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The mathematics achievement discrepancy between girls and boys, with its subsequent occupational consequences, is an issue that has received considerable attention in the literature. It is often referred to as the 'math-gap' and favours boys. A major component of the explanation of this gap resides in determining its age of onset. We analyse here data from more than 10,000 (cross-sectional study) and 2000 (longitudinal study) French students aged 4-7 years, tested in the framework of the Etude Longitudinale Française depuis l'Enfance (ELFE). The results allow to precisely determine the age of onset, since the gender difference, non-existent (or even slightly in favour of girls) in kindergarten (4-5 years), is clearly in favour of boys in first grade (6-7 years). They could therefore provide an important element in the controversial debate on the origin of gender-differentiated performance in mathematics.

Summary Background Statins inhibit the cholesterol biosynthesis and are used as cholesterol-lowering agents in fat-metabolism disorders. Furthermore, several studies state that statins have supportive functions in breast cancer treatment. Therefore, simvastatin (SVA) as a potential radiosensitizer should be investigated on the basis of human breast cells. Methods First, an optimal concentration of SVA for normal (MCF10A) and cancer (MCF-7) cells was identified via growth and cytotoxicity assays that, according to the definition of a radiosensitizer in the narrower sense, enhances the effect of radiation therapy but has no cytotoxic effect. Next, in combination with radiation SVA’s influence on DNA repair capacity and clonogenic survival in 2D and 3D was determined. Furthermore cell cycle distribution, expression of survivin and connective tissue growth factor (CTGF) as well as ERK1 map kinase were analysed. Results 1 μM SVA was identified as highest concentration without an influence on cell growth and cytotoxicity and was used for further analyses. In terms of early and residual γH2AX-foci, SVA affected the number of foci in both cell lines with or without irradiation. Different radiation responses were detected in 2D and 3D culture conditions. During the 2D cultivation, a radiosensitizing effect within the clonogenic survival was observable, but not in 3D. Conclusion The present study suggests that SVA may have potential for radiosensitization. Therefore, it is important to further investigate the role of SVA in relation to the extent of radiosensitization and how it could be used to positively influence the therapy of breast cancer or other entities. Electronic supplementary material The online version of this article (10.1007/s10637-020-01046-6) contains supplementary material, which is available to authorized users.

Channelrhodopsins (ChRs) are algal light-gated ion channels widely used as optogenetic tools for manipulating neuronal activity. ChRs desensitize under continuous bright-light illumination, resulting in a significant decline of photocurrents. Here we describe a metagenomically identified family of phylogenetically distinct anion-conducting ChRs (designated MerMAIDs). MerMAIDs almost completely desensitize during continuous illumination due to accumulation of a late non-conducting photointermediate that disrupts the ion permeation pathway. MerMAID desensitization can be fully explained by a single photocycle in which a long-lived desensitized state follows the short-lived conducting state. A conserved cysteine is the critical factor in desensitization, as its mutation results in recovery of large stationary photocurrents. The rapid desensitization of MerMAIDs enables their use as optogenetic silencers for transient suppression of individual action potentials without affecting subsequent spiking during continuous illumination. Our results could facilitate the development of optogenetic tools from metagenomic databases and enhance general understanding of ChR function., Channelrhodopsins (ChRs) are algal light-gated ion channels used as optogenetic tools for manipulating neuronal activity. Here authors present a metagenomically identified family of phylogenetically distinct anion-conducting ChRs (MerMAIDs) which desensitize during continuous illumination due to accumulation of a non-conducting photointermediate.

Short-term exposure to air pollution has been associated with cardiovascular and respiratory mortality and morbidity. Little is known about associations between air pollution caused by firework events and daily mortality. We investigated whether particulate matter from fireworks during New Year’s celebrations was associated with daily mortality. We analyzed the celebrations of the years 1995–2012. PM10 concentrations increased dramatically during the firework events. Countrywide, the daily average PM10 concentrations from 27–30 December was 29 μg/m3 and increased during the first hour of the New Year by 277 μg/m3. In the more densely populated areas of the Netherlands the increase was even steeper, 598 μg/m3 in the first hour of the New Year. No consistent associations were found using linear regression models between PM10 concentrations during the first six hours of 1 January and daily mortality in the general population. Yet, using a case-crossover analysis firework-days and PM10 concentrations were associated with daily mortality. Therefore, in light of the contradictory results obtained with the different statistical analyses, we recommend further epidemiological research on the health effects of exposure to firework emissions.

Checkpoint inhibitors target the inhibitory receptors expressed by tumor-infiltrating T cells in order to reinvigorate an anti-tumor immune response. Therefore, understanding T cell composition and phenotype in human tumors is crucial. We analyzed by flow cytometry tumor-infiltrating lymphocytes (TILs) from two independent cohorts of patients with different cancer types, including RCC, lung, and colon cancer. In healthy donors, peripheral T cells are usually either CD4+ or CD8+ with a small percentage of CD4+ CD8+ DP cells (5%, reaching 30–50% of T cells in some patients). These DP T cells have an effector memory phenotype and express CD38, 4-1BB, and HLA-DR, suggesting antigen-driven expansion. In fact, TCR sequencing analysis revealed a high degree of clonality in DP T cells. Additionally, there were high levels of PD-1 and TIM-3 expression on DP T cells, which correlated with higher expression of PD-1 and TIM-3 in conventional single positive CD8 T cells from the same patients. These results suggest that DP T cells could be dysfunctional tumor-specific T cells with the potential to be reactivated by checkpoint inhibitors.

Agents targeting the PD1-PDL1 axis have transformed cancer therapy. Factors that influence clinical response to PD1-PDL1 inhibitors include tumor mutational burden, immune infiltration of the tumor and local PDL1 expression. To identify peripheral correlates of the anti-tumor immune response in the absence of checkpoint blockade, we performed a retrospective study of circulating T cell subpopulations and matched tumor gene expression in melanoma and non-small cell lung carcinoma (NSCLC) patients. Notably, both melanoma and NSCLC patients whose tumors exhibited increased inflammatory gene transcripts presented high CD4+ and CD8+ central memory T cell (CM) to effector T cell (Eff) ratios in blood. Consequently, we evaluated CM/Eff T cell ratios in a second cohort of NSCLC. The data showed that high CM/Eff T cell ratios correlated with increased tumor PDL1 expression. Furthermore, of the 22 patients within this NSCLC cohort who received nivolumab, those with high CM/Eff T cell ratios, had longer progression-free survival (PFS) (median survival: 91 vs. 215 days). These findings show that by providing a window into the state of the immune system, peripheral T cell subpopulations inform about the state of the anti-tumor immune response and identify potential blood biomarkers of clinical response to checkpoint inhibitors in melanoma and NSCLC.

BACKGROUND: Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants. METHODS: We used data from 22 European cohort studies, which created a total study population of 367,251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and between 10 μm and 2.5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis. FINDINGS: The total study population consisted of 367,251 participants who contributed 5,118,039 person-years at risk (average follow-up 13.9 years), of whom 29,076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2.5 of 1.07 (95% CI 1.02-1.13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0.95). HRs for PM2.5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1.06, 95% CI 1.00-1.12) or below 20 μg/m(3) (1.07, 1.01-1.13). INTERPRETATION: Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value. FUNDING: European Community's Seventh Framework Program (FP7/2007-2011).

