The MESANGE model: re-estimation on National Accounts base 2000 / Part 2 Version with chained-linked volumes

Mesange is a medium-size quarterly macro-econometric model of the French economy (about 500 equations, three sectors). The model describes short-term Keynesian dynamics and its long-term equilibrium is driven by supply-side determinants. Its reestimation on data from the national accounts base 2000 with fixed-base volumes is presented in a recent working paper (Klein and Simon, 2010). This first version of the model has been optimized for simulation use. Other applications of the Mesange model (short-term forecasting, analyses of the past) required its adaptation to the published data from the quarterly accounts with chained-linked volumes, as well as the integration of the recent crisis episode. A second version of the Mesange model has, therefore, been developed for this purpose. This version is presented in this working paper. First, the problems raised for macroeconomic modelling by national accounts with chained-linked volumes are explained and the solutions chosen to adapt the model to these new conventions are discussed. The applications of the version of the model with chained-linked volumes are, then, explained and illustrated with examples. Last, the main reestimated equations are detailed. The differences with respect to the version of the model with fixed-base volumes are commented. They stem from estimations based on non-identical data, but also from the different uses made of the two versions of Mesange and the resulting various needs and constraints that have conditioned the methodological choices that have been made. As for the version of the model with chained-linked volumes, priority has been given to the quality of the adjustment to the data rather than to the underlying theoretical framework. Nonetheless, the philosophy and general structure of the two versions of the model remain very much alike.macroeconometric model, estimation, chained-linked volumes, short-term forecasting, contribution analysis

HIV infected adults do not have an excess of colonising bacteria in their large airways

BACKGROUND: HIV infected adults have increased susceptibility to bacterial pneumonia but the underlying immune defect is poorly understood. We tested the hypothesis that HIV infection might be associated with increased bacterial colonisation of distal airways by nasal flora, which would then predispose patients to bacterial pneumonia. METHODS: Healthy volunteer adults with normal chest radiographs were recruited. Bronchoscopy was carried out and uncontaminated mucosal samples were collected from proximal and distal sites in the large airways using a protected specimen brush. Samples were cultured to detect typical respiratory tract colonising organisms, and the proportion of samples found to contain colonising bacteria compared between HIV infected and uninfected subjects using non-parametric tests. RESULTS: Forty-nine subjects were studied of whom 27 were HIV infected. Colonising bacteria were identified in the nasopharynx of all subjects including Streptococcus pneumoniae in 6/49 subjects (5 HIV uninfected). Colonising bacteria were found in the distal airway of 6 subjects (3/27 HIV infected vs 3/22 HIV uninfected ; χ(2 )= 0.07, p = 0.8). Streptococcus pneumoniae was identified in the trachea of all subjects with nasal colonisation but in the distal airway of only 1 subject. CONCLUSIONS: There was no evidence to support a hypothesis of increased airway bacterial colonisation in healthy HIV infected subjects

Intergenerational inequalities since baby-boom

Cohorts born until the late 1940s benefited from a clear generational progress: from one generation to the next, the conditions for entering the labour market were more favourable, living standards increased regularly, access to education and homeownership was more common. These progresses strongly slowed down and even stopped, for generations born in the 1950s and 1960s. Early in their life course, the latter had to face the two oil shocks and the bad economic context that followed. The most recent generations are experiencing a mixed picture. Several years of good economic performance at the turn of the 2000s helped to increase again their standard of living in comparison to previous generations at the same age. Then, they benefited from low interest rates that facilitated again access to the property, despite rising property prices. However, this improvement appears to be very dependent on the macroeconomic environment, which can easily turn around. Inequalities between generations go together with inequalities within generations. In particular, access to employment is closely linked to educational level. Graduate people are more protected from unemployment and get a stable job more easily, but such an improvement is at the cost of a downgrading as regards wages and employment position. Non-graduates, meanwhile, are more dependent on economic conditions, not only at the end of their studies but also during the beginning of their careers. Finally, the fragility of this generational progress, and the increased importance of intergenerational transfers of wealth, could possibly lead to a widening of the gap between social classes or social origins. For instance, since the beginning of the 2000s, the access of younger generations to property has been improving again but the gap in property rates between social categories has been increasing.intergenerational inequalities, social inequalities, cohorts

Severity-Related Changes of Bronchial Microbiome in Chronic Obstructive Pulmonary Disease

