Luottamusmiesten sitoutuminen yritykseen ja ammattijärjestöönsä

Tutkimuksen tavoitteena on kartoittaa luottamusmiesten organisaatio- ja ammattijärjestösitoutumiseen liittyviä tekijöitä sekä kuvata eri tavoin sitoutuneita ryhmiä. Keskeisiä tutkimuskysymyksiä ovat siten: Rapauttavatko hyvät esimies-alaissuhteet ja sujuviksi koetut neuvottelusuhteet työnantajan ja ammattiyhdistyksen välillä perustaa luottamusmiesten ammattijärjestösitoutumiselta? Mitkä tekijät vaikuttavat luottamusmiehen organisaatio- ja ammattijärjestösitoutumisen taustalla? Tutkimustulokset osoittavat, että oman johtajan/esimiehen ja luottamusmiehen välinen molemminpuolinen hyväksyntä ja siitä syntynyt motivoituneisuus ja työtyytyväisyys yhdistyneenä pitkän työsuhteen antamaan turvallisuuden tunteeseen ovat voimakkaammin pääkonttorien luottamusmiesten organisaatiositoutumisen taustalla. Kun taas kentän luottamusmiesten työssään kokema epävarmuus, oman työn autonomian puute, haasteeton työnjohtoilmasto tuntuivat aiheuttavan enemmän kritiikkiä työorganisaatiota kohtaan ja suuntaavan samaistumista oman ammattijärjestön suuntaan. Enemmistö tutkimuksen luottamusmiehistä oli kuitenkin kaksoissitoutuneita ja he kokivat ammattiliittonsa ja työnantajansa välisten suhteiden perustuvan yhteistyöhön ja luottamukseen organisaation johtoon. Luottamusmiesten sitoutuminen professioon ja työnantajaan näyttäisi olevan toinen vaihtoehtoinen tulevaisuuden kaksoissidoksen malli.

Galilein ja Miltonin ihmeellinen tapaaminen

Tarkastelun kohteena on Galileo Galilein ja John Miltonin tapaaminen 1638 sekä Galilein inkvisitio-oikeudenkäynnin vaikutus John Miltonin käsitykseen sananvapaudesta. Artikkelia on täydennetty 2009.

Grönlannin mannerjäätikön tulevaisuus: merenpinnan nousu maailmanlaajuisesti ja Itämerellä

Sea level rise is among the most worrying consequences of climate change, and the biggest uncertainty of sea level predictions lies in the future behaviour of the ice sheets of Greenland and Antarctica. In this work, a literature review is made concerning the future of the Greenland ice sheet and the effect of its melting on Baltic Sea level. The relation between sea level and ice sheets is also considered more generally from a theoretical and historical point of view. Lately, surprisingly rapid changes in the amount of ice discharging into the sea have been observed along the coastal areas of the ice sheets, and the mass deficit of Greenland and West Antarctic ice sheets which are considered vulnerable to warming has been increasing from the 1990s. The changes are probably related to atmospheric or oceanic temperature variations which affect the flow speed of ice either via meltwater penetrating to the bottom of the ice sheet or via changes in the flow resistance generated by the floating parts of an ice stream. These phenomena are assumed to increase the mass deficit of the ice sheets in the warming climate; however, there is no comprehensive theory to explain and model them. Thus, it is not yet possible to make reliable predictions of the ice sheet contribution to sea level rise. On the grounds of the historical evidence it appears that sea level can rise rather rapidly, 1 2 metres per century, even during warm climate periods. Sea level rise projections of similar magnitude have been made with so-called semiempirical methods that are based on modelling the link between sea level and global mean temperature. Such a rapid rise would require considerable acceleration of the ice sheet flow. Stronger rise appears rather unlikely, among other things because the mountainous coastline restricts ice discharge from Greenland. The upper limit of sea level rise from Greenland alone has been estimated at half a metre by the end of this century. Due to changes in the Earth s gravity field, the sea level rise caused by melting ice is not spatially uniform. Near the melting ice sheet the sea level rise is considerably smaller than the global average, whereas farther away it is slightly greater than the average. Because of this phenomenon, the effect of the Greenland ice sheet on Baltic Sea level will probably be rather small during this century, 15 cm at most. Melting of the Antarctic ice sheet is clearly more dangerous for the Baltic Sea, but also very uncertain. It is likely that the sea level predictions will become more accurate in the near future as the ice sheet models develop.

