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Search Results: 1 - 10 of 8347 matches for " Fran?ois Maltais "
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Responsiveness of Various Exercise-Testing Protocols to Therapeutic Interventions in COPD
Benoit Borel,Steeve Provencher,Didier Saey,Franois Maltais
Pulmonary Medicine , 2013, DOI: 10.1155/2013/410748
Abstract: Exercise intolerance is a key element in the pathophysiology and course of Chronic Obstructive Pulmonary Disease (COPD). As such, evaluating exercise tolerance has become an important part of the management of COPD. A wide variety of exercise-testing protocols is currently available, each protocol having its own strengths and weaknesses relative to their discriminative, methodological, and evaluative characteristics. This paper aims to review the responsiveness of several exercise-testing protocols used to evaluate the efficacy of pharmacological and nonpharmacological interventions to improve exercise tolerance in COPD. This will be done taking into account the minimally important difference, an important concept in the interpretation of the findings about responsiveness of exercise testing protocols. Among the currently available exercise-testing protocols (incremental, constant work rate, or self-paced), constant work rate exercise tests (cycle endurance test and endurance shuttle walking test) emerge as the most responsive ones for detecting and quantifying changes in exercise capacity after an intervention in COPD. 1. Introduction Chronic airflow limitation is the defining physiological feature of Chronic Obstructive Pulmonary Disease (COPD) whose main symptom is dyspnea. Exercise intolerance is another major consequence of COPD, leading to a sedentary life style and poor quality of life [1, 2]. In fact, exercise intolerance is central to the progression of the downward spiral of COPD [3]. Considering the key role of exercise intolerance in the pathophysiology and course of COPD, the evaluation of exercise tolerance should now be included in the assessment of this disease [4], especially for the evaluation of the response to pharmacological and nonpharmacological interventions [5–7]. Also, the heterogeneity in the mechanisms of exercise intolerance in COPD highlights the importance of comprehensive exercise testing, assessing all systems potentially involved [8]. Exercise testing is currently included in the follow-up of chronic diseases like COPD. Exercise testing can be used to document the severity of pulmonary disease, the functional impact of altered respiratory function and to better understand the physiopathological mechanisms involved in exercise intolerance; this refers to the discriminative characteristic of the test. Exercise testing can also be used to quantify the impact of an intervention to improve exercise tolerance [9, 10] or dyspnea [11, 12] and in the preoperative and pre rehabilitation assessments of patients, corresponding to
Assessment of Daily Life Physical Activities in Pulmonary Arterial Hypertension
Vincent Mainguy, Steeve Provencher, Franois Maltais, Simon Malenfant, Didier Saey
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0027993
Abstract: Background In pulmonary arterial hypertension (PAH), the six-minute walk test (6MWT) is believed to be representative of patient's daily life physical activities (DLPA). Whether DLPA are decreased in PAH and whether the 6MWT is representative of patient's DLPA remain unknown. Methods 15 patients with idiopathic PAH (IPAH) and 10 patients with PAH associated with limited systemic sclerosis (PAH-SSc) were matched with 15 healthy control subjects and 10 patients with limited systemic sclerosis without PAH. Each subject completed a 6MWT. The mean number of daily steps and the mean energy expenditure and duration of physical activities >3 METs were assessed with a physical activity monitor for seven consecutive days and used as markers of DLPA. Results The mean number of daily steps and the mean daily energy expenditure and duration of physical activities >3 METs were all reduced in PAH patients compared to their controls (all p<0.05). The mean number of daily steps correlated with the 6MWT distance for both IPAH and PAH-SSc patients (r = 0.76, p<0.01 and r = 0.85, p<0.01), respectively. Conclusion DLPA are decreased in PAH and correlate with the 6MWT distance. Functional exercise capacity may thus be a useful surrogate of DLPA in PAH.
Physiological Correlates of Endurance Time Variability during Constant-Workrate Cycling Exercise in Patients with COPD
Isabelle Vivodtzev,Philippe Gagnon,Véronique Pepin,Didier Saey,Louis Laviolette,Cynthia Brouillard,Franois Maltais
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0017007
Abstract: The endurance time (Tend) during constant-workrate cycling exercise (CET) is highly variable in COPD. We investigated pulmonary and physiological variables that may contribute to these variations in Tend.
