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1.  Tumour necrosis factor receptor 1 and mortality in a multi-ethnic cohort: the Northern Manhattan Study 
Age and Ageing  2013;42(3):385-390.
Objective: to study the association between soluble tumour necrosis factor receptor 1 (sTNFR1) levels and mortality in the population-based Northern Manhattan Study (NOMAS).
Methods: NOMAS is a multi-ethnic, community-based cohort study with mean 8.4 years of follow-up. sTNFR1 was measured using ELISA. Cox proportional hazards models were used to calculate hazard ratios and 95% confidence intervals (HR, 95% CI) for the association of sTNFR1 with risk of all-cause mortality after adjusting for relevant confounders.
Results: sTNFR1 measurements were available in 1,862 participants (mean age 69.2 ± 10.2 years) with 512 all-cause deaths. Median sTNFR1 was 2.28 ng/ml. Those with sTNFR1 levels in the highest quartile (Q4), compared with those with sTNFR1 in the lowest quartile (Q1), were at an increased risk of all-cause mortality (adjusted HR: 1.8, 95% CI: 1.4–2.4) and non-vascular mortality (adjusted HR: 2.5, 95% CI: 1.5–3.6), but not vascular mortality (adjusted HR: 1.3, 95% CI: 0.9–1.9). There were interactions between sTNFR1 quartiles and medical insurance-status [likelihood ratio test (LRT) with 3 degrees of freedom, Pinteraction = 0.02] and alcohol consumption (LRT with 3 degrees of freedom, Pinteraction < 0.01) for all-cause mortality. In participants with no insurance or Medicaid, those with sTNFR1 in the top quartile had nearly a threefold increased risk of total mortality than the lowest quartile (adjusted HR: 2.9, 95% CI: 1.9–4.4).
Conclusion: in this multi-ethnic cohort, sTNFR1 was associated with all-cause and non-vascular mortality, particularly among those of a lower socioeconomic status.
doi:10.1093/ageing/afs175
PMCID: PMC3693433  PMID: 23321203
inflammation; insurance status; mortality risk; alcohol use; older people
2.  Infectious Burden and Carotid Plaque Thickness: The Northern Manhattan Study 
Background
The overall burden of prior infections may contribute to atherosclerosis and stroke risk. We hypothesized that serological evidence of common infections would be associated with carotid plaque thickness in a multi-ethnic cohort.
Methods
Antibody titers to five common infectious microorganisms (i.e. Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpesvirus 1 and 2) were measured among stroke-free community participants, and a weighted index of infectious burden (IB) was calculated based on Cox models previously derived from for the association of each infection with stroke risk. High-resolution carotid duplex Doppler studies were used to assess maximum carotid plaque thickness (MCPT). Weighted least squares regression was used to measure the association between IB and MCPT after adjusting for other risk factors.
Results
Serological results for all five infectious organisms were available in 861 participants with MCPT measurements available (mean age 67.2+/−9.6 yrs). Each individual infection was associated with stroke risk after adjusting for other risk factors. The IB index (n=861) had a mean of 1.00 ± standard deviation 0.35, median 1.08. Plaque was present in 52% of participants (mean 0.90+/−1.04 mm). IB was associated with MCPT (adjusted increase in MCPT 0.09 mm, 95% confidence interval 0.03–0.15 mm, per standard deviation increase of IB).
Conclusion
A quantitative weighted index of infectious burden, derived from the magnitude of association of individual infections with stroke, was associated with carotid plaque thickness in this multi-ethnic cohort. These results lend support to the notion that past or chronic exposure to common infections, perhaps by exacerbating inflammation, contributes to atherosclerosis. Future studies are needed to confirm this hypothesis and to define optimal measures of infectious burden as a vascular risk factor.
doi:10.1161/STROKEAHA.109.571299
PMCID: PMC2830875  PMID: 20075350
3.  Private Practice Administrative Costs Influenced by Insurance Payer Mix 
Journal of Oncology Practice  2009;5(6):291-297.
This report provides a foundation for analysis and study design of an examination of administrative costs associated with insurance and billing processing in private hematology-oncology practices and measurement of financial exposure by predominant payer mix.
Background:
Increased staffing and oncology drug costs per physician, combined with decreased drug revenue, have made private hematology-oncology practices susceptible to increased financial risk. We hypothesized that practices with a higher combined commercial insurance (CCI) mix would experience greater inefficiencies in insurance billing (IB) processes and higher IB administrative costs.
Methods:
A cross-sectional survey was administered to a national pool of private hematology-oncology practices. Practices were identified through the ASCO online registry. Participants self-reported insurance information. T and Wilcoxon rank sum tests were used to compare high (50% or more) Medicare payer mix groups and high (50% or more) CCI payer mix groups for practice operation indicators. These tests were also used to compare denial processing cost per Medicare patient and CCI patient.
Results:
Among the 33 practices that responded to the survey, the mean total IB administrative cost for high Medicare payer mix groups was $191,646.25 (standard deviation [SD], $173,031.63), significantly lower (P = .0454) than the mean for high CCI groups at $476,280.00 (SD, $475,408.57). The mean annual cost per IB support staff member was significantly higher (P = .0453) in the high CCI group at $49,778.67 (SD = $14,896.32) compared with the mean cost in the high Medicare group, which was $39,413.08 (SD, $12,068.17). Medicare patient denial processing cost was significantly lower (P = .0237) than that for CCI patients.
Conclusion:
Practices with a high Medicare payer mix experience both lower mean cost per FTE IB support staff member and total overall IB administrative cost. Processing denials for reimbursement for Medicare patients requires fewer practice resources than does processing for CCI patients.
doi:10.1200/JOP.091052
PMCID: PMC2775410  PMID: 19949446

Results 1-3 (3)