Synthesis dataset of physical and ecosystem properties from pan-arctic wetland sites using peat core analysis

Permafrost dynamics play an important role in high-latitude peatland carbon balance and are key to understanding the future response of soil carbon stocks. Permafrost aggradation can control the magnitude of the carbon feedback in peatlands through effects on peat properties. We compiled peatland plant macrofossil records for the northern permafrost zone (515 cores from 280 sites) and classified samples by vegetation type and environmental class (fen, bog, tundra and boreal permafrost, thawed permafrost). We examined differences in peat properties (bulk density, carbon (C), nitrogen (N) and organic matter content, C/N ratio) and C accumulation rates among vegetation types and environmental classes.

Sustained neuronal activity generated by glial plasticity

Astrocytes release gliotransmitters, notably glutamate, that can affect neuronal and synaptic activity. In particular, astrocytic glutamate release results in the generation of NMDA receptor (NMDA-R)-mediated slow inward currents (SICs) in neurons. However, factors underlying the emergence of SICs and their physiological roles are essentially unknown. Here we show that, in acute slices of rat somatosensory thalamus, stimulation of lemniscal or cortical afferents results in a sustained increase of SICs in thalamocortical (TC) neurons that outlasts the duration of the stimulus by 1 h. This long-term enhancement of astrocytic glutamate release is induced by group I metabotropic glutamate receptors and is dependent on astrocytic intracellular calcium. Neuronal SICs are mediated by extrasynaptic NR2B subunit-containing NMDA-Rs and are capable of eliciting bursts. These are distinct from T-type Ca2+ channel-dependent bursts of action potentials and are synchronized in neighboring TC neurons. These findings describe a previously unrecognized form of excitatory, nonsynaptic plasticity in the CNS that feeds forward to generate local neuronal firing long after stimulus termination.

Glutamatergic input-output properties of thalamic astrocytes

Astrocytes in the somatosensory ventrobasal (VB) thalamus of rats respond to glutamatergic synaptic input with metabotropic glutamate receptor (mGluR) mediated intracellular calcium ([Ca²?](i)) elevations. Astrocytes in the VB thalamus also release the gliotransmitter (GT) glutamate in a Ca²?-dependent manner. The tripartite synapse hypothesis posits that astrocytic [Ca²?](i) elevations resulting from synaptic input releases gliotransmitters that then feedback to modify the synapse. Understanding the dynamics of this process and the conditions under which it occurs are therefore important steps in elucidating the potential roles and impact of GT release in particular brain activities. In this study, we investigated the relationship between VB thalamus afferent synaptic input and astrocytic glutamate release by recording N-methyl-D-aspartate (NMDA) receptor-mediated slow inward currents (SICs) elicited in neighboring neurons. We found that Lemniscal or cortical afferent stimulation, which can elicit astrocytic [Ca²?](i) elevations, do not typically result in the generation of SICs in thalamocortical (TC) neurons. Rather, we find that the spontaneous emergence of SICs is largely resistant to acute afferent input. The frequency of SICs, however, is correlated to long-lasting afferent activity. In contrast to short-term stimulus-evoked GT release effects reported in other brain areas, astrocytes in the VB thalamus do not express a straightforward input-output relationship for SIC generation but exhibit integrative characteristics.

Non-neuronal, slow GABA signalling in the ventrobasal thalamus targets δ-subunit-containing GABA(A) receptors