The impact of obesity on walking and cycling performance and response to pulmonary rehabilitation in COPD
Francesco Sava, Louis Laviolette, Sarah Bernard, Marie-Josée Breton, Jean Bourbeau, Franois Maltais
BMC Pulmonary Medicine , 2010, DOI: 10.1186/1471-2466-10-55
Abstract: 261 patients with COPD were divided into three groups: normal body mass index (BMI), overweight and obese. Baseline and post rehabilitation pulmonary function, 6-min walking test (6MWT), endurance time during a constant workrate exercise test (CET) and St. George's Respiratory Questionnaire (SGRQ) scores were compared between all three classes of BMI.At baseline, obese and overweight patients had less severe airflow obstruction compared to normal BMI patients. There was no baseline difference in CET performance or SGRQ scores across BMI classes and 6MWT was reduced in the presence of obesity (p < 0.01). Compared to baseline, post-rehabilitation 6MWT, CET performance and SGRQ scores improved significantly in each group (p < 0.01), but 6MWT was still significantly lower in the presence of obesity.Walking, but not cycling performance was worse in obese patients. This difference was maintained post rehabilitation despite significant improvements. Weight excess may counterbalance the effect of a better preserved respiratory function in the performance of daily activities such as walking. However, obesity and overweight did not influence the magnitude of improvement after pulmonary rehabilitation.Chronic obstructive pulmonary disease (COPD) is associated with dyspnea and exercise intolerance, two major impediments to quality of life. Although low body weight[1] and muscle wasting[2] have traditionally been the focus of nutritional management in COPD, recent data indicate that obesity is becoming frequent in this disease[3]. On one hand, a high body mass index (BMI) appears to convey a survival advantage to patients with COPD[1,4]. On the other hand, obesity by itself may compromise lung function[5], decrease exercise tolerance particularly during weight bearing activities[6,7], and quality of life[8], leading to greater disability[9,10].The effects of obesity in combination with COPD on exercise tolerance and dyspnea have received little attention. In one study, obese pat
Variability of protein level and phosphorylation status caused by biopsy protocol design in human skeletal muscle analyses
Marc-André Caron, Steve J Charette, Franois Maltais, Richard Debigaré
BMC Research Notes , 2011, DOI: 10.1186/1756-0500-4-488
Abstract: Akt and p70 S6K phosphorylation levels were increased by 83% when AF biopsy was compared to R1. Mob condition induced important phosphorylation of p70 S6K when compared to R2. Comparison of R1 and R2 biopsies revealed a relative stability of the signal for both total and phosphorylated proteins.This study highlights the importance to standardize muscle biopsy protocols in order to minimize the method-induced variation when analyzing Western blot signals.Skeletal muscle atrophy is a common clinical component of numerous diseases including AIDS, cancer, chronic heart failure, chronic obstructive pulmonary disease, and diabetes [1-3]. Muscle atrophy has a wide spectrum of consequences for chronically ill patients, ranging from an aggravated morbidity to a seriously impaired survival prognostic [4,5]. Since there is currently no effective treatment for atrophy [6], there is a crucial need for a clear comprehension of muscle depletion at the molecular level.Fundamentally, muscle mass maintenance relies on a tight regulation of protein synthesis and degradation, two fundamental processes influenced by numerous signaling pathways. The phosphatidylinositol-3 kinase/Akt pathway has been pointed out as a key coordinator of synthesis and degradation. Akt, the central protein of this pathway, is an upstream kinase to several targets implicated in both processes [7,8]. With the discovery of the muscle-specific E3 ligases Muscle RING finger 1 (MuRF1) and Muscle Atrophy F-box in 2001 [9], the ubiquitin-proteasome pathway has also emerged as an important putative player in the atrophying process. Historically, these two pathways have been predominantly investigated in cells and animal models. However, to ascertain consistency with human muscle biology, these pathways have been repeatedly studied directly in human samples [10,11].Human muscle samples required for biochemical studies have been obtained repeatedly with a Bergstr?m biopsy needle [12]. A concern with this technique is t
