3 and 4 The prime role of the coronary arteries is to supply blood into the heart; hence its blockage results into

a serious shortage of blood in the heart muscles, which in turn deprives the myocardial tissues of oxygen. Such a lack of oxygen in the heart muscles results into a painful indication known as angina. The hardening of the plaques may even stop the total blood supply into the heart which then results into a heart attack.5 Low density lipoprotein (LDL) and the cholesterol Selleckchem Enzalutamide are the prime contributors in the formation of such plaques inside the blood vessels.6 The high-density lipoprotein (HDL) however also contributes to the formation of the plaques.7 Cholesteryl ester transfer protein (CETP) is a plasma glycoprotein that facilitates the transfer of cholesteryl esters (CE) and triglycerides from HDL to LDL/VLDL.8 HDL transports the cholesterol into the liver, where it is finally broken down, while LDL helps in deposition of the cholesterol into the inner walls of the arteries. Hence high quantities of LDL and lower quantities of the HDL inside the blood stream increase the risk of heart attack. LDL carries much more Cholesterol than HDL. CETP is one such plasma glycoprotein that transfers buy EPZ-6438 the CE from the HDL to the LDL, thereby

increasing the risk of the cholesterol deposition in the inner walls of the arteries.9 CETP inhibition has hence been proven as a potential target in the war against heart diseases.10 and 11 Recent works have revealed that CETP may be inhibited by the drugs such as Dalcetrapib, Torcetrapib, JIT-705 and Anacetrapib.8 After inhibition of CETP the cholesterol level of HDL increases which in turn controls the cholesterol transportation.12 However, Torcetrapib was rejected in phase III of clinical trials due to its enormous side effects.11 Quantitative structure–activity relationship (QSAR) has been proven as the most fruitful tool in the comparative evaluation of the structure of a drug with its biological activity.13

The physicochemical properties of a drug are related to its structure which helps us correlate and optimize the therapeutic effects and MycoClean Mycoplasma Removal Kit minimize the toxicity of the drug substance.14 The tool has been utilized by the medicinal chemists to investigate new drug substance or optimization of the existing ones.15 and 16 A series of N–N-disubstituted trifluoro-3-amino-2-propanol derivatives were retrieved from published study.17 These compounds were evaluated as cholesteryl ester transfer protein (CETP) inhibitors. Authors have extensively studied structure–activity relationship (SAR) by substituting various functional groups at the 1- and 2-positions to achieve an effective CETP inhibition. Eighty one structures (H explicit 2D and 3D) of N–N-disubstituted trifluoro-3-amino-2-propanol were sketched and optimized using Marvin Sketch (developed by ChemAxon Company).

5 vs. 2.95 for 6-month persistent infection; 0.20 vs. 0.39 for CIN2+). In a FUTURE I/II analyses of HPV6, 11,16, and/or 18 DNA positive women, Gardasil®

was 100% (95% CI: 78.6–100) effective in preventing incident CIN2+ associated with a vaccine type for which the women were DNA negative at enrollment [33]. Efficacy against vaccine type-related external genital and vaginal lesions in this study group was 93.8% (95% CI: 80.7–98.8). Gardasil® was also shown to protect seropositive women against subsequent disease from the corresponding vaccine type [35]. In a MITT analysis of combined FUTURE I, FUTURE II and 007 data, efficacy in women DNA negative and seropositive for the corresponding type was 100% (95% CI: 28.7–100.0) find more against CIN1+ and 100% (95% CI: 28.3–100.0) against EGLs. However attack rates in controls, Gefitinib and therefore rate reductions, were low, 0.2 for CIN1+ and external genital lesions and 0.1 for CIN2+.