The rodent ventrobasal (VB) thalamus contains a relatively uniform population of thalamocortical (TC) neurons that receive glutamatergic input from the vibrissae and the somatosensory cortex, and inhibitory input from the nucleus reticularis thalami (nRT). In this study we describe ?-aminobutyric acid (GABA)(A) receptor-dependent slow outward currents (SOCs) in TC neurons that are distinct from fast inhibitory postsynaptic currents (IPSCs) and tonic currents. SOCs occurred spontaneously or could be evoked by hypo-osmotic stimulus, and were not blocked by tetrodotoxin, removal of extracellular Ca(2+) or bafilomycin A1, indicating a non-synaptic, non-vesicular GABA origin. SOCs were more common in TC neurons of the VB compared with the dorsal lateral geniculate nucleus, and were rarely observed in nRT neurons, whilst SOC frequency in the VB increased with age. Application of THIP, a selective agonist at d-subunit-containing GABA(A) receptors, occluded SOCs, whereas the benzodiazepine site inverse agonist ß-CCB had no effect, but did inhibit spontaneous and evoked IPSCs. In addition, the occurrence of SOCs was reduced in mice lacking the d-subunit, and their kinetics were also altered. The anti-epileptic drug vigabatrin increased SOC frequency in a time-dependent manner, but this effect was not due to reversal of GABA transporters. Together, these data indicate that SOCs in TC neurons arise from astrocytic GABA release, and are mediated by d-subunit-containing GABA(A) receptors. Furthermore, these findings suggest that the therapeutic action of vigabatrin may occur through the augmentation of this astrocyte-neuron interaction, and highlight the importance of glial cells in CNS (patho) physiology.

Astrocytic GABA transporter GAT-1 dysfunction in experimental absence seizures

An enhanced tonic GABA-A inhibition in the thalamus plays a crucial role in experimental absence seizures, and has been attributed, on the basis of indirect evidence, to a dysfunction of the astrocytic GABA transporter-1 (GAT-1). Here, the GABA transporter current was directly investigated in thalamic astrocytes from a well-established genetic model of absence seizures, the Genetic Absence Epilepsy Rats from Strasbourg (GAERS), and its non-epileptic control (NEC) strain. We also characterized the novel form of GABAergic and glutamatergic astrocyte-to-neuron signalling by recording slow outward currents (SOCs) and slow inward currents (SICs), respectively, in thalamocortical (TC) neurons of both strains. In patch-clamped astrocytes, the GABA transporter current was abolished by combined application of the selective GAT-1 and GAT-3 blocker, NO711 (30µM) and SNAP5114 (60µM), respectively, to GAERS and NEC thalamic slices. NO711 alone significantly reduced (41%) the transporter current in NEC, but had no effect in GAERS. SNAP5114 alone reduced by half the GABA transporter current in NEC, whilst it abolished it in GAERS. SIC properties did not differ between GAERS and NEC TC neurons, whilst moderate changes in SOC amplitude and kinetics were observed. These data provide the first direct demonstration of a malfunction of the astrocytic thalamic GAT-1 transporter in absence epilepsy and support an abnormal astrocytic modulation of thalamic ambient GABA levels. Moreover, while the glutamatergic astrocyte-neuron signalling is unaltered in the GAERS thalamus, the changes in some properties of the GABAergic astrocyte-neuron signaling in this epileptic strain may contribute to the generation of absence seizures.

α7 nicotinic receptor-mediated astrocytic gliotransmitter release:Aβ effects in a preclinical Alzheimer's mouse model

It is now recognized that astrocytes participate in synaptic communication through intimate interactions with neurons. A principal mechanism is through the release of gliotransmitters (GTs) such as ATP, D-serine and most notably, glutamate, in response to astrocytic calcium elevations. We and others have shown that amyloid-β (Aβ), the toxic trigger for Alzheimer's disease (AD), interacts with hippocampal α7 nicotinic acetylcholine receptors (nAChRs). Since α7nAChRs are highly permeable to calcium and are expressed on hippocampal astrocytes, we investigated whether Aβ could activate astrocytic α7nAChRs in hippocampal slices and induce GT glutamate release. We found that biologically-relevant concentrations of Aβ1-42 elicited α7nAChR-dependent calcium elevations in hippocampal CA1 astrocytes and induced NMDAR-mediated slow inward currents (SICs) in CA1 neurons. In the Tg2576 AD mouse model for Aβ over-production and accumulation, we found that spontaneous astrocytic calcium elevations were of higher frequency compared to wildtype (WT). The frequency and kinetic parameters of AD mice SICs indicated enhanced gliotransmission, possibly due to increased endogenous Aβ observed in this model. Activation of α7nAChRs on WT astrocytes increased spontaneous inward currents on pyramidal neurons while α7nAChRs on astrocytes of AD mice were abrogated. These findings suggest that, at an age that far precedes the emergence of cognitive deficits and plaque deposition, this mouse model for AD-like amyloidosis exhibits augmented astrocytic activity and glutamate GT release suggesting possible repercussions for preclinical AD hippocampal neural networks that contribute to subsequent cognitive decline. © 2013 Pirttimaki et al.

