes in the protein profile of quadriceps dystrophic muscles of exercised versus sedentary mdx mice. Four protein spots were found to be significantly changed and were identified as three isoforms of Carbonic anhydrase 3 (CA3) and superoxide dismutase [Cu-Zn] (SODC). Protein levels of CA3 isoforms were significantly up-regulated in quadriceps of sedentary mdx mice and were completely restored to wild type mice values, both sedentary and exercised, in quadriceps of exercised mdx mice. Protein levels of SODC were down-regulated in quadriceps of sedentary mdx mice and were significantly restored to wild type mice values, both sedentary and exercised, in quadriceps of exercised mdx mice. Western blot data were in agreement with those obtained using proteomic analysis and revealed the presence of one more CA3 isoform that was significantly changed. Based on data found in the present study, it seems that low-intensity endurance exercise may in part contribute to reduce cell degeneration process in mdx muscles, by counteracting oxidative stress

Hemopoietic and angiogenetic progenitors in healthy athletes: different responses to endurance and maximal exercise

J Appl Physiol. 2010 Jul;109(1):60-7. Epub 2010 May 6. Hemopoietic and angiogenetic progenitors in healthy athletes: different responses to endurance and maximal exercise. Bonsignore MR, Morici G, Riccioni R, Huertas A, Petrucci E, Veca M, Mariani G, Bonanno A, Chimenti L, Gioia M, Palange P, Testa U. SourceBiomedical Department, Internal and Specialistic Medicine (DIBIMIS), Section of Pneumology, University of Palermo, Via Trabucco, 180, 90146 Palermo, Italy. [email protected] Abstract The effects of endurance or maximal exercise on mobilization of bone marrow-derived hemopoietic and angiogenetic progenitors in healthy subjects are poorly defined. In 10 healthy amateur runners, we collected venous blood before, at the end of, and the day after a marathon race (n = 9), and before and at the end of a 1.5-km field test (n = 8), and measured hemopoietic and angiogenetic progenitors by flow cytometry and culture assays, as well as plasma or serum concentrations of several cytokines/growth factors. After the marathon, CD34(+) cells were unchanged, whereas clonogenetic assays showed decreased number of colonies for both erythropoietic (BFU-E) and granulocyte-monocyte (CFU-GM) series, returning to baseline the morning post-race. Conversely, CD34(+) cells, BFU-E, and CFU-GM increased after the field test. Angiogenetic progenitors, assessed as CD34(+)KDR(+) and CD133(+)VE-cadherin(+) cells or as adherent cells in culture expressing endothelial markers, increased after both endurance and maximal exercise but showed a different pattern between protocols. Interleukin-6 increased more after the marathon than after the field test, whereas hepatocyte growth factor and stem cell factor increased similarly in both protocols. Plasma levels of angiopoietin (Ang) 1 and 2 increased after both types of exercise, whereas the Ang-1-to-Ang-2 ratio or vascular endothelial growth factor-A were little affected. These data suggest that circulating hemopoietic progenitors may be utilized in peripheral tissues during prolonged endurance exercise. Endothelial progenitor mobilization after exercise in healthy trained subjects appears modulated by the type of exercise. Exercise-induced increase in growth factors suggests a physiological trophic effect of exercise on the bone marrow. PMID:20448032[PubMed - indexed for MEDLINE