In comparison, a similar analysis of seronegatives in this combined study group reported a CIN2+ attack rate of 0.5 in controls [20]. From these studies, it is clear that prevalent infection by one type does not impede vaccine-induced protection from incident infection by another vaccine type. In addition, the results also seemingly indicate that the antibody responses to natural infection do not fully protect women from reinfection, Carnitine palmitoyltransferase II in contrast to antibodies induced by vaccination. The generally much lower antibody titers detected after infection

likely account for this difference in protection (discussed below). Consistent with this explanation, most seropositive controls who subsequently became DNA positive had antibody titers that were below the geometric mean titer [32] and [35]. Also supporting this interpretation, a recent analysis of seropositive controls in the CVT found that women with relatively high antibody titers at enrollment were mostly protected from incident infection (as measured by DNA detection) whereas those with low titers were not [36]. The 2- to 5-fold lower attack rates in seropositives vs. seronegatives supports the conclusion that antibodies induced by infection play a substantial role in protection from reinfection, or are a surrogate marker for cell-mediated immune protection. It is important to note that the above analyses might be subject to substantial misclassification. Relatively low cut points for seropositivity were used in the vaccine trials, because of the desire to exclude, as much as possible, women with prior exposure to the vaccine types in the primary ATP analyses. It is possible that the low titers in some women might be due to non-specific or cross-reactive antibody rather than indications of prior vaccine-type infection.

However, no review has specifically sought factors associated with the first episode of low back pain. This may be why no studies have evaluated how modification of risk factors affects the incidence of low back pain in children (Burton et al 2005). Therefore, this review specifically focuses on risk factors for the first episode of low back pain. Of particular interest is the identification of potentially modifiable risk factors, as these may indicate possible strategies

to protect young people from developing low back pain. Earlier studies and reviews into risk factors for low back pain in children and adolescents have implicated genetic factors, environmental factors (El-Metwally Rucaparib mw et al 2008), psychosocial factors such as negative psychosocial experiences

in childhood (Cardon and Balague 2004, Jones and Macfarlane 2005), and levels of physical activity (Duggleby and Kumar 1997, Leboeuf-Yde 2004). The only risk factor established by these reviews for an episode of low back pain is a previous episode (Battie and Bigos 1991, Burton et al 2005, Hestbaek et al 2006, Hestbaek et al 2003, Jones and Macfarlane 2005). Only one of these reviews was a systematic review (Cardon and Balague 2004), and it searched only one database, searched and publications in only a 9-year period, and was published in 2004. Furthermore, none of the reviews investigated risk factors for selleck screening library the first episode of low back pain specifically. Therefore an up-todate systematic review is required. Such a review should consider children and adolescents up to 18 years of age, because children appear more prone to low back pain during times of increased growth (Fairbank et al 1984, Feldman et al 2001, Harreby et al 1996, Olsen et al

1992). Rapid growth in males begins at around 12.5 years, with completion typically between 13.5 and 17.5 years. Females commence and finish growth spurts on average two years prior to this (Duggleby and Kumar 1997). Therefore, the specific study questions for this systematic review were: 1. What modifiable and non-modifiable risk factors have been identified for the first episode of low back pain in children and adolescents? The method of this review was based on the Cochrane Handbook for Systematic Reviews of Interventions (Higgins and Green 2006), adapted for the systematic review of longitudinal and cross-sectional studies), and the MOOSE Statement (Stroup et al 2000). A grid of search terms and definitions of interest was developed and converted to a sensitive search strategy for each database searched.

His relaxed and personable style is reflected on the BiM website. Technically, the site itself has a professional feel, is easy to navigate, visually appealing and is kept up to date. In this respect, the website benefits greatly from the input of Heidi Allen, a professional social media consultant with an interest in health care whose role involves day-to-day running of the site. The site sees some 15 000 visitors each month and almost all blog posts generate some degree of discussion. That discussion is at times controversial probably attests to

