Riittääkö, että opettaja on motivoitunut?

Tämän tutkimuksen tarkoituksena oli selvittää, mitkä asiat vaikuttavat varhaiskasvatuksen opettajien motivaatioon ja millä tavalla varhaiskasvatuksen opettajien psykologiset perustarpeet täyttyvät heidän työssään. Tässä tutkimuksessa varsinaisia tutkimuskysymyksiä oli kaksi: 1. Mikä varhaiskasvatuksen opettajia motivoi työssään? ja 2. Millä tavalla varhaiskasvatuksen opettajien psykologiset perustarpeet täyttyvät työssä? Tämän tutkimuksen teoreettisena viitekehyksenä toimivat Decin ja Ryanin itsemääräämisteoria ja Maslow’n tarvehierarkia. Tutkimus toteutettiin puolistrukturoiduilla yksilöhaastatteluilla. Haastateltavana oli neljä varhaiskasvatuksen opettajaa, jotka työskentelivät samassa yksikössä, mutta olivat keskenään erilaisissa ryhmissä. Haastatteluvastaukset analysoitiin teorialähtöisellä analyysillä. Tulosten mukaan varhaiskasvatuksen opettajien motivaation orientaatiolaji oli autonominen motivaatio. Varhaiskasvatuksen opettajat pitivät työnsä sisältöä mielekkäänä, mikä edesauttoi arvoihin ja tavoitteisiin sitoutumista. Motivaatiota heikentäviksi tekijöiksi sanoitettiin sellaisia asioita, kuten vajaavaiset resurssit niin henkilöstössä, kuin materiaalissakin, yhteiskunnallisen ja rahallisen arvostuksen puute, sekä yksikön arvojen piiloon jääminen. Varhaiskasvatuksen opettajien psykologiset perustarpeet täyttyivät vaihtelevasti. Haastateltavat eivät kyenneet luomaan turvallisuudentunnetta itselleen työstä saatavalla rahallisella korvauksella, elleivät olleet erityisen säästäväisiä. Jokainen haastateltavista koki me-henkeä oman tiiminsä kanssa, mutta ei koko yksikön kesken. Suurin osa haastateltavista tunsi saavansa tarpeeksi arvostusta työstänsä, mutta samalla enemmistö myös tunsi, ettei heidän täysi potentiaalinsa toteudu heidän nykyisessä työssään. Tämä tutkimus toi esiin sen, millä tasolla varhaiskasvatuksen opettajien motivaatio oli, ja miten heidän psykologiset perustarpeensa täyttyvät työssään. Tämän tutkimuksen tulokset eivät kuitenkaan ole yleistettävissä pienen otannan takia

Tumor-derived exosomes confer antigen-specific immunosuppression in a murine delayed-type hypersensitivity model

Exosomes are endosome-derived small membrane vesicles that are secreted by most cell types including tumor cells. Tumor-derived exosomes usually contain tumor antigens and have been used as a source of tumor antigens to stimulate anti-tumor immune responses. However, many reports also suggest that tumor-derived exosomes can facilitate tumor immune evasion through different mechanisms, most of which are antigen-independent. In the present study we used a mouse model of delayed-type hypersensitivity (DTH) and demonstrated that local administration of tumor-derived exosomes carrying the model antigen chicken ovalbumin (OVA) resulted in the suppression of DTH response in an antigen-specific manner. Analysis of exosome trafficking demonstrated that following local injection, tumor-derived exosomes were internalized by CD11c+ cells and transported to the draining LN. Exosome-mediated DTH suppression is associated with increased mRNA levels of TGF-β1 and IL-4 in the draining LN. The tumor-derived exosomes examined were also found to inhibit DC maturation. Taken together, our results suggest a role for tumor-derived exosomes in inducing tumor antigen-specific immunosuppression, possibly by modulating the function of APCs. © 2011 Yang et al

Hadronization properties of b quarks compared to light quarks in e+e- -> q qbar from 183 to 200 GeV

The DELPHI detector at LEP has collected 54 pb^{-1} of data at a centre-of-mass energy around 183 GeV during 1997, 158 pb^{-1} around 189 GeV during 1998, and 187 pb^{-1} between 192 and 200 GeV during 1999. These data were used to measure the average charged particle multiplicity in e+e- -> b bbar events, _{bb}, and the difference delta_{bl} between _{bb} and the multiplicity, _{ll}, in generic light quark (u,d,s) events: delta_{bl}(183 GeV) = 4.55 +/- 1.31 (stat) +/- 0.73 (syst) delta_{bl}(189 GeV) = 4.43 +/- 0.85 (stat) +/- 0.61 (syst) delta_{bl}(200 GeV) = 3.39 +/- 0.89 (stat) +/- 1.01 (syst). This result is consistent with QCD predictions, while it is inconsistent with calculations assuming that the multiplicity accompanying the decay of a heavy quark is independent of the mass of the quark itself.Comment: 13 pages, 2 figure