IntroductionInformation on the relationship between levels of particulate matter (PM) smaller than 2.5μm and mortality rates in Europe is relatively sparse because of limited availability of PM2.5 measurement data. Even less information is available on the health effects attributable to PM2.5–10, especially for North-West Europe.ObjectivesTo investigate the relationship between various PM size fractions and daily mortality rates.MethodsDaily concentrations of PM from the Dutch National Ambient Air Quality Monitoring Network as well as all cause and cause-specific mortality rates in the Netherlands were obtained for the period 2008–2009. Poisson regression analysis using generalized additive models was used, with adjustment for potential confounding including long-term and seasonal trends, influenza incidence, meteorological variables, day of the week, and holidays.Different measures of PM (PM2.5, PM10 and PM2.5–10) were analysed.ResultsPM10 and PM2.5 levels were statistically significantly (p

Outdoor air pollution has been associated with decrements in lung function and growth of lung function in school-age children. Lung function effects have not been examined in preschoolers, with the exception of one study on minute ventilation in newborns. Our goal was to assess the relationship between long- and short-term exposure to traffic-related air pollution and interrupter resistance in 4-year-old children.Lung function was measured using the interrupter resistance method in children participating in a Dutch birth cohort study. Long-term average air pollution concentrations of fine particulate matter, nitrogen dioxide and soot at the residential address at birth were assessed using land-use regression models. Daily average air pollution concentrations on the day of clinical examination were obtained from the Dutch National Air Quality Monitoring Network.Significant associations were found between long-term average air pollution concentrations and interrupter resistance. Interrupter resistance increased by 0.04 kPa.s.L-1 (95% CI 0.01-0.07) per interquartile range increase (3.3 mu g.m(-3)) in fine particle concentration. Short-term exposure was not associated with interrupter resistance.Long-term exposure to traffic-related air pollution was associated with increased interrupter resistance in 4-year-old children, supporting previous birth cohort studies reporting effects of air pollution on subjectively reported respiratory symptoms in preschool children.

We studied the spatial distribution of cancer incidence rates around a large steel plant and its association with historical exposure. The study population was close to 600,000. The incidence data was collected for 1995–2006. From historical emission data the air pollution concentrations for polycyclic aromatic hydrocarbons (PAH) and metals were modelled. Data were analyzed using Bayesian hierarchical Poisson regression models. The standardized incidence ratio (SIR) for lung cancer was up to 40% higher than average in postcodes located in two municipalities adjacent to the industrial area. Increased incidence rates could partly be explained by differences in socioeconomic status (SES). In the highest exposure category (approximately 45,000 inhabitants) a statistically significant increased relative risk (RR) of 1.21 (1.01–1.43) was found after adjustment for SES. The elevated RRs were similar for men and women. Additional analyses in a subsample of the population with personal smoking data from a recent survey suggested that the observed association between lung cancer and plant emission, after adjustment for SES, could still be caused by residual confounding. Therefore, we cannot indisputably conclude that past emissions from the steel plant have contributed to the increased risk of lung cancer.

We examined the effects of the sulfonylurea compound NS5806 on neuronal A-type channel function. Using whole-cell patch-clamp we studied the effects of NS5806 on the somatodendritic A-type current (ISA) in cultured hippocampal neurons and the currents mediated by Kv4.2 channels coexpressed with different auxiliary β-subunits, including both Kv channel interacting proteins (KChIPs) and dipeptidyl aminopeptidase-related proteins (DPPs), in HEK 293 cells. The amplitude of the ISA component in hippocampal neurons was reduced in the presence of 20 μM NS5806. ISA decay kinetics were slowed and the recovery kinetics accelerated, but the voltage dependence of steady-state inactivation was shifted to more negative potentials by NS5806. The peak amplitudes of currents mediated by ternary Kv4.2 channel complexes, associated with DPP6-S (short splice-variant) and either KChIP2, KChIP3 or KChIP4, were potentiated and their macroscopic inactivation slowed by NS5806, whereas the currents mediated by binary Kv4.2 channels, associated only with DPP6-S, were suppressed, and the NS5806-mediated slowing of macroscopic inactivation was less pronounced. Neither potentiation nor suppression and no effect on current decay kinetics in the presence of NS5806 were observed for Kv4.2 channels associated with KChIP3 and the N-type inactivation-conferring DPP6a splice-variant. For all recombinant channel complexes, NS5806 slowed the recovery from inactivation and shifted the voltage dependence of steady-state inactivation to more negative potentials. Our results demonstrate the activity of NS5806 on native ISA and possible molecular correlates in the form of recombinant Kv4.2 channels complexed with different KChIPs and DPPs, and they shed some light on the mechanism of NS5806 action.

Background: Maternal exposure to air pollution has been associated with adverse pregnancy outcomes. Few studies took into account the spatial and temporal variation of air pollution levels.Objectives: To evaluate the impact of maternal exposure to traffic-related air pollution during pregnancy on preterm birth and term birth weight using a spatio-temporal exposure model.Methods: We estimated maternal residential exposure to nitrogen dioxide (NO2), particulate matter (PM2.5) and soot during pregnancy (entire pregnancy, 1st trimester, and last month) for 3853 singleton births within the Dutch PIAMA prospective birth cohort study by means of temporally adjusted land-use regression models. Associations between air pollution concentrations and preterm birth and term birth weight were analyzed by means of logistic and linear regression models with and without adjustment for maternal physical, lifestyle, and socio-demographic characteristics.Results: We found positive, statistically non-significant associations between exposure to soot during entire pregnancy and during the last month of pregnancy and preterm birth [adj. OR (95% CI) per interquartile range increase in exposure 1.08 (0.88-1.34) and 1.09 (0.93-1.27), respectively]. There was no indication of an adverse effect of air pollution exposure on term birth weight.Conclusions: In this study, maternal exposure to traffic-related air pollution during pregnancy was not associated with term birth weight. There was a tendency towards an increased risk of preterm birth with increasing air pollution exposure, but statistical power was low. (C) 2010 Elsevier Inc. All rights reserved.

Apolipoprotein A-I (apoA-I) mimetic peptides have been pursued as new therapeutic agents for the treatment of atherosclerosis, yet their precise mechanism responsible for atheroprotection remains unclear. Like apoA-I itself, most of these peptides are capable of stimulating cholesterol efflux from macrophages or foam cells, and some of them stimulate lecithin cholesterol acyltransferase (LCAT) activity in the reverse cholesterol transport (RCT) pathway. However, the ability of mimetic peptides to deliver cholesterol into hepatocytes (off-loading), the last step of the RCT pathway, has not been demonstrated. In this study, we compared a mimetic peptide D-4F to purified apoA-I, to address the role that mimetics play during the off-loading process. Both D-4F and apoA-I formed spherical nano-particles when reconstituted with cholesteryl ester and phospholipids. Compared to apoA-I, D-4F particles were 20 times more efficient in off-loading cholesterol to HepG2 hepatocytes with an apparent K(t) (transport) of 0.74 mug/mL. Furthermore, D-4F also facilitated cholesteryl ester offloading from HDL particles into HepG2 cells when it was pre-incubated with these HDL particles. Using an inducible HEK293 cell line, we demonstrated that these nano-particles were able to be taken up through SR-BI, a HDL selective receptor. Cholesterol uptake by HepG2 cells was completely blocked by a neutralizing monoclonal antibody against SR-BI, demonstrating that D-4F particles, similar to HDL, specifically off-loaded cholesterol through SR-BI. Overall our data provides evidence that D-4F is capable of mimicking apoA-I to form HDL-like particles, and off-loads cholesterol for catabolism and excretion, thus completing RCT.