Are transglutaminase 2 inhibitors able to reduce gliadin-induced toxicity related to celiac disease? A proof-of-concept study

Purpose Celiac disease is an autoimmune-mediated enteropathy characterized by adaptive and innate immune responses to dietary gluten in wheat, rye and barley in genetically susceptible individuals. Gluten-derived gliadin peptides are deamidated by transglutaminase 2 (TG2), leading to an immune response in the small-intestinal mucosa. TG2 inhibitors have therefore been suggested as putative drugs for celiac disease. In this proof-of-concept study we investigated whether two TG2 inhibitors, cell-impermeable R281 and cell-permeable R283, can prevent the toxic effects of gliadin in vitro and ex vivo. Methods Intestinal epithelial Caco-2 cells were treated with peptic-tryptic-digested gliadin (PT-gliadin) with or without TG2 inhibitors and thereafter direct toxic effects (transepithelial resistance, cytoskeletal rearrangement, junction protein expression and phoshorylation of extracellular-signal-regulated kinase 1/2) were determined. In an organ culture of celiacpatient- derived small-intestinal biopsies we measured secretion of TG2-autoantibodies into the culture medium and the densities of CD25- and interleukin (IL) 15-positive cells, forkhead box P3 (FOXP3)-positive regulatory Tcells (Tregs) and Ki-67- positive proliferating crypt cells. Results Both TG2 inhibitors evinced protective effects against gliadin-induced detrimental effects in Caco-2 cells but the cellimpermeableR281seemedslightlymorepotent. Inaddition,TG2 inhibitor R281 modified the gluten-induced increase in CD25- and IL15-positive cells,Tregs and crypt cell proliferation, but had no effect on antibody secretion in celiac-patient-derived biopsies. Conclusions Our results suggest that TG2 inhibitors are able to reduce certain gliadin-induced effects related to responses in vitro and ex vivo. © Springer Science+Business Media, LLC 2012.

Astrocyte plasticity:implications for synaptic and neuronal activity

Astrocytes are increasingly implicated in a range of functions in the brain, many of which were previously ascribed to neurons. Much of the prevailing interest centers on the role of astrocytes in the modulation of synaptic transmission and their involvement in the induction of forms of plasticity such as long-term potentiation and long-term depression. However, there is also an increasing realization that astrocytes themselves can undergo plasticity. This plasticity may be manifest as changes in protein expression which may modify calcium activity within the cells, changes in morphology that affect the environment of the synapse and the extracellular space, or changes in gap junction astrocyte coupling that modify the transfer of ions and metabolites through astrocyte networks. Plasticity in the way that astrocytes release gliotransmitters can also have direct effects on synaptic activity and neuronal excitability. Astrocyte plasticity can potentially have profound effects on neuronal network activity and be recruited in pathological conditions. An emerging principle of astrocyte plasticity is that it is often induced by neuronal activity, reinforcing our emerging understanding of the working brain as a constant interaction between neurons and glial cells. © The Author(s) 2013.

GABAB receptor-mediated activation of astrocytes by gamma-hydroxybutyric acid

The gamma-aminobutyric acid (GABA) metabolite gamma-hydroxybutyric acid (GHB) shows a variety of behavioural effects when administered to animals and humans, including reward/addiction properties and absence seizures. At the cellular level, these actions of GHB are mediated by activation of neuronal GABAB receptors (GABABRs) where it acts as a weak agonist. Because astrocytes respond to endogenous and exogenously applied GABA by activation of both GABAA and GABABRs, here we investigated the action of GHB on astrocytes on the ventral tegmental area (VTA) and the ventrobasal (VB) thalamic nucleus, two brain areas involved in the reward and proepileptic action of GHB, respectively, and compared it with that of the potent GABABR agonist baclofen. We found that GHB and baclofen elicited dose-dependent (ED50: 1.6 mM and 1.3 µM, respectively) transient increases in intracellular Ca2+ in VTA and VB astrocytes of young mice and rats, which were accounted for by activation of their GABABRs and mediated by Ca2+ release from intracellular store release. In contrast, prolonged GHB and baclofen exposure caused a reduction in spontaneous astrocyte activity and glutamate release from VTA astrocytes. These findings have key (patho)physiological implications for our understanding of the addictive and proepileptic actions of GHB.