Search for supersymmetric particles in scenarios with a gravitino LSP and stau NLSP

Sleptons, neutralinos and charginos were searched for in the context of scenarios where the lightest supersymmetric particle is the gravitino. It was assumed that the stau is the next-to-lightest supersymmetric particle. Data collected with the DELPHI detector at a centre-of-mass energy near 189 GeV were analysed combining the methods developed in previous searches at lower energies. No evidence for the production of these supersymmetric particles was found. Hence, limits were derived at 95% confidence level.Comment: 31 pages, 14 figure

Strategy for Treating Motor Neuron Diseases Using a Fusion Protein of Botulinum Toxin Binding Domain and Streptavidin for Viral Vector Access: Work in Progress

Although advances in understanding of the pathogenesis of amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) have suggested attractive treatment strategies, delivery of agents to motor neurons embedded within the spinal cord is problematic. We have designed a strategy based on the specificity of botulinum toxin, to direct entry of viral vectors carrying candidate therapeutic genes into motor neurons. We have engineered and expressed fusion proteins consisting of the binding domain of botulinum toxin type A fused to streptavidin (SAv). This fusion protein will direct biotinylated viral vectors carrying therapeutic genes into motor nerve terminals where they can enter the acidified endosomal compartments, be released and undergo retrograde transport, to deliver the genes to motor neurons. Both ends of the fusion proteins are shown to be functionally intact. The binding domain end binds to mammalian nerve terminals at neuromuscular junctions, ganglioside GT1b (a target of botulinum toxin), and a variety of neuronal cells including primary chick embryo motor neurons, N2A neuroblastoma cells, NG108-15 cells, but not to NG CR72 cells, which lack complex gangliosides. The streptavidin end binds to biotin, and to a biotinylated Alexa 488 fluorescent tag. Further studies are in progress to evaluate the delivery of genes to motor neurons in vivo, by the use of biotinylated viral vectors

IκBβ acts to inhibit and activate gene expression during the inflammatory response

The activation of pro-inflammatory gene programs by nuclear factor-κB (NF-κB) is primarily regulated through cytoplasmic sequestration of NF-κB by the inhibitor of κB (IκB) family of proteins1. IκBβ, a major isoform of IκB, can sequester NF-κB in the cytoplasm2, although its biological role remains unclear. Although cells lacking IκBβ have been reported3, 4, in vivo studies have been limited and suggested redundancy between IκBα and IκBβ5. Like IκBα, IκBβ is also inducibly degraded; however, upon stimulation by lipopolysaccharide (LPS), it is degraded slowly and re-synthesized as a hypophosphorylated form that can be detected in the nucleus6, 7, 8, 9, 10, 11. The crystal structure of IκBβ bound to p65 suggested this complex might bind DNA12. In vitro, hypophosphorylated IκBβ can bind DNA with p65 and c-Rel, and the DNA-bound NF-κB:IκBβ complexes are resistant to IκBα, suggesting hypophosphorylated, nuclear IκBβ may prolong the expression of certain genes9, 10, 11. Here we report that in vivo IκBβ serves both to inhibit and facilitate the inflammatory response. IκBβ degradation releases NF-κB dimers which upregulate pro-inflammatory target genes such as tumour necrosis factor-α (TNF-α). Surprisingly, absence of IκBβ results in a dramatic reduction of TNF-α in response to LPS even though activation of NF-κB is normal. The inhibition of TNF-α messenger RNA (mRNA) expression correlates with the absence of nuclear, hypophosphorylated-IκBβ bound to p65:c-Rel heterodimers at a specific κB site on the TNF-α promoter. Therefore IκBβ acts through p65:c-Rel dimers to maintain prolonged expression of TNF-α. As a result, IκBβ^(−/−) mice are resistant to LPS-induced septic shock and collagen-induced arthritis. Blocking IκBβ might be a promising new strategy for selectively inhibiting the chronic phase of TNF-α production during the inflammatory response

