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- Bång, Magnus, 1967-, et al.
(författare)
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Distributed user interfaces for clinical ubiquitous computing applications
- 2005
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Ingår i: International Journal of Medical Informatics. - : Elsevier BV. - 1386-5056 .- 1872-8243. ; 74:7-8, s. 545-551
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: Ubiquitous computing with multiple interaction devices requires new interface models that support user-specific modifications to applications and facilitate the fast development of active workspaces.Methods: We have developed NOSTOS, a computer-augmented work environment for clinical personnel to explore new user interface paradigms for ubiquitous computing. NOSTOS uses several devices such as digital pens, an active desk, and walk-up displays that allow the system to track documents and activities in the workplace.Results: We present the distributed user interface (DUI) model that allows standalone applications to distribute their user interface components to several devices dynamically at run-time. This mechanism permit clinicians to develop their own user interfaces and forms to clinical information systems to match their specific needs. We discuss the underlying technical concepts of DUIs and show how service discovery, component distribution, events and layout management are dealt with in the NOSTOS system.Conclusion: Our results suggest that DUIs - and similar network-based user interfaces - will be a prerequisite of future mobile user interfaces and essential to develop clinical multi-device environments. © 2005 Elsevier Ireland Ltd. All rights reserved.
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- Friberg, P. Anders, 1976, et al.
(författare)
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Apoptotic effects of a progesterone receptor antagonist on rat granulosa cells are not mediated via reduced protein isoprenylation.
- 2007
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Ingår i: Molecular reproduction and development. - : Wiley. - 1040-452X .- 1098-2795. ; 74:10, s. 1317-26
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Tidskriftsartikel (refereegranskat)abstract
- Progesterone is a survival factor in rat periovulatory granulosa cells. The mechanisms involved are unclear but progesterone receptor (PGR) antagonists have been shown to inhibit cholesterol synthesis and induce apoptosis. Furthermore, reports suggest that statins induce apoptosis by inhibition of protein isoprenylation. Statins inhibit the rate-limiting step of the cholesterol synthesis, thereby reducing availability of intermediates used for the post-translational isoprenylation process. It has been suggested that PGR antagonists in a similar manner induce apoptosis by decreasing cholesterol synthesis and thereby protein isoprenylation. In this study we hypothesized that the mechanism by which the nuclear PGR antagonist Org 31,710 induces apoptosis in rat periovulatory granulosa cells, is by decreasing cholesterol synthesis and thereby general cell protein isoprenylation. Incubation of isolated granulosa cells with Org 31,710 or simvastatin for 22 hr resulted in increased apoptosis and reduced cholesterol synthesis. However, simvastatin caused a substantial inhibition of cholesterol synthesis after 6 hr in culture without inducing apoptosis. In contrast, Org 31,710 had only a modest effect on cholesterol synthesis after 6 hr while it significantly induced apoptosis. Addition of isoprenylation substrates partially reversed apoptosis induced by simvastatin and to a lesser extent apoptosis induced by Org 31,710. In addition, and in contrast to Org 31,710, simvastatin caused a decrease in isoprenylation of a selected isoprenylation marker protein, the Ras-related protein RAB11. In conclusion, we demonstrate that the PGR antagonist inhibits cholesterol synthesis in granulosa cells but reduced protein isoprenylation is not the mediating mechanism of increased apoptosis as previously hypothesized.
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- Friberg, P. Anders, 1976, et al.
(författare)
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Dominant role of nuclear progesterone receptor in the control of rat periovulatory granulosa cell apoptosis.
- 2009
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Ingår i: Biology of reproduction. - : Oxford University Press (OUP). - 0006-3363 .- 1529-7268. ; 80:6, s. 1160-7
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Tidskriftsartikel (refereegranskat)abstract
- In this study, it was hypothesized that progesterone (P4) acts as a survival factor primarily by actions of the classic nuclear progesterone receptor (PGR) signaling pathway in rat periovulatory granulosa cells. Granulosa cells were isolated from immature female rats primed with equine chorionic gonadotropin/human chorionic gonadotropin and treated in vitro with PGR antagonists. As little as 10 nM of two different PGR antagonists (Org 31710 and RU 486) increased apoptosis measured as caspase 3/7 activity, which was reversed by cotreatment with the progestin R5020. Concurrently, P4 synthesis was decreased. Inhibition of P4 synthesis by cyanoketone similarly induced apoptosis but required greater inhibition of P4 synthesis than that seen after treatment with PGR antagonists. Therefore, the induction of apoptosis by PGR antagonists cannot be explained by decreased P4 synthesis alone. Low concentrations of R5020 also completely reversed the effects of cyanoketone. Inhibition of P4 synthesis was more effective in inducing apoptosis than treatment with PGR antagonists. However, cotreatment with PGR antagonists protected cells from the additional effects of cyanoketone, indicating partial agonist effects of the antagonists and a dominating role for PGR in P4-mediated regulation of apoptosis. Progesterone receptor membrane component 1 (PGRMC1) was expressed in granulosa cells; however, an anti-PGRMC1 antibody did not induce apoptosis in periovulatory granulosa cells. Neither anti-PGRMC1 nor P4 or cyanoketone affected apoptosis of immature granulosa cells. In conclusion, we show that P4 regulates apoptosis in periovulatory granulosa cells by acting via the classic nuclear receptor.
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