Objectives: Associations between cardiovascular mortality and air pollution and noise together were investigated. Methods: Data from the ongoing Netherlands Cohort Study on Diet and Cancer (120 852 subjects; follow-up 1987–1996) were used. Cox proportional hazard analyses were conducted for the association between cardiovascular mortality and exposure to black smoke, traffic intensity on the nearest road and road traffic noise at the home address. Results: The correlations between traffic noise and background black smoke, and traffic intensity on the nearest road were moderate at 0.24 and 0.30, respectively. Traffic intensity was associated with cardiovascular mortality, with highest relative risk (95% confidence interval) for ischaemic heart disease (IHD) mortality being 1.11 (1.03 to 1.20) (increment 10 000 motor vehicles/24 h). Relative risks for black smoke concentrations were elevated for cerebrovascular (1.39 (0.99 to 1.94)) and heart failure mortality (1.75 (1.00 to 3.05)) (increment 10 μg/m 3 ). These associations were insensitive to adjustment for traffic noise. There was an excess of cardiovascular mortality in the highest noise category (>65 dB(A)), with elevated risks for IHD (1.15 (0.86 to 1.53)) and heart failure mortality (1.99 (1.05 to 3.79)). After adjustment for black smoke and traffic intensity, noise risk reduced to unity for IHD mortality and was slightly reduced for heart failure mortality. Conclusions: Associations between black smoke concentrations and traffic intensity on the nearest road with specific cardiovascular causes of death were not explained by traffic noise in this study.

International audience; Non-pathological, spontaneous mirror writing, whether complete or partial, has long been associated with writing with the left hand and attributed to the fact that abductive writing, which most people find easier, is from right to left when people write with their left hand. However, recent research suggests another explanation: children who do not know the orientation of the letters and digits may apply an implicit right-writing rule which causes them to invert mainly left-oriented characters (e.g., J, 3). But would left-hand writers apply such a rule? The present study examines the relationship between these two explanations of mirror writing and asks whether they coexist in children who write with their left hand. Is the abductive writing explanation specific to mirror writing by left-hand writers and the implicit right-writing rule specific to right-hand writers? A comparison of 59 children who wrote with their left hand and 59 children who wrote with their right hand (matched for age and school experience) provided clear evidence against the abductive-writing explanation and in favour of the right-writing rule for both groups. Therefore, spontaneous mirror writing in typical 5- to 6-year-olds does not seem to be a function of preferred writing hand.

Sphingosine-1-phosphate (S1P) receptor agonists are novel immunosuppressive agents. The selectivity of S1P1 against S1P3 is strongly correlated with lymphocyte sequestration and minimum acute toxicity and bradycardia. This study describes molecular modeling, site-directed mutagenesis, and affinity studies exploring the molecular basis for selectivity between S1P1 and S1P3 receptors. Computational models of human S1P1 and S1P3 receptors bound with two nonselective agonists or two S1P1-selective agonists were developed based on the X-ray crystal structure of bovine rhodopsin. The models predict that S1P1 Leu276 and S1P3 Phe263 contribute to the S1P1/S1P3 selectivity of the two S1P1-selective agonists. These residues were subjected to site-directed mutagenesis. The wild-type and mutant S1P receptors were expressed in Chinese hamster ovary cells and examined for their abilities to bind to and be activated by agonists in vitro. The results indicate that the mutations have minimal effects on the activities of the two nonselective agonists, although they have dramatic effects on the S1P1-selective agonists. These studies provide a fundamental understanding of how these two receptor-selective agonists bind to the S1P1 and S1P3 receptors, which should aid development of more selective S1P1 receptor agonists with immunosuppressive properties and improved safety profiles.

Exposure to environmental stressors can impair children's health and their cognitive development. The effects of air pollution, lead, and chemicals have been studied, but there has been less emphasis on the effects of noise. Our aim, therefore, was to assess the effect of exposure to aircraft and road traffic noise on cognitive performance and health in children.We did a cross-national, cross-sectional study in which we assessed 2844 of 3207 children aged 9-10 years who were attending 89 schools of 77 approached in the Netherlands, 27 in Spain, and 30 in the UK located in local authority areas around three major airports. We selected children by extent of exposure to external aircraft and road traffic noise at school as predicted from noise contour maps, modelling, and on-site measurements, and matched schools within countries for socioeconomic status. We measured cognitive and health outcomes with standardised tests and questionnaires administered in the classroom. We also used a questionnaire to obtain information from parents about socioeconomic status, their education, and ethnic origin.We identified linear exposure-effect associations between exposure to chronic aircraft noise and impairment of reading comprehension (p=0.0097) and recognition memory (p=0.0141), and a non-linear association with annoyance (p0.0001) maintained after adjustment for mother's education, socioeconomic status, longstanding illness, and extent of classroom insulation against noise. Exposure to road traffic noise was linearly associated with increases in episodic memory (conceptual recall: p=0.0066; information recall: p=0.0489), but also with annoyance (p=0.0047). Neither aircraft noise nor traffic noise affected sustained attention, self-reported health, or overall mental health.Our findings indicate that a chronic environmental stressor-aircraft noise-could impair cognitive development in children, specifically reading comprehension. Schools exposed to high levels of aircraft noise are not healthy educational environments.

Studies have suggested that children living close to busy roads may have impaired respiratory health. This study was designed to test the hypothesis that exposure to exhaust from heavy traffic in particular is related to childhood respiratory health. Children attending 24 schools located within 400 m from busy motorways were investigated. The motorways carried between 5,190 and 22,326 trucks per weekday and between 30,399 and 155,656 cars per day. Locations were chosen so that the correlation between truck and car traffic counts was low. Air pollution measurements were performed at the schools for 1 year. Respiratory symptoms were collected by parent-completed questionnaire. Sensitization to common allergens was measured by serum immunoglobulin E and skin prick tests. Bronchial hyperresponsiveness (BHR) was measured with a hypertonic saline challenge. Respiratory symptoms were increased near motorways with high truck but not high car traffic counts. They were also related to air pollutants that increased near motorways with high truck traffic counts. Lung function and BHR were not related to pollution. Sensitization to pollen increased in relation to truck but not car traffic counts. The relation between symptoms and measures of exposure to (truck) traffic-related air pollution were almost entirely restricted to children with BHR and/or sensitization to common allergens, indicating that these are a sensitive subgroup among all children for these effects.

