Engineering of interworking TINA-based telecommunication services

This paper describes a Service Creation approach being developed in the EU funded ACTS TOSCA (TINA Open Service Creation Architecture) project to rapidly develop validated TINA based multimedia telecommunications services. The approach is based around object-oriented software frameworks in SDL which are specialized towards services by means of graphical paradigm tools. Further, in TOSCA, the need for service interworking across service provider domains via federation has been recognized in order to allow users to join service sessions offered by providers they are not customers of. However, service interworking may cause undesired behavior - the so called service interaction phenomenon. This paper focuses on this issue and the underlying technology of the service creation approach with emphasis on how service federation has been implemented

Hybrid solutions to the feature interaction problem

In this paper we assume a competitive marketplace where the features are developed by different enterprises, which cannot or will not exchange information. We present a classification of feature interaction in this setting and introduce an on-line technique which serves as a basis for the two novel <i>hybrid</i> approaches presented. The approaches are hybrid as they are neither strictly off-line nor on-line, but combine aspects of both. The two approaches address different kinds of feature interactions, and thus are complimentary. Together they provide a complete solution by addressing interaction detection and resolution. We illustrate the techniques within the communication networks domain

The First Word

Does the President get the last word in the legislative process when he issues a signing statement? Those angry about President Bush\u27s December 2005 signing statement on the Detainee Treatment Act thought he did just that. Implying that the statute\u27s prohibitions on cruel, inhuman, or degrading treatment would not apply in certain circumstances, President Bush\u27s statement provoked an outcry. Critics claimed that the President did not have the political muscle to defeat the statute, so he instead announced that he would sometimes ignore it. Having the last word has its advantages. But so does having the first word. Signing statements come at the end of the legislative process, but they also come at the beginning of the life of a law. President Bush\u27s signing statement was controversial not only because it was the last word, but because his words mattered. In the absence of a definitive judicial interpretation of the statute, the signing statement would guide those in the executive branch who were bound to follow the law. This Article, using signing statements as one example, analyzes the various tools available to Presidents to exert influence over actors in the executive branch. Signing statements are notable because they permit the President to instruct subordinates ex ante. They are, that is, the first word --the first step in the process of turning laws into on-the-ground reality. But they are just one of many instruments Presidents can rely on to manage, direct, and supervise subordinate officials. The Article identifies a variety of circumstances in which Presidents might worry about the actions of subordinates and examines presidential responses in order to assess their efficacy. The President can appoint key personnel; he can provide ex ante instructions; and he can review major agency actions ex post. These strategies are not equally effective. As this Article will show, the effectiveness of a given strategy depends both on the task assigned to the subordinate official and the nature of that official\u27s potential drift away from the White House. An important lesson of the analysis is that ex ante instructions, like signing statements, have some distinct advantages over ex post review in controlling certain kinds of discretionary actions by subordinates. In particular, ex ante methods of control could allow the White House to control exercises of discretion by subordinate actors that are difficult to control through ex post means. Some of the exercises of discretion that may be most effectively controlled by ex ante mechanisms are also generally immune from judicial review. In the absence of judicial control of these administrative actions, the President may be able to exercise particularly strong control over an agency

Temporary Accidents?

In Part I of this Review, I will summarize Croley\u27s book, focusing on his powerful critique of public choice theory and the alternative account that he develops and defends. Part II assesses the book, arguing that Croley is successful in demonstrating agency autonomy but less successful in showing that either administrator motivations or the administrative process tend to make agencies regulate in welfare-enhancing ways. As is often the case, the critique is more powerful than the construction of the alternative account. Even so, Croley\u27s book should alter debates over the possibility of good government by placing the agency and how it does its business at the center of our understanding of government regulation

