In health care the reimbursement of medical providers is an important topic and can influence the overall outcome. We present the agent-based GAP-DRG model, which allows a comparison of reimbursement schemes in outpatient care. It models patients and medical providers as agents. In the simulation patients develop medical problems (i.e., diseases) and a need for medical services. This leads to utilization of medical providers. The reimbursement system receives information on the patients' visits via its generic interface, which facilitates an easy replacement. We describe the assumptions of the model in detail and show how it makes extensive use of available Austrian routine care data for its parameterization. The model design is optimized for utilizing as much of these data as possible. However, many assumptions have to be simplifications. Further work and detailed comparisons with health care data will provide insight on which assumptions are valid descriptions of the real process.
To establish a qualitative and quantitative model of blood glucose response to stress hormone exposure, healthy subjects (HS) on and off somatostatin (250 micrograms/h) as well as insulin dependent diabetic patients were infused with either epinephrine (E), glucagon (G), cortisol (F), growth hormone (GH) or with a cocktail of these hormones raising plasma stress hormones to values seen in severe diabetic ketoacidosis. The developed input/output model consists of two submodels interconnected in series plus two additional submodels for correction of gains describing both sensitivity of tissue response and utilisation as well as provision of glucose. It was shown and confirmed experimentally that blood glucose response to stress hormones was essentially nonlinear. Furthermore, the mathematical models for healthy subjects and for insulin dependent diabetic patients proved to be of the same structure and differed only in the values of some typical parameters. The model raises the possibility to describe and in part to predict blood glucose response to stress hormone exposure in healthy man and insulin dependent diabetic patients.
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