Charting the landscape of enterprise architecture management

Todays enterprises are faced with the challenge of an everchanging environment, which they continuously have to adaptto. A commonly accepted means to support an enterprisein the transformation process and furthermore enhance thealignment between business and IT is enterprise architecture(EA) management, which provides a holistic perspectiveon the enterprise. In order to support an enterprise inthe transformation process, EA management creates architecturaldescriptions of current, planned, and future statesof the enterprise. Reecting the aforementioned importanceof EA management a plurality of approaches for establishingan EA management function in an enterprise have beenproposed by researchers, practitioners, and standardizationbodies. The approaches vary widely in respect to the proposedmethods, models, and languages.The objective of this article is to analyze the state-of-theartin EA and EA management respectively. Therefore, anextensive literature survey on publications in the area is performed.Criteria for the analysis are inter alia the distribution of papers over time, their regional distribution, type ofpublication, number of references of an article, and the involvedauthors groups. Thereby the article seeks to give anoverview on the current research occupation in the eld ofEA management

Loss of pain perception in diabetes is dependent on a receptor of the immunoglobulin superfamily

Molecular events that result in loss of pain perception are poorly understood in diabetic neuropathy. Our results show that the receptor for advanced glycation end products (RAGE), a receptor associated with sustained NF-κB activation in the diabetic microenvironment, has a central role in sensory neuronal dysfunction. In sural nerve biopsies, ligands of RAGE, the receptor itself, activated NF-κBp65, and IL-6 colocalized in the microvasculature of patients with diabetic neuropathy. Activation of NF-κB and NF-κB–dependent gene expression was upregulated in peripheral nerves of diabetic mice, induced by advanced glycation end products, and prevented by RAGE blockade. NF-κB activation was blunted in RAGE-null (RAGE(–/–)) mice compared with robust enhancement in strain-matched controls, even 6 months after diabetes induction. Loss of pain perception, indicative of long-standing diabetic neuropathy, was reversed in WT mice treated with soluble RAGE. Most importantly, loss of pain perception was largely prevented in RAGE(–/–) mice, although they were not protected from diabetes-induced loss of PGP9.5-positive plantar nerve fibers. These data demonstrate, for the first time to our knowledge, that the RAGE–NF-κB axis operates in diabetic neuropathy, by mediating functional sensory deficits, and that its inhibition may provide new therapeutic approaches