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Value-based insurance design (VBID) has shown promise for improving medication adherence by lowering or eliminating patients' payments for some medications. Yet the business case for VBID remains unclear. VBID is based on the premise that higher medication and administrative expenses incurred by insurers will be offset by lower nonmedication expenditures that result from better disease control. This article examines Blue Cross Blue Shield of North Carolina's VBID program, which began in 2008. The program eliminated copayments for generic medications and reduced copays for brand-name medications. Patient adherence improved 2.7-3.4 percent during the two-year study period. Hospital admissions decreased modestly, but there were no significant changes in emergency department use or total health expenditures. The insurer incurred$6.4 million in higher medication expenditures; total nonmedication expenditures for the study population decreased $ 5.7 million. Our results provide limited support for the idea that VBID can be cost-neutral in specific subpopulations. The business case for VBID may be more compelling over the long term and in high risk subgroups for whose members cost is an important barrier to improved medication adherence. [PUBLICATION ABSTRACT]

Inflammatory processes within the central nervous system are challenging for the clinician, radiologist, and pathologist alike. They often can mimic other more well-known and defined disease processes. We present the case of a patient with a newly described inflammatory process that primarily involves the pons and adjacent structures, which is called chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS). An 80-year-old man presented with numbness of his right hand that ultimately progressed to involve both lower extremities and face and was associated with mild dysarthria and ataxia. He had received the influenza vaccination 2 weeks prior. The biopsy revealed primarily reactive T-cell lymphocytic infiltrates with macrophages and gliosis. Treatment required long-term immunosuppressive therapy. CLIPPERS is a recently described central nervous system inflammatory condition that should be considered in the differential diagnosis when a prominent lymphocytic inflammatory infiltrate is encountered in brainstem, spinal cord, midbrain, or cerebellar biopsies.

We report a case of an intraventricular tumor with features of atypical central neurocytoma with a sarcomatous component in a 44-year-old woman who presented with headaches and vomiting. Magnetic resonance imaging revealed a 3.4-cm lobulated enhancing mass in the occipital horn of the left lateral ventricle, and the patient subsequently underwent a left occipital-parietal craniotomy for debulking. The tumor contained 2 cell populations: round cells with perinuclear halos in a fibrillary background, and spindle cells with oval nuclei arranged in interlacing fascicles with focal necrosis. The round cells had diffuse synaptophysin immunopositivity, while the spindle cells were diffusely immunopositive for vimentin and had intercellular reticulin. The mitotic activity (8 mitotic figures per 10 high-power fields) and the high Ki-67 proliferation index (15.0%) were consistent with atypical central neurocytoma with a sarcomatous component. Although different histologic variants have been described, this is the first reported case, to our knowledge, of central neurocytoma with spindle cell sarcomatous features.

AimTo evaluate the sensitivity of a commercial autoantibody screening method (Phadia EliA connective tissue disease (CTD) screen) for the detection of less common antibody specificities associated with connective tissue disease.Methods399 sera positive for anti-PM/Scl (n=102), anti-RNA polymerase III (n=199), anti-fibrillarin (n=50), anti-Mi-2 (n=12), anti-proliferating cell nuclear antigen (PCNA) (n=13) and anti-ribosomal P (n=23) were analysed using the solid phase assay. Each well was coated with the respective antigens for these autoantibodies and also with the antigens Ro, La, Jo-1, Scl-70, CENP-B, U1-RNP, Sm and native DNA.ResultsAll the anti-ribosomal P, anti-PCNA and anti-Mi-2 sera and 94% of the anti-PM/Scl sera were positive. For anti-fibrillarin, 36 (68%) were positive and 12 (22%) were equivocal. For anti-RNA polymerase III, 131 (67%) were positive, 23 (11%) were equivocal and 45 (22%) were negative.ConclusionsThe sensitivity of the Phadia EliA CTD screen is currently insufficient for the assay to be used as a screening test for anti-fibrillarin and anti-RNA polymerase III, but appears to be satisfactory for the other autoantibodies tested.

