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Now is the time for the science of epidemiology to embrace its pragmatic roots. The article by Galea in this issue of the Journal (Am J Epidemiol. 2013;178(8):1185-1191) calls for us to become more "consequentialist." The Affordab...
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Now is the time for the science of epidemiology to embrace its pragmatic roots. The article by Galea in this issue of the Journal (Am J Epidemiol. 2013;178(8):1185-1191) calls for us to become more "consequentialist." The Affordable Care Act allows us to access population-level databases from which we can examine how to deliver care more efficiently and cost-effectively. Asking the questions "so what" and "how much" will increase our relevance over the next decade.
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Rhinovirus, influenza, parainfluenza or respiratory syncytial virus not only provoke upper respiratory tract infections (URI) but also can precipitate asthma in adults and children, many of whom also manifest allergic respiratory ...
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Rhinovirus, influenza, parainfluenza or respiratory syncytial virus not only provoke upper respiratory tract infections (URI) but also can precipitate asthma in adults and children, many of whom also manifest allergic respiratory disease. It has been postulated that patients with allergic rhinitis experience more pronounced symptoms and pathophysiology during URI than individuals without allergy. These observations have provided limited insight into the pathogenesis of URI in allergic patients. To better define these relationships several groups of investigators have examined the effect of experimental virus infection on volunteers, with and without allergic rhinitis and with and without asthma. Lemanski et al. showed that Rhinovirus-16 (RV16) was able to modify bronchial hyperreactivity and late phase allergic asthmatic reactions. Calhoun et al. demonstrated that RV16 potentiated airway inflammation after segmental allergen bronchoprovocation in allergic subjects. Experimental RV16 infection also provoked a modest increase in histamine responsiveness accompanied by a modest increase in bronchial and intranasal lymphocytes and eosinophils. Yet, experimental RV16 infection did not trigger asthma or changes in spirometry or changes in bronchial reactivity to histamine or bradykinin in normal subjects. Studies in our laboratories using experimental Rhinovirus 39 (RV39) infection did not-alter pulmonary measurements or methacholine responses in normal healthy allergic subjects. These results were surprising, as enhanced WBC histamine release was observed in the same RV39-infected allergic subjects and was similar to that observed in RV16 infection described by others. The RV39-infected allergic subjects also showed acute increases in serum IgE as well as changes of cellular immune parameters. Bardin et al. described more severe nasal symptoms as well as increased nasal albumin in allergic rhinitis subjects experimentally infected with RV16. However, allergic subjects infected with RV39 did not show a physiologic hyper-responsiveness during a nonallergy season. Analysis of nasal secretions during RV39 infection did show more vascular permeability in allergic subjects. Experimental infection with RV39 and Influenza A has provoked eustachian tube obstruction, otitis media and rarely acute otitis. These studies of volunteers experimentally infected with virus suggest that atopy alone does not predispose to more severe symptoms but combining URI with allergen exposure enhanced allergen-induced inflammation. Recent studies implicate cytokines as participants in these virus-provoked responses. Increases in nasal lavage concentrations of IL-6 were found during experimental URIs caused by RV39, Influenza A and respiratory syncytial virus and coincide with peaks in symptomatology and pathophysiology. Moreover, IL-6 applied directly to the nasal mucosa in noninfected allergic subjects reproduced symptoms of rhinitis. Other studies have shown that IL-10 secretion from peripheral blood white cells was impaired in allergic subjects after experimental infection with Influenza A. It is anticipated that future studies using natural infection as well as experimental virus infection model will further define the mechanisms and relationships of virus infection to allergy and asthma.
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Epidemiology is the branch of science that investigates the causes and distribution of disease in populations in order to provide preventative measures and promote human health. The fields of genetic and environmental epidemiology...
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Epidemiology is the branch of science that investigates the causes and distribution of disease in populations in order to provide preventative measures and promote human health. The fields of genetic and environmental epidemiology primarily seek to identify genetic and environmental risk factors for disease, respectively. Epigenetics is emerging as an important piece of molecular data to include in these studies because it can provide mechanistic insights into genetic and environmental risk factors for disease, identify potential intervention targets, provide biomarkers of exposure, illuminate gene-environment interactions and help localize disease-relevant genomic regions. Here, we describe the importance of including epigenetics in genetic and environmental epidemiology studies, provide a conceptual framework when considering epigenetic data in population-based studies and touch upon the many challenges that lie ahead.
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Public and occupational exposures to microwave (RF) radiation are of two main types. The first type of exposures are those connected with military and industrial uses and, to someextent, broadcast exposures. It is this type that m...
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Public and occupational exposures to microwave (RF) radiation are of two main types. The first type of exposures are those connected with military and industrial uses and, to someextent, broadcast exposures. It is this type that most of the data cited in this study draw upon. The second type, cellular telephones and their associated broadcast requirements, have raised concerns about current exposures because of their increasingly widespread use.
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Respiratory-related morbidity and mortality were evaluated in relation to incident prescription oral synthetic cannabinoid (nabilone, dronabinol) use among older adults with chronic obstructive pulmonary disease (COPD).This was a ...