the relevance and timeliness of the material presented. Similarly the fact that discussion comes from selleckchem researchers, clinicians, and the public indicates the broad significance of the material. The field of pain science is an emerging area of PF 2341066 interest to physiotherapists, and according to a survey on the site, approximately 45% of users identify themselves as physiotherapists. The content of the site has clear relevance for the physiotherapy profession. This website provides a worthwhile resource for clinicians treating patients with painful conditions and in doing so serves multiple purposes. It presents relevant information

in one place, provides concise and user-friendly summaries, and offers a forum for discussion and debate as to the significance and utility of the findings. Poor accessibility of scientific information has been identified as a barrier to evidence-based

practice (Iles and Davidson, 2006). Accessibility issues include difficulties in finding relevant information, costs involved in procuring published studies, and also the capacity of non-academic users to appraise and process study reports. Sites such as Body in Mind provide an invaluable tool for overcoming these barriers. I have no substantial issues with the content, the structure, or tone of the site. One remark however, attends to a question of interpretation of some of the research presented. While the focus is on oxyclozanide highlighting the potential clinical applicability of research, there is the risk that preliminary or experimental findings may not be treated with the appropriate degree of circumspection before implementation into clinical practice. The extent to which the authors of the posts are responsible for this is of course debatable, but it is an issue that should be borne in mind by users of the site. Body in Mind is an excellent website with clear relevance and utility for physiotherapists whose caseload includes patients with pain conditions. The blog posts are concise and easy to read, and the discussions frequently interesting and enlightening. The website performs an important function in bringing pain research in a digestible form to a broad audience.

Hemagglutination inhibition (HI) antibody titers against the vaccine strains were assessed

at GlaxoSmithKline Vaccines central laboratory using validated assay methods as previously described [18]. The primary objective was to assess the lot-to-lot consistency of three QIV lots based on GMTs at Day 21 post-vaccination. Secondary objectives were to evaluate: the superiority of GMTs at Day 21 for QIV versus TIV-Vic against the Yamagata B strain, and QIV versus TIV-Yam against the Victoria B strain (i.e. B strains absent CT99021 research buy from each TIV); and the non-inferiority of GMTs at Day 21 for QIV versus TIV-Vic + TIV-Yam against all four strains, QIV versus TIV-Vic against the Victoria B strain, and QIV versus TIV-Yam against the Yamagata B strain (i.e. shared strains). Immunogenicity was described at Day 0, 21, and 180

(sub-cohort) including GMTs, seroprotection rate (SPR; proportion with post-vaccination titer ≥1:40), seroconversion rate (SCR; proportion with antibody titer <1:10 at baseline and with post-vaccination titer of ≥1:40, or pre-vaccination titer of ≥1:10 and a ≥4-fold post-vaccination increase in titer), and seroconversion factor (SCF; geometric mean of the ratio between pre-vaccination and post-vaccination reciprocal HI titers). Subjects with HI antibody Trichostatin A cost titers of ≥1:10 were considered to be seropositive. Immunogenicity was also assessed according to US

Center for Biologics Evaluation and Research (CBER) licensure criteria. The occurrence and intensity of solicited adverse events (AEs) was recorded Metalloexopeptidase by subjects on diary cards and included local symptoms (pain, redness, and swelling) and general symptoms (arthralgia, fatigue, gastrointestinal symptoms, headache, generalised myalgia, shivering, and fever). Unsolicited AEs were assessed prospectively at each study visit. Injection site reactions were considered to be related to the vaccine and investigators provided causality assessments for solicited general symptoms and unsolicited events. Reactogenicity and safety outcome measures (secondary objectives) were local and general solicited adverse events during the 7-day post-vaccination period, unsolicited AEs during the 21-day post-vaccination period, and medically attended events (MAEs) and serious adverse events (SAEs) during the 6 months study period. The target sample size for the QIV group was 400 subjects assigned to each of the three QIV lots; assuming 6% will be non-evaluable and equivalence among the lots, 375 evaluable subjects per lot would have 92% power using Bonferroni’s adjustment to meet the consistency criterion. The target sample size for each TIV group was 200 subjects, giving 190 evaluable subjects assuming 5% will be non-evaluable.

