Euran emännän neulakintaat : Tutkielma Luistarin haudan 56 neulakinnasfragmenteista

Tutkielman tavoitteena on tuottaa neulakinnasrekonstruktio Euran Luistarin kalmiston haudan 56 neulakinnasfragmenttien pohjalta. Hauta on tutkittu vuonna 1969, jolloin kalmistoalueen arkeologiset kaivaukset aloitettiin. Haudan löytöjen perusteella on aikaisemmin tehty kokonainen pukurekonstruktio, Euran muinaispuku. Luistarin hauta 56 on ruumishauta ja se on tehty naisvainajalle rautakaudella, 1000-luvun alkupuolella jKr. Neulakinnastekniikalla on valmistettu neuloksia jo tuhansia vuosia. Eri neulakinnastekniikoita on yritetty kuvata useilla teorioilla, joista paras lienee Egon H. Hansenin merkintätapa. Suomalaisen kansanperinteen mukaan maassamme on tehty neuleita kolmella erilaisella neulakinnastekniikalla: suomeksi , venäjäksi ja pyöräyttäen . Luistarin haudan 56 neulakinnastekniikalla valmistetut tekstiilifragmentit löytyivät vainajan vatsalta suuren puukontupen päältä sekä kämmenluiden ja sormusten yhteydestä. Fragmentteja saatiin kaivauksissa talteen yhteensä kuusi, joista suurin on kooltaan 6x9 cm. Fragmentit on sijaintinsa perusteella tulkittu kintaiden jäänteiksi. Hautaustilanteessa kintaat ovat ilmeisesti sijainneet vainajan vatsalla, eivätkä käsiin puettuina, sillä fragmentteja ei löytynyt kaikkien sormusten yhteydestä. Myös eräistä muista rautakautisista ruumishaudoista on löydetty neulakintaiden jäänteitä. Luistarin haudan 56 neulakinnasfragmenteista on tutkittu valmistustekniikka, lankojen paksuudet ja kierteisyydet. Selkeänä erottuvat kolme väriä on tulkittu mikroskooppitarkastelussa siniseksi, punaiseksi ja keltaiseksi. Pieni punaisen kerroksen pätkä aivan suurimman fragmentin reunassa on tulkittu peukalon tyveksi. Muita Suomesta löytyneitä rautakautisia neulakinnasfragmentteja ja niistä saatuja tietoja on käytetty vertailuaineistona. Kinnasrekonstruktioon käytetyt langat on värjätty luonnonväreillä. Värjäyksessä on käytetty osittain nykypäivän keinoja, mutta niin, että lopputulos poikkeaisi mahdollisimman vähän muinaistekniikoilla tehdystä. Punainen lanka on värjätty värimataralla eli krapilla, keltainen kanervalla ja sininen luonnonindigolla. Kintaiden muotoilu perustuu suomalaiseen neulakinnastraditioon ja lähialueiltamme löytyneisiin keskiaikaisiin neulakintaisiin.

N-syndecan and HB-GAM in neural migration and differentiation : Modulation of growth factor activity in brain