Abstract Unique among the vascular beds, loss of endothelial integrity in the pulmonary microcirculation due to injury can lead to rapidly fatal hypoxemia. The ability to regain confluence and re-establish barrier function is central to restoring proper gas exchange. The adult respiratory distress syndrome (ARDS) is a heterogeneous disease, however, meaning that endothelial cells within different regions of the lung do not likely see the same oxygen tension as they attempt to proliferate and re-establish an intact endothelial monolayer; the effect of hypoxia on the integrity of this newly formed endothelial monolayer is not clear. Immortalized human pulmonary microvascular endothelial cells (PMVEC) (ST1.6R cells) were sparsely plated and grown to confluence over 4 days in either normoxia (21% oxygen) or hypoxia (5% oxygen). Confluence attained in a hypoxic environment resulted in a tighter, less permeable endothelial monolayer (as determined by an increase in transendothelial electrical resistance, decreased permeability to fluorescently labeled macromolecules, and decreased hydraulic conductance). PMVEC grown to confluence under hypoxia had decreased RhoA activity; consistent with this finding, inhibition of Rho kinase, a well-described downstream target of RhoA, markedly increased electrical resistance in normoxic, but not hypoxic, PMVEC. These results were confirmed in primary human and rat PMVEC. These data suggest that PMVEC grown to confluence under hypoxia form a tighter monolayer than similar cells grown under normoxia. This tighter barrier appears to be due, in part, to the inhibition of RhoA activity in hypoxic cells.

Simplified models have been proposed to describe dense nonaqueous phase liquids (DNAPL) source mass discharge versus time assuming that aqueous mass transfer is proportional to the DNAPL mass remaining raised to the power of a “source architecture” coefficient. Recent studies suggest that source discharge predictions may be improved using multiple functions for different architectures. However, multiple‐source functions require estimation of additional parameters, which can be difficult to do from available field data. A hypothetical problem was considered that involves a DNAPL source zone consisting of seven discrete trichloroethylene (TCE) sources within a roughly 120,000 m2 area, each having different release dates, masses, and rate parameters. A transport model was used to simulate dissolved TCE concentrations in 22 monitoring wells over a 23 year period. “Noise” representing conceptual model errors and sampling or measurement error was applied to produce synthetic monitoring data. Source mass and dissolution rates were computed for the total source and for various depth intervals for a 5 year period and were also overlaid with suitable “noise.” Data sets consisting of various subsets of the noisy monitoring and source data were employed to calibrate various model formulations. Results indicate that calibration using only near‐source discharge rates yield highly uncertain estimates of future mass discharge rates. Prediction accuracy is improved and uncertainty is reduced by calibrating to whole plume data in conjunction with source discharge estimates, especially if the latter are available for multiple depths. More complex models reduce prediction uncertainty up to a point beyond which added complexity was a liability unless additional or more accurate data are available.

A multiphase flow model (ARMOS) was used to evaluate the effects of subsurface heterogeneities on the recover of light, nonaqueous phase liquids (LNAPLs or simply \"oil\"). Stochastic inputs for the model included the saturated hydraulic conductivity (Ksw), van Genuchten alpha and n, the water saturation at field capacity (Sm), and the maximum residual oil saturations in the saturated (Sor) and the unsaturated zones (Sog). The turning bands method was used to generate stochastic soil parameters representing three hypothetical sandy loam soils. Oil recovery in the three heterogeneous cases was compared to an \"equivalent\" homogeneous soil with effective parameters computed as the geometric means of the stochastic parameters. Distributions of the free oil plumes were described over time using statistical and spatial moment analysis. Due to the smoothing effect of the flow process, the predicted well oil thickness (Ho) and free oil specific volume (Vof) were less variable than the input stochastic parameter ln (Ksw). However, Ho and Vof became more variable as free oil volume diminished and the oil distribution was controlled more by soil variability than gradients in the fluid levels. At the onset of oil recovery, the free oil area was greater in all three heterogeneous soils than the homogeneous soil. Nevertheless, soil heterogeneities did not greatly affect oil recovery or trapping in the saturated and unsaturated zones. Heterogeneities may have had a greater influence on oil recovery if a smaller spill had been studied or if the vertical dimension had been simulated explicitly. The results suggest that the geometric mean soil properties provide a useful estimate of the potential for oil recovery from oil spills that span a large number of correlation scales

Samples of myocardium from four areas of ischemic and infarcted canine ventricle were examined over a 20-day period for content of the three adenine nucleotides as well as inosine, hypoxanthine, adenosine, and inosine monophosphate. The adenosine triphosphate (ATP) content of central and peripheral areas within the infarct fell to 11% and 8% of control, respectively, 1 day after coronary occlusion. The total adenine nucleotide (TAN) content in these areas fell to 17% of control and showed no significant recovery during the period of study. In the functional myocardium immediately surrounding the infarct the ATP content was depressed to 58% of control after 1 day, and the TAN content was also depressed. In the healthy myocardium near the apex, the ATP content was significantly depressed only at the 3-day sample period. Adenine nucleotide derivatives were detected only at 30 min in the central ischemic area. The absence of the nucleoside and nucleobase compounds formed during adenine nucleotide degradation is attributed to their high membrane diffusibility. Loss of these compounds is considered a contributing factor in the prolonged depression of adenine nucleotide content in both ischemic and non-ischemic regions.