CD8 positive T cells express IL-17 in patients with chronic obstructive pulmonary disease
Ying Chang, Jessica Nadigel, Nicholas Boulais, Jean Bourbeau, Franois Maltais, David H Eidelman, Qutayba Hamid
Respiratory Research , 2011, DOI: 10.1186/1465-9921-12-43
Abstract: Bronchoscopic biopsies of the airway were obtained from 16 COPD subjects (GOLD stage 1-4) and 15 control subjects. Paraffin sections were used for the investigation of IL-17A and IL-17F expression in the airways by immunohistochemistry, and frozen sections were used for the immunofluorescence double staining of IL-17A or IL-17F paired with CD4 or CD8. In order to confirm the expression of IL-17A and IL-17F at the mRNA level, a quantitative RT-PCR was performed on the total mRNA extracted from entire section or CD8 positive cells selected by laser capture microdissection.IL-17F immunoreactivity was significantly higher in the bronchial biopsies of COPD patients compared to control subjects (P < 0.0001). In the submucosa, the absolute number of both IL-17A and IL-17F positive cells was higher in COPD patients (P < 0.0001). After adjusting for the total number of cells in the submucosa, we still found that more cells were positive for both IL-17A (P < 0.0001) and IL-17F (P < 0.0001) in COPD patients compared to controls. The mRNA expression of IL-17A and IL-17F in airways of COPD patients was confirmed by RT-PCR. The expression of IL-17A and IL-17F was co-localized with not only CD4 but also CD8, which was further confirmed by RT-PCR on laser capture microdissection selected CD8 positive cells.These findings support the notion that Th17 cytokines could play important roles in the pathogenesis of COPD, raising the possibility of using this mechanism as the basis for novel therapeutic approaches.Chronic obstructive pulmonary disease (COPD), a progressive and irreversible chronic inflammatory disease of the lung caused predominantly by cigarette smoking, is one of the most important causes of mortality globally [1]. The inflammatory response in the lungs of COPD patients has been found to be strongly linked to tissue destruction and alveolar airspace enlargement, which lead to disease progression [2].The inflammatory response reflects both the innate immune response to ci
Responsiveness of Various Exercise-Testing Protocols to Therapeutic Interventions in COPD
Benoit Borel,Steeve Provencher,Didier Saey,François Maltais
Pulmonary Medicine , 2013, DOI: 10.1155/2013/410748
Abstract:
Satellite Cells Senescence in Limb Muscle of Severe Patients with COPD
Marie-Eve Thériault, Marie-ève Paré, Franois Maltais, Richard Debigaré
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0039124
Abstract: Rationale The maintenance of peripheral muscle mass may be compromised in chronic obstructive pulmonary disease (COPD) due to premature cellular senescence and exhaustion of the regenerative potential of the muscles. Methods Vastus lateralis biopsies were obtained from patients with COPD (n = 16) and healthy subjects (n = 7). Satellite cell number and the proportion of central nuclei, as a marker of muscle regenerative events, were assessed on cryosections. Telomere lengths, used as a marker of cellular senescence, were determined using Southern blot analyses. Results Central nuclei proportion was significantly higher in patients with COPD with a preserved muscle mass compared to controls and patients with COPD with muscle atrophy (p<0.001). In COPD, maximal telomere length was significantly decreased compared to controls (p<0.05). Similarly, minimal telomere length was significantly reduced in GOLD III–IV patients with muscle atrophy compared to controls (p<0.005). Minimal, mean and maximum telomere lengths correlated with mid-thigh muscle cross-sectional area (MTCSA) (R = 0.523, p = 0.005; R = 0.435, p = 0.019 and R = 0.491, p = 0.009, respectively). Conclusions Evidence of increased regenerative events was seen in GOLD III–IV patients with preserved muscle mass. Shortening of telomeres in GOLD III–IV patients with muscle atrophy is consistent with an increased number of senescent satellite cells and an exhausted muscle regenerative capacity, compromising the maintenance of muscle mass in these individuals.
