Opiskelija-asuntojen tuotantotarvelaskelma 2003-2012

Suomen opiskelija-asuntotarve on vuosia jatkuneen opiskelija-asuntopulan jälkeen tasaantunut muun muassa viimeaikaisen uudisrakentamisen ansiosta. Määrällisesti kysyntä ja tarjonta ovat useimmilla suurillakin paikkakunnilla lähes tasapainossa, mutta asuntojen tyyppi, sijainti ja hinta eivät täysin vastaa kysyntää. Pääkaupunkiseudulla on lisäksi edelleen merkittävää uustuotantotarvetta. Kokonaisuutena tämän selvityksen mukaan opiskelija-asuntojen tuotantotarve Suomessa vuosina 2003–2012 on 16 500 asuntopaikkaa, asuntoina ilmaistuna 9 700 asuntoa. Näistä enemmän kuin puolet tulisi rakentaa pääkaupunkiseudulle. Peruskorjausta tarvitsee noin 8 500 asuntoa. Selvityksen perusteella opiskelija-asuntoihin liittyvät tärkeimmät toimenpiteet voidaan jakaa kahteen osaan: 1. olemassa olevien asuntojen peruskorjaamiseen ja niiden muuttamiseen yksiöiksi ja perheasunnoiksi, ja 2. uustuotannon keskittämiseen oppilaitosten lähelle ja mahdollisuuksien mukaan kaupunkien keskusta-alueille. Oppilaitoksen voidaan katsoa sijaitsevan lähietäisyydellä asunnosta, jos matkan voi tehdä kevyen liikenteen keinoin. Kysyntä kohdistuu kohdan 2) mukaisiin asuntoihin, mutta niiden rakentaminen on hinnaltaan ja sijainniltaan sopivien tonttien puuttumisen vuoksi vähäistä. Tämän selvityksen mukaan juuri tontteihin liittyvät seikat ovat nousseet suurimmaksi esteeksi opiskelija-asuntojen rakentamiselle. Toinen yhtä tärkeä tekijä opiskelijoiden asumisessa on asumisen kalleus. Opintotuen ja asumislisän ei katsota riittävästi kattavan opiskelijoiden asumiskustannuksia etenkään suurilla paikkakunnilla. Siten opiskelija-asuntojen merkitys opiskeluedellytysten turvaamisessa säilyy tulevaisuudessakin tärkeänä. Opiskelija-asuntoja tuottavien yhteisöjen kannalta ongelmallisia ovat aravalainojen ehdot

JAK Inhibitors AG-490 and WHI-P154 Decrease IFN-γ-Induced iNOS Expression and NO Production in Macrophages

In inflammation, inducible nitric oxide synthase (iNOS) produces nitric oxide (NO), which modulates inflammatory processes. We investigated the effects of Janus kinase (JAK) inhibitors, AG-490 and WHI-P154, on iNOS expression and NO production in J774 murine macrophages stimulated with interferon-γ (IFN-γ). JAK inhibitors AG-490 and WHI-P154 decreased IFN-γ-induced nuclear levels of signal transducer and activator of transcription 1α (STAT1α). JAK inhibitors AG-490 and WHI-P154 decreased also iNOS protein and mRNA expression and NO production in a concentration-dependent manner. Neither of the JAK inhibitors affected the decay of iNOS mRNA when determined by actinomycin D assay. Our results suggest that the inhibition of JAK-STAT1-pathway by AG-490 or WHI-P154 leads to the attenuation of iNOS expression and NO production in IFN-γ-stimulated macrophages

Sosiaali- ja terveyspalveluiden kehittämisen prosessimalli, esimerkkinä Lahti

ln Lahti it was decided that cost cutting in itstraditional sense and rationalisation measureswithout a clear framework for development andclearly set objectives had come to its end.Management of Lahti decided to launch acomprehensive program for the development of thesecondary health care and welfare services. lnLahti region the death rate due to illnesses, forwhich a normal person of over 65 years of ageshould not die, is higher than normal. Whenanalysed in more detail, it was discovered thatsocio-economic factors were the cause of thesepremature deaths. Because of this, it was decidedthat it is crucial to start developing the services inco-operation with the service providers in bothhealth care and welfare sectors. This studyanalyses the aims and the realisation of thedevelopment project carried out in Lahti'ssecondary health care and welfare services

Anti-Inflammatory Effects of β2-Receptor Agonists Salbutamol and Terbutaline Are Mediated by MKP-1

Mitogen-activated protein kinase phosphatase 1 (MKP-1) expression is induced by inflammatory factors, and it is an endogenous suppressor of inflammatory response. MKP-1 expression is increased by PDE4 inhibitor rolipram suggesting that it is regulated by cAMP-enhancing compounds. Therefore, we investigated the effect of β2-receptor agonists on MKP-1 expression and inflammatory response. We found that β2-receptor agonists salbutamol and terbutaline, as well as 8-Br-cAMP, increased MKP-1 expression. Salbutamol and terbutaline also inhibited p38 MAPK phosphorylation and TNF production in J774 mouse macrophages. Interestingly, salbutamol suppressed carrageenan-induced paw inflammation in wild-type mice, but the effect was attenuated in MKP-1(-/-) mice. In conclusion, these data show that β2-receptor agonists increase MKP-1 expression, which seems to mediate, at least partly, the observed anti-inflammatory effects of β2-receptor agonists.Public Library of Science open acces

Dual Specificity Phosphatase 1 Regulates Human Inducible Nitric Oxide Synthase Expression by p38 MAP Kinase

The role of dual specificity phosphatase 1 (DUSP1) in inducible nitric oxide synthase (iNOS) expression in A549 human pulmonary epithelial cells, J774 mouse macrophages and primary mouse bone marrow-derived macrophages (BMMs) was investigated. iNOS expression was induced by a cytokine mixture (TNF, IFNγ and IL-1β) in A549 cells and by LPS in J774 cells, