Modeling of the Earth's gravity field using the New Global Earth Model (NEWGEM)

Traditionally, the global gravity field was described by representations based on the spherical harmonics (SH) expansion of the geopotential. The SH expansion coefficients were determined by fitting the Earth's gravity data as measured by many different methods including the use of artificial satellites. As gravity data have accumulated with increasingly better accuracies, more of the higher order SH expansion coefficients were determined. The SH representation is useful for describing the gravity field exterior to the Earth but is theoretically invalid on the Earth's surface and in the Earth's interior. A new global Earth model (NEWGEM) (KIM, 1987 and 1988a) was recently proposed to provide a unified description of the Earth's gravity field inside, on, and outside the Earth's surface using the Earth's mass density profile as deduced from seismic studies, elevation and bathymetric information, and local and global gravity data. Using NEWGEM, it is possible to determine the constraints on the mass distribution of the Earth imposed by gravity, topography, and seismic data. NEWGEM is useful in investigating a variety of geophysical phenomena. It is currently being utilized to develop a geophysical interpretation of Kaula's rule. The zeroth order NEWGEM is being used to numerically integrate spherical harmonic expansion coefficients and simultaneously determine the contribution of each layer in the model to a given coefficient. The numerically determined SH expansion coefficients are also being used to test the validity of SH expansions at the surface of the Earth by comparing the resulting SH expansion gravity model with exact calculations of the gravity at the Earth's surface

Tectonic deformation on icy satellites: A model of compensating horsts

Voyager images demonstrate that the icy satellites have been shaped by a variety of magmatic and tectonic processes, of which ridge and trough terrain is a manifestation. This terrain is observed on Ganymede, Enceladus, Miranda, and Ariel, and many models have been proposed to explain its origin. A likely model is horst and graben style normal faulting, in which horizontal extension results in a series of downdropped grabens and relatively uplifted horsts. The apparent negative elevation of ridges and troughs relative to surrounding terrain has been used to argue such an extensional-tectonic origin for ridge and trough terrain on Ganymede and Enceladus. A ridge or ridge set which stands above a presumed original base level, thus, might be suspect of having a magmatic or compressional origin. It has been shown that rotation of domino-style normal faulting, which involves rotation of fault blocks about a fulcrum, can allow ridges to stand slightly above the original base level, and this relative uplift may be amplified by isostatic uplift. Compensation might also be accomplished through uplift of adjacent horsts. These theories are defended with dynamical equations

