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1.  Reduced myotube diameter, atrophic signalling and elevated oxidative stress in cultured satellite cells from COPD patients 
The mechanisms leading to skeletal limb muscle dysfunction in chronic obstructive pulmonary disease (COPD) have not been fully elucidated. Exhausted muscle regenerative capacity of satellite cells has been evocated, but the capacity of satellite cells to proliferate and differentiate properly remains unknown. Our objectives were to compare the characteristics of satellite cells derived from COPD patients and healthy individuals, in terms of proliferative and differentiation capacities, morphological phenotype and atrophy/hypertrophy signalling, and oxidative stress status. Therefore, we purified and cultivated satellite cells from progressively frozen vastus lateralis biopsies of eight COPD patients and eight healthy individuals. We examined proliferation parameters, differentiation capacities, myotube diameter, expression of atrophy/hypertrophy markers, oxidative stress damages, antioxidant enzyme expression and cell susceptibility to H2O2 in cultured myoblasts and/or myotubes. Proliferation characteristics and commitment to terminal differentiation were similar in COPD patients and healthy individuals, despite impaired fusion capacities of COPD myotubes. Myotube diameter was smaller in COPD patients (P = 0.015), and was associated with a higher expression of myostatin (myoblasts: P = 0.083; myotubes: P = 0.050) and atrogin-1 (myoblasts: P = 0.050), and a decreased phospho-AKT/AKT ratio (myoblasts: P = 0.022). Protein carbonylation (myoblasts: P = 0.028; myotubes: P = 0.002) and lipid peroxidation (myotubes: P = 0.065) were higher in COPD cells, and COPD myoblasts were significantly more susceptible to oxidative stress. Thus, cultured satellite cells from COPD patients display characteristics of morphology, atrophic signalling and oxidative stress similar to those described in in vivo COPD skeletal limb muscles. We have therefore demonstrated that muscle alteration in COPD can be studied by classical in vitro cellular models.
PMCID: PMC4288361  PMID: 25339614
COPD; muscle dysfunction; cellular model; atrophy; oxidative stress; satellite cells
2.  A short questionnaire for the assessment of quality of life in patients with chronic obstructive pulmonary disease: psychometric properties of VQ11 
There is a need for a validated short instrument that can be used in routine practice to quantify potential short-term change in Health-Related Quality of Life (HRQoL) in patients with chronic obstructive pulmonary disease (COPD). Our aim is to determine the validity and reliability of the VQ11 questionnaire dedicated to the routine assessment of HRQoL.
181 COPD patients (40–85 yrs, I to IV GOLD stages) completed the VQ11, and several tests. One week later, 49 of these patients completed the VQ11 again.
Confirmatory factor analysis supported the two-level hierarchical structure of the VQ11 with 11 items covering three components and HRQoL at a higher level. The VQ11 showed good internal consistency and good reproducibility (r = 0.88). Concurrent validity showed significant correlations between VQ11 total scores and St George’s Respiratory Questionnaire-C (r = 0.70), Short Form-36 (r = -0.66 for the physical component and -0.63 for the mental component). We obtained significant correlations with MRC Dyspnea Grades (r = 0.59), the Hospital Anxiety and Depression Scale total score (r = 0.62), and the BODE index (r = 0.53).
The VQ11 has good measurement properties and provides a valid and reliable measure of COPD-specific HRQoL. It is ready for use in routine practice.
Clinical registration
The study was approved by the University of Montpellier 1 Ethics Committee and the Regional Ethics Committee (authorization number: A00332-53).
PMCID: PMC3842624  PMID: 24160852
Chronic obstructive pulmonary disease; Brief questionnaire; Health-related quality of life; Validity; VQ11
3.  Systems medicine and integrated care to combat chronic noncommunicable diseases 
Genome Medicine  2011;3(7):43.
We propose an innovative, integrated, cost-effective health system to combat major non-communicable diseases (NCDs), including cardiovascular, chronic respiratory, metabolic, rheumatologic and neurologic disorders and cancers, which together are the predominant health problem of the 21st century. This proposed holistic strategy involves comprehensive patient-centered integrated care and multi-scale, multi-modal and multi-level systems approaches to tackle NCDs as a common group of diseases. Rather than studying each disease individually, it will take into account their intertwined gene-environment, socio-economic interactions and co-morbidities that lead to individual-specific complex phenotypes. It will implement a road map for predictive, preventive, personalized and participatory (P4) medicine based on a robust and extensive knowledge management infrastructure that contains individual patient information. It will be supported by strategic partnerships involving all stakeholders, including general practitioners associated with patient-centered care. This systems medicine strategy, which will take a holistic approach to disease, is designed to allow the results to be used globally, taking into account the needs and specificities of local economies and health systems.
