Healthcare Reform Through Redesign

This thesis will focus on the study of a complex redesign plan that healthcare organizations can utilize through healthcare reform. Research has indicated that there are numerous individuals who are uninsured or underinsured. In addition, research has supported the rising costs of healthcare today . Because of these two elements, the federal government has launched a healthcare reform campaign. Therefore, healthcare facilities must be able to reengineer the way they currently conduct business. There have been several redesign plans developed through research. However, the five common components are the delivery services, financial management and cost containment, marketing development, physician relations, and employee structure. Each of these components need dramatic changes in order for healthcare institutions to survive reform. The purpose of this study is to apply each of the five basic components in a typical healthcare setting. Each of the areas studied examined typical problems existing within the components. Specifically, it is hypothesized that by redesigning the five major components the healthcare facility will dramatically improve in performance. This study consists of secondary data. There were no subjects used in this process. The data collected was analyzed on an independent basis. Results of the analysis collected demonstrated considerable evidence to support the hypothesis. In conclusion, healthcare institutions need to redesign their current methodology in order to remain constant in the future

A β-Peptide Agonist of the GLP-1 Receptor, a Class B GPCR

[Image: see text] Previous work has shown that certain β(3)-peptides can effectively mimic the side chain display of an α-helix and inhibit interactions between proteins, both in vitro and in cultured cells. Here we describe a β(3)-peptide analog of GLP-1, CC-3(Act), that interacts with the GLP-1R extracellular domain (nGLP-1R) in vitro in a manner that competes with exendin-4 and induces GLP-1R-dependent cAMP signaling in cultured CHO-K1 cells expressing GLP-1R