Background Studies have shown associations between mortality and long-term exposure to particulate matter air pollution. Few cohort studies have estimated the effects of the elemental composition of particulate matter on mortality. Objectives Our aim was to study the association between natural-cause mortality and long-term exposure to elemental components of particulate matter. Methods Mortality and confounder data from 19 European cohort studies were used. Residential exposure to eight a priori–selected components of particulate matter (PM) was characterized following a strictly standardized protocol. Annual average concentrations of copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc within PM size fractions ≤ 2.5 μm (PM2.5) and ≤ 10 μm (PM10) were estimated using land-use regression models. Cohort-specific statistical analyses of the associations between mortality and air pollution were conducted using Cox proportional hazards models using a common protocol followed by meta-analysis. Results The total study population consisted of 291,816 participants, of whom 25,466 died from a natural cause during follow-up (average time of follow-up, 14.3 years). Hazard ratios were positive for almost all elements and statistically significant for PM2.5 sulfur (1.14; 95% CI: 1.06, 1.23 per 200 ng/m3). In a two-pollutant model, the association with PM2.5 sulfur was robust to adjustment for PM2.5 mass, whereas the association with PM2.5 mass was reduced. Conclusions Long-term exposure to PM2.5 sulfur was associated with natural-cause mortality. This association was robust to adjustment for other pollutants and PM2.5. Citation Beelen R, Hoek G, Raaschou-Nielsen O, Stafoggia M, Andersen ZJ, Weinmayr G, Hoffmann B, Wolf K, Samoli E, Fischer PH, Nieuwenhuijsen MJ, Xun WW, Katsouyanni K, Dimakopoulou K, Marcon A, Vartiainen E, Lanki T, Yli-Tuomi T, Oftedal B, Schwarze PE, Nafstad P, De Faire U, Pedersen NL, Östenson C-G, Fratiglioni L, Penell J, Korek M, Pershagen G, Eriksen KT, Overvad K, Sørensen M, Eeftens M, Peeters PH, Meliefste K, Wang M, Bueno-de-Mesquita HB, Sugiri D, Krämer U, Heinrich J, de Hoogh K, Key T, Peters A, Hampel R, Concin H, Nagel G, Jaensch A, Ineichen A, Tsai MY, Schaffner E, Probst-Hensch NM, Schindler C, Ragettli MS, Vilier A, Clavel-Chapelon F, Declercq C, Ricceri F, Sacerdote C, Galassi C, Migliore E, Ranzi A, Cesaroni G, Badaloni C, Forastiere F, Katsoulis M, Trichopoulou A, Keuken M, Jedynska A, Kooter IM, Kukkonen J, Sokhi RS, Vineis P, Brunekreef B. 2015. Natural-cause mortality and long-term exposure to particle components: an analysis of 19 European cohorts within the Multi-Center ESCAPE Project. Environ Health Perspect 123:525–533; http://dx.doi.org/10.1289/ehp.1408095

Rationale: Prospective cohort studies have shown that chronic exposure to particulate matter and traffic-related air pollution is associated with reduced survival. However, the effects on nonmalignant respiratory mortality are less studied, and the data reported are less consistent. Objectives: We have investigated the relationship of long-term exposure to air pollution and nonmalignant respiratory mortality in 16 cohorts with individual level data within the multicenter European Study of Cohorts for Air Pollution Effects (ESCAPE). Methods: Data from 16 ongoing cohort studies from Europe were used. The total number of subjects was 307,553. There were 1,559 respiratory deaths during follow-up. Measurements and Main Results: Air pollution exposure was estimated by land use regression models at the baseline residential addresses of study participants and traffic-proximity variables were derived from geographical databases following a standardized procedure within, the ESCAPE study. Cohort-specific hazard ratios obtained by Cox proportional hazard models from standardized individual cohort analyses were combined using metaanalyses. We found no significant associations between air pollution exposure and nonmalignant respiratory mortality. Most hazard ratios were slightly below unity, with the exception of the traffic-proximity indicators. Conclusions: In this study of 16 cohorts, there was no-association between air pollution exposure and nonmalignant respiratory mortality.

We studied the association of daily mortality with short-term variations in the ambient concentrations of major gaseous pollutants and PM in the Netherlands. The magnitude of the association in the four major urban areas was compared with that in the remainder of the country. Daily cause-specific mortality counts, air quality, temperature, relative humidity, and influenza data were obtained from 1986 to 1994. The relationship between daily mortality and air pollution was modeled using Poisson regression analysis. We adjusted for potential confounding due to long-term and seasonal trends, influenza epidemics, ambient temperature and relative humidity, day of the week, and holidays, using generalized additive models. Influenza episodes were associated with increased mortality up to 3 weeks later. Daily mortality was significantly associated with the concentration of all air pollutants. An increase in the PM10 concentration by 100 micrograms/m3 was associated with a relative risk (RR) of 1.02 for total mortality. The largest RRs were found for pneumonia deaths. Ozone had the most consistent, independent association with mortality. Particulate air pollution (e.g., PM10, black smoke [BS]) was not more consistently associated with mortality than were the gaseous pollutants SO2 and NO2. Aerosol SO4(-2), NO3-, and BS were more consistently associated with total mortality than was PM10. The RRs for all pollutants were substantially larger in the summer months than in the winter months. The RR of total mortality for PM10 was 1.10 for the summer and 1.03 for the winter. There was no consistent difference between RRs in the four major urban areas and the more rural areas.

Item does not contain fulltext BACKGROUND:: Air pollution has been associated with respiratory health effects. There is little direct evidence that reductions in air pollution related to abatement policies lead to actual improvement in respiratory health. We assessed whether a reduction in (traffic policy-related) air pollution concentrations was associated with changes in respiratory health. METHODS:: Air pollution concentrations and respiratory health were measured in 2008 and 2010 at eight busy urban streets and at four suburban background control locations. Respiratory function was assessed twice in 661 residents by spirometry and measurements of airway resistance. Nitric oxide (NO) in exhaled air was measured as a marker for airway inflammation. RESULTS:: Air pollution concentrations were lower in 2010 than in 2008. The declines in pollutants varied among locations, with the largest decline observed in a street with a large reduction in traffic intensity. In regression analyses adjusted for important covariates, reductions in concentrations of soot, NO2, NOx, Cu, and Fe were associated with increases in forced vital capacity (FVC) ( approximately 1% increase per interquartile range [IQR] decline). Airway resistance decreased with a decline in particulate matter (PM10) and PM2.5 (9% per IQR), although these associations were somewhat less consistent. No associations were found with exhaled NO. Results were driven largely by one street where traffic-related air pollution showed the largest reduction. Forced expiratory volume and FVC improved by 3% to 6% in residents of this street compared with suburban background residents. This was accompanied by a suggestive reduction in airway resistance. CONCLUSIONS:: Reductions in air pollution may lead to small improvements in respiratory function.

The medieval mystic altarpiece towers above the altar table. It is linked to the evocation of a religious mystery beyond our faculty of reasoning. Symbolism of an enclosed garden evokes the image of the Heavenly Garden isolated by a wall from the rest of earthly world. In this mystic chiefly Rhenan altarpiece the enclosed garden is that of Virgin Mary who in the Middle Ages was likened to the spouse in the song of songs. The Blessed Virgin is painted with flowers, lily, rose, violet, lily of the valley. Most of these are medicinal plants in order to implore a faith healing for the believers. All in all about fifty plants are showed on Rhenan altarpieces and on 14th century mystic altarpieces almost contemporary of Issenheim's altarpiece, some Italian, some Rhenan.

In the 4th century A.D. the first unicorn was shown as a little horse with a twisted horn and was completely different from the Oriental one described by Marco Polo. The new unicorn appeared during the 4th century A.D. in Alexandria. This animal enamoured of purity was used as a Christian symbol of purity and sacrifice and adornment of churches like in Lyons in the 13th century. In the 15th17th centuries the unicorn was found again in famous tapestries like La Dame B la Licorne as it meant courage, speed and purity. Since the 6th century the powder of unicorn horn was used as a medicine or a drug against poisoning. Depictions of unicorn can be found in chemist's signs, engravings or paintings until the 19th century.