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Respiratory-related morbidity and mortality were evaluated in relation to incident prescription oral synthetic cannabinoid (nabilone, dronabinol) use among older adults with chronic obstructive pulmonary disease (COPD).This was a retrospective, population-based, data-linkage cohort study, analysing health administrative data from Ontario, Canada, from 2006 to 2016. We identified individuals aged 66 years and older with COPD, using a highly specific, validated algorithm, excluding individuals with malignancy and those receiving palliative care (n=185?876 after exclusions). An equivalent number (2106 in each group) of new cannabinoid users (defined as individuals dispensed either nabilone or dronabinol, with no dispensing for either drug in the year previous) and controls (defined as new users of a non-cannabinoid drug) were matched on 36 relevant covariates, using propensity scoring methods. Cox proportional hazard regression was used.Rate of hospitalisation for COPD or pneumonia was not significantly different between new cannabinoid users and controls (HR 0.87; 95% CI 0.61–1.24). However, significantly higher rates of all-cause mortality occurred among new cannabinoid users compared with controls (HR 1.64; 95%?CI 1.14–2.39). Individuals receiving higher-dose cannabinoids relative to controls were observed to experience both increased rates of hospitalisation for COPD and pneumonia (HR 2.78; 95%?CI 1.17–7.09) and all-cause mortality (HR 3.31; 95%?CI 1.30–9.51).New cannabinoid use was associated with elevated rates of adverse outcomes among older adults with COPD. Although further research is needed to confirm these observations, our findings should be considered in decisions to use cannabinoids among older adults with COPD.
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PURPOSE. To determine whether there is an association between polymorphisms of the AKR1B1 gene and cortical cataract in the presence of hyperglycemia.
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Five species of Bolivian carnivores, including nine Geoffroy's cats (Oncifelis geoffroyi), ten ocelots (Leopardus pardalis), one jaguarundi (Herpailurus yaguarondi), nine pampas foxes (Pseudalopex gymnocercus), and five crab-eatin...
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Five species of Bolivian carnivores, including nine Geoffroy's cats (Oncifelis geoffroyi), ten ocelots (Leopardus pardalis), one jaguarundi (Herpailurus yaguarondi), nine pampas foxes (Pseudalopex gymnocercus), and five crab-eating foxes (Cerdocyon thous) were sampled between March 2001 and April 2005 and tested for antibodies to common pathogens of domestic carnivores. Carnivores were trapped in three areas: a village, the region between human settlements and a protected area, and within Kaa-Iya National Park, Bolivia. Antibodies to canine distemper virus were detected in ocelots and pampas foxes. Antibodies to canine parvovirus were detected in pampas foxes and crab-eating foxes. Geoffroy's cats and all of the ocelots tested positive for antibodies to feline calicivirus (FCV), while fewer than half of Geoffroy's cats and no ocelots had antibodies to feline panleukopenia (FPV). These results confirm that these species of Bolivian carnivores are not naive to common pathogens of domestic carnivores, and seropositive animals were found in villages as well as in the national park..
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Heat exposure has been related to increased morbidity and mortality for several health outcomes. There is little evidence whether this is also true for COPD. This study quantified the relationship between ambient heat and hospital...
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Heat exposure has been related to increased morbidity and mortality for several health outcomes. There is little evidence whether this is also true for COPD. This study quantified the relationship between ambient heat and hospitalisation for COPD in the Brazilian population.Data on hospitalisations for COPD and weather conditions were collected from 1642 cities during the 2000–2015 hot seasons. A time-stratified, case-crossover design was used for city-specific analyses, which were then pooled at the regional and national levels using random-effect meta-analyses. Stratified analyses were performed by sex, age group and early/late hot season. Annual change in the association was examined using a random-effect meta-regression model.The OR of hospitalisation was 1.05 (95% CI 1.04 to 1.06) for every 5℃ increase in daily mean temperature at the national level, with the effect estimate stronger in the late hot season compared with the early hot season. The effect was similar in women and in men but was greatest for those aged ≥75 years. The association was stronger in the central west and southeast regions and minimal in the northeast. Assuming a causal relationship, 7.2% of admissions were attributable to heat exposure. There was no significant temporal decline in the impact of ambient heat over the 16-year study period.In Brazil, exposure to ambient heat was positively associated with hospitalisation for COPD, particularly during the late hot season. These data add to the growing evidence base implicating global warming as being an important contributor to the future healthcare burden.
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В статье обсуждаются основные элементы научного познания в эпидемиологии, а именно — ее предметная область, цели и методы Обо...
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В статье обсуждаются основные элементы научного познания в эпидемиологии, а именно — ее предметная область, цели и методы Обосновывается утверждение, что основным предметом эпидемиологии, определяющим ее специфику, является заболеваемость населения и раскрывается содержание цели и используемых методов. Дано определение термина <<эпидемиологический подход>>. Приводится схема, отражающая структуру эпидемиологии.
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