26 research outputs found

    Adjusting Medicare capitation payments using prior hospitalization data

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    The diagnostic cost group approach to a reimbursement model for health maintenance organizations is presented. Diagnostic information about previous hospitalizations is used to create empirically determined risk groups, using only diagnoses involving little or no discretion in the decision to hospitalize. Diagnostic cost group and other models (including Medicare\u27s current formula and other prior-use models) are tested for their ability to predict future costs, using R2 values and new measures of predictive performance. The diagnostic cost group models perform relatively well with respect to a range of criteria, including administrative feasibility, resistance to provider manipulation, and statistical accuracy

    B0 meson decays to rho0 K*0, f0 K*0, and rho-K*+, including higher K* resonances

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    We present branching fraction measurements for the decays B0 -> rho0 K*0, B0 -> f0 K*0, and B0 -> rho- K*+, where K* is an S-wave (K pi)_0* or a K*(892) meson; we also measure B0 -> f0 K_2*(1430)^0. For the K*(892) channels, we report measurements of longitudinal polarization fractions (for rho final states) and direct CP-violation asymmetries. These results are obtained from a sample of (471.0 +/- 2.8) x 10^6 BBbar pairs collected with the BaBar detector at the PEP-II asymmetric-energy e+ e- collider at the SLAC National Accelerator Laboratory. We observe rho0 K*(892)^0, rho0 (K pi)_0^{*0}, f0 K*(892)^0, and rho- K*(892)+ with greater than 5 sigma significance, including systematics. We report first evidence for f0 (K pi)_0^{*0} and f0 K_2*(1430)^0, and place an upper limit on rho- (K pi)_0^{*+}. Our results in the K*(892) channels are consistent with no direct CP-violation.Comment: 17 pages, 6 postscript figures, submitted to Phys. Rev.

    PACE and the Medicare+Choice Risk-Adjusted Payment Model

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    This paper investigates the impact of the Medicare principal inpatient diagnostic cost group (PIP-DCG) payment model on the Program of All-Inclusive Care for the Elderly (PACE). Currently, more than 6,000 Medicare beneficiaries who are nursing home certifiable receive care from PACE, a program poised for expansion under the Balanced Budget Act of 1997. Overall, our analysis suggests that the application of the PIP-DCG model to the PACE program would reduce Medicare payments to PACE, on average, by 38%. The PIP-DCG payment model bases its risk adjustment on inpatient diagnoses and does not capture adequately the risk of caring for a population with functional impairments

    Adjusting Medicare capitation payments using prior hospitalization data

    No full text
    The diagnostic cost group approach to a reimbursement model for health maintenance organizations is presented. Diagnostic information about previous hospitalizations is used to create empirically determined risk groups, using only diagnoses involving little or no discretion in the decision to hospitalize. Diagnostic cost group and other models (including Medicare\u27s current formula and other prior-use models) are tested for their ability to predict future costs, using R2 values and new measures of predictive performance. The diagnostic cost group models perform relatively well with respect to a range of criteria, including administrative feasibility, resistance to provider manipulation, and statistical accuracy

    Dimerization of Toll-like Receptor 3 (TLR3) Is Required for Ligand Binding*

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    TLR3 (Toll-like receptor 3) recognizes dsRNA, a potent indicator of viral infection. The extracellular domain of TLR3 dimerizes when it binds dsRNA, and the crystal structure of the dimeric complex reveals three sites of interaction on each extracellular domain, two that bind dsRNA and one that is responsible for dimer formation. The goal of this study was to determine which amino acid residues are essential for forming a stable receptor·ligand complex and whether dimerization of TLR3 is required for dsRNA binding. Using a novel ELISA to analyze dsRNA binding by mutant TLR3 constructs, we identified the essential interacting residues and determined that the simultaneous interaction of all three sites is required for ligand binding. In addition, we show that TLR3 is unable to bind dsRNA when dimerization is prevented by mutating residues in the dimerization site or by immobilizing TLR3 at low density. We conclude that dimerization of TLR3 is essential for ligand binding and that the three TLR3 contact sites individually interact weakly with their binding partners but together form a high affinity receptor·ligand complex
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