Anaphylaxis has been defined as a 'severe, life-threatening generalized or systemic hypersensitivity reaction'. However, data indicate that the vast majority of foodtriggered anaphylactic reactions are not life-threatening. Nonetheless, severe lifethreatening reactions do occur and are unpredictable. We discuss the concepts surrounding perceptions of severe, life-threatening allergic reactions to food by different stakeholders, with particular reference to the inclusion of clinical severity as a factor in allergy and allergen risk management. We review the evidence regarding factors that might be used to identify those at most risk of severe allergic reactions to food, and the consequences of misinformation in this regard. For example, a significant proportion of food-allergic children also have asthma, yet almost none will experience a fatal food-allergic reaction; asthma is not, in itself, a strong predictor for fatal anaphylaxis. The relationship between dose of allergen exposure and symptom severity is unclear. While dose appears to be a risk factor in at least a subgroup of patients, studies report that individuals with prior anaphylaxis do not have a lower eliciting dose than those reporting previous mild reactions. It is therefore important to consider severity and sensitivity as separate factors, as a highly sensitive individual will not necessarily experience severe symptoms during an allergic reaction. We identify the knowledge gaps that need to be addressed to improve our ability to better identify those most at risk of severe food-induced allergic reactions.

Objectives We examined the outcomes of a cognitive-behavioral therapy (CBT) intervention for pain in pediatric sickle cell disease (SCD) using smartphones as a novel delivery method. Methods Forty-six children with SCD received CBT coping skills training using a randomized, waitlist control design. The intervention involved a single-session of CBT training and home-based practice using smartphones for eight weeks. Pre-post questionnaires between the randomized groups were used to evaluate changes in active psychological coping and negative thinking using the Coping Strategies Questionnaire. Daily diaries completed by the full sample during the treatment period were used to assess if CBT skill use was related to reductions in next day pain intensity and increases in same day functional activity. Results The pre-post group comparison suggested that youth increased active psychological coping attempts with the intervention. Daily diary data indicated that when children used CBT skills on days with higher pain, there were reductions in next day pain intensity. There was no such association between skill use and functional activity. Discussion CBT coping skills training supported via smartphones can increase coping and reduce pain intensity for children with SCD; however, additions to the study protocols are recommended in future studies. Advantages and caveats of using smartphones are also discussed.

Posttraumatic growth (PTG), positive change resulting from the struggle with trauma, has garnered significant attention in the literature on adults. Recently, the research base has begun to extend downward, and this literature indicates that youth also evidence PTG-like changes. Researchers have sought to assess the construct, examine its correlates, and understand the factors that contribute to PTG in youth. Drawing from this work, this article considers clinical implications for youth. After briefly describing the PTG construct, its hypothesized process, and its distinction from resilience, the article focuses on key themes in the literature and, with those findings as backdrop, ways in which professionals can facilitate growth in youth who have experienced trauma. This discussion situates PTG within the broader trauma literature and includes specific applications used to date as well as the role of cultural factors. Future directions--salient to practitioners and researchers alike--are considered.

Environmental carcinogenic exposures are major contributors to global disease burden yet how they promote cancer is unclear. Over 70 years ago, the concept of tumour promoting agents driving latent clones to expand was rst proposed. In support of this model, recent evidence suggests that human tissue contains a patchwork of mutant clones, some of which harbour oncogenic mutations, and many environmental carcinogens lack a clear mutational signature. We hypothesised that the environmental carcinogen, <2.5μm particulate matter (PM2.5), might promote lung cancer promotion through nonmutagenic mechanisms by acting on pre-existing mutant clones within normal tissues in patients with lung cancer who have never smoked, a disease with a high frequency of EGFR activating mutations. We analysed PM2.5 levels and cancer incidence reported by UK Biobank, Public Health England, Taiwan Chang Gung Memorial Hospital (CGMH) and Korean Samsung Medical Centre (SMC) from a total of 463,679 individuals between 2006-2018. We report associations between PM2.5 levels and the incidence of several cancers, including EGFR mutant lung cancer. We nd that pollution on a background of EGFR mutant lung epithelium promotes a progenitor-like cell state and demonstrate that PM accelerates lung cancer progression in EGFR and Kras mutant mouse lung cancer models. Through parallel exposure studies in mouse and human participants, we nd evidence that in ammatory mediators, such as interleukin-1 , may act upon EGFR mutant clones to drive expansion of progenitor cells. Ultradeep mutational pro ling of histologically normal lung tissue from 247 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 33% of normal tissue samples, respectively. These results support a tumour-promoting role for PM acting on latent mutant clones in normal lung tissue and add to evidence providing an urgent mandate to address air pollution in urban areas.