PMCID: PMC3221551  PMID: 21745417
4.  Does Prior Training Affect Acute O2 Supply Responses During Exercise in Desaturator COPD Patients? 
This study investigated the effects of a prior individualized training program (TP) on the response to acute oxygen supply during exercise in chronic obstructive pulmonary disease (COPD) patients showing exercise-induced desaturation.
Twenty-two COPD patients (mean [SD] FEV1 = 52.1 [3]% predicted) who desaturated on exercise participated in a TP. Exercise tolerance while breathing compressed air or oxygen was assessed using a walking test (WT) before and after TP. Oxygen flow was individualized.
Before TP, acute oxygen supply improved mean exercise tolerance. But this response was heterogeneous as only 8 patients increased their walking distance with oxygen. TP improved exercise tolerance in the entire population. However, a greater affect of oxygen administration during exercise was not observed after TP. The response to oxygen again showed great disparity as only 6 patients increased their walking distance with oxygen after TP.
The response to oxygen supply during exercise varied among COPD patients. Moreover, despite the clinical benefits of TP, no cumulative effect of TP and oxygen supply was observed during exercise performance.
PMCID: PMC2606654  PMID: 19340322
COPD; training program; oxygen; exercise.
5.  The effect of respiratory muscle training with CO2 breathing on cellular adaptation of mdx mouse diaphragm 
Neuromuscular Disorders   2005;15(6):427-436.
The aim of our study was to investigate the cellular mechanisms induced by hypercapnic stimulation of ventilation, during 6 weeks/30 min per day, in 10 mdx and 8 C57BL10 mice (10G0.2 months old). Ten mdx and eight C57BL10 mice served as control group. This respiratory training increases in vitro maximal tetanic tension of the diaphragm only in mdx mice. Western blot analysis of diaphragm showed: (1) an over-expression of a-dystrobrevin in mdx and C57BL10 training group compared to control group (8100G710 versus 6100G520 and 2800G400 versus 2200G250 arbitrary units); (2) a decrease in utrophin expression only in mdx training group compared to control group (2100G320 versus 3100G125 arbitrary units). Daily respiratory muscle training in mdx mice, induces a beneficial effect on diaphragm strength, with an over-expression of a-dystrobrevin. Further studies are needed to determine if, in absence of dystrophin, the over-expression of a-dystrobrevin could be interpreted as a possible pathway to improve function of dystrophic muscle.
PMCID: PMC1978214  PMID: 15907290
Ventilatory responses; Hypercapnia; alpha-dystrobrevin; Utrophin; Adaptation, Physiological; Animals; Blotting, Western; Body Weight; Breathing Exercises; Carbon Dioxide; pharmacology; Citrate (si)-Synthase; metabolism; Diaphragm; cytology; physiology; Dystrophin; metabolism; Dystrophin-Associated Proteins; metabolism; Female; Hematoxylin; Hypercapnia; physiopathology; Hyperventilation; physiopathology; Isometric Contraction; physiology; Male; Mice; Mice, Inbred C57BL; Mice, Inbred mdx; Muscle Fibers; metabolism; Muscular Dystrophy, Animal; physiopathology; therapy; Organ Size; Respiratory Mechanics; physiology; Utrophin; metabolism
6.  Ventilation during air breathing and in response to hypercapnia in 5 and 16 month-old mdx and C57 mice 
Previous studies have shown a blunted ventilatory response to hypercapnia in mdx mice older than 7 months. We test the hypothesis that in the mdx mice ventilatory response changes with age, concomitantly with the increased functional impairment of the respiratory muscles. We thus studied the ventilatory response to CO2 in 5 and 16 month-old mdx and C57BL10 mice (n = 8 for each group). Respiratory rate (RR), tidal volume (VT), and minute ventilation (VE) were measured, using whole-body plethysmography, during air breathing and in response to hypercapnia (3, 5 and 8% CO2). The ventilatory protocol was completed by histological analysis of the diaphragm and intercostals muscles. During air breathing, the 16 month-old mdx mice showed higher RR and, during hypercapnia (at 8% CO2 breathing), significantly lower RR (226 ± 26 vs. 270 ± 21 breaths/min) and VE (1.81 ± 0.35 vs. 3.96 ± 0.59 ml min−1 g−1)(P < 0.001) in comparison to C57BL10 controls. On the other hand, 5 month-old C57BL10 and mdx mice did not present any difference in their ventilatory response to air breathing and to hypercapnia. In conclusion, this study shows similar ventilation during air breathing and in response to hypercapnia in the 5 month-old mdx and control mice, in spite of significant pathological structural changes in the respiratory muscles of the mdx mice. However in the 16 month-old mdx mice we observed altered ventilation under air and blunted ventilation response to hypercapnia compared to age-matched control mice. Ventilatory response to hypercapnia thus changes with age in mdx mice, in line with the increased histological damage of their respiratory muscles.
PMCID: PMC1974787  PMID: 17431804
Age; Duchenne muscular dystrophy; Hypercapnia mdx mouse; Ventilatory response

Results 1-6 (6)