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Background Heatwaves affect human health and global heatwave-related disease burden will continue to rise as climate change proceeds, but the effects of heatwaves on cardiovascular and respiratory diseases have not yet been investigated globally and nationally. Objectives This systematic review and meta-analysis aim to quantify heatwave effects on four major health outcomes: cardiovascular and respiratory morbidity and mortality. Methods We searched PubMed, Scopus, Embase, and Web of Science for relevant studies from database inception to November 2018. Categories of morbidity included hospital admissions, emergency department visits, and ambulance attendances/call-outs. A random-effects meta-analysis model was used to pool previous estimates of heatwave effects on mortality and morbidity due to cardiovascular and respiratory diseases. Subgroup analyses by gender, age, and disease cause were conducted. Sensitivity analyses were performed by the categories of morbidity, heatwave definitions, study design, and using a leave-one-out cross validation approach. This study is registered with PROSPERO (number: CRD42018101964). Results We identified 54 studies conducted in 20 countries. In total, there were significant associations between heatwaves and cardiovascular mortality (risk estimates (RE): 1.149, 95% confidence interval (CI): 1.090, 1.210) and respiratory mortality (RE: 1.183, 95%CI: 1.092, 1.282), but the magnitude of these associations varied across countries and studies. Heatwaves appeared to be marginally associated with cardiovascular and respiratory morbidities (RE: 0.999, 95%CI: 0.996, 1.002, p-value = 0.61 for cardiovascular morbidity; RE: 1.043, 95%CI: 0.995, 1.093; p-value = 0.08 for respiratory morbidity). For mortality, significant associations were observed for the elderly, ischemic heart disease, stroke, heart failure, and chronic obstructive pulmonary disease. Sensitivity analyses suggested that these findings were robust. Conclusion Mortality of ca

The recent advances in biotechnology in the plant industry have led to increasing crop production and yield that in turn has increased the usage of genetically modified (GM) food in the human food chain. The usage of GM foods for human consumption has raised a number of fundamental questions including the ability of GM foods to elicit potentially harmful immunological responses, including allergic hypersensitivity. To assess the safety of foods derived from GM plants including allergenic potential, the US FDA, Food and Agriculture Organization of the United Nations (FAO)/World Health Organization (WHO), and the EU have developed approaches for evaluation assessment. One assessment approach that has been a very active area of research and debate is the development and usage of animal models to assess the potential allergenicity of GM foods. A number of specific animal models employing rodents, pigs, and dogs have been developed for allergenicity assessment. However, validation of these models is needed and consideration of the criteria for an appropriate animal model for the assessment of allergenicity in GM plants is required. We have recently employed a BALB/c mouse model to assess the potential allergenicity of GM plants. We have been able to demonstrate that this model is able to detect differences in antigenicity and identify aspects of protein post-translational modifications that can alter antigenicity. Furthermore, this model has also enabled us to examine the usage of GM plants as a therapeutic approach for the treatment of allergic diseases. This review discusses the current approaches to assess the allergenic potential of GM food and particularly focusing on the usage of animal models to determine the potential allergenicity of GM foods and gives an overview of our recent findings and implications of these studies.

Individuals with food allergy often present with uritcaria and atopic dermatitis. Indeed, susceptibility to food allergy may predispose to the development of these cutaneous allergic disorders. Recently, we developed a model of food allergy, whereby oral

Background & Aims: Eosinophil-associated gastrointestinal diseases are frequently associated with extraintestinal features, including bronchopulmonary manifestations. The factors predisposing to bronchial hyperresponsiveness in eosinophil-associated gastrointestinal diseases are unknown. To elucidate the mechanistic link between eosinophil-associated gastrointestinal diseases and bronchial hyperresponsiveness, we used murine models of eosinophil-associated gastrointestinal diseases and eotaxin-1/transgene-induced eosinophil-associated gastrointestinal diseases. Methods: Mice were sensitized and orally challenged with ovalbumin-coated encapsulated particles to induce eosinophil-associated gastrointestinal disease, and bronchial responsiveness was examined. Furthermore, transgenic mice expressing eotaxin in the intestine (with the rat fatty acid-binding promoter) were used to specifically elucidate the contribution of this chemokine in eosinophil-associated gastrointestinal disease-associated bronchial hyperresponsiveness. Results: The induction of allergen-induced eosinophil-associated gastrointestinal disease was directly correlated with the development of bronchial hyperresponsiveness. The development of bronchial hyperresponsiveness in mice with allergen-induced eosinophil-associated gastrointestinal disease was dependent on eotaxin expression in the gastrointestinal tract. Expression of eotaxin in the gastrointestinal tract of transgenic mice was sufficient to promote bronchial hyperresponsiveness. Bronchial hyperresponsiveness was shown to be directly linked to the aberrant CD4+ T helper 2 lymphocyte production of interleukin-13. It is interesting to note that transgenic expression of eotaxin was linked with enhanced T helper 2 lymphocyte/cytokine synthesis (interleukin-4, -5, and -13) and the production of mucosal immunoglobulin G1 in the gastrointestinal lumen. We also showed that eotaxin treatment of CD4+ T cells enhanced interleukin-13 production in vitro. C

Eosinophil-associated gastrointestinal disorders (EGDs) are characterized by a pronounced cellular inflammation. Recent clinical and experimental investigations have implicated a family of molecules known as chemokines in the regulation of leukocyte recruitment in these diseases. The underlying cellular and molecular mechanisms involved in chemokine-mediated cellular infiltration are largely unknown. In this review, we describe the role of CD4+ T cells and eosinophils in the clinical manifestations of EGDs and discuss the current understanding of the role of chemokines in the recruitment of these cells in the expression of diseases.