MIRACLE Handbook : Guidelines for Mixed Reality Applications for Culture and Learning Experiences

Siirretty Doriast

Tuulivoimarakentamisen edistäminen : Keinoja sujuvaan hankekehitykseen ja eri tavoitteiden yhteensovitukseen

Tuulivoimaloiden määrä Suomessa on kasvanut viimeisen vuosikymmenen aikana voimakkaasti ja tavoitteena on edelleenkin kasvattaa tuulivoiman osuutta energiantuotannosta. Tuulivoiman lisääminen edesauttaa Suomen uusiutuvan energian tavoitteiden saavuttamista. Tässä selvityksessä on tutkittu tapoja edistää tuulivoimarakentamista kolmen osakokonaisuuden kautta: tuulivoimarakentamista koskevien viranomaismenettelyiden sujuvoittaminen ja selkeyttäminen; merituulivoiman kannattavuuden parantaminen; tuulivoimarakentamisen ja aluevalvonnan yhteensovittaminen. Kukin osakokonaisuus koostuu nykytilanteen kuvauksesta sekä johtopäätöksinä esitetyistä toimenpide-ehdotuksista. Viranomaismenettelyiden sujuvoittamisehdotukset koostuvat ohjeistuksen ja toimijoiden välisen vuoropuhelun lisäämisestä sekä yksityiskohtaisemmista ehdotuksista koskien YVA-menettelyä, kaavoitusta, vaikutusten arviointia sekä eräitä muita lupa- ja lausuntomenettelyitä. Viranomaismenettelyiden osalta työssä on kiinnitetty erityistä huomiota siihen, että myös talousvyöhykkeellä edellytetyt viranomaismenettelyt on kuvattu kattavasti. Merituulivoiman kannattavuuden edistämiseksi ehdotetaan muun muassa tarkempaa selvitystä valtion takauksien hyödyntämisestä pitkäaikaisissa sähkönostosopimuksissa. Puolustusvoimien aluevalvonnan ja tuulivoiman yhteensovittamisen teknologisia mahdollisuuksia on kuvattu kattavasti. Yhteensovittamisen kehittämiseksi esitetään, että tuulivoimaloiden tarvitsemasta Puolustusvoimien hyväksynnästä säädetään lailla. Selvitykseen ei ole sisältynyt esitettyjen toimenpiteiden vaikutustenarviointi.Tämä julkaisu on toteutettu osana valtioneuvoston selvitys- ja tutkimussuunnitelman toimeenpanoa. (tietokayttoon.fi) Julkaisun sisällöstä vastaavat tiedon tuottajat, eikä tekstisisältö välttämättä edusta valtioneuvoston näkemystä

The expression and prognostic relevance of programmed cell death protein 1 in tongue squamous cell carcinoma

Programmed cell death protein 1 (PD-1) is an immune checkpoint receptor which plays an important role in a patient's immune responses to microbial and cancer antigens. It is expressed in tumor-infiltrating lymphocytes (TILs) with many different malignancies. The aim of the study was to evaluate PD-1 expression and its prognostic value in tongue cancer. The data of tongue squamous cell carcinoma (TSCC) patients (N = 81) treated in Tampere University Hospital between 1999 and 2013 were used. Control data consisted of patients with non-malignant tongue mucous membrane lesions (N = 48). The formalin-fixed paraffin-embedded samples were stained immunohistochemically and scanned via digital microscope. The staining of PD-1 was examined semi-quantitatively. The density and intensity of PD-1 + cells were significantly higher in TSCC than in control samples. The expression of PD-1 correlated with better survival. The expression of PD-1 could be a potential prognostic marker in TSCC. Further research using larger sample size is needed.Peer reviewe

SHARPIN is an endogenous inhibitor of beta 1-integrin activation

Regulated activation of integrins is critical for cell adhesion, motility and tissue homeostasis. Talin and Kindlins activate β1-integrins, but the counteracting inhibiting mechanisms are poorly defined. Here we identified SHARPIN as an important inactivator of β1-integrins in an RNAi-screen. SHARPIN inhibited β1-integrin functions in human cancer cells and primary leukocytes. Fibroblasts, leukocytes and keratinocytes from SHARPIN-deficient mice exhibited increased β1-integrin activity which was fully rescued by re-expression of SHARPIN. SHARPIN directly bound to a conserved cytoplasmic region of integrin α-subunits and inhibited recruitment of Talin and Kindlin to the integrin. Therefore, SHARPIN inhibits the critical switching of β1-integrins from inactive to active conformations

FinnGen provides genetic insights from a well-phenotyped isolated population.

Population isolates such as those in Finland benefit genetic research because deleterious alleles are often concentrated on a small number of low-frequency variants (0.1% ≤ minor allele frequency < 5%). These variants survived the founding bottleneck rather than being distributed over a large number of ultrarare variants. Although this effect is well established in Mendelian genetics, its value in common disease genetics is less explored1,2. FinnGen aims to study the genome and national health register data of 500,000 Finnish individuals. Given the relatively high median age of participants (63 years) and the substantial fraction of hospital-based recruitment, FinnGen is enriched for disease end points. Here we analyse data from 224,737 participants from FinnGen and study 15 diseases that have previously been investigated in large genome-wide association studies (GWASs). We also include meta-analyses of biobank data from Estonia and the United Kingdom. We identified 30 new associations, primarily low-frequency variants, enriched in the Finnish population. A GWAS of 1,932 diseases also identified 2,733 genome-wide significant associations (893 phenome-wide significant (PWS), P < 2.6 × 10-11) at 2,496 (771 PWS) independent loci with 807 (247 PWS) end points. Among these, fine-mapping implicated 148 (73 PWS) coding variants associated with 83 (42 PWS) end points. Moreover, 91 (47 PWS) had an allele frequency of <5% in non-Finnish European individuals, of which 62 (32 PWS) were enriched by more than twofold in Finland. These findings demonstrate the power of bottlenecked populations to find entry points into the biology of common diseases through low-frequency, high impact variants

Evidence of a causal effect of genetic tendency to gain muscle mass on uterine leiomyomata

Uterine leiomyomata (UL) are the most common tumours of the female genital tract and the primary cause of surgical removal of the uterus. Genetic factors contribute to UL susceptibility. To add understanding to the heritable genetic risk factors, we conduct a genome-wide association study (GWAS) of UL in up to 426,558 European women from FinnGen and a previous UL meta-GWAS. In addition to the 50 known UL loci, we identify 22 loci that have not been associated with UL in prior studies. UL-associated loci harbour genes enriched for development, growth, and cellular senescence. Of particular interest are the smooth muscle cell differentiation and proliferation-regulating genes functioning on the myocardin-cyclin dependent kinase inhibitor 1A pathway. Our results further suggest that genetic predisposition to increased fat-free mass may be causally related to higher UL risk, underscoring the involvement of altered muscle tissue biology in UL pathophysiology. Overall, our findings add to the understanding of the genetic pathways underlying UL, which may aid in developing novel therapeutics.Peer reviewe