Developmental-like responses in injured mature central neurons

Traumatic insults to the central nervous system are frequently followed by profound and irreversible neuronal loss as well as the inability of the damaged neurons to regenerate. One of the major therapeutic challenges is to increase the amount of surviving neurons after trauma. Thus it is crucial to understand how injury affects neuronal responses and which conditions are optimal for survival to prevent neuronal loss. During development neuronal survival is thought to be dependent on the competition for the availability of survival-promoting molecules called neurotrophic factors. Much less is known on the survival mechanisms of mature neurons under traumatic conditions. Increasing amount of evidence points towards the possibility that after injury neuronal responses might aquire some developmental characteristics. One of the important examples is the change in the responses to the neurotransmitter GABA: it is inhibitory in the intact mature neurons, but can induce excitation during development and after trauma. An important step in the maturation of GABAergic transmission in the CNS is the developmental shift in the action of GABAA receptor from depolarization in immature neurons to hyperpolarization in mature neurons. GABAA-mediated responses are tightly linked to the homeostasis of the chloride anion (Cl-), which in neurons is mainly regulated by Na+-K+-2Cl- cotransporter NKCC1 and K+-Cl- cotransporter KCC2. Trauma-induced functional downregulation of KCC2 promotes a shift from hyperpolarizing GABAA-mediated responses to depolarizing. Other important consequences of neuronal trauma are the emergence of dependency of central neurons on brain-derived neuro¬trophic factor (BDNF) for survival, as well as the upregulation of neurotrophin receptor p75NTR. Our aim was to answer the question whether these post-traumatic events are interrelated, and whether the regulation of BDNF and KCC2 expression is different under traumatic conditions and in intact neurons. To study responses of injured mature central neurons, we used an in vitro and in vivo axotomy models. For in vitro studies, we lesioned organotypic hippocampal slices between CA3 and CA1 regions, which resulted in selective axotomy of the CA3 neurons and denervation of the CA1 neurons. Some experiments were repeated in vivo by lesioning the neurons of the corticospinal tract at the internal capsule level, or by lesioning spinal motoneurons at the ventral root. We show that intact mature neurons do not require BDNF for survival, whereas in axotomized neurons apoptosis is induced upon BDNF deprivation. We further show that post-traumatic dependency on BDNF is mediated by injury-induced upregulation of p75NTR. Post-traumatic increase in p75NTR is induced by GABAA-mediated depolarization, consequent opening of voltage-gated Ca2+ channels, and the activation of Rho kinase ROCK. Thus, post-traumatic KCC2 downregulation leads to the dependency on BDNF through the induction of p75NTR upregulation. Neurons that survive after axotomy over longer period of time lose BDNF dependency and regain normal KCC2 levels. This phenomenon is promoted by BDNF itself, since after axotomy contrary to normal conditions KCC2 is upregulated by BDNF. The developmentally important thyroid hormone thyroxin regulates BDNF expression during development. We show that in mature intact neurons thyroxin downregulates BDNF, whereas after axotomy thyroxin upregulates BDNF. The elevation of BDNF expression by thyroxin promoted survival of injured neurons. In addition, thyroxin also enhanced axonal regeneration and promoted the regaining of normal levels of KCC2. Thus we show that this hormone acts at several levels on the axotomy-initiated chain of events described in the present work, and could be a potential therapeutic agent for the injured neurons. We have also characterized a previously unknown downregulatory interaction between thyroxin and KCC2 in intact neurons. In conclusion, we identified several important interactions at the neurotrophin-protein and hormone-neurotrophin level that acquire immature-like characteristics after axotomy and elucidated an important part of the mechanism by which axotomy leads to the requirement of BDNF trophic support. Based on these findings, we propose a new potential therapeutic strategy where developmentally crucial agents could be used to enhance survival and regeneration of axotomized mature central neurons.