Bronchial colonization by potentially pathogenic microorganisms (PPMs) is often demonstrated in chronic obstructive pulmonary disease (COPD), but culture-based techniques identify only a portion of the bacteria in mucosal surfaces. The aim of the study was to determine changes in the bronchial microbiome of COPD associated with the severity of the disease. The bronchial microbiome of COPD patients was analyzed by 16S rRNA gene amplification and pyrosequencing in sputum samples obtained during stable disease. Seventeen COPD patients were studied (forced expiratory volume in the first second expressed as a percentage of the forced vital capacity [FEV1%] median, 35.0%; interquartile range [IQR], 31.5 to 52.0), providing a mean of 4,493 (standard deviation [SD], 2,598) sequences corresponding to 47 operational taxonomic units (OTUs) (SD, 17) at a 97% identity level. Patients were dichotomized according to their lung function as moderate to severe when their FEV1% values were over the median and as advanced when FEV1% values were lower. The most prevalent phyla in sputum were Proteobacteria (44%) and Firmicutes (16%), followed by Actinobacteria (13%). A greater microbial diversity was found in patients with moderate-to-severe disease, and alpha diversity showed a statistically significant decrease in patients with advanced disease when assessed by Shannon (ρ = 0.528; P = 0.029, Spearman correlation coefficient) and Chao1 (ρ = 0.53; P = 0.028, Spearman correlation coefficient) alpha-diversity indexes. The higher severity that characterizes advanced COPD is paralleled by a decrease in the diversity of the bronchial microbiome, with a loss of part of the resident flora that is replaced by a more restricted microbiota that includes PPMs

Associations of airway inflammation and responsiveness markers in non asthmatic subjects at start of apprenticeship

<p>Abstract</p> <p>Background</p> <p>Bronchial Hyperresponsiveness (BHR) is considered a hallmark of asthma. Other methods are helpful in epidemiological respiratory health studies including Fractional Exhaled Nitric Oxide (FENO) and Eosinophils Percentage (EP) in nasal lavage fluid measuring markers for airway inflammation along with the Forced Oscillatory Technique measuring Airway resistance (AR). Can their outcomes discriminate profiles of respiratory health in healthy subjects starting apprenticeship in occupations with a risk of asthma?</p> <p>Methods</p> <p>Rhinoconjunctivitis, asthma-like symptoms, FEV1 and AR post-Methacholine Bronchial Challenge (MBC) test results, FENO measurements and EP were all investigated in apprentice bakers, pastry-makers and hairdressers not suffering from asthma. Multiple Correspondence Analysis (MCA) was simultaneously conducted in relation to these groups and this generated a synthetic partition (EI). Associations between groups of subjects based on BHR and EI respectively, as well as risk factors, symptoms and investigations were also assessed.</p> <p>Results</p> <p>Among the 441 apprentice subjects, 45 (10%) declared rhinoconjunctivitis-like symptoms, 18 (4%) declared asthma-like symptoms and 26 (6%) suffered from BHR. The mean increase in AR post-MBC test was 21% (sd = 20.8%). The median of FENO values was 12.6 ppb (2.6-132 range). Twenty-six subjects (6.7%) had EP exceeding 14%. BHR was associated with atopy (p < 0.01) and highest FENO values (p = 0.09). EI identified 39 subjects with eosinophilic inflammation (highest values of FENO and eosinophils), which was associated with BHR and atopy.</p> <p>Conclusions</p> <p>Are any of the identified markers predictive of increased inflammatory responsiveness or of development of symptoms caused by occupational exposures? Analysis of population follow-up will attempt to answer this question.</p

Expression of Toll-like receptor 2 is up-regulated in monocytes from patients with chronic obstructive pulmonary disease

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterised by pulmonary and systemic inflammation which flare-up during episodes of acute exacerbation (AECOPD). Given the role of Toll-like receptors (TLRs) in the induction of inflammatory responses we investigated the involvement of TLRs in COPD pathogenesis. METHODS: The expression of TLR-2, TLR-4 and CD14 in monocytes was analyzed by flow cytometry. To study the functional responses of these receptors, monocytes were stimulated with peptidoglycan or lipopolysaccharide and the amounts of TNFα and IL-6 secreted were determined by ELISA. RESULTS: We found that the expression of TLR-2 was up-regulated in peripheral blood monocytes from COPD patients, either clinically stable or during AECOPD, as compared to never smokers or smokers with normal lung function. Upon stimulation with TLR-2 ligand monocytes from COPD patients secreted increased amounts of cytokines than similarly stimulated monocytes from never smokers and smokers. In contrast, the expressions of TLR-4 and CD14 were not significantly different between groups, and the response to lipopolysaccharide (a TLR-4 ligand) stimulation was not significantly different either. At discharge from hospital TLR-2 expression was down-regulated in peripheral blood monocytes from AECOPD patients. This could be due to the treatment with systemic steroids because, in vitro, steroids down-regulated TLR-2 expression in a dose-dependent manner. Finally, we demonstrated that IL-6, whose plasma levels are elevated in patients, up-regulated in vitro TLR-2 expression in monocytes from never smokers. CONCLUSION: Our results reveal abnormalities in TLRs expression in COPD patients and highlight its potential relationship with systemic inflammation in these patients