OBJECTIVES: The Swiss Cohort Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) was designed to investigate the health effects from long-term exposure to air pollution. METHODS: The health assessment at recruitment (1991) and at the first reassessment (2001-3) consisted of an interview about respiratory health, occupational and other exposures, spirometry, a methacholine bronchial challenge test, end-expiratory carbon monoxide (CO) measurement and measurement for atopy. A bio bank for DNA and blood markers was established. Heart rate variability was measured using a 24-hour ECG (Holter) in a random sample of participants aged 50 years and older. Concentrations of nitrogen dioxide (NO2), sulphur dioxide (SO2), ozone (O3) and particulates in ambient air have been monitored in all study areas since 1991. Residential histories collected over the 11 year follow-up period coupled with GIS modelling will provide individual long-term air pollutant exposure estimates. RESULTS: Of 9651 participants examined in 1991, 8715 could be traced for the cohort study and 283 died. Basic information about health status was obtained for 8047 individuals (86% of alive persons), 6 528 individuals (70%) agreed to the health examination and 5 973 subjects (62%) completed the entire protocol. Non-participants in the reassessment were on average younger than participants and more likely to have been smokers and to have reported respiratory symptoms in the first assessment. Average weight had increased by 5.5 kg in 11 years and 28% of smokers in 1991 had quit by the time of the reassessment. The most powerful approach for studying long-term effects from ambient air pollution on health is the long-term prospective follow-up of well-defined population-based cohorts with well-characterized air pollution exposure information (European Science Foundation 1998). There are currently only five cohort studies in adults, with published results, that address the long-term impact of air pollution (Abbey et al. 1999;Dockery et al. 1993;Finkelstein et al. 2004;Hoek et al. 2002; Pope et al. 2002;. All studies but one are based in the US and three of them (Dockery et al. 1993;Hoek et al. 2002; Pope et al. 2002), have only published findings related to mortality. The relation of longterm exposure to air pollution with respiratory and cardiovascular health and morbidity has yet to be measured in a large prospective cohort study in Europe. The large European Community Respiratory Health Survey (ECRHS) de- Probst-Hensch NM, et al. Follow-up of SAPALDIA 2, 1991-2003 signed to measure natural history and risk factors for respiratory diseases (particularly asthma and allergy) across Europe has recently included air pollution exposure assessment in its protocol (Burney et al. 1994;Hazenkamp-von Arx et al. 2004). However, the Swiss Cohort Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) is the only prospective cohort study of respiratory and cardiovascular health in adults in Europe with detailed individual residential exposure hi...
TSH concentrations are elevated in obese children but are not correlated with the amount of excess body weight or fat. During weight loss, independent of changes in body weight or composition, decreases in elevated serum TSH predict decreases in fasting insulin and HOMA. These findings suggest interventions that target high TSH concentrations during weight loss in obese subjects may improve insulin sensitivity.
CD137 (ILA / 4‐1BB) is a member of the TNF / NGF receptor family, and has previously been suggested to be involved in T cell activation and differentiation. Here, we demonstrate that blood neutrophils from control individuals and patients with cystic fibrosis express CD137 mRNA and surface protein. In contrast, lung neutrophils derived from patients with cystic fibrosis did not express detectable CD137 levels. Such CD137‐deficient neutrophils could also be generated from normal neutrophils by TNF‐α stimulation in vitro. TNF‐α was found to be highly expressed in epithelial cells from cystic fibrosis but not normal lungs, suggesting that TNF‐α might account for reduced neutrophil CD137 levels under inflammatory conditions in vivo. To investigate whether CD137 is involved in the regulation of apoptosis, neutrophils were activated with functional anti‐CD137 antibody in the presence or absence of different neutrophil survival factors in vitro. Activation of CD137 abrogated GM‐CSF‐mediated anti‐apoptosis in normal but not in CD137‐deficient neutrophils. Moreover, G‐CSF‐ and IFN‐γ‐mediated neutrophil anti‐apoptosis was not affected by anti‐CD137 antibody treatment. In conclusion, these data suggest that CD137 activation may limit GM‐CSF‐mediated anti‐apoptosis of neutrophils. The absence of this anti‐inflammatory mechanism in inflammatory responses might be associated with massive neutrophil accumulation and consequent tissue damage.
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