Estrogen and Vitamin D Control of Transcription in MCF-7 Cells

Abstract The Extracellular Signal-Regulated Kinase (ERK) is part of a key, signaling pathway that regulates both transcription and translation in many cell types. Increases in intracellular calcium levels results in the CaM Kinase-dependent activation of ERK and cell growth in MCF-7 breast cancer cells. ERK has also been shown to play a role in the regulation of MCF-7 cell proliferation through control of downstream transcription factors including Elk-1. The hormone, Vitamin D has been suggested to play an inhibitory role on cancer cells by blocking ERK activation. Our goal was to evaluate the ability of E2 to activate Elk-1, through a CaM Kinase/ERK dependent pathway, in MCF-7 cells. We also examined Vitamin D’s inhibitory regulation of ERK and Elk-1 activation. Interestingly, E2 stimulation of MCF-7 cells triggered Elk-1 phosphorylation an effect that was blocked by inhibiting either CaM KK or ERK. Similarly, E2 treatment of MCF-7 cells also triggered a significant increase in Elk-1-dependent luciferase activity. siRNA inhibition of CaM KK or ERK blocked E2-stimulated Elk-1 luciferase activity. Additionally, E2 triggered a sustained increase in ERK and Elk-1 phosphorylation, both of which were blocked by Vitamin D treatment. Vitamin D treatment of cells also inhibited Elk-1 luciferase activity downstream of E2 stimulation. In summary, our data suggests that E2 utilizes both CaM KK and ERK to activate Elk-1 transcriptional activity an effect that is blocked by the hormone Vitamin D

TRP Channel Regulation of Estrogen Signaling

Abstract Calcium regulates numerous cell functions including growth and development. Calcium can enter cells through transient receptor potential channels (TRPCs). Previous studies in MCF-7 cells have suggested that the expression of one particular TRPC, TRPC6, correlates with cell transformation and disease progression. Calcium has several cellular targets including the Calcium/Calmodulin-dependent protein kinases (CaM Ks) and ERK. Previous work has shown that estrogen (E2) may utilize CaM Ks and ERK to promote breast cancer cell proliferation, however the possible involvement of TRPCs in this pathway is currently unknown. Our objective was to understand which E2 receptor is used in our system and if TRPCs participate in the control of CaM Kinase activation of ERK in MCF-7 cells. Specifically, we wanted to explore if E2 may utilize TRPCs particularly, TRPC6, upstream of the ERK pathway in MCF-7 cells. E2 stimulation of MCF-7 cells and the estrogen receptor alpha (α) inhibitor, MPP, completely blocked ERK activity. In contrast, MPP did not block EGF stimulation of ERK. MCF-7 cells express endogenous TRPC6 protein and TRPC inhibitors, APB and SK&F, both blocked ERK activation downstream of E2. In addition, neither APB or SK&F inhibited EGF activation of ERK. Results from these studies suggest that E2 is capable of activating ERK through the specifically through the alpha form of the estrogen receptor and TRPCs

Transcription Factor Regulation of ERK and Estrogen in MCF-7 Cells

Abstract ERK is activated by increased intracellular calcium downstream of the hormone estrogen (E2). E2 activates ERK via the CaM Kinases, specifically CaM KK and CaM KI in MCF-7 cells. ERK may control cell growth and proliferation through Elk-1, Rsk, SRF, CREB, and numerous other molecules and nuclear targets. Vitamin D, a hormone, has proven to be an effective antagonist of ERK and MCF-7 breast cancer cell growth. Our goal was to evaluate if the E2 pathway working through CaM KK and ERK regulated the transcription factors Elk-1, CREB, and SRF. We also examined the ability of vitamin D to antagonize ERK activation of its downstream targets. Interestingly, E2 stimulation of MCF-7 cells activated both ERK and Elk-1 an effect that was blocked by inhibiting both CaM KK and ERK. E2 treatment of MCF-7 cells also triggered a significant increase in SRF and CREB phosphorlation in a CaM KK- and ERK-dependent manner. Dimerization of transcription factors may enhance DNA binding and gene expression. E2 stimulation of MCF-7 cells promoted the formation of a molecular complex between endogenous Elk-1 and SRF. Finally, E2 triggered a prolonged increased in ERK and Elk-1 phosphorylation, both of which were blocked by vitamin D treatment. Taken together our data demonstrates several transcriptional targets for E2 working through CaM KK and their inhibition by vitamin D signaling