The challenge of accurately describing the epidemiology of bronchopulmonary dysplasia (BPD) based on the various current definitions of BPD.

Despite marked improvements in the survival of extremely low birth weight preterm infants, bronchopulmonary dysplasia (BPD) remains a prevalent morbidity. BPD has evolved pathologically and epidemiologically but the definition has failed to keep up. The majority of the definitions of BPD still use the respiratory support provided to the infants at a single timepoint. The lack of a uniform definition of BPD presently reflects the changing BPD pathogenesis and phenotype and limits defining the epidemiology. To address the epidemiology of BPD, the definition should be clarified; even the newer definitions have not been validated entirely. The definition needs to be meaningful clinically and be predictive of long-term respiratory outcomes. We believe the definition should have a composite assessment like a score (quantitative measurement) and include the different phenotypes (qualitative measurements) so that optimally they can be applied to the different phases of BPD and at different timepoints. Furthermore, the definitions need to be easy to measure and assess so that generalizability is enhanced.

Ewing's Sarcoma of the Cervical Spine.

In this article, we present the case of a 6-year-old female presented to the emergency department with progressive ascending motor weakness leading to cardiac arrest. The recent medical history included neck trauma 1 month prior to admission, 2 weeks of subjective fevers, and 1 day of urinary incontinence. After stabilization, and a review of the recent signs and symptoms, a magnetic resonance imaging of the neck revealed a posterior neck mass from C2 to T2. Neurosurgical removal of the mass was consistent with Ewing's sarcoma. Neck pain is a common presentation in the pediatric population, with the most common cause being traumatic. When coupled with neurological deficits, further studies are warranted to evaluate for organic causes.

Effect of antigen sensitization and challenge on oscillatory mechanics of the lung and pulmonary inflammation in obese carboxypeptidase E-deficient mice.

Atopic, obese asthmatics exhibit airway obstruction with variable degrees of eosinophilic airway inflammation. We previously reported that mice obese as a result of a genetic deficiency in either leptin (ob/ob mice) or the long isoform of the leptin receptor (db/db mice) exhibit enhanced airway obstruction in the presence of decreased numbers of bronchoalveolar lavage fluid (BALF) eosinophils compared with lean, wild-type mice following antigen (ovalbumin; OVA) sensitization and challenge. To determine whether the genetic modality of obesity induction influences the development of OVA-induced airway obstruction and OVA-induced pulmonary inflammation, we examined indices of these sequelae in mice obese as a result of a genetic deficiency in carboxypeptidase E, an enzyme that processes prohormones and proneuropeptides involved in satiety and energy expenditure (Cpe(fat) mice). Accordingly, Cpe(fat) and lean, wild-type (C57BL/6) mice were sensitized to OVA and then challenged with either aerosolized PBS or OVA. Compared with genotype-matched, OVA-sensitized and PBS-challenged mice, OVA sensitization and challenge elicited airway obstruction and increased BALF eosinophils, macrophages, neutrophils, IL-4, IL-13, IL-18, and chemerin. However, OVA challenge enhanced airway obstruction and pulmonary inflammation in Cpe(fat) compared with wild-type mice. These results demonstrate that OVA sensitization and challenge enhance airway obstruction in obese mice regardless of the genetic basis of obesity, whereas the degree of OVA-induced pulmonary inflammation is dependent on the genetic modality of obesity induction. These results have important implications for animal models of asthma, as modeling the pulmonary phenotypes for subpopulations of atopic, obese asthmatics critically depends on selecting the appropriate mouse model.