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1.  Inpatient Healthcare Trends Among Adult Cystic Fibrosis Patients in the U.S 
Pediatric pulmonology  2011;47(3):245-251.
Summary
Background
Adult cystic fibrosis (CF) patients are an expanding cohort that is taken care of in a variety of hospital settings including adult centers located within pediatric institutions. This study compared costs and discharge rates among adult CF patient hospitalizations in terms of location of hospitalization.
Methods
The 2007 Nationwide Inpatient Sample was utilized to identify adult CF patient admission data on patients aged 18–44. Data were separated into pediatric and adult facilities based on percentage discharge rate for patients >18. Primary outcomes measures were length of stay (LOS) and total hospital charges. Secondary predictors were geographic, primary payer, and co-morbidity effects on LOS and total hospital charges.
Results
LOS was higher for adult CF patient admissions in pediatric facilities compared to adult facilities by a mean of 2.5 days. Mean total hospital charges were not significantly different. Adult hospitals in the Western U.S. had a mean total charge more than $50,000 greater than any region in the U.S. Self-pay patients had significantly fewer hospital days and charges across all hospital types. Adult facilities had 7% more CF patients discharged home with home healthcare use. Depressed CF patients had longer LOS by 1.5 days regardless of facility type.
Conclusions
LOS for adult CF inpatient admissions was significantly lower in adult facilities compared to pediatric facilities without a significant difference in hospital charges and is influenced by geographic hospital location. Depressed patients had longer lengths of stay regardless of facility type. Self-insured adult CF patients have a significant reduction in LOS and hospital charges when compared to all other payers regardless of hospital type.
doi:10.1002/ppul.21535
PMCID: PMC3805019  PMID: 21901854
healthcare utilization; socioeconomic factors; geographic factors
2.  EXAGGERATED INFLAMMATORY RESPONSES MEDIATED BY BURKHOLDERIA CENOCEPACIA IN HUMAN MACROPHAGES DERIVED FROM CYSTIC FIBROSIS 
Cystic Fibrosis (CF) is accompanied with heightened inflammation worsened by drug resistant Burkholderia cenocepacia. Human CF macrophage responses to B. cenocepacia are poorly characterized and variable in the literature. Therefore, we examined human macrophage responses to the epidemic B. cenocepacia J2315 strain in order to identify novel anti-inflammatory targets. Peripheral blood monocyte derived macrophages were obtained from 23 CF and 27 non-CF donors. Macrophages were infected with B. cenocepacia J2315 and analyzed for cytokines, cytotoxicity, and microscopy. CF macrophages demonstrated significant increases in IL-1β, IL-10, MCP-1, and IFN-γ production in comparison to non-CF controls. CF patients on prednisone exhibited globally diminished cytokines compared to controls and other CF patients. CF macrophages also displayed increased bacterial burden and cell death. In conclusion, CF macrophages demonstrate exaggerated IL-1β, IL-10, MCP-1, and IFN-γ production and cell death during B. cenocepacia infection. Treatment with corticosteroids acutely suppressed cytokine responses.
doi:10.1016/j.bbrc.2012.06.066
PMCID: PMC3408781  PMID: 22728038
cystic fibrosis; burkholderia; macrophage; IL-1β; corticosteroids
3.  Elevated high-sensitivity C-reactive protein in preterm infants with pulmonary colonization with Ureaplasma 
Journal of Thoracic Disease  2013;5(3):223-227.
Background
A link between pulmonary Ureaplasma spp. colonization in premature infants and bronchopulmonary dysplasia (BPD) exists and could possibly contribute to systemic inflammation.
Methods
A prospective cohort study was performed from July 2006 to July 2007 where very low birth weight (VLBW) premature infants were screened at birth. Serum and tracheal aspirate samples were collected during the first 28 days of life that represented the early high-sensitivity C-reactive protein (hs-CRP) group, and follow-up samples obtained between 28-42 days of life were the late hs-CRP group. An Enzyme-linked immunosorbent assay (ELISA) for hs-CRP was performed on serum samples while tracheal aspirates underwent polymerase chain reaction (PCR) analysis for Ureaplasma spp.
Results
A total of 65 patients were screened. 30 patients completed full analysis, 15 died before early and late hs-CRP samples could be obtained, and 20 had incomplete data due to early discharge or transfer. There was no significant difference between all early and late hs-CRP group levels (mg/L), median [interquartile range] 1.019 [0.242, 5.844] vs. 0.773 [0.143, 8.954] (P=0.3958); however, there was a significant difference when comparing Ureaplasma spp. positivity vs. negativity between both groups, median 2.223 [0.398, 7.099] vs. 0.675 [0.219, 4.038] (P=0.0131) for the early group and median 2.335 [0.359, 14.91] vs. 0.2155 [0.122, 2.296] (P=0.03) for the late group, respectively.
Conclusions
VLBW premature infants colonized with Ureaplasma spp. have an elevated hs-CRP, suggestive of a chronic low-grade systemic inflammatory response.
doi:10.3978/j.issn.2072-1439.2013.04.14
PMCID: PMC3698281  PMID: 23825751
High-sensitivity C-reactive protein (hs-CRP); Ureaplasma; preterm infant; bronchopulmonary dysplasia (BPD)
4.  Autophagy stimulation by rapamycin suppresses lung inflammation and infection by Burkholderia cenocepacia in a model of cystic fibrosis 
Autophagy  2011;7(11):1359-1370.
Cystic fibrosis (CF) is the most common inherited lethal disease in Caucasians which results in multiorgan dysfunction. However, 85% of the deaths are due to pulmonary infections. Infection by Burkholderia cenocepacia (B. cepacia) is a particularly lethal threat to CF patients because it causes severe and persistent lung inflammation and is resistant to nearly all available antibiotics. In CFTR ΔF508 (ΔF508) mouse macrophages, B. cepacia persists in vacuoles that do not fuse with the lysosomes and mediates increased production of IL-1β. It is believed that intracellular bacterial survival contributes to the persistence of the bacterium. Here we show for the first time that in wild-type but not in ΔF508 macrophages, many B. cepacia reside in autophagosomes that fuse with lysosomes at later stages of infection. Accordingly, association and intracellular survival of B. cepacia are higher in CFTR-ΔF508 macrophages than in WT macrophages. An autophagosome is a compartment that engulfs nonfunctional organelles and parts of the cytoplasm then delivers them to the lysosome for degradation to produce nutrients during periods of starvation or stress. Furthermore, we show that B. cepacia downregulates autophagy genes in WT and ΔF508 macrophages. However, autophagy dysfunction is more pronounced in ΔF508 macrophages since they already have compromised autophagy activity. We demonstrate that the autophagystimulating agent, rapamycin markedly decreases B. cepacia infection in vitro by enhancing the clearance of B. cepacia via induced autophagy. In vivo, rapamycin decreases bacterial burden in the lungs of CF mice and drastically reduces signs of lung inflammation. Together, our studies reveal that if efficiently activated, autophagy can control B. cepacia infection and ameliorate the associated inflammation. Therefore, autophagy is a novel target for new drug development for CF patients to control B. cepacia infection and accompanying inflammation.
doi:10.4161/auto.7.11.17660
PMCID: PMC3359483  PMID: 21997369
autophagy; rapamycin; cystic fibrosis; host-pathogen interaction; Burkholderia cenocepacia; inflammation; macrophages

Results 1-4 (4)