1000 resultados para Kurki, Johanna


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The design methods and languages targeted to modern System-on-Chip designs are facing tremendous pressure of the ever-increasing complexity, power, and speed requirements. To estimate any of these three metrics, there is a trade-off between accuracy and abstraction level of detail in which a system under design is analyzed. The more detailed the description, the more accurate the simulation will be, but, on the other hand, the more time consuming it will be. Moreover, a designer wants to make decisions as early as possible in the design flow to avoid costly design backtracking. To answer the challenges posed upon System-on-chip designs, this thesis introduces a formal, power aware framework, its development methods, and methods to constraint and analyze power consumption of the system under design. This thesis discusses on power analysis of synchronous and asynchronous systems not forgetting the communication aspects of these systems. The presented framework is built upon the Timed Action System formalism, which offer an environment to analyze and constraint the functional and temporal behavior of the system at high abstraction level. Furthermore, due to the complexity of System-on-Chip designs, the possibility to abstract unnecessary implementation details at higher abstraction levels is an essential part of the introduced design framework. With the encapsulation and abstraction techniques incorporated with the procedure based communication allows a designer to use the presented power aware framework in modeling these large scale systems. The introduced techniques also enable one to subdivide the development of communication and computation into own tasks. This property is taken into account in the power analysis part as well. Furthermore, the presented framework is developed in a way that it can be used throughout the design project. In other words, a designer is able to model and analyze systems from an abstract specification down to an implementable specification.

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Dedicatio: Anders Ringbom [ruots. pr.], Eva Johanna Ringbom s. Rungia [ruots. pr.].

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Dedicatio: Daniel Walle, Johanna Magdalena Walle, s. Gylling.

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Invocatio: M.G.H.

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Invocatio: I.G.N.

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Invocatio: D.O.M.D.

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Prostate cancer is generally a slowly developing disease. However, some cancers develop into an aggressive, metastasic and consequently life-threatening state. The mechanisms of prostate cancer spread are still mainly unidentified but hormones and growth factors are known to been involved. The forming of new blood vessels i.e. angiogenesis is crucial for tumor growth. Blood vessels and lymphatic vessels are also prominent routes for metastasis. Both angiogenic and lymphangiogenic factors are overexpressed in prostate cancer. We established an in vivo model to study the factors effecting human prostate cancer growth and metastasis. Tumors were produced by the orthotopic inoculation of PC-3 prostate cancer cells into the prostates of immunodeficient mice. Like human prostate tumors, these tumors metastasized to prostate-draining lymph nodes. Treatment of the mice with the bisphosphonate alendronate known to decrease prostate cancer cell invasion in vitro inhibited metastasis and decreased tumor growth. Decreased tumor growth was associated with decreased angiogenesis and increased apoptosis of tumor cells. To elucidate the role of angiogenesis in prostate cancer progression, we studied the growth of orthotopic PC-3 tumors overexpressing fibroblast growth factor b (FGF8b) known to be expressed in human prostate cancer. FGF8b increased tumor growth and angiogenesis, which were both associated with a characteristic gene expression pattern. To study the role of lymphangiogenesis, we produced orthotopic PC-3 tumors overexpressing vascular endothelial growth factor C (VEGF-C). Blocking of VEGF-C receptor (VEGFR3) completely inhibited lymph node metastasis whereas overexpression of VEGF-C increased tumor growth and angiogenesis. VEGF-C also increased lung metastases but, surprisingly, decreased spread to lymph nodes. This suggests that the expanded vascular network was primarily used as a route for tumor spreading. Finally, the functionality of the capillary network in subcutaneous FGF8b-overexpressing PC-3 tumors was compared to that of tumors overexpressing VEGF. Both tumors showed angiogenic morphology and grew faster than control tumors. However, FGF8b tumors were hypoxic and their perfusion and oxygenation was poor compared with VEGF tumors. This suggests that the growth advantage of FGF8b tumors is more likely due to stimulated proliferation than effective angiogenesis. In conclusion, these results show that orthotopic prostate tumors provide a useful model to explore the mechanisms of prostate cancer growth and metastasis.

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Artikkelissa kerrotaan Porin kaupungin koulutoimen vuonna 1997 alkaneesta Iltis-projektista, joka on koulujen uusi iltapäivätoiminnan muoto.

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