Effect of median household income on surgical approach and survival in renal cell carcinoma.

PURPOSE: We sought to determine whether median household income (MHI) independently predicts surgical approach (partial vs. radical nephrectomy) and survival in patients with renal cell carcinoma. METHODS: The U.S. Surveillance Epidemiology and End Results Database (1988-2011) was queried to examine kidney cancer cases and linked to the Area Health Resources File. We correlated surgical approach and survival, both overall and cancer-specific, with tumor stage, age, race, sex, and income data. RESULTS: Of 152,589 patients diagnosed with renal cell carcinoma, 24,221 (16%) patients underwent partial nephrectomy, 102,771 (67%) patients underwent radical nephrectomy, and 25,597 (17%) patients had no surgery. There was no significant difference in stage of presentation between the wealthiest and poorest MHI quartiles, with approximately 35% of patients in each quartile presenting with T1aN0M0 disease and 17% of patients presenting with metastatic disease. Despite this, 18% of patients in the wealthiest quartile underwent partial nephrectomy compared to 14% of patients in the poorest quartile. Although the percentage of patients undergoing partial nephrectomy rose over the timeframe studied in both the wealthiest and poorest quartiles, the rate of rise was highest in the wealthier group. Those in the poorest quartile were 0.10 times more likely to die of all causes (95% CI: 1.09-1.11, P<0.001) and 0.09 times more likely to die of kidney cancer (95% CI: 1.05-1.10, P<0.001) than those in the wealthiest quartile over the timeframe studied. CONCLUSIONS: Despite presenting with similar stage, patients with lower MHI less commonly undergo partial nephrectomy and are more likely to die of kidney cancer than those in the highest MHIs.

Cellular responses of A549 alveolar epithelial cells to serially collected Pseudomonas aeruginosa from cystic fibrosis patients at different stages of pulmonary infection.

Pseudomonas aeruginosa is the major cause of chronic pulmonary disease in cystic fibrosis (CF) patients. During chronic infection, P. aeruginosa lose certain virulence factors, transform into a mucoid phenotype, and develop antibiotic resistance. We hypothesized that these genetic and phenotypic alterations of P. aeruginosa affect the airway epithelial responses. A549 cells were infected with 27 well-characterized isolates of P. aeruginosa from CF patients obtained during longitudinal observation, or with P. aeruginosa mutant strains lacking flagella, pili, lipopolysaccharide, or pyocyanin. Pseudomonas aeruginosa isolates from the early stages of the infection exhibited high adherence to A549 cells, were readily internalized, and able to induce reactive oxygen species (ROS) production, apoptosis of infected cells, and the release of granulocyte macrophage colony-stimulating factor. Late P. aeruginosa isolates collected from patients with chronic lung infection were shown to have reduced adherence to and internalization into A549 cells compared with bacteria from patients with intermittent P. aeruginosa colonization, and induced lower production of ROS and apoptosis, but caused high proinflammatory cytokine and adhesion molecule expression. Our findings suggest that despite the loss of virulence factors during the adaptation process in the CF lung by late P. aeruginosa strains, they retain high proinflammatory abilities that likely contribute to the disease pathogenesis.

Chromosomal gfp labelling of Pseudomonas aeruginosa using a mini-Tn7 transposon: application for studies of bacteria-host interactions.

Analysis of bacterial interactions with host cells using multiple techniques is essential for studies on microbial pathogenesis and for the development of new antimicrobial therapies. Pseudomonas aeruginosa is an important opportunistic pathogen that can cause severe, often life-threatening pulmonary infections in individuals with impaired host defense mechanisms. Using a mini-Tn7 transposon delivery system, we have chromosomally labelled the strain P. aeruginosa PAK with a green fluorescent protein gene (gfp) and tested PAKgfp as a research tool for studies of bacteria-host interactions. We were able to reliably and rapidly measure the interactions of PAKgfp with A549 human lung epithelial cells by using flow cytometry, a fluorometric microplate reader-based assay, and fluorescence microscopy. With these analytical tools, we have demonstrated the adhesion of PAKgfp to the extracellular matrix protein fibronectin and the involvement of fibronectin in PAKgfp-A549 cell interactions. PAKgfp can be successfully used to explore the effects of various pharmacological compounds on P. aeruginosa - host cell interactions in both in vitro and in vivo systems, with potentially important medical applications.