For our current study, we used wound-healing assays to examine the rates of migration of cell lines established from LD 10–87 VERO cells and HD 10–87 VERO cells at 10 passage intervals. After the monolayer was scratched with a pipette tip, the migration of cells

into the wounded area were photographed every 3 h for 15 h. Representative photomicrographs are shown of wounded cell-culture monolayers at 0 and 12 h. Red arrows represent absence of cell migration into the wounds. The non-tumorigenic LD 10–87 VERO cells at p151 and tumorigenic check details LD 10–87 VERO cells at p256 were used as references lines for slowly and rapidly migrating cells, respectively. The tumorigenic LD 10–87 VERO cells at p256 started filling the wound around 9 h and completely closed the wound by 12 h, whereas little or no motility was observed with LD 10–87 VERO at p151 ( Fig. 3A). When we tested LD 10–87 VERO cells at 10-passage intervals between p151 to p256, the cells displayed a progressive EGFR inhibitor increase in migration rates from p165 to p186, and the wound was completely closed by LD 10–87 VERO cells at p194. In a similar fashion, HD 10–87 VERO cells displayed a progressive increase in migration rate from p165 to p195 (Fig. 3B). The rate at which the HD 10–87 VERO cells migrate was somewhat faster than the LD VERO cells, since as the wound completely closed at p185 as opposed to p194 for LD VERO cells. Both LD

and HD VERO cells appeared to migrate predominantly

MTMR9 as tightly packed sheets in a wound-healing assay. Since doubling times for both LD (26 h) and HD VERO (20 h) cells are greater than the assay time (12 h), it is unlikely that the differences in migration observed were affected by the rate of proliferation of the respective cells. In our earlier study, 10 specific signature miRNAs were identified that correlated with the transition of LD 10–87 VERO cells from a non-tumorigenic phenotype at p148 to a tumorigenic phenotype at p256 [28]. The 10 signature miRNAs were differentially overexpressed in tumorigenic, high-passage LD 10–87 VERO cells compared with non-tumorigenic, low-passage LD 10–87 VERO cells. Based on their level of expression, six miRNAs (miR-376a, miR-654-3p, miR-543, miR-299-3p, miR-134 and miR-369-3p) were chosen for evaluation of their use as potential biomarkers to track the progression of neoplastic development in VERO cells. Using RNA samples prepared from LD 10–87 VERO cell banks established at every 10 passages from p150 to p254, the level of expression of the selected miRNAs was examined by quantitative RT-PCR. The expression levels of these miRNAs in non-tumorigenic LD 10–87 VERO cells (p154) were slightly above background levels of pAGMK cells. In contrast, the expression levels of these miRNAs increased progressively by at least 2-10 fold at p174 and by greater than 8-42 fold (p < 0.

The test organisms were Rhizopus oryzae (MTCC 262), Chrysosporium tropicum (MTCC) and Aspergillus niger buy Dabrafenib (MTCC 281). The readymade potato dextrose agar medium (39 g) was suspended in distilled water (1000 ml) and heated to boiling until it dissolved completely. The medium and the petri dishes were autoclaved at a pressure of 15 ib/inch for 20 min.

Stock solutions were prepared by dissolving compound in DMSO and different concentrations were prepared (30 μg/ml). Agar cup bioassay was employed for testing antifungal activity of plant extract following the standard procedure. 14 The Panobinostat in vitro medium was poured into petri dishes under aseptic conditions in a laminar flow chamber. When the medium in the plates solidified, 0.5 ml of 24 h old culture of test organism was inoculated. After inoculation, cups were scooped out with 6 mm sterile cork borer and the lids of the dishes were replaced. To each cup different concentration of test solutions (30, 100 μg) were added. Controls were maintained with DMSO using sample Clotrimazole. The treated and the control samples were kept at RT for 24–96 h