Effect of obesity on constant workrate exercise in hyperinflated men with COPD
Louis Laviolette, Francesco Sava, Denis E O'Donnell, Katherine A Webb, Alan L Hamilton, Steven Kesten, Franois Maltais
BMC Pulmonary Medicine , 2010, DOI: 10.1186/1471-2466-10-33
Abstract: Men with COPD and hyperinflation were divided according to World Health Organization BMI classification: 84 normal BMI (NBMI), 130 overweight (OW) and 64 obese (OB). Patients underwent spirometric and lung volumes assessment and an incremental cycling exercise test. This was followed by a constant workrate exercise test (CET) at 75% of peak capacity. Inspiratory capacity and Borg dyspnea scores were measured at baseline, during and at the end of CET.FEV1 % predicted was not different across BMI classes. Total lung capacity and functional residual capacity were significantly lower in OB and OW compared to NBMI patients. Peak VO2 in L·min-1 was significantly higher in OB and OW patients than in NBMI patients. CET time was not different across BMI classes (p = 0.11). Changes in lung volumes and dyspnea during CET were not different between BMI categories.OB and OW patients with COPD had a higher peak VO2 than their lean counterparts. Endurance time, dyspnea and changes in lung volumes during CET were similar between BMI categories.COPD is characterized by reduced exercise tolerance [1], which is determined by a multitude of factors whose individual contribution may vary between patients[2]. Obesity is now an important issue in COPD: it is reported in 18% [3] to 54% [4] of patients with COPD and is associated with a better prognosis[5,6]. Both conditions, when taken individually, are characterized by physiological alterations in breathing mechanics along with functional limitations. The precise combined effects of COPD and obesity on such a multidimensional issue as exercise tolerance remain ambiguous. Clinical experience dictates that their combination would lead to a worsening of functional limitations and symptoms[7,8]. However, there are complex interactions between the two conditions that could mitigate a negative synergic effect on exercise performance.On one hand, obesity is associated with an increased work of breathing [9], increased breathing resistive load [1
Cigarette smoke increases TLR4 and TLR9 expression and induces cytokine production from CD8+ T cells in chronic obstructive pulmonary disease
Jessica Nadigel, David Préfontaine, Carolyn J Baglole, Franois Maltais, Jean Bourbeau, David H Eidelman, Qutayba Hamid
Respiratory Research , 2011, DOI: 10.1186/1465-9921-12-149
Abstract: Endobronchial biopsies and peripheral blood were obtained from COPD patients and control subjects. TLR4 and TLR9 expression was assessed by immunostaining of lung tissue and flow cytometry of the peripheral blood. CD8+ T cells isolated from peripheral blood were treated with or without cigarette smoke condensate (CSC) as well as TLR4 and TLR9 inhibitors. PCR and western blotting were used to determine TLR4 and TLR9 expression, while cytokine secretion from these cells was detected using electrochemiluminescence technology.No difference was observed in the overall expression of TLR4 and TLR9 in the lung tissue and peripheral blood of COPD patients compared to control subjects. However, COPD patients had increased TLR4 and TLR9 expression on lung CD8+ T cells. Exposure of CD8+ T cells to CSC resulted in an increase of TLR4 and TLR9 protein expression. CSC exposure also caused the activation of CD8+ T cells, resulting in the production of IL-1β, IL-6, IL-10, IL-12p70, TNFα and IFNγ. Furthermore, inhibition of TLR4 or TLR9 significantly attenuated the production of TNFα and IL-10.Our results demonstrate increased expression of TLR4 and TLR9 on lung CD8+ T cells in COPD. CD8+ T cells exposed to CSC increased TLR4 and TLR9 levels and increased cytokine production. These results provide a new perspective on the role of CD8+ T cells in COPD.Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide [1], with more than 80% of COPD cases caused by cigarette smoking [2]. Chronic inflammation observed in COPD is characterized by pro-inflammatory cytokine production and recruitment of several cell types to the lungs, including cells of the innate immune response, such as neutrophils and macrophages [3], as well as those of adaptive immune response, namely T and B lymphocytes [4,5]. CD8+ T cells are regarded as a hallmark cell of COPD, and are increased in both the central [6] and peripheral [7] airways of COPD patients. CD8+ T cells foun
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