Background Children living close to roads are exposed to both traffic noise and traffic-related air pollution. There are indications that both exposures affect cognitive functioning. So far, the effects of both exposures have only been investigated separately. Objectives To investigate the relationship between air pollution and transportation noise on the cognitive performance of primary schoolchildren in both the home and school setting. Methods Data acquired within RANCH from 553 children (aged 9–11 years) from 24 primary schools were analysed using multilevel modelling with adjustment for a range of socio-economic and life-style factors. Results Exposure to NO2 (which is in urban areas an indicator for traffic-related air pollution) at school was statistically significantly associated with a decrease in the memory span length measured during DMST (χ2=6.8, df=1, p=0.01). This remained after additional adjustment for transportation noise. Statistically significant associations were observed between road and air traffic noise exposure at school and the number of errors made during the ‘arrow’ (χ2=7.5, df=1, p=0.006) and ‘switch’ (χ2=4.8, df=1, p=0.028) conditions of the SAT. This remained after adjustment for NO2. No effects of air pollution exposure or transportation noise exposure at home were observed. Combined exposure of air pollution and road traffic noise had a significant effect on the reaction times measured during the SRTT and the ‘block’ and the ‘arrow’ conditions of the SAT. Conclusions Our results provide some support that prolonged exposure to traffic-related air pollution as well as to noise adversely affects cognitive functioning.

This study sought to evaluate treatment outcomes of implant-prosthetic rehabilitation with implants in the edentulous maxilla or mandible that were immediately loaded by fixed prostheses. Special consideration was given to the time of implantation (immediate, delayed, or late implant placement).Twenty-five patients who received 283 immediately loaded screw-type implants were included in this retrospective study. Data captured included patient file information, panoramic and periapical radiographs obtained during treatment, and clinical parameters examined during the recall period. Clinical and radiographic status of peri-implant soft and hard tissue was evaluated, as well as the function of prostheses and subjective assessment by the patients of the treatment. Survival/success rates were analyzed with respect to the time of implantation.Following a maximum observation period of 120 months (median 29 months) postimplantation and subsequent immediate functional loading, implant survival was 99.6% (one implant failed after 20 months). The success rates were 98.2% for implants and 88% for patients; five implants in three patients did not meet success criteria. Neither the implant site nor the time of implantation were associated with unsuccessful outcomes. Implant-related evaluations revealed a significant association between implant success and implant length of 10 mm or less (P.018).Within the limits of this study, immediate loading of rough-surfaced, screw-type implants supporting fixed dentures for the treatment of edentulous maxilla or mandible appears to be a reliable treatment option with a high probability of success. The time of implantation did not influence implant survival or success rates.

Objectives Land use regression (LUR) modelling is a popular method to estimate outdoor air pollution concentrations at the home and/or work addresses of individual subjects in epidemiological studies. Typically, such models are constructed using measurements from dedicated monitoring campaigns lasting up to 1 year. It is unknown to what extent such models can adequately predict concentrations in earlier or later time periods. We tested the stability of measured and modelled spatial contrasts in outdoor nitrogen dioxide (NO 2 ) pollution across the Netherlands over 8 years. Methods NO 2 measurements were conducted at 40 locations in the Netherlands in 1999–2000. In 2007, NO 2 was again measured at 144 locations, of which 35 were the same as in 1999–2000. This enabled us to compare measurements as well as model predictions between the two time periods. Results NO 2 measurements conducted in 2007 agreed well with NO 2 measurements taken in 1999–2000 at the same locations (R 2 =0.86). LUR models from 1999–2000 and 2007 explained 85% and 86% of observed spatial variance, respectively. The 2007 LUR model explained 77% of spatial variability in the 1999–2000 measurements and the 1999–2000 model explained 81% of variability in the 2007 measurements. Conclusion We found good agreement between measured spatial contrasts in outdoor NO 2 in 1999–2000 and 2007. LUR models predicted spatial contrast 8 years in the past (2007 model) and 8 years in the future (1999–2000 model) well. This supports the use of LUR models in epidemiological studies with health data available for a later or earlier timepoint.

Background: Current air quality standards for particulate matter (PM) use the PM mass concentration [PM with aerodynamic diameters ≤ 10 μm (PM10) or ≤ 2.5 μm (PM2.5)] as a metric. It has been suggested that particles from combustion sources are more relevant to human health than are particles from other sources, but the impact of policies directed at reducing PM from combustion processes is usually relatively small when effects are estimated for a reduction in the total mass concentration. Objectives: We evaluated the value of black carbon particles (BCP) as an additional indicator in air quality management. Methods: We performed a systematic review and meta-analysis of health effects of BCP compared with PM mass based on data from time-series studies and cohort studies that measured both exposures. We compared the potential health benefits of a hypothetical traffic abatement measure, using near-roadway concentration increments of BCP and PM2.5 based on data from prior studies. Results: Estimated health effects of a 1-μg/m3 increase in exposure were greater for BCP than for PM10 or PM2.5, but estimated effects of an interquartile range increase were similar. Two-pollutant models in time-series studies suggested that the effect of BCP was more robust than the effect of PM mass. The estimated increase in life expectancy associated with a hypothetical traffic abatement measure was four to nine times higher when expressed in BCP compared with an equivalent change in PM2.5 mass. Conclusion: BCP is a valuable additional air quality indicator to evaluate the health risks of air quality dominated by primary combustion particles.

Background Air pollution may promote type 2 diabetes by increasing adipose inflammation and insulin resistance. This study examined the relation between long-term exposure to traffic-related air pollution and type 2 diabetes prevalence among 50- to 75-year-old subjects living in Westfriesland, the Netherlands. Methods Participants were recruited in a cross-sectional diabetes screening-study conducted between 1998 and 2000. Exposure to traffic-related air pollution was characterized at the participants' home-address. Indicators of exposure were land use regression modeled nitrogen dioxide (NO2) concentration, distance to the nearest main road, traffic flow at the nearest main road and traffic in a 250 m circular buffer. Crude and age-, gender- and neighborhood income adjusted associations were examined by logistic regression. Results 8,018 participants were included, of whom 619 (8%) subjects had type 2 diabetes. Smoothed plots of exposure versus type 2 diabetes supported some association with traffic in a 250 m buffer (the highest three quartiles compared to the lowest also showed increased prevalence, though non-significant and not increasing with increasing quartile), but not with the other exposure metrics. Modeled NO2-concentration, distance to the nearest main road and traffic flow at the nearest main road were not associated with diabetes. Exposure-response relations seemed somewhat more pronounced for women than for men (non-significant). Conclusions We did not find consistent associations between type 2 diabetes prevalence and exposure to traffic-related air pollution, though there were some indications for a relation with traffic in a 250 m buffer.

In a time series study, air pollution was associated with specific cardiovascular causes of death. Deaths due to heart failure (ICD-9 428), arrhythmia (ICD-9 427), cerebrovascular causes (ICD-9 430-436), and thrombocytic causes (ICD-9 415.1, 433-4, 444, 452-3) were more strongly associated with air pollution than cardiovascular deaths (ICD-9 390-448) in general. Excess relative risks were 2.5 to 4 times larger for these categories than for total cardiovascular disease mortality. Heart failure deaths, which made up 10% of all cardiovascular deaths, were found to be responsible for about 30% of the cardiovascular deaths related to particulate matter, SO2, CO, and NO2.