and inhibition zones were measured and diameter was calculated. Clotrimazole is taken as standard reference agent. (6a) 5-(phenyl)-4-methyl-3yl-(Imidazolidin-1ylmethyl, 2-ylidene nitro imine) isoxazole IR: νmax: 3310, 1580, 1590, 1410, 1297 cm−1, 1H NMR: δ 5.3 (s, 2H, –CH2–N–), 2.3 (s, 3H, isoxazole–CH3), 2.1 (brs, 1H, –NH), 2.8–3.1 (m, 4H, CH2), 7.4–7.55 (m, 3H, Ar.H), 7.7–7.8 (m, 2H, Ar.H), EI mass (m/z) 301 (M+), 247, 216. (6b) 5-(4-chlorophenyl)4- methyl-3yl-(Imidazolidin-1ylmethyl, 2-ylidene nitro imine) isoxazole IR: νmax: 3310, 2998, 1580 cm−1, 1H NMR: δ 5.5 (s, 2H, –CH2–N), 2.3 (s, 3H, isoxazole–CH3), 2.1 (brs, 1H, -NH), 2.9–3.2 (m, 4H), 7.4 (d, 2H, Ar.H, J = 8.0 Hz),7.65 (d, 2H, Ar.H = 8.2 Hz), EI mass (m/z) 335 (M+), 262, 247, 111. (6c) 5-(4-bromophenyl)-4-methyl-3yl-(Imidazolidin-1yl methyl, 2-ylidene nitro imine) isoxazole either IR: νmax: 3310, 1580, 1415, 1297 cm−1, 1H NMR: δ

4.6 (s, 2H, –CH2N–), 2.4 (s, 3H, isoxazole–CH3), 2.2 (brs, 1H, –NH), 2.7–3.1 (m, 4H), 7.5 (dd, J = 7.9 and 2.5 Hz, 2H, Ar.H), 7.8 (dd, J = 8.1 and 2.4 Hz 2H, Ar.H), EI mass (m/z) 379 (M+), 262, 225. (6d) 5-(4-flourophenyl)-4-methyl-3yl-(Imidazolidin-1ylmethyl, 2-ylidenenitroImine)isoxazole. IR: νmax: 3411, 1586, 1417, 1296 cm−1, 1H NMR: δ 5.5 (s, 2H, –CH2–N–), 2.3 (s, 3H, isoxazole–CH3), 2.10 (brs, 1H, –NH), 2.55–2.8 (m, 4H), 7.15 (m, 2H, Ar.H), J = 8.5 Hz, 7.75 (m, 2H, Ar.H), EI mass (m/z) 319 (M+), 270, 245. (6e) 5-(4-methyl phenyl)-4-methyl-3yl-(Imidazolidin-1ylmethyl, 2-ylidene nitro imine) isoxazole IR: νmax: 3406, 1555, 1410 cm−1, NMR: δ 2.4 (s, 3H, –ArCH3), 5.4 (s, 2H, –CH2–N), 2.2 (s, 3H, isoxazole–CH3), 2.1 (brs, 1H, –NH), 2.6–3.1 (m, 4H), 7.3 (d, 2H, Ar.H, J = 7.5 Hz), 7.7 (d, 2H, Ar.H = 7.

If the placebo recipients were found rotavirus positive by ELISA, further confirmation for the presence of HRV vaccine strain was done using the appropriate molecular technique (e.g. Reverse Polymerase Chain Reaction [RT-PCR], sequencing). If an ELISA positive stool sample from placebo recipients for which the vaccine strain is not confirmed, the stool sample was tested for rotavirus G- and P-type using reverse hybridization assay at DDL laboratories, the Netherlands or by any other appropriate molecular technique

