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The prevalence and complexity of allergic diseases have increased in recent decades, leading to a significant burden for patients and their families. However, training in Allergy and Clinical Immunology (ACI) varies worldwide, with significant heterogeneity between countries. This variability may limit the number of healthcare professionals and researchers undergoing ACI training in the future. To address this, the European Academy of Allergy and Clinical Immunology (EAACI) has developed a mentorship program to support young professionals in enhancing their skills and network. The program has been successful and may serve as a model for other scientific organizations in the ACI field. [Extracted from the article]

Heat waves are increasing in intensity, frequency, and duration causing significant heat stress in all living organisms. Heat stress has multiple negative effects on plants affecting photosynthesis, respiration, growth, development, and reproduction. It also impacts animals leading to physiological and behavioral alterations, such as reduced caloric intake, increased water intake, and decreased reproduction and growth. In humans, epidemiological studies have shown that heat waves are associated with increased morbidity and mortality. There are many biological effects of heat stress (structural changes, enzyme function disruption, damage through reactive oxygen or nitrogen species). While plants and animals can mitigate some of these effects through adaptive mechanisms such as the generation of heat shock proteins, antioxidants, stress granules, and others, these mechanisms may likely be inadequate with further global warming. This review summarizes the effects of heat stress on plants and animals and the adaptative mechanisms that have evolved to counteract this stress. [ABSTRACT FROM AUTHOR]

Keywords: airway epithelium; cryopreservation; human rhinovirus EN airway epithelium cryopreservation human rhinovirus 1486 1489 4 06/01/20 20200601 NES 200601 To the Editor, Human epithelial cell lines (eg, A549 and BEAS-2B cells), as well as primary nasal and bronchial epithelial cells, have been used extensively to explore the role of virus-host interactions in respiratory allergic diseases.[1] In vitro cell cultures of primary airway epithelial cells from patients are a key model for these studies. In RV-infected cells, 45 genes were differentially expressed (36 higher and 9 lower in fresh compared to cryopreserved cells) (Figure C, Table S2B). In the last decades, epithelial infection models have evolved from using cell lines[5] to submerged primary cells[6] to air-liquid interphase differentiated cells.[7] At the same time, utilization of cryopreserved cells or tissues has increased considerably. [Extracted from the article]

Current data indicate that the "bronchiolitis" diagnosis comprises more than one condition. Clinically, pathophysiologically, and even genetically three main clusters of patients can be identified among children suffering from severe bronchiolitis (or first wheezing episode): (a) respiratory syncytial virus (RSV)‐induced bronchiolitis, characterized by young age of the patient, mechanical obstruction of the airways due to mucus and cell debris, and increased risk of recurrent wheezing. For this illness, an effective prophylactic RSV‐specific monoclonal antibody is available; (b) rhinovirus‐induced wheezing, associated with atopic predisposition of the patient and high risk of subsequent asthma development, which may, however, be reversed with systemic corticosteroids in those with severe illness; and (c) wheeze due to other viruses, characteristically likely to be less frequent and severe. Clinically, it is important to distinguish between these partially overlapping patient groups as they are likely to respond to different treatments. It appears that the first episode of severe bronchiolitis in under 2‐year‐old children is a critical event and an important opportunity for designing secondary prevention strategies for asthma. As data have shown bronchiolitis cannot simply be diagnosed using a certain cutoff age, but instead, as we suggest, using the viral etiology as the differentiating factor. Respiratory syncytial virus‐induced bronchiolitis and rhinovirus‐induced first wheezing episode are the main clusters of severe bronchiolitis in less than 2‐year‐old children. It is important to distinguish these overlapping patient groups since they differ clinically, pathophysiologically, and genetically and are likely to respond to different treatments. The first episode of severe bronchiolitis appears to be a critical event and an opportunity for designing secondary prevention strategies for asthma. [ABSTRACT FROM AUTHOR]