Machine tools need to be tested to check they behave correctly while machining. A bigger production (capacity), improving the accuracy in final products (quality) or reducing costs are some of the main goals. Reducing the maintenance of the machines, their nonproductive time and a higher quality of the final parts, have a strong influence in the costs. Even machines built to the same specification present different properties and behaviours, which leads into a reduction of the flexibility when it comes to move operations among them. This study is focused on the measurement and modelling of four machine tools (M1, M2, M3 and M4), with same specifications, from the static point of view. Methods used to measure all these properties are the circular tests under loaded conditions, with the device Loaded Double Ball Bar (LDBB), which measures positional accuracy and static stiffness. Different pressures (0.5, 1, 3, 5, 6, 7 bar) and locations for the LDBB have been used.   After the tests were performed, all the machines shown good properties with the detail of M4, which had a lower stiffness than the other three ones due to its table attachments. / Maskinverktyg måste testas för att kontrollera att de beter sig korrekt vid bearbetning. En större produktion (kapacitet), förbättra noggrannheten i slutprodukterna (kvalitet) eller sänka kostnaderna är några av huvudmålen. Att minska underhållet av maskinerna, deras icke-produktiva tid och en högre kvalitet på de slutliga delarna har ett starkt inflytande i kostnaderna. Även maskiner konstruerade för samma specifikation presenterar olika egenskaper och beteenden, vilket leder till en minskning av flexibiliteten när det gäller att flytta verksamheten bland dem. Denna studie är inriktad på mätning och modellering av fyra verktygsmaskiner (M1, M2, M3 och M4), med samma specifikationer, ur statisk synvinkel. Metoder som används för att mäta alla dessa egenskaper är de cirkulära testerna under laddade förhållanden, med enheten Loaded Double Ball Bar (LDBB), som mäter positionsnoggrannhet och statisk styvhet. Olika tryck (0,5, 1, 3, 5, 6, 7 bar) och platser för LDBB har använts.   Efter testerna visade alla maskiner goda egenskaper med detaljerna i M4, som hade en lägre styvhet än de andra tre på grund av dess bordsfästanordningar.

LIM Kinase 1 (LIMK1), a modulator of actin and microtubule dynamics, has been shown to be involved in cell cycle progression. In this study we examine the role of LIMK1 in G1 phase and mitosis. We found ectopic expression of LIMK1 resulted in altered expression of p27Kip1, the G1 phase Cyclin D1/Cdk4 inhibitor. Overexpression of LIMK1 resulted in lower levels of p27Kip1 and p27Kip1-pY88 (inactive p27Kip1). Knockdown of LIMK1 resulted in elevated levels of p27Kip1 and p27Kip1-pY88. Together, these results suggest LIMK1 regulates progression of G1 phase through modulation of p27Kip1 expression. LIMK1 is involved in the mitotic process through inactivating phosphorylation of Cofilin. Aurora kinase A (Aur-A), a mitotic kinase, regulates initiation of mitosis through centrosome separation and proper assembly of bipolar spindles. Phosphorylated LIMK1 is recruited to the centrosomes during early prophase, where it colocalizes with ?-tubulin. Here, we report a novel functional cooperativity between Aur-A and LIMK1 through mutual phosphorylation. LIMK1 is recruited to the centrosomes during early prophase and then to the spindle poles, where it colocalizes with Aur-A. Aur-A physically associates with LIMK1 and activates it through phosphorylation, which is important for its centrosomal and spindle pole localization. Aur-A also acts as a substrate of LIMK1, and the function of LIMK1 is important for its specific localization and regulation of spindle morphology. Taken together, the novel molecular interaction between these two kinases and their regulatory roles on one other's function may provide new insight on the role of Aur-A in manipulation of actin and microtubular structures during spindle formation. The substrates of LIMK1, Aur-A and Cofilin, are also involved in the mitotic process. Aur-A kinase regulates early mitotic events through phosphorylation and activation of a variety of proteins. Specifically, Aur-A is involved in centrosomal separation and formation of mitotic spindles in early prophase. The effect of Aur-A on mitotic spindles is mediated by modulation of microtubule dynamics and association with microtubule binding proteins. In this study we show that Aur-A exerts its effects on spindle organization through regulation of the actin cytoskeleton. Aur-A phosphorylates Cofilin at multiple sites including S3 resulting in inactivation of its actin depolymerizing function. Aur-A interacts with Cofilin in early mitotic phases and regulates its phosphorylation status. Cofilin phosphorylation follows a dynamic pattern during progression of prophase to metaphase. Inhibition of Aur-A activity altered subcellular localization of Cofilin and induced a delay in the progression of prophase to metaphase. Aur-A inhibitor also disturbed the pattern of Cofilin phosphorylation, which correlated with the mitotic delay. Our results establish a novel function of Aur-A in the early mitotic stage through regulation of actin cytoskeleton reorganization. ?

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<p>Based on the concept that the tactile hypersensitivity and the central sensitization observed in animal models of peripheral neuropathy are maintained by peripheral drive from primary sensory neurons, the present project measured the changes in electrophysiological, immunohistochemical, and pharmacological properties of the dorsal root ganglia (DRG) neurons induced by a peripheral neuropathy. The aim of this study was to make a systematic survey and a unique understanding of changes that occur in primary sensory neurons that can sustain peripheral drive in this model. The data of this study indicate a prominent role of large diameter Aβ-fibers, including low threshold mechanoreceptors in peripheral neuropathy.</p> / Doctor of Philosophy (Medical Science)