(e.g. RT-PCR, sequencing) [11]. If rotavirus vaccine strain was detected from the twin receiving placebo, stool samples were further tested to estimate the presence of infectious viral particles (direct culture of stool Selleckchem Alectinib samples on MA-104 cells for which results were expressed

qualitatively). If applicable, full genome of rotavirus was sequenced from twin pairs receiving placebo or the HRV vaccine to evaluate genetic variation. At pre-vaccination and 7 weeks post-Dose 2 of HRV vaccine/placebo, serum samples were collected from all the twins for the analysis of anti-rotavirus IgA antibody concentration using ELISA methodology designed by Ward et Pifithrin-�� concentration al. [12] and [13] at GSK Biologicals Laboratory, Rixensart, Belgium with an assay cut-off of 20 U/ml. Serious adverse events and all episodes of gastroenteritis (diarrhea [three or more looser than normal stools per day] with or without vomiting) occurring throughout the study period (until 7-weeks after Dose 2 of HRV vaccine/placebo) were recorded by the parents/guardians in the dairy cards. In case

of a gastroenteritis episode until 7-weeks after Dose 2, and if the stool sample that is temporally closest to the onset day of the gastroenteritis episode is positive for rotavirus by ELISA, then presence of HRV vaccine strain was evaluated using the appropriate molecular technique (e.g. RT-PCR, sequencing). If the vaccine strain is not confirmed, the stool sample was tested for rotavirus G- and P-type using reverse hybridization assay at DDL laboratories, the Netherlands or by any other appropriate molecular technique (e.g. RT-PCR, sequencing). A randomization list was generated ALOX15 at GlaxoSmithKline (GSK) Biologicals, Rixensart, using a standard SAS® program. A randomization blocking scheme (1:1 ratio, block size = 2) was used to ensure balance between the treatment arms; a treatment number uniquely identified the vaccine doses to be administered to the same infant. The study was double-blinded and the parents/guardians of infants, investigator and the study personnel were unaware of the study vaccine administered. No investigator or any person involved in the clinical trial (including laboratory personnel, statisticians and data management) was aware of the treatment groups during the course of the study.

CASTS contributed to analysis and interpretation of the data; MdaGLCT contributed to interpretation of the data; SR did the initial analysis of the data; SMAM contributed to prepare the data to analysis; JPGL contributed with the design of the study and interpretation Enzalutamide of the data; MLB contributed

with the design of the study, analysis and interpretation of the data. All the authors contributed to edit the paper. The manuscript has been read and approved by all named authors and that there are no other persons who satisfied the criteria for authorship but are not listed. The order of authors listed in the manuscript has been approved by all of us. All authors have given due consideration to the protection of intellectual property associated with this work and that there are no impediments to publication, including the timing of publication, with respect to intellectual property. In so doing the authors confirm that they have followed the regulations of their institutions concerning intellectual property. This study was approved by the Committee of Institute of Collective Health, Federal University of Bahia (Protocol 017-08/CEP/ISC-2008), by four local ethics committees. Consent to participate was obtained from selleck products all the hospitals. Carers of participating children signed written an informed consent form. This work was supported by Health Surveillance of Ministry of Health of Brazil who collaborated

in recruitment of sites but no role in study design, in collection, analysis, interpretation of data, in the writing of the report or in the decision of submit the article for publication. We recognize the contribution of the ROTAVAC Group which includes all the professionals enrolled in the rotavirus AD Surveillance System who participated in the conduction of the study: Alessandra Araújo Siqueira, Greice Madeleine, Rejane Maria de Souza Alves, Viviane Martins, Marli Costa, Ernani Renoir, Eduardo