Cyclin Dependent Kinase 5 in Endothelial Cell Migration

Cyclin dependent kinase 5 (Cdk5) is studied to take part in the migration neurons and development of brain. It is proven to participate also in the mediation of endothelial cell migration and angiogenesis. Angiogenesis is a crucial physiological mechanism in mediating wound healing and menstrual cycle among other functions. It is also important in some patophysiological processes like diabetic retinopathy and tumour outgrow. Tumour is shown to need its own vascularisation after reaching a size of 2-3 mm as a diameter in order to proceed growing. This makes Cdk5 a potential therapeutic target in regulating angiogenesis. In order to be activated, Cdk5 forms a complex together with its neuronal activator p35 or p39, or with their respective cleavage products p25 or p29. The mechanisms, how Cdk5 is activated in human ehdothelial cells has not been studied before. This master thesis is to evaluate the existence of Cdk5 activators p35 and p39 and their respective cleavage products in spreading human umbilical vein endothelial cells (HUVECs) to mimic the cell migration by freshly plating the cells. In our studies we performed western blot analysis and quantitative PCR analysis to investigate the expression of p35 and p25 in spreading HUVECs in different time points. We also performed an immunofluorescence assay to investigate the localisation of p35 and p25 in spreading HUVECs using confocal laser scanning microscopy (CLSM). The expression of p35 and p25 was also studied after growth factor stimulation (VEGF, FGF). The expression of the activator p39 in spreading HUVECs was studied using quantitative PCR method. Finally we investigated the interaction of Cdk5 with its activator p35 and its cleavage product p25 in spreading HUVECs using immunoprecipitation (IP). We were able to show in our studies that the activators p35 and p25 are expressed in HUVECs and that their expression is changing in spreading HUVECs in different time points. Additionally we were able to show, that p35 and p25 are partly localized in periphery in spreading cells. We were able to show that also the activator p39 is expressed in spreading HUVECs, but its relative amount was shown to be only a small portion of p35 in HUVECs. We were able to prove the interaction of Cdk5 with its activator p35 and p25 using immunoprecipitation, although the result could not be completely verified. Stimulation with growth factors showed no appreciable changes in the expression of p35 or p25. Based on the results, we can state that both the activator p35 and p39, and at least p25, the cleavage product p35, are expressed also in HUVECs. As they are neuronal activators of Cdk5 and Cdk5 has shown to participate in the mediation of angiogenesis and endothelial cell migration, the results amplify our hypothesis that also these activators might have a role in mediating endothelial cell migration and angiogenesis. Nevertheless to assure it, to specify the possible different roles of each activators and their interaction with Cdk5, further studies are needed.Sykliineistä riippuvainen kinaasi 5 (Cdk5) on todettu osallistuvan neuronien migraation ja aivojen kehittymisen säätelyyn. Sen osallisuus on todistettu myös endoteelisolujen migraation ja angiogeneesin säätelyssä. Angiogeneesi on tärkeä fysiologinen mekanismi mm. haavan paranemisen ja kuukautiskierron yhteydessä. Sillä on todettu olevan rooli myös joissakin patofysiologisissa prosesseissa kuten diabeettisessa retinopatiassa ja syöpäkasvainten kasvussa. Syöpäkasvain tarvitsee oman verisuonistuksensa, jotta se voi jatkaa kasvuaan saavuttaessaan 2-3 mm halkaisijan läpimitan. Tämä tekee Cdk5 roolista potentiaalisen terapeuttisen kohteen angiogeneesin säätelyssä. Aktivoituakseen Cdk5:n on muodostettava kompleksi sen neuronaalisen aktivaattorin p35:n tai p39:n kanssa, tai niiden pilkkoutumistuotteiden p25:n tai p29:n kanssa. Cdk5 aktivoitumismekanismeja ei ole ennen tutkittu endoteelisoluissa, joten tämän Pro gradu tutkielman tarkoituksena oli tutkia Cdk5 aktivaattoreiden ja niiden pilkkoutumistuotteiden ilmentymistä humaani endoteelisoluissa. Tutkimuksissa pyrittiin selvittämään aktivaattoreiden ilmentymistä napanuoran laskimosta eristetyissä humaani endoteelisoluissa (HUVEC) imitoimalla solumigraatiota jakamalla solut levittäytymään solumaljoille. Tutkimuksessa selvitettiin p35:n ja p25:n ilmentymistä eri aikapisteissä mitattuina levittäytyvissä endoteelisoluissa western blot menetelmän ja kvantitatiivisen PCR menetelmän avulla. Lisäksi tutkittiin p35:n ja p25:n lokalisaatiota levittäytyvissä soluissa fluoresenssivärjäyksen ja konfokaalimikroskopoinnin avulla. P35:n ja p25:n ilmentymistä tutkittiin myös stimuloimalla soluja eri kasvutekijöillä (VEGF, FGF). Toisen aktivaattorin p39 ilmentymistä tutkittiin levittäytyvissä soluissa kvantitatiivisen PCR menetelmän avulla. Lisäksi p35:n ja p25:n interaktiota Cdk5:n levittäytyvissä soluissa tutkittiin immunosaostuksen avulla. Kokeiden avulla voitiin osoittaa että aktivaattoreiden p35 ja p25 pitoisuudet muuttuvat levittäytyvissä soluissa eri aika pisteissä mitattuna. Lisäksi voitiin osoittaa, että p35 ja p25 paikantuvat levittäytyvissä soluissa solujen reuna-alueille. p39:n ilmentymisen todettiin olevan vain pieni osa p35:n määrästä. Immunosaostuksen avulla voitiin osoittaa interaktio kinaasin ja p35:n välillä, joskin tulosta ei voitu täysin varmistaa. Kasvutekijöillä stimuloiduissa soluissa ei voitu osoittaa muutosta aktivaattoreiden p35 ja p25 ilmentymisessä. Tulosten pohjalta voidaan todeta, että aktivaattorit p35 ja p39, sekä ainakin p35:n pilkkoutumistuote p25 ilmentyvät myös humaani endoteelisoluissa, joissa Cdk5 on todettu osallistuvan angiogeneesin ja endoteelisolujen migraation säätelyyn. Tulokset vahvistvat hypoteesia, että näillä aktivaattoreilla on rooli endoteelisolujen migraatiossa, joskin sen varmistaminen, eri aktivaattoreiden rooli sekä yhteys Cdk5:n aktivoitumiseen vaativat vielä lisätutkimuksia