The juvenile sea squirt wanders through the sea searching for a suitable rock or hunk of coral to cling to and make its home for life. For this task it has a rudimentary nervous system. When it finds its spot and takes root, it doesn't need its brain any more so it eats it. It's rather like getting tenure. Daniel C. Dennett (from Consciousness Explained, 1991) The little sea squirt needs its brain for a task that is very simple and short. When the task is completed, the sea squirt starts a new life in a vegetative state, after having a nourishing meal. The little brain is more tightly structured than our massive primate brains. The number of neurons is exact, no leeway in neural proliferation is tolerated. Each neuroblast migrates exactly to the correct position, and only a certain number of connections with the right companions is allowed. In comparison, growth of a mammalian brain is a merry mess. The reason is obvious: Squirt brain needs to perform only a few, predictable functions, before becoming waste. The more mobile and complex mammals engage their brains in tasks requiring quick adaptation and plasticity in a constantly changing environment. Although the regulation of nervous system development varies between species, many regulatory elements remain the same. For example, all multicellular animals possess a collection of proteoglycans (PG); proteins with attached, complex sugar chains called glycosaminoglycans (GAG). In development, PGs participate in the organization of the animal body, like in the construction of parts of the nervous system. The PGs capture water with their GAG chains, forming a biochemically active gel at the surface of the cell, and in the extracellular matrix (ECM). In the nervous system, this gel traps inside it different molecules: growth factors and ECM-associated proteins. They regulate the proliferation of neural stem cells (NSC), guide the migration of neurons, and coordinate the formation of neuronal connections. In this work I have followed the role of two molecules contributing to the complexity of mammalian brain development. N-syndecan is a transmembrane heparan sulfate proteoglycan (HSPG) with cell signaling functions. Heparin-binding growth-associated molecule (HB-GAM) is an ECM-associated protein with high expression in the perinatal nervous system, and high affinity to HS and heparin. N-syndecan is a receptor for several growth factors and for HB-GAM. HB-GAM induces specific signaling via N-syndecan, activating c-Src, calcium/calmodulin-dependent serine protein kinase (CASK) and cortactin. By studying the gene knockouts of HB-GAM and N-syndecan in mice, I have found that HB-GAM and N-syndecan are involved as a receptor-ligand-pair in neural migration and differentiation. HB-GAM competes with the growth factors fibriblast growth factor (FGF)-2 and heparin-binding epidermal growth factor (HB-EGF) in HS-binding, causing NSCs to stop proliferation and to differentiate, and affects HB-EGF-induced EGF receptor (EGFR) signaling in neural cells during migration. N-syndecan signaling affects the motility of young neurons, by boosting EGFR-mediated cell migration. In addition, these two receptors form a complex at the surface of the neurons, probably creating a motility-regulating structure.

Heparin-binding growth-associated molecule (HB-GAM) in activity-dependent neuronal plasticity in hippocampus

Cell adhesion and extracellular matrix (ECM) molecules play a significant role in neuronal plasticity both during development and in the adult. Plastic changes in which ECM components are implicated may underlie important nervous system functions, such as memory formation and learning. Heparin-binding growthassociated molecule (HB-GAM, also known as pleiotrophin), is an ECM protein involved in neurite outgrowth, axonal guidance and synaptogenesis during perinatal period. In the adult brain HB-GAM expression is restricted to the regions which display pronounced synaptic plasticity (e.g., hippocampal CA3-CA1 areas, cerebral cortex laminae II-IV, olfactory bulb). Expression of HB-GAM is regulated in an activity-dependent manner and is also induced in response to neuronal injury. In this work mutant mice were used to study the in vivo function of HB-GAM and its receptor syndecan-3 in hippocampal synaptic plasticity and in hippocampus-dependent behavioral tasks. Phenotypic analysis of HBGAM null mutants and mice overexpressing HB-GAM revealed that opposite genetic manipulations result in reverse changes in synaptic plasticity as well as behavior in the mutants. Electrophysiological recordings showed that mice lacking HB-GAM have an increased level of long-term potentiation (LTP) in the area CA1 of hippocampus and impaired spatial learning, whereas animals with enhanced level of HB-GAM expression have attenuated LTP, but outperformed their wild-type controls in spatial learning. It was also found that GABA(A) receptor-mediated synaptic transmission is altered in the transgenic mice overexpressing HB-GAM. The results suggest that these animals have accentuated hippocampal GABAergic inhibition, which may contribute to the altered glutamatergic synaptic plasticity. Structural studies of HB-GAM demonstrated that this protein belongs to the thrombospondin type I repeat (TSR) superfamily and contains two β-sheet domains connected by a flexible linker. It was found that didomain structure is necessary for biological activity of HB-GAM and electrophysiological phenotype displayed by the HB-GAM mutants. The individual domains displayed weaker binding to heparan sulfate and failed to promote neurite outgrowth as well as affect hippocampal LTP. Effects of HB-GAM on hippocampal synaptic plasticity are believed to be mediated by one of its (co-)receptor molecules, namely syndecan-3. In support of that, HB-GAM did not attenuate LTP in mice deficient in syndecan-3 as it did in wild-type controls. In addition, syndecan-3 knockout mice displayed electrophysiological and behavioral phenotype similar to that of HB-GAM knockouts (i.e. enhanced LTP and impaired learning in Morris water-maze). Thus HB-GAM and syndecan-3 are important modulators of synaptic plasticity in hippocampus and play a role in regulation of learning-related behavior.