Do as I say, not as I do: a survey of public impressions of queue-jumping and preferential access.

OBJECTIVES: The Canada Health Act legislates that Canadian citizens have access to healthcare that is publicly administered, universal, comprehensive, portable, and accessible (i.e. unimpeded by financial, clinical, or social factors). We surveyed public impressions and practices regarding preferential access to healthcare and queue jumping. METHODS: Households were randomly selected from the Toronto telephone directory. English speakers aged 18 years or older were solicited for a standardized telephone survey. Statistical analysis was performed using SPSS and SAS. RESULTS: Fifteen percent (n=101) of 668 solicited were surveyed. Ninety-five percent advocated equal access based on need. Support for queue jumping in the emergency department (ED) was strong for cases of emergency, severe pain, and pediatrics, equivocal for police, and minimal for the homeless, doctors, hospital administrators, and government officials. To improve a position on a waiting list, approximately half surveyed would call a friend who is a doctor, works for a doctor, or is a hospital administrator. Sixteen percent reported having done this. The likelihoods of offering material inducement for preferential access were 30 and 51% for low and high-impact medical scenarios, respectively. The likelihoods of offering nonmaterial inducement were 56 and 71%, respectively. Responses were not associated with sex, occupation, or education. CONCLUSIONS: Respondents expressed support for equal access based on need. Policy and scenario-type questions elicited different responses. Expressed beliefs may vary from personal practice. Clearly defined and enforced policies at the hospital and provincial level might enhance principles of fairness in the ED queue.

Expression of S100A8 correlates with inflammatory lung disease in congenic mice deficient of the cystic fibrosis transmembrane conductance regulator.

BACKGROUND: Lung disease in cystic fibrosis (CF) patients is dominated by chronic inflammation with an early and inappropriate influx of neutrophils causing airway destruction. Congenic C57BL/6 CF mice develop lung inflammatory disease similar to that of patients. In contrast, lungs of congenic BALB/c CF mice remain unaffected. The basis of the neutrophil influx to the airways of CF patients and C57BL/6 mice, and its precipitating factor(s) (spontaneous or infection induced) remains unclear. METHODS: The lungs of 20-day old congenic C57BL/6 (before any overt signs of inflammation) and BALB/c CF mouse lines maintained in sterile environments were investigated for distinctions in the neutrophil chemokines S100A8 and S100A9 by quantitative RT-PCR and RNA in situ hybridization, that were then correlated to neutrophil numbers. RESULTS: The lungs of C57BL/6 CF mice had spontaneous and significant elevation of both neutrophil chemokines S100A8 and S100A9 and a corresponding increase in neutrophils, in the absence of detectable pathogens. In contrast, BALB/c CF mouse lungs maintained under identical conditions, had similar elevations of S100A9 expression and resident neutrophil numbers, but diverged in having normal levels of S100A8. CONCLUSION: The results indicate early and spontaneous lung inflammation in CF mice, whose progression corresponds to increased expression of both S100A8 and S100A9, but not S100A9 alone. Moreover, since both C57BL/6 and BALB/c CF lungs were maintained under identical conditions and had similar elevations in S100A9 and neutrophils, the higher S100A8 expression in the former (or suppression in latter) is a result of secondary genetic influences rather than environment or differential infection.