Keravan Energia Oy:n ja Etelä-Suomen Energia Oy:n sähköverkkojen yleissuunnitelma

Työn tavoitteena on ollut laatia Keravan Energia Oy:n ja Etelä-Suomen Energia Oy:n keskijänniteverkkoja koskeva yleissuunnitelma. Tutkimustyön painopiste on ollut verkkojen nykytilan selvityksen ohella ajankohtaisissa verkkojärjestelykysymyksissä. Kuormitusennusteiden laadinnan pohjana on ollut kunnista saatavat väestö- ja työpaikkaennusteet. Verkkojen vahvistusta koskevat toimenpide-ehdotukset sijoittuvat vahvoille kasvualueille Etelä-Sipooseen ja Alikeravalle. Eräs keskeisimmistä tehtävistä on ollut Etelä-Suomen Energia Oy:n verkkoon sijoittuvan Östersundomin alueen sähkönjakelun kehittäminen. Työssä on tarkasteltu ja vertailtu uuden sähköaseman rakentamista keskijänniteverkon saneeraamisvaihtoehtoon. Alueen kuormituksen nopea kasvu edellyttää verkoston kehittämissuunnitelmien pikaista toimeenpanoa jo seuraavien 1-2 vuoden kuluessa. Toinen merkittävistä verkostohankkeista sijoittuu Keravan Energia Oy:n sähköverkkoon. Työssä on selvitetty 110 kV:n verkon uudelleenjärjestelyjen vaikutuksia nykyisen keskijänniteverkon rakenteeseen. Savion ja Alikeravan asemien korvaaminen uudella asemalla aiheuttaisi asemainvestoinnin lisäksi noin kahden miljoonan markan lisäinvestoinnin kaapeliyhteyksien rakentamista varten sekä lähes miljoonan markan lisähäviökustannukset tarkasteluajalta.

Effects of vacancy-type defects in silicon based particle detectors

The semiconductor particle detectors used at CERN experiments are exposed to radiation. Under radiation, the formation of lattice defects is unavoidable. The defects affect the depletion voltage and leakage current of the detectors, and hence affect on the signal-to-noise ratio of the detectors. This shortens the operational lifetime of the detectors. For this reason, the understanding of the formation and the effects of radiation induced defects is crucial for the development of radiation hard detectors. In this work, I have studied the effects of radiation induced defects-mostly vacancy related defects-with a simulation package, Silvaco. Thus, this work essentially concerns the effects of radiation induced defects, and native defects, on leakage currents in particle detectors. Impurity donor atom-vacancy complexes have been proved to cause insignificant increase of leakage current compared with the trivacancy and divacancy-oxygen centres. Native defects and divacancies have proven to cause some of the leakage current, which is relatively small compared with trivacancy and divacancy-oxygen.

β-Adrenergic modulation of skeletal muscle contraction: key role of excitation-contraction coupling.

Our aim is to describe the acute effects of catecholamines/β-adrenergic agonists on contraction of non-fatigued skeletal muscle in animals and humans, and explain the mechanisms involved. Adrenaline/β-agonists (0.1-30 μm) generally augment peak force across animal species (positive inotropic effect) and abbreviate relaxation of slow-twitch muscles (positive lusitropic effect). A peak force reduction also occurs in slow-twitch muscles in some conditions. β2 -Adrenoceptor stimulation activates distinct cyclic AMP-dependent protein kinases to phosphorylate multiple target proteins. β-Agonists modulate sarcolemmal processes (increased resting membrane potential and action potential amplitude) via enhanced Na(+) -K(+) pump and Na(+) -K(+) -2Cl(-) cotransporter function, but this does not increase force. Myofibrillar Ca(2+) sensitivity and maximum Ca(2+) -activated force are unchanged. All force potentiation involves amplified myoplasmic Ca(2+) transients consequent to increased Ca(2+) release from sarcoplasmic reticulum (SR). This unequivocally requires phosphorylation of SR Ca(2+) release channels/ryanodine receptors (RyR1) which sensitize the Ca(2+) -induced Ca(2+) release mechanism. Enhanced trans-sarcolemmal Ca(2+) influx through phosphorylated voltage-activated Ca(2+) channels contributes to force potentiation in diaphragm and amphibian muscle, but not mammalian limb muscle. Phosphorylation of phospholamban increases SR Ca(2+) pump activity in slow-twitch fibres but does not augment force; this process accelerates relaxation and may depress force. Greater Ca(2+) loading of SR may assist force potentiation in fast-twitch muscle. Some human studies show no significant force potentiation which appears to be related to the β-agonist concentration used. Indeed high-dose β-agonists (∼0.1 μm) enhance SR Ca(2+) -release rates, maximum voluntary contraction strength and peak Wingate power in trained humans. The combined findings can explain how adrenaline/β-agonists influence muscle performance during exercise/stress in humans.