The Beyond the Standard Model Working Group: Summary Report

Report of the "Beyond the Standard Model" working group for the Workshop `Physics at TeV Colliders', Les Houches, France, 21 May - 1 June 2001. It consists of 18 separate parts: 1. Preface; 2. Theoretical Discussion; 3. Numerical Calculation of the mSUGRA and Higgs Spectrum; 4. Theoretical Uncertainties in Sparticle Mass Predictions; 5. High Mass Supersymmetry with High Energy Hadron Colliders; 6. SUSY with Heavy Scalars at LHC; 7. Inclusive Study of MSSM in CMS; 8. Establishing a No-Lose Theorem for NMSSM Higgs Boson Discovery at the LHC; 9. Effects of Supersymmetric Phases on Higgs Production in Association with Squark Pairs in the Minimal Supersymmetric Standard Model; 10. Study of the Lepton Flavour Violating Decays of Charged Fermions in SUSY GUTs; 11. Interactions of the Goldstino Supermultiplet with Standard Model Fields; 12. Attempts at Explaining the NuTeV Observation of Di-Muon Events; 13. Kaluza-Klein States of the Standard Model Gauge Bosons: Constraints From High Energy Experiments; 14. Kaluza-Klein Excitations of Gauge Bosons in the ATLAS Detector; 15. Search for the Randall Sundrum Radion Using the ATLAS Detector; 16. Radion Mixing Effects on the Properties of the Standard Model Higgs Boson; 17. Probing Universal Extra Dimensions at Present and Future Colliders; 18. Black Hole Production at Future Colliders.Report of the Beyond the Standard Model working group for the Workshop `Physics at TeV Colliders', Les Houches, France, 21 May - 1 June 2001. It consists of 18 separate parts: 1. Preface: 2. Theoretical Discussion: 3. Numerical Calculation of the mSUGRA and Higgs Spectrum: 4. Theoretical Uncertainties in Sparticle Mass Predictions: 5. High Mass Supersymmetry with High Energy Hadron Colliders: 6. SUSY with Heavy Scalars at LHC: 7. Inclusive Study of MSSM in CMS: 8. Establishing a No-Lose Theorem for NMSSM Higgs Boson Discovery at the LHC: 9. Effects of Supersymmetric Phases on Higgs Production in Association with Squark Pairs in the Minimal Supersymmetric Standard Model: 10. Study of the Lepton Flavour Violating Decays of Charged Fermions in SUSY GUTs: 11. Interactions of the Goldstino Supermultiplet with Standard Model Fields: 12. Attempts at Explaining the NuTeV Observation of Di-Muon Events: 13. Kaluza-Klein States of the Standard Model Gauge Bosons: Constraints From High Energy Experiments: 14. Kaluza-Klein Excitations of Gauge Bosons in the ATLAS Detector: 15. Search for the Randall Sundrum Radion Using the ATLAS Detector: 16. Radion Mixing Effects on the Properties of the Standard Model Higgs Boson: 17. Probing Universal Extra Dimensions at Present and Future Colliders: 18. Black Hole Production at Future Colliders

MAVS-Mediated Apoptosis and Its Inhibition by Viral Proteins

BACKGROUND: Host responses to viral infection include both immune activation and programmed cell death. The mitochondrial antiviral signaling adaptor, MAVS (IPS-1, VISA or Cardif) is critical for host defenses to viral infection by inducing type-1 interferons (IFN-I), however its role in virus-induced apoptotic responses has not been elucidated. PRINCIPAL FINDINGS: We show that MAVS causes apoptosis independent of its function in initiating IFN-I production. MAVS-induced cell death requires mitochondrial localization, is caspase dependent, and displays hallmarks of apoptosis. Furthermore, MAVS(-/-) fibroblasts are resistant to Sendai virus-induced apoptosis. A functional screen identifies the hepatitis C virus NS3/4A and the Severe Acute Respiratory Syndrome coronavirus (SARS-CoV) nonstructural protein (NSP15) as inhibitors of MAVS-induced apoptosis, possibly as a method of immune evasion. SIGNIFICANCE: This study describes a novel role for MAVS in controlling viral infections through the induction of apoptosis, and identifies viral proteins which inhibit this host response

Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis

Rheumatoid arthritis is an autoimmune disease characterized by hyperplasia of the synovial lining and destruction of cartilage and bone. Recent studies have suggested that a lack of apoptosis contributes to the hyperplasia of the synovial lining and to the failure in eliminating autoreactive cells. Mice lacking Fas or Bim, two pro-apoptotic proteins that mediate the extrinsic and intrinsic death cascades, respectively, develop enhanced K/BxN serum transfer-induced arthritis. Since the pro-apoptotic protein Bid functions as an intermediate between the extrinsic and intrinsic apoptotic pathways, we examined the role that it plays in inflammatory arthritis. Mice deficient in Bid (Bid-/-) show a delay in the resolution of K/BxN serum transfer-induced arthritis. Bid-/- mice display increased inflammation, bone destruction, and pannus formation compared to wild-type mice. Furthermore, Bid-/- mice have elevated levels of CXC chemokine and IL-1β in serum, which are associated with more inflammatory cells throughout the arthritic joint. In addition, there are fewer apoptotic cells in the synovium of Bid-/- compared to Wt mice. These data suggest that extrinsic and intrinsic apoptotic pathways cooperate through Bid to limit development of inflammatory arthritis