ObjectivesThere is growing evidence for an adverse effect of maternal exposure to air pollution on pregnancy outcomes. As European data on this topic are limited, the aim of this study was to evaluate the impact of maternal exposure to traffic-related air pollution during different periods of pregnancy on preterm birth and fetal growth.MethodsWe estimated maternal residential exposure to NO2during pregnancy (entire pregnancy and trimesters) for 7600 singleton births participating in the Amsterdam Born Children and their Development (ABCD) prospective birth cohort study by means of a temporally adjusted land-use regression model. Associations between air pollution concentrations and preterm birth and fetal growth (expressed as small for gestational age and term birth weight) were analysed by means of logistic and linear regression models with and without adjustment for maternal physiological, lifestyle and sociodemographic characteristics.ResultsThere was no indication of an increase in preterm birth among highly exposed women. Children of mothers with NO2levels in the highest exposure category on average had the highest term birth weight of all children and were among those with the lowest risk of being small for gestational age with little indication of a dose–response relationship.ConclusionsIn this study, there is no evidence for a harmful effect of estimated maternal exposure to traffic-related air pollution during pregnancy on pregnancy outcomes such as preterm birth, small for gestational age and term birth weight.

Typically developing 5- to 6-year-old children often reverse some digits (e.g., ɛ for 3) or single (capital) letters (e.g., Я for R) when they are required to write them under dictation. A theoretical approach to this phenomenon, based on an implicit right writing rule and that postulates an influence of the preceding writing, was tested in an experimental study of 300 children aged 5–6 years. The data support the implicit right writing rule and show the considerable influence of the preceding writing. For example, 73% of the children who correctly wrote the letter C mirror wrote an immediately following digit 3, whereas only 10% of the children who mirror wrote the letter C also mirror wrote an immediately following digit 3.

Jules Guiart was born in Château-Thierry in 1870. He took over from Louis Lortet at the chair of Parasitology and Natural History in Lyons while Jules Courmont took over at the chair of Medicine and Bacteriology in 1906. Guiart taught History of Medicine in Lyons and in Romania. He succeeded Lacassagne as chairman of the Academy of Lyons in 1926. Nowadays he looks like a symbolical link between the Society and the historians of medicine.

In 1943, René Guillet, a young surgeon in the Department of Professor Mallet-Guy, took part in the Resistance as he helped the wounded men in the hospital of Edouard Herriot. René Guillet joined the French Army of the Resistance on June 6, 1944. Then, in July 1944, he took care of the wounded men in the hospital of Oyonnax with doctor Parker, an English surgeon in the French hospital in London. Although it was very dangerous, the two doctors managed to transfer the wounded to Geneva.

Background Daily variations in the levels of air pollution are well known to be associated with daily variations in mortality counts. Given the large number of time-series studies, there is little need for simple replication of these results in additional locations. However, additional analyses of time-series data might be useful in elucidating remaining questions on the role of air pollution on mortality. Objectives Because of ongoing issues related to causality, changing toxicity, the difficulty in isolating the independent effects of individual pollutants, the availability of new methods to detect effect thresholds, and questions about the extent to which effects are restricted to frail members of the population, additional analyses of time-series data might be helpful in addressing these issues. We show an example where additional time-series analyses can be helpful in elucidating specific questions in the field of air pollution epidemiology. Methods We analysed daily mortality and air pollution data using Poisson regression in generalised additive models. Air pollution data for the overall period 1992–2006 and for four different periods were analysed to assess the overall risk estimates for the whole period and to assess variability over time for the different effect estimates. Results and Conclusion We found some statistically significant upward trends, but this was only the case for a few associations without a consistent pattern over the cause-specific deaths. Whether these findings are consistent over time or whether our findings are merely the result of statistical chance can only be elucidated by continuation of monitoring of the relative risks over time in the future. Although these results may indicate that both photochemical and particulate matter air pollution might have become more toxic, the lack of a clear pattern in the results makes these conclusions speculative.

Evidence is increasing that long-term exposure to ambient air pollution is associated with deaths from cardiopulmonary diseases. In a 2002 pilot study, we reported clear indications that traffic-related air pollution, especially at the local scale, was related to cardiopulmonary mortality in a randomly selected subcohort of 5000 older adults participating in the ongoing Netherlands Cohort Study (NLCS) on diet and cancer. In the current study, referred to as NLCS-AIR, our objective was to obtain more precise estimates of the effects of traffic-related air pollution by analyzing associations with cause-specific mortality, as well as lung cancer incidence, in the full cohort of approximately 120,000 subjects. Cohort members were 55 to 69 years of age at enrollment in 1986. Follow-up was from 1987 through 1996 for mortality (17,674 deaths) and from late 1986 through 1997 for lung cancer incidence (2234 cases). Information about potential confounding variables and effect modifiers was available from the questionnaire that subjects completed at enrollment and from publicly available data (including neighborhood-scale information such as income distributions). The NLCS was designed for a case-cohort approach, which makes use of all the cases in the full cohort, while data for the random subcohort are used to estimate person-time experience in the study. Full information on confounders was available for the subjects in the random subcohort and for the emerging cases of mortality and lung cancer incidence during the follow-up period, and in NLCS-AIR we used the case-cohort approach to examine the relation between exposure to air pollution and cause-specific mortality and lung cancer. We also specified a standard Cox proportional hazards model within the full cohort, for which information on potential confounding variables was much more limited. Exposure to air pollution was estimated for the subjects' home addresses at baseline in 1986. Concentrations were estimated for black smoke (a simple marker for soot) and nitrogen dioxide (NO2) as indicators of traffic-related air pollution, as well as nitric oxide (NO), sulfur dioxide (SO2), and particulate matter with aerodynamic diameteror = 2.5 microm (PM2.5), as estimated from measurements of particulate matter with aerodynamic diameteror = 10 microm (PM10). Overall long-term exposure concentrations were considered to be a function of air pollution contributions at regional, urban, and local scales. We used interpolation from data obtained routinely at regional stations of the National Air Quality Monitoring Network (NAQMN) to estimate the regional component of exposure at the home address. Average pollutant concentrations were estimated from NAQMN measurements for the period 1976 through 1996. Land-use regression methods were used to estimate the urban exposure component. For the local exposure component, geographic information systems (GISs) were used to generate indicators of traffic exposure that included traffic intensity on and distance to nearby roads. A major effort was made to collect traffic intensity data from individual municipalities. The exposure variables were refined considerably from those used in the pilot study, but we also analyzed the data for the full cohort in the current study using the exposure indicators of the pilot study. We analyzed the data in models with the estimated overall pollutant concentration as a single variable and with the background concentration (the sum of regional and urban components) and the local exposure estimate from traffic indicators as separate variables. In the full-cohort analyses adjusted for the limited set of confounders, estimated overall exposure concentrations of black smoke, NO2, NO, and PM2.5 were associated with mortality. For a 10-microg/m3 increase in the black smoke concentration, the relative risk (RR) (95% confidence interval [CI]) was 1.05 (1.00-1.11) for natural-cause (nonaccidental) mortality, 1.04 (0.95-1.13) for cardiovascular mortality, 1.22 (0.99-1.50) for respiratory mortality, 1.03 (0.88-1.20) for lung cancer mortality, and 1.04 (0.97-1.12) for noncardiopulmonary, non-lung cancer mortality. Results were similar for NO2, NO, and PM2.5. For a 10-microg/m3 increase in PM2.5 concentration, the RR for natural-cause mortality was 1.06 (95% CI, 0.97-1.16), the same as in the results of the American Cancer Society Study reported by Pope and colleagues in 2002. The highest relative risks were found for respiratory mortality, though confidence intervals were wider for this less-frequent cause of death. No associations with mortality were found for SO2. Some of the associations between the traffic indicator variables used to assess traffic intensity near the home and mortality reached statistical significance in the full cohort. For an increase in traffic intensity of 10,000 motor vehicles in 24 hours (motor vehicles/day) on the road nearest a subject's residence, the RR was 1.03 (95% CI, 1.00-1.08) for natural-cause mortality, 1.05 (0.99-1.12) for cardiovascular mortality, 1.10 (0.95-1.26) for respiratory mortality, 1.07 (0.96-1.19) for lung cancer mortality, and 1.00 (0.94-1.06) for noncardiopulmonary, non-lung cancer mortality. Results were similar for traffic intensity in a 100-m buffer around the subject's residence and living near a major road (a road with more than 10,000 motor vehicles/day). Distance in meters to the nearest major road and traffic intensity on the nearest major road were not associated with any of the mortality outcomes. We did not find an association between cardiopulmonary mortality and living near a major road as defined using the methods of the pilot study. In the case-cohort analyses adjusted for all potential confounders, we found no associations between background air pollution and mortality. The associations between traffic intensity and mortality were weaker than in the full cohort, and confidence intervals were wider, consistent with the smaller number of subjects. The lower relative risks of mortality associated with traffic variables in the case-cohort study population could be related to the particular subcohort that was randomly selected from the full cohort, as the risks estimated with the actual subcohort were well below the average estimates obtained for 100 new case-cohort analyses with 100 alternative subcohorts of 5000 subjects each that we randomly selected from the full cohort. Differences in adjusted relative risks between the full-cohort and the case-cohort analyses could be explained by random error introduced by sampling from the full cohort and by a selection effect resulting from the relatively large number of missing data for variables in the extensive confounder model used in the case-cohort analyses. More complete control for confounding probably did not contribute much to the lower relative risks in the case-cohort analyses, especially for the traffic variables, as results were similar when the limited confounder model for the full cohort was used in analyses of the subjects in the case-cohort study population. In additional analyses using black smoke concentrations as the exposure variables, we found that the association between overall black smoke and cardiopulmonary mortality was somewhat stronger for case-cohort subjects who did not change residence during follow-up, and in the full cohort, there was a tendency for relative risks to be higher for subjects living in the three major cities included in the study. Adjustment for estimated exposure to traffic noise did not affect the associations of background black smoke and traffic intensity with cardiovascular mortality. There was some indication of an association between traffic noise and cardiovascular mortality only for the 1.6% of the subjects in the full cohort who were exposed to traffic noise in the highest category of65 A-weighted decibels (dB(A); decibels with the sound pressure scale adjusted to conform with the frequency response of the human ear). Examination of sex, smoking status, educational level, and vegetable and fruit intake as possible effect modifiers showed that for overall black smoke concentrations, associations with mortality tended to be stronger in case-cohort subjects with lower levels of education and those with low fruit intake, but differences between strata were not statistically significant. For lung cancer incidence, we found essentially no relation to exposure to NO2, black smoke, PM2.5, SO2, or several traffic indicators. Associations of overall air pollution concentrations and traffic indicator variables with lung cancer incidence were, however, found in subjects who had never smoked, with an RR of 1.47 (95% CI, 1.01-2.16) for a 10-microg/m3 increase in overall black smoke concentration. In the current study, the mortality risks associated with both background air pollution and traffic exposure variables were much smaller than the estimate previously reported in the pilot study for risk of cardiopulmonary mortality associated with living near a major road (RR, 1.95; 95% CI, 1.09-3.51). The differences are most likely due to the extension of the follow-up period in the current study and to random error in the pilot study related to sampling from the full cohort. Though relative risks were generally small in the current study, long-term average concentrations of black smoke, NO2, and PM2.5 were related to mortality, and associations of black smoke and NO2 exposure with natural-cause and respiratory mortality were statistically significant. Traffic intensity near the home was also related to natural-cause mortality. The highest relative risks associated with background air pollution and traffic variables were for respiratory mortality, though the number of deaths was smaller than for the other mortality categories. (ABSTRACT TRUNCATED)

