a b s t r a c tObjectives: Parapneumonic pleural effusions/empyema (PPE/PE) are severe complications of communityacquired pneumonia. We investigated the bacterial aetiology and incidence of paediatric PPE/PE in Germany after the introduction of universal pneumococcal conjugate vaccine (PCV) immunization for infants. Methods: Children <18 years of age hospitalized with pneumonia-associated PPE/PE necessitating pleural drainage or persisting >7 days were reported to the German Surveillance Unit for Rare Diseases in Childhood between October 2010 and June 2017. All bacteria detected in blood or pleural fluid (by culture/PCR) were included, with serotyping for Streptococcus pneumoniae. Results: The median age of all 1447 PPE/PE patients was 5 years (interquartile range 3e10). In 488 of the 1447 children with PPE/PE (34%), 541 bacteria (>40 species) were detected. Aerobic gram-positive cocci accounted for 469 of 541 bacteria detected (87%); these were most frequently Streptococcus pneumoniae (41%), Streptococcus pyogenes (19%) and Staphylococcus aureus (6%). Serotype 3 accounted for 45% of 78 serotyped S. pneumoniae strains. Annual PPE/PE incidence varied between 14 (95%CI 12e16) and 18 (95%CI 16e21) PPE/PE per million children. Incidence of S. pneumoniae PPE/PE decreased from 3.5 (95%CI 2.5e4.6) per million children in 2010/11 to 1.5 (95%CI 0.9e2.4) in 2013/14 (p 0.002), followed by a reincrease to 2.2 (95%CI 1.5e3.2) by 2016/17 (p 0.205). Conclusions: In the era of widespread PCV immunization, cases of paediatric PPE/PE were still caused mainly by S. pneumoniae and, increasingly, by S. pyogenes. The re-increase in the incidence of PPE/PE overall and in S. pneumoniae-associated PPE/PE indicates ongoing changes in the bacterial aetiology and requires further surveillance.

Purpose To assess the clinical feasibility of self-gated non-contrast-enhanced functional lung (SENCEFUL) magnetic resonance (MR) imaging for quantitative ventilation (QV) imaging in patients with cystic fibrosis (CF). Materials and Methods Twenty patients with CF and 20 matched healthy volunteers underwent functional 1.5-T lung MR imaging with the SENCEFUL imaging approach, in which a two-dimensional fast low-angle shot sequence is used with quasi-random sampling. The lungs were manually segmented on the ventilation-weighted images to obtain QV measurements, which were compared between groups. QV values of the patients were correlated with results of pulmonary function testing. Three radiologists rated the images for presence of ventilation deficits by means of visual inspection. Mann-Whitney U tests, receiver operating characteristic analyses, Spearman correlations, and Gwet agreement coefficient analyses were used for statistical analysis. Results QV of the entire lungs was lower for patients with CF than for control subjects (mean ± standard deviation, 0.09 mL/mL ± 0.03 vs 0.11 mL/mL ± 0.03, respectively; P = .007). QV ratios of upper to lower lung halves were lower in patients with CF than in control subjects (right, 0.84 ± 0.2 vs 1.16 ± 0.2, respectively [P < .001]; left, 0.88 ± 0.3 vs 1.11 ± 0.1, respectively [P = .017]). Accordingly, ventilation differences between the groups were larger in the upper halves (Δ = 0.04 mL/mL, P ≤ .001-.002). QV values of patients with CF correlated with forced vital capacity (r = 0.7; 95% confidence interval [CI]: 0.21, 0.91), residual volume (static hyperinflation, r = -0.8; 95% CI: -0.94, 0.42), and forced expiratory volume in 1 second (airway obstruction, r = 0.7; 95% CI: 0.21, 0.91). Disseminated small ventilation deficits were the most frequent involvement pattern, present in 40% of the functional maps in CF versus 8% in the control subjects (P < .001). Conclusion SENCEFUL MR imaging is feasible for QV assessment. Less QV, especially in upper lung parts, and correlation to vital capacity and to markers for hyperinflation and airway obstruction were found in patients with CF. RSNA, 2016.

Abstract-Renal perfusion pressure (RPP) regulates renin release with a reduction of RPP stimulating and an elevation inhibiting renin secretion. The precise sensing and effector mechanisms by which changes in arterial pressure are linked to the exocytosis of renin are not well-defined. The present experiments were designed to study the potential role of adenosine as a mediator of this renal baroreceptor mechanism. In isolated perfused mouse kidneys a stepwise reduction of RPP from 90 mm Hg to 65 and 40 mm Hg stimulated renin secretion rates (RSR) 1.4-fold and 3.6-fold, whereas stepwise elevations of RPP from 90 mm Hg to 115 and 140mm Hg suppressed RSR to 64% or 40% of baseline. Inactivation of A1 adenosine receptors by either pharmacological blockade (DPCPX 1mol/L) or genetic deletion (A1AR Ϫ/Ϫ mice) did not modify the stimulation of renin release by a low RPP, but completely prevented the suppression of renin secretion by higher perfusion pressures. In vivo, the induction of arterial hypertension by either acute (single subcutaneous injection) or chronic (osmotic minipump for 72 hours) application of phenylephrine significantly reduced plasma renin concentration (PRC) in wild-type mice to Ϸ40% of control, whereas it did not significantly affect PRC in A1ARϪ/Ϫ mice. Together these data demonstrate that A1 adenosine receptors are indispensable for the inhibition of renin secretion by an increase in blood pressure, suggesting that formation and action of adenosine is responsible for baroreceptor-mediated inhibition of renin release. In contrast, the stimulation of the renin system by a low blood pressure appears to follow different pathways.