do Carmo Hage (Health Surveillance of Ministry of Health, Brasilia, Brazil); Alexandre Madi Fialho, Rosane Santos Maria de Assis (Regional Reference Laboratory, FIOCRUZ, Rio de Janeiro, Brazil); Rita Cássia Compagnoli Carmona (Regional Reference Laboratory, Adolfo Lutz, Sao Paulo, Brazil); Joana D’Arc Pereira Mascarenhas, Luana da Silva Soares (National Reference Laboratory/Evandro Chagas, Belém, Brazil); Acácia too Perolina Resende Setton, Adelaide da Silva Nascimento, Ana Gabriela de Andrade Carreira, Ângela Maria Rodrigues Ferreira, Fabíula Maria de Almeida de Holanda Tormenta, Janete Xavier dos Santos, Teonília Loula Dourado, Mara Espíndola Cardoso Araújo, Marco Aurelio de Oliveira Goes, Maria Elisa Paula de Oliveira, Marília Reichelt Barbosa, Maria Cristina Toledo Coelho, Sandra Cristina Deboni (AD Surveillance System of the States and Municipalities, Brazil); Ivana R. S. Varella, Elenice Brandão Cunha, Emerson Henklain Ferruzz, Marícia de Macedo Mory Kuroki, Maria de Fátima Rezende Dória Pinto, Maria Roseilda B.

Elle doit être proposée dès le stade 2 en cas de dyspnée malgré un traitement médicamenteux optimal. La période au décours immédiat d’une hospitalisation Veliparib pour exacerbation semble un moment privilégié ; en effet, l’exacerbation entraîne une sédentarité accrue

pendant au moins un mois après l’hospitalisation et une réhabilitation précoce diminuerait le nombre de ré-adminissions voire la mortalité. L’intérêt de débuter la réhabilitation au cours de l’hospitalisation pour exacerbation est incertain [41]. La réhabilitation réduit la dyspnée, améliore la tolérance à l’effort et la qualité de vie, l’anxiété et la dépression, diminue la consommation de soins en réduisant les exacerbations, les consultations en urgence et la durée des hospitalisations [1]. C’est un programme multidisciplinaire, individualisé selon les besoins et demandes du patient, incluant un réentraînement à l’effort, une prise en charge nutritionnelle, psychologique et sociale, et une éducation thérapeutique. Cette approche multidisciplinaire est nécessaire en regard des conséquences systémiques de la BPCO (dénutrition, atteinte musculaire, syndrome dépressif, sédentarité)

qui retentissent sur la dyspnée, la qualité de vie, la tolérance à l’effort et contribuent à la spirale du déconditionnement. La réhabilitation ne modifie pas la sévérité de l’obstruction bronchique mais peut SAR405838 mouse permettre d’inverser à long terme la spirale du déconditionnement en modifiant le comportement du patient. La prescription d’une réhabilitation peut émaner du pneumologue mais aussi du médecin traitant, voire être sollicitée par le patient. Dans tous les cas, un bilan préalable notamment cardiovasculaire est indispensable (idéalement, une épreuve d’effort cardiorespiratoire VO2 max) ; un test de marche de six minutes, une évaluation nutritionnelle et psychosociale avec un diagnostic éducatif permettent de définir avec le patient ses objectifs. Les modalités de la réhabilitation respiratoire doivent répondre aux besoins, contraintes et sévérité du

patient ; le stage initial peut être réalisé en hospitalisation ou en ambulatoire, voire à domicile dans le cadre de réseaux de soins [1], [2], [3] and [6]. Les bronchodilatateurs de longue durée d’action et les associations fixes d’un MTMR9 β2-adrénergique et d’un corticoïde, prescrits dans le respect de leurs indications, peuvent contribuer à augmenter les résultats de la réhabilitation sur la tolérance à l’effort. Le stage initial comporte au moins 12 séances (habituellement 20), sur une période de 6 à 12 semaines. Le rythme est de deux à trois séances par semaine en ambulatoire et jusqu’à cinq séances par semaine en hospitalisation. Ces séances comportent un réentraînement des membres inférieurs, mais aussi des membres supérieurs, en associant des exercices d’endurance et de force et, selon le résultat du bilan, un entraînement des muscles inspirateurs.