Germline MSH2 and MLH1 mutational spectrum in HNPCC families from Poland and the Baltic States.

Peer reviewe

Systematic review with meta-analysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema

<p>Abstract</p> <p>Background</p> <p>Smoking is a known cause of the outcomes COPD, chronic bronchitis (CB) and emphysema, but no previous systematic review exists. We summarize evidence for various smoking indices.</p> <p>Methods</p> <p>Based on MEDLINE searches and other sources we obtained papers published to 2006 describing epidemiological studies relating incidence or prevalence of these outcomes to smoking. Studies in children or adolescents, or in populations at high respiratory disease risk or with co-existing diseases were excluded. Study-specific data were extracted on design, exposures and outcomes considered, and confounder adjustment. For each outcome RRs/ORs and 95% CIs were extracted for ever, current and ex smoking and various dose response indices, and meta-analyses and meta-regressions conducted to determine how relationships were modified by various study and RR characteristics.</p> <p>Results</p> <p>Of 218 studies identified, 133 provide data for COPD, 101 for CB and 28 for emphysema. RR estimates are markedly heterogeneous. Based on random-effects meta-analyses of most-adjusted RR/ORs, estimates are elevated for ever smoking (COPD 2.89, CI 2.63-3.17, n = 129 RRs; CB 2.69, 2.50-2.90, n = 114; emphysema 4.51, 3.38-6.02, n = 28), current smoking (COPD 3.51, 3.08-3.99; CB 3.41, 3.13-3.72; emphysema 4.87, 2.83-8.41) and ex smoking (COPD 2.35, 2.11-2.63; CB 1.63, 1.50-1.78; emphysema 3.52, 2.51-4.94). For COPD, RRs are higher for males, for studies conducted in North America, for cigarette smoking rather than any product smoking, and where the unexposed base is never smoking any product, and are markedly lower when asthma is included in the COPD definition. Variations by sex, continent, smoking product and unexposed group are in the same direction for CB, but less clearly demonstrated. For all outcomes RRs are higher when based on mortality, and for COPD are markedly lower when based on lung function. For all outcomes, risk increases with amount smoked and pack-years. Limited data show risk decreases with increasing starting age for COPD and CB and with increasing quitting duration for COPD. No clear relationship is seen with duration of smoking.</p> <p>Conclusions</p> <p>The results confirm and quantify the causal relationships with smoking.</p

Air pollution and respiratory health of children: the PEACE panel study in Katowice, Poland.

This study was carried out within the framework of the multicentre Pollution Effects on Asthmatic Children in Europe (PEACE) project. Two panels of mildly asthmatic children were studied. Seventy two children living in the Upper Silesia (the largest Polish industrial agglomeration) and 73 children in the control panel were followed up during two winter months in 1994. Ambient concentration of particles with a 50% cut-off aerodynamic diameter of 10 μm (PM10) black smoke, SO2 and NO2 were measured and peak respiratory flows and respiratory symptoms were recorded on a daily basis. There were no substantial differences in exposure to air pollution and the prevalence of respiratory symptoms between the urban and the control panels. No severe smog episodes were observed. No consistent association between daily changes of air pollution levels and daily variations of peak expiratory flows or respiratory symptoms prevalence and incidence was found. In conclusion, no clear effect of air pollution on respiratory health could be observed

Inter-laboratory comparison of flow-volume curve measurements as quality control procedure in the framework of an international epidemiological study (PEACE project)

The aim of this work was to describe the results of a simple quality control procedure for the flow-volume curve adopted in a multicentre epidemiological study (PEACE). In 14 centres, 8-15 individuals (n = 157) performed forced vital capacity (FVC) manoeuvres following a standard protocol with both the local spirometer/pneumotachograph and a portable spirometer (i.e. the 'reference instrument' for this study). Deviances of measurements were assessed by computing the differences (Delta d) between the former and the latter, the ratios of such differences on portable spirometer values (Delta%) and the coefficients of variation (CV). The portable spirometer yielded lower mean Delta FVC and Delta FEV1 (forced in 1 sec) than local instruments (except for two and four centres, respectively). In most instances, differences were statistically significant. Absolute mean Delta%FVC ranged from 4.9-18.2%, while Delta%FEV1 ranged from 2.3-18.5%. The Bland and Altman analysis showed a good agreement between the portable and local instruments, except for two centres, where a systematic trend towards higher individual absolute Delta FVC and Delta FEV1 was observed. The overall variability, assessed by CV, was within 6.2% and 5.1% for FVC and FEV1, respectively: it was similar to other quality control studies ranging from 2.0-5.5% for FVC and 2.2-5.8% for FEV1. Our results point out the importance of performing interlaboratory comparisons as a quality control procedure in multicentre epidemiological studies on lung function, and of stimulating manufacturers to extend the accuracy and precision of the instruments

Angiotensin-(1-7) receptor Mas agonist ameliorates progress of atherosclerosis in apoE-knockout mice

Our interest focused on an open question whether AT-(1-7), nonpeptide receptor agonist: AVE 0991, is able to ameliorate atherosclerosis. We used an apolipoprotein E (apoE) - knockout mice model of atherosclerosis. Experimental groups received the same diet as control, mixed with: AVE 0991 at a dose of 0.58 μmol/kg b.w./day, perindopril at a dose of 0.4 mg/kg b.w./day or with tiorphan at a dose of 2.5 mg/kg b.w./day. A-779 [(D-alanine)-angiotensin (1-7)] was given at a dose of 3.3 mg/kg b.w., 3 times a week i.p. Measured by "en face" method, the percentage of occupied by Sudan IV-stained surfaces were as follows: 14.2±1.9 % in control group, whereas in AVE 0991-treated as well as in perindopril-treated groups percentages were statistically significantly lower. In tiorphan group there was no change comparing to control group, whereas in A-779 group percentage was statistically significantly higher. "Cross-section" of aortic roots revealed also the difference in atherosclerotic lesions. The mean surfaces, occupied by oil red O-stained changes were: 91.213±8.123 μm(2) in control group, while in AVE 0991-treated as well as in perindopril-treated groups lesions were statistically significantly lower. In tiorphan group there was no change; however, in A-779 group lesions were statistically significantly higher. Measured by real time RT-PCR relative p22phox (submit of NADPH oxidase) expression was significantly decreased in AVE 0991-treated mice. As revealed by flow cytometry, the expression of co-stimulatory molecules: CD86, CD80 and CD40 on both dendritic cells (CD11c+) and macrophages (F4/80+) was reduced in AVE 0991-treated group, which correlated with decreased expression of CD69 activation marker on CD4+T cells. In our report we showed the beneficial effect of AVE 0991 on atherogenesis in gene-targeted mice