Experiences on dynamic simulation software in chemical engineering education

Commercial process simulators are increasing interest in the chemical engineer education. In this paper, the use of commercial dynamic simulation software, D-SPICE® and K-Spice®, for three different chemical engineering courses is described and discussed. The courses cover the following topics: basic chemical engineering, operability and safety analysis and process control. User experiences from both teachers and students are presented. The benefits of dynamic simulation as an additional teaching tool are discussed and summarized. The experiences confirm that commercial dynamic simulators provide realistic training and can be successfully integrated into undergraduate and graduate teaching, laboratory courses and research. © 2012 The Institution of Chemical Engineers.

Estudio sobre la contribución de la radio al envejecimiento activo. Fase incial: análisis cuantitativo de la presencia de la vejez en los magazines de radio

Este trabajo aborda la posible contribución de la radio al envejecimiento activo. La ética comunicativa actual debe tener presentes los colectivos más vulnerables de la sociedad y uno de ellos es el de la vejez. Se recogen en el artículo los principales datos demográficos sobre población mayor, cuyo crecimiento es tal que se hace necesario un cambio de paradigma a la hora de abordar estos cambios, lo que se conoce como envejecimiento activo. Se plantea que la radio, por sus peculiares características, puede contribuir a promover dicho paradigma. Pero es necesario partir de datos objetivos y el artículo concluye presentando los datos y gráficos de la investigación realizada sobre la presencia de la vejez en los magazines matinales de las cuatro emisoras más importantes del país.

Valtatien 13 parantaminen välillä Lappeenranta–Nuijamaa : Hanke-esite

Valtatien 13 osuus Lappeenrannasta Nuijamaalle kuuluu Euroopan komission päättämään Suomen kattavaan liikenneverkkoon TEN-T. Tieosuus on maan toiseksi tärkein kansainvälisen liikenteen yhteys kuljetuksille ja henkilöliikenteelle. Valtatie 13 kulkee maan poikki länsirannikolta Kokkolasta Lappeenrantaan ja siitä edelleen Nuijamaan rajanylityspaikan kautta Venäjän puolelle Viipuriin. Valtatie 13 palvelee osaltaan myös paikallista liikkumista Nuijamaan kylätaajaman ja Lappeenrannan välillä. Erityisesti Mustolan alueelle ja myös osittain Nuijamaan raja-aseman läheisyyteen suunnitellut ja jo osittain toteutuneet maankäytön kaupalliset palvelut lisäävät voimakkaasti kasvaessaan myös seudullista liikennettä suunnitteluosuudella. Nuijamaan raja-asema on ollut Suomen itärajan toiseksi vilkkain tieliikenteen rajanylityspaikka. Rajanylityspaikan kautta kulki vuonna 2015 noin miljoona ajoneuvoa ja 2,4 miljoonaa matkustajaa. Venäjän ja Suomen valtioiden välisen liikenteen kasvu on ollut voimakkainta Kaakkois-Suomessa ja sille on edelleen perusteltuja kasvuodotuksia, vaikka viime aikoina liikenne on merkittävästi vähentynyt. Myös tavaraliikenteellä on potentiaalia lisääntyä viimeaikaisesta. Suunnittelualueeseen kuuluu valtatien 13 (16,6 km) lisäksi valtatien 6 länsipuolinen valtatien 13 jatke Karjalantie (mt 3821) (1,2 km). Yleissuunnitelmassa on selvitetty valtatien 13 puutteet ja ongelmat, palvelutasotavoitteet, valtatien 13 ja muiden väylien periaateratkaisut tilantarpeineen, suhde ympäröivään maankäyttöön, vaikutukset sekä mahdollisuudet vaiheittain toteuttamiseksi. Päätavoitteena on ollut selvittää valtatien 13 ja muiden väylien kehittämisen periaatteet niin, että palvelutasopuutteet saadaan poistettua ja valtatie 13 vastaa sille asetettuja vaatimuksia liikenteen sujuvuuden ja turvallisuuden kannalta. Osana suunnitelmaa on esitetty toimenpiteet meluhaittojen torjumiseksi ja ympäristövaikutusten lieventämiseksi. Valtatie 13 parannetaan nykyisellä paikallaan korkealuokkaiseksi nelikaistaiseksi valtatieksi tarvittavine tie-, katu- ja liittymäjärjestelyineen. Vastakkaiset ajosuunnat on erotettu toisistaan rakenteellisesti ja kaikki valtatien liittymät ovat eritasoliittymiä.