Sophie Delaporte's book, Philippe Paillard's, Chantal Roussels's novels and Dupeyron's movie underline the difficulties of repairing physical and moral sufferings of the "disfigured men" wounded during the Great War. Beside medical and technical didactic aimed drawings the exhibition of wasted, mutilated or out of repair faces remains little known. In France, Germany or Great Britain there are many artists who took part in war. Among the artists the French painter Raphael Freida and some German expressionists like Otto Dix, Max Beckmann or George Grosz are the most famous. Their works are often confidential, set apart in the museums and showed in rare exhibitions in Great Britain and the United States of America. The sight of ruined faces inspired such horror that the artists depicted it only exceptionally and with discretion, before 1914. Without doubt it is the fear of touching the privacy of the face which is a part of the human identity. There are no "disfigured men" in the countless religious paintings of torture, neither in the Disasters of Warfrom painters or engravers like Goya or Jacques Callot.

Mean flow predictions obtained from a host of turbulence models were found to be in poor agreement with recent direct numerical simulation results for turbulent flow distal to an idealized eccentric stenosis. Many of the widely used turbulence models, including a large eddy simulation model, were unable to accurately capture the poststenotic transition to turbulence. The results suggest that efforts toward developing more accurate turbulence models for low-Reynolds number, separated transitional flows are necessary before such models can be used confidently under hemodynamic conditions where turbulence may develop.

BACKGROUND: Several studies have found an effect on mortality of between-city contrasts in long-term exposure to air pollution. The effect of within-city contrasts is still poorly understood. OBJECTIVES: We studied the association between long-term exposure to traffic-related air pollution and mortality in a Dutch cohort. METHODS: We used data from an ongoing cohort study on diet and cancer with 120,852 subjects who were followed from 1987 to 1996. Exposure to black smoke (BS), nitrogen dioxide, sulfur dioxide, and particulate matter < or = 2.5 microm (PM(2.5)), as well as various exposure variables related to traffic, were estimated at the home address. We conducted Cox analyses in the full cohort adjusting for age, sex, smoking, and area-level socioeconomic status. RESULTS: Traffic intensity on the nearest road was independently associated with mortality. Relative risks (95% confidence intervals) for a 10-microg/m(3) increase in BS concentrations (difference between 5th and 95th percentile) were 1.05 (1.00-1.11) for natural cause, 1.04 (0.95-1.13) for cardiovascular, 1.22 (0.99-1.50) for respiratory, 1.03 (0.88-1.20) for lung cancer, and 1.04 (0.97-1.12) for mortality other than cardiovascular, respiratory, or lung cancer. Results were similar for NO(2) and PM(2.5), but no associations were found for SO(2). CONCLUSIONS: Traffic-related air pollution and several traffic exposure variables were associated with mortality in the full cohort. Relative risks were generally small. Associations between natural-cause and respiratory mortality were statistically significant for NO(2) and BS. These results add to the evidence that long-term exposure to ambient air pollution is associated with increased mortality.

As a military surgeon Henry Gabrielle had a heroic behaviour during the World War I. He was appointed professor of surgery at the hospital Val-de-Grâce in 1919 and in 1926 he became professor of anatomy at the Faculty of Medicine in Lyon. His action in the French Resistance was so significant that he was appointed Health Director of the Region Rhône Alpes. As president of the hospitals of Lyon from 1952 his role of organisation was important.

