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The article presents a case study of a 19-year-old female who suffered from a panic/anxiety attack for three hours. It discusses results of her physical examination, chest X-ray, computed tomography angiogram, an esophagogram, and elective bronchoscopy. The patient was diagnosed of spontaneous pneumomediastinum (SPM) with speedy capacity breaths in a few hours next to a panic attack.

Introduction: Injury is a major public health issue in the USA. In 2017, unintentional injury was the leading cause of death for ages 1 through 44. Unfortunately, there is evidence that the sciences of injury prevention and control may not fully and widely integrated into medical school curriculum. This paper describes a novel injury prevention and control summer programme that was implemented in 2002 and is ongoing., Methods: The main component of the Series includes at least seven injury-related lectures and discussions designed to provoke students' interest and understanding of injury as a biopsychosocial disease. These lectures are organised in a seminar fashion and are 2-4 hours in duration. Kirkpatrick's four-part model guides evaluation specific to our four programme objectives. Trainee satisfaction with the programme, knowledge and outcome (specific to career goals) is evaluated using several mixed-methods tools., Results: A total of 318 students have participated in the Series. Evaluation findings show an increase in knowledge of injury-related concepts as well as an increase in interest in pursuing injury-related research topics in the future., Implications: The Series is a novel and innovative programme that provides training in injury and injury prevention and control-related topics to medical students, as well as undergraduate, graduate and pharmacy students. We hope that by increasing students' knowledge and understanding of injury prevention and control we are contributing to a physician workforce that understands the importance of a public health approach to injury prevention, that implements public health principles in practice and that advocates for policies and practices that positively impact injury prevention and control to help make our communities healthier and safer., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Alcohol use disorders (AUDs), including alcohol abuse and dependence, and cigarette smoking are widely acknowledged and common risk factors for pneumococcal pneumonia. Reasons for these associations are likely complex but may involve an imbalance in pro- and anti-inflammatory cytokines within the lung. Delineating the specific effects of alcohol, smoking, and their combination on pulmonary cytokines may help unravel mechanisms that predispose these individuals to pneumococcal pneumonia. We hypothesized that the combination of AUD and cigarette smoking would be associated with increased bronchoalveolar lavage (BAL) proinflammatory cytokines and diminished anti-inflammatory cytokines, compared with either AUDs or cigarette smoking alone. Acellular BAL fluid was obtained from 20 subjects with AUDs, who were identified using a validated questionnaire, and 19 control subjects, matched on the basis of age, sex, and smoking history. Half were current cigarette smokers; baseline pulmonary function tests and chest radiographs were normal. A positive relationship between regulated and normal T cell expressed and secreted (RANTES) with increasing severity of alcohol dependence was observed, independent of cigarette smoking (P = 0.0001). Cigarette smoking duration was associated with higher IL-1β (P = 0.0009) but lower VEGF (P = 0.0007); cigarette smoking intensity was characterized by higher IL-1β and lower VEGF and diminished IL-12 (P = 0.0004). No synergistic effects of AUDs and cigarette smoking were observed. Collectively, our work suggests that AUDs and cigarette smoking each contribute to a proinflammatory pulmonary milieu in human subjects through independent effects on BAL RANTES and IL-1β. Furthermore, cigarette smoking additionally influences BAL IL-12 and VEGF that may be relevant to the pulmonary immune response.