Kommunikaatio-ongelmat tilaus-toimitusketjun rajapinnoissa

Tässä tutkielmassa tavoitteena on tunnistaa ja etsiä ratkaisuja yrityksen tilaus-toimitusketjun rajapinnoissa toimivien ihmisten välisiin kommunikaatio-ongelmiin. Tutkimusongelmaan haettiin vastausta sekä kirjallisuudesta että empiriasta. Tutkimuksen lähestymistapa on abduktiivinen tapaustutkimus, joka suoritetaan laadullisena tutkimuksena. Tapausyrityksenä oli kansainvälisesti toimiva teollisuudenalan suuryritys, jonka henkilöstöstä valittiin tutkimuksen haastateltavat harkinnanvaraisella otoksella. Kirjallisuuden mukaan tilaus-toimitusketjun toimivuuden on todettu vaikuttavan liiketoiminnan kannattavuuteen, kun taas kommunikaatiolla on vaikutusta tilaus-toimitusketjun suorituskykyyn. Tästä syystä kommunikaatio-ongelmien kartoittaminen tilaus-toimitusketjun rajapinnoissa on relevanttia. Tilaus-toimitusketjulla tarkoitetaan tässä tutkielmassa sitä toimintaa, mitä tapahtuu tilauksen vastaanottamisen ja tilauksen jälkeiseen suoritusmittauksen välissä. Kommunikaation rajapinnat tapausyrityksessä sijoittuvat tilaus-toimitusketjun sisäisesti logistiikan, rahoituksen, myynnin ja markkinoinnin, oston, asiakaspalvelun sekä tuotannon välille. Tilaus-toimitusketjun ulkopuolelle tapahtuva kommunikaatio tapahtuu edellä mainittujen sekä toimittajien, viranomaisten, kuljetusyritysten ja asiakkaiden välillä. Empiirinen aineisto tuki osittain aiemman kirjallisuuden näkökulmia kommunikaatio-ongelmiin kansainvälisessä työympäristössä. Tutkimuksen mukaan voidaan päätellä, että ongelmat liittyvät esimerkiksi henkilökemioihin, tiedon läpinäkyvyyteen, kommunikoijien taustoista johtuviin väärinymmärryksiin, tiedon väärään sijaintiin, epätarkkuuksiin ja epätäsmällisyyksiin, palaverien epäjärjestelmällisyyteen, kiireeseen, hierarkiaan, kielellisiin eroihin, kulttuurieroihin sekä kuuntelun puutteeseen. Suuri osa ongelmista ratkeaisi sillä, että kommunikoitava viesti muotoiltaisi riittävän selkeästi ja yksityiskohtaisesti väärinymmärrysten välttämiseksi, sekä sillä, että määriteltäisiin sisällön lisäksi tarkemmin myös se, kuka tarvitsee tietoa, millaista tietoa tarvitaan ja milloin sitä tarvitaan. Suunnitelmattomuus ja epämääräinen kommunikointi eivät edistä liiketoimintaa ja tilaus-toimitusketjun toimintaa, vaan kommunikaatiota on käytettävä ja ohjailtava oikein, jotta siitä saadaan paras mahdollinen hyöty. Lisäksi on muistettava, että vaikka kommunikaatio on tärkeä osa tilaus-toimitusketjua, se ei saa olla koko toiminnan tarkoitus.