Three mummies--one of a woman and two of a woman and a child--are nowadays presented in the Museum of Anatomy Testut-Latarjet in Lyon. They have been brought in 1901 from Egypt to the Museum Guimet of Lyon and after a few years, they have been given to Professor Testut and studied by Louis Paul Fisher and Frederique Cantero in a thesis of medicine of Lyon (1991). They have been examined by x-rays non-invasive scanning by Professor Michel Bochut. Finally Professor Jean-Claude Goyon, chairman in the "Maison de l'Orient", proposed to date them from the end of the 5th or the beginning of the 6th century, after the designs and the ornaments of the clothes.

Background: Conclusions that can be drawn from earlier studies on noise and children’s blood pressure are limited due to inconsistent results, methodological problems, and the focus on school noise exposure. Objectives: To investigate the effects of aircraft and road traffic noise exposure on children’s blood pressure and heart rate. Methods: Participants were 1283 children (age 9–11 years) attending 62 primary schools around two European airports. Data were pooled and analysed using multilevel modelling. Adjustments were made for a range of socioeconomic and lifestyle factors. Results: After pooling the data, aircraft noise exposure at school was related to a statistically non-significant increase in blood pressure and heart rate. Aircraft noise exposure at home was related to a statistically significant increase in blood pressure. Aircraft noise exposure during the night at home was positively and significantly associated with blood pressure. The findings differed between the Dutch and British samples. Negative associations were found between road traffic noise exposure and blood pressure, which cannot be explained. Conclusion: On the basis of this study and previous scientific literature, no unequivocal conclusions can be drawn about the relationship between community noise and children’s blood pressure.

Background: In epidemiological studies of the potential health effects of traffic related air pollution, self reported traffic intensity is a commonly used, but rarely validated, exposure variable. Methods: As part of a study on the impact of Traffic Related Air Pollution on Childhood Asthma (TRAPCA), data from 2633 and 673 infants from the Dutch and the German-Munich cohorts, respectively, were available. Parents subjectively assessed traffic intensity at the home address. Objective exposures were estimated by a combination of spatial air pollution measurements and geographic information system (GIS) based modelling using an identical method for both cohorts. Results: The agreement rates between self reported and GIS modelled exposure—accumulated over the three strata of self assessed traffic intensity—were 55-58% for PM2.5, filter absorbance (PM2.5 abs), and nitrogen dioxide in Munich and 39-40% in the Netherlands. Of the self reported low traffic exposed group, 71-73% in Munich and 45-47% in the Netherlands had low modelled exposure to these three air pollutants. Of the self assessed high exposed subgroups in Munich (15% of the total population) and the Netherlands (22% of the total population), only 22-33% and 30-32% respectively had high modelled exposure to the three air pollutants. The subjective assessments tend to overestimate the modelled estimates for PM2.5 and NO2 in both study areas. When analysis was restricted to the portion of the Dutch cohort living in non-urban areas, the agreement rates were even lower. Conclusions: Self reported and modelled assessment of exposure to air pollutants are only weakly associated.

In order to estimate the spatial variation within well-defined study areas, nitrogen dioxide was measured with diffusion samplers (Palmes tube) in 40-42 sites each in Germany (Munich), the Netherlands and Sweden (Stockholm County). Each site was measured over four 2-week periods during 1 year (spring 1999 to summer 2000). In each country, one reference site was measured during all periods and the results were used to adjust for seasonal variability, to improve the estimates of the annual average. Comparisons between the chemiluminescence method (European reference method) and Palmes tube measurement indicated a good agreement in Germany (with a ratio of 1.0 for Palmes tube/chemiluminescence) but underestimation for Palmes tube measurement in the Netherlands and Sweden (0.8 for both countries). The r2 values were between 0.86 and 0.90 for all three countries. The annual average values for NO2 for different sampling sites were between 15.9 and 50.6 (mean 28.8 microg/m3) in Germany, between 12.1 and 50.8 (mean 28.9 microg/m3) in the Netherlands and between 6.1 and 44.7 (mean 18.5 microg/m3) in Sweden. Comparing spatial variation between similar sites in the three countries, we did not find any significant differences between annual average levels for urban traffic sites. In Sweden, annual average levels in urban background and suburban backgrounds sites were about 8 microg/m3 lower than comparable sites in Germany and the Netherlands. Comparing site types within each country only urban traffic sites and suburban background sites differed in Germany. In the Netherlands and Sweden, the urban traffic sites differed from all other sites and in Sweden also the urban background sites differed from the other background sites. The observed contribution from local traffic was similar in the Netherlands and Sweden (10 and 8 microg/m3, corresponding to 26-27% of the NO2 concentration found in the urban traffic sites). In Germany, the contribution from local traffic was only 3 microg/m3, corresponding to 9% of the NO2 concentration found in the urban traffic sites. The spatial variation was substantially larger for NO2 than the variation for PM2.5 and similar to PM2.5 absorbance, measured in the same locations.

As part of a multicenter study relating traffic-related air pollution with incidence of asthma in three birth cohort studies (TRAPCA), we used a measurement and modelling procedure to estimate long-term average exposure to traffic-related particulate air pollution in communities throughout the Netherlands; in Munich, Germany; and in Stockholm County, Sweden.In each of the three locations, 40-42 measurement sites were selected to represent rural, urban background and urban traffic locations. At each site and fine particles and filter absorbance (a marker for diesel exhaust particles) were measured for four 2-week periods distributed over approximately 1-year periods between February 1999 and July 2000. We used these measurements to calculate annual average concentrations after adjustment for temporal variation. Traffic-related variables (eg, population density and traffic intensity) were collected using Geographic Information Systems and used in regression models predicting annual average concentrations. From these models we estimated ambient air concentrations at the home addresses of the cohort members.Regression models using traffic-related variables explained 73%, 56% and 50% of the variability in annual average fine particle concentrations for the Netherlands, Munich and Stockholm County, respectively. For filter absorbance, the regression models explained 81%, 67% and 66% of the variability in the annual average concentrations. Cross-validation to estimate the model prediction errors indicated root mean squared errors of 1.1-1.6 microg/m for PM(2.5) and 0.22-0.31 *10(-5) m for absorbance.A substantial fraction of the variability in annual average concentrations for all locations was explained by traffic-related variables. This approach can be used to estimate individual exposures for epidemiologic studies and offers advantages over alternative techniques relying on surrogate variables or traditional approaches that utilize ambient monitoring data alone.

BACKGROUND: Long-term exposure to particulate matter air pollution has been associated with increased cardiopulmonary mortality in the USA. We aimed to assess the relation between traffic-related air pollution and mortality in participants of the Netherlands Cohort study on Diet and Cancer (NLCS), an ongoing study. METHODS: We investigated a random sample of 5000 people from the full cohort of the NLCS study (age 55-69 years) from 1986 to 1994. Long-term exposure to traffic-related air pollutants (black smoke and nitrogen dioxide) was estimated for the 1986 home address. Exposure was characterised with the measured regional and urban background concentration and an indicator variable for living near major roads. The association between exposure to air pollution and (cause specific) mortality was assessed with Cox's proportional hazards models, with adjustment for potential confounders. FINDINGS: 489 (11%) of 4492 people with data died during the follow-up period. Cardiopulmonary mortality was associated with living near a major road (relative risk 1.95, 95% CI 1.09-3.52) and, less consistently, with the estimated ambient background concentration (1.34, 0.68-2.64). The relative risk for living near a major road was 1.41 (0.94-2.12) for total deaths. Non-cardiopulmonary, non-lung cancer deaths were unrelated to air pollution (1.03, 0.54-1.96 for living near a major road). INTERPRETATION: Long-term exposure to traffic-related air pollution may shorten life expectancy.