60 research outputs found

    Simplicity is not Simple: How Business Architecture in One of Belgium’s Biggest Companies Can Be Simple and Easy-to-Use

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    Part 9: Engineering MethodsInternational audienceAs organizations are becoming more complex, Enterprise Architecture (EA) serves as an important means to align the strategy with the operations and to achieve business/IT (i.e., Information Technology) alignment. Although numerous approaches have been designed for large enterprises, little EA research was oriented towards small- and medium-sized enterprises (SMEs). However, both organizational types are fundamentally different and require a tailored approach. Therefore, CHOOSE was designed as an EA approach that is in accordance with the needs of SMEs. By performing a case study in the department of a large enterprise, this paper aims to investigate how CHOOSE can be used outside its original context. More specifically, it will be examined how the metamodel and modeling method could be extended to deliver an overview and valuable insights about a complex business reality. To realize this, potential solutions for the encountered issues are formulated and evaluated by the involved business stakeholders

    Invasiveness, proliferative activity and ultrastructural phenotypes of hepatocytes from diethylnitrosamine‐induced neoplastic nodules and hepacarcinomas in vitro

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    The invasive behavior of hepatocytes from diethylnitrosamine (DENA) induced neoplastic nodules and hepatocarcinomas was studied in a confronting culture system in vitro. These observations confirm our previous report, demonstrating that hepatocytes from hepatocarcinomas and from neoplastic nodules invaded into embryonic chick precultured heart fragments (PHF), a property associated with malignancy (Mareel, 1979). We now further demonstrate that: (1) Invasiveness was expressed by the hepatocytes in 10 out of 12 samples from hepatocarcinomas, and in 13 out of 36 confronted nodular samples. The hepatocytes from the other two‐thirds of nodule samples died off in the confrontation as did all normal hepatocytes. (2) Invasive hepatocytes from tumors and from nodules showed the same arrangement of invasive liver cells in relation to the heart tissue, and the same ultrastructural phenotypes. The latter did not differ from those in the non‐invading subpopulations, with the exception perhaps of a higher proportion of cells with an indented nucleus. (3) None of the scored ultrastructural alterations was present in all the invasive cells, thus excluding any specific requisite in this respect. (4) When 3H‐TdR was made continuously available to the cultures, starting at the time of confrontation between heart and liver tissues, unlabelled as well as labelled invasive hepatocytes were found inside the PHF in about equal proportions. It is concluded that nodular hepatocytes deviate from normality by at least 2 different properties that may or may not be related to each other and are revealed under in vitro conditions, namely the ability to survive and to proceed through S‐phase and mitosis under such conditions and to actively invade precultured chick heart fragments. The latter property indicates that at least some of the nodules contain hepatocytes that have performed one step in malignant progression. Copyright © 1987 Wiley‐Liss, Inc. A Wiley CompanySCOPUS: ar.jFLWNAinfo:eu-repo/semantics/publishe

    The effect of ischemia and reperfusion on mitochondrial contact sites in isolated rat hearts

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    Contact sites may be described as energy channels between the mitochondria and the cytosol, created by fusion of the inner and the outer mitochondrial membranes, and their number depends highly on the energy state of the cell. The aim of the present study was to examine the early changes of ischemia and reperfusion on the number of mitochondrial contact sites. Therefore isolated rat hearts were subjected to short periods of ischemia followed by reperfusion. The left ventricular pressure (LVP), the contractility (dPIdt,, ) and the heart rate were measured. The number o? contact sites was morphometrically evaluated. As the flow was stopped, LVP, dP/dt and HR declined rapidly and became undetectable a P2 min of ischemia. The number of contact sites fe11 to a minimum after 10 min of ischemia after an initial increase (1 min of ischemia). A 15 min ischemic period resulted in a high number of contact sites which decreased again after 20 min of ischemia. Reperfusion after 2 rnin of ischemia caused an immediate functional recovery and a high presence of contact sites. After 15 rnin of reperfusion, al1 values returned to control values. Reperfusion after 10 rnin of ischemia resulted in a slow recovery of the number of contact sites and after 15 rnin of ischemia the number of contact sites remained low upon reperfusion. We may conclude that mitochondria lose the ability to form contact sites after more than 15 min of ischemia and this might be a first indication of irreversible injury
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