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1.  Epidemiology and Predictors of Failure of the Infant Car Seat Challenge 
Pediatrics  2013;131(5):951-957.
The American Academy of Pediatrics recommends all neonates born at <37 weeks’ gestation receive a predischarge Infant Car Seat Challenge (ICSC), a resource-intensive test with little information on failure rates and risk factors. We sought to determine incidence and predictors of failure to allow more selective testing.
We conducted a retrospective medical record review of 1173 premature neonates qualifying for the ICSC between 2009 and 2010. We looked at ICSC result and potential risk factors and then performed bivariate and multivariable logistic analyses to evaluate for predictors of failure.
Overall incidence of failure was 4.3%. Infants who failed were less premature and had higher birth weights. Late-preterm infants made up 60% of our study population but accounted for 78% of failures (P = .019). Infants who passed had older chronologic ages at time of testing, were more likely to have been exposed to caffeine, and were more likely to have required some type of respiratory support than those that failed. Final multivariable model demonstrated that increasing birth gestational age (GA) increased the odds of failure when corrected for gender, race, and small for GA status. For every 1-day increase in birth GA the odds ratio of failure was 1.03 (95% confidence interval 1.01–1.05).
We found that increasing birth GA was a significant predictor of failure, and that late-preterm infants comprised a significant percentage of infants who failed. This suggests that limiting testing to extremely premature infants would miss most cases of ICSC failure.
PMCID: PMC3967776  PMID: 23545379
apnea; Car Seat Test; Infant Car Seat Challenge; intermittent desaturations; prematurity
2.  Th17 cytokines are critical for RSV associated airway hyperreponsiveness through regulation by complement C3a and tachykinins1 
Respiratory syncytial virus (RSV) infection is associated with serious lung disease in infants and immunocompromised individuals and is linked to development of asthma. In mice, acute RSV infection causes airway hyperresponsiveness (AHR), inflammation, and mucus hypersecretion. Infected cells induce complement activation, producing the anaphylatoxin C3a. Here we show RSV infected wild type mice produce Th17 cytokines, a response not previously associated with viral infections. Mice deficient in the C3aR (C3aR1−/−) fail to develop AHR following acute RSV infection, and production of Th17 cytokines was significantly attenuated. Tachykinin production has also been implicated in RSV pathophysiology, and tachykinin receptor null mice (TACR1−/−) were similarly protected from developing AHR. These animals were also deficient in production of Th17 cytokines. Tachykinin release was absent in C3aR1−/− mice, while C3a levels were unchanged in TACR1−/− animals. Thus, our data reveal a crucial sequence following acute RSV infection where initial C3a production causes tachykinin release, followed by activation of the IL-17A pathway. Deficiency of either receptor affords protection from AHR, identifying two potential therapeutic targets.
PMCID: PMC3186836  PMID: 21918196
respiratory syncytial virus; C3a anaphylatoxin; complement; inflammation; IL17A; airway hyperresponsiveness; tachykinins; substance P; hemokinin-1
3.  Patient characteristics associated with in-hospital mortality in children following tracheotomy 
Archives of disease in childhood  2010;95(9):703-710.
To identify children at risk for in-hospital mortality following tracheotomy.
Retrospective cohort study.
25 746 876 US hospitalisations for children within the Kids’ Inpatient Database 1997, 2000, 2003 and 2006.
18 806 hospitalisations of children ages 0–18 years undergoing tracheotomy, identified from ICD-9-CM tracheotomy procedure codes.
Main outcome measure
Mortality during the initial hospitalisation when tracheotomy was performed in relation to patient demographic and clinical characteristics (neuromuscular impairment (NI), chronic lung disease, upper airway anomaly, prematurity, congenital heart disease, upper airway infection and trauma) identified with ICD-9-CM codes.
Between 1997 and 2006, mortality following tracheotomy ranged from 7.7% to 8.5%. In each year, higher mortality was observed in children undergoing tracheotomy who were aged <1 year compared with children aged 1–4 years (mortality range: 10.2–13.1% vs 1.1–4.2%); in children with congenital heart disease, compared with children without congenital heart disease (13.1–18.7% vs 6.2–7.1%) and in children with prematurity, compared with children who were not premature (13.0–19.4% vs 6.8–7.3%). Lower mortality was observed in children with an upper airway anomaly compared with children without an upper airway anomaly (1.5–5.1% vs 9.1–10.3%). In 2006, the highest mortality (40.0%) was observed in premature children with NI and congenital heart disease, who did not have an upper airway anomaly.
Congenital heart disease, prematurity, the absence of an upper airway anomaly and age <1 year were characteristics associated with higher mortality in children following tracheotomy. These findings may assist provider communication with children and families regarding early prognosis following tracheotomy.
PMCID: PMC3118570  PMID: 20522454
4.  FcγRIII Is Protective against Pseudomonas aeruginosa Pneumonia 
Defenses against bacterial infections involve activation of multiple systems of innate immunity, including complement, Toll-like receptors, and defensins. Reactions to chronic infections bring adaptive immune mechanisms into play as well, with the introduction of modulatory interactions between the two. In humans with chronic lung infections, the severity of inflammation and disease correlate with elevated levels of pathogen-specific immune complexes and complement activation. In mice with genetic deficiency in C5, or targeted deletion of the C5a receptor, Pseudomonas lung infections reveal a role for the C5a anaphylatoxin in disease severity. Deficient animals exhibit significantly reduced survival and clearance of infecting bacteria, simultaneous with greatly increased pulmonary influx of inflammatory cells. Among the actions of C5a on inflammatory cells mediated through the C5a receptor is a shift in the relative expression of Fcγ receptors to increase FcγRIII relative to FcγRII. This shift may significantly impact defenses against chronic infection, reflecting the cellular activation profiles of these IgG receptors. We addressed the role of FcγRIII in defense against Pseudomonas lung infection, and found that, like C5aR-deficient mice, animals with targeted deletion of FcγRIII are more susceptible to mortality upon infection and exhibit reduced clearance of the pathogen. Pseudomonas infection was associated with an increase in the FcγRIII/FcγRII ratio in wild-type mice, and the data support its role as an additional mechanism of host defense against bacterial infection.
PMCID: PMC2274945  PMID: 17975174
Fcγ; receptors; host defense; bacterial infection; Pseudomonas; pneumonia

Results 1-4 (4)