A theoretical and empirical study of physician compensation arrangements

It has been suggested by researchers that fixed fee contracts are generally used to shift the full cost of resource inefficiencies to the agent. What is not clear, however, is why firms do not always use fixed fee contracts to discourage the agent\u27s resource inefficiencies but, instead, use other types of contracting approaches, such as cost reimbursement or fee-for-service. There has been little work so far which has both theoretically addressed this issue and then tested the implications of the theory. In this work agency theory is used to study this issue. The focus of study are HMOs because of the clear separation of their compensation methods into predetermined payment contracts (known as capitation) and fee-for-service contracts. In the model developed in this work, the final decisions of a risk averse primary care physician are observable by the HMO (although neither the physician\u27s reason for making his decisions nor his underlying effort in diagnosing the patient are observable by the HMO). Also the physician\u27s decisions involve different costs to the HMO and potentially different levels of effort to the physician. A specification of an optimal compensation scheme is derived. The theory from this model predicts that when there are more patients in the HMO who require greater amounts of the primary care physician\u27s time and effort to diagnose and treat, the HMO is more likely to pay its physicians fee-for-service rather than capitation. Both a reduced form equation and a structural equation system are used to test this prediction. The results under both approaches are consistent with the theory. For example, the value of the variable measuring the proportion of the population in the HMO\u27s county which is 65 or older in the reduced form equation and an instrumental variable measuring the number of hospital days per 1000 in the HMO from the structural equation system are significantly correlated in a positive direction with the HMO\u27s choice of fee-for-service (vs. capitation)

Astrocytes follow ganglion cell axons to establish an angiogenic template during retinal development.

Immature astrocytes and blood vessels enter the developing mammalian retina at the optic nerve head and migrate peripherally to colonize the entire retinal nerve fiber layer (RNFL). Retinal vascularization is arrested in retinopathy of prematurity (ROP), a major cause of bilateral blindness in children. Despite their importance in normal development and ROP, the factors that control vascularization of the retina remain poorly understood. Because astrocytes form a reticular network that appears to provide a substrate for migrating endothelial cells, they have long been proposed to guide angiogenesis. However, whether astrocytes do in fact impose a spatial pattern on developing vessels remains unclear, and how astrocytes themselves are guided is unknown. Here we explore the cellular mechanisms that ensure complete retinal coverage by astrocytes and blood vessels in mouse. We find that migrating astrocytes associate closely with the axons of retinal ganglion cells (RGCs), their neighbors in the RNFL. Analysis of Robo1; Robo2 mutants, in which RGC axon guidance is disrupted, and Math5 (Atoh7) mutants, which lack RGCs, reveals that RGCs provide directional information to migrating astrocytes that sets them on a centrifugal trajectory. Without this guidance, astrocytes exhibit polarization defects, fail to colonize the peripheral retina, and display abnormal fine-scale spatial patterning. Furthermore, using cell type-specific chemical-genetic tools to selectively ablate astrocytes, we show that the astrocyte template is required for angiogenesis and vessel patterning. Our results are consistent with a model whereby RGC axons guide formation of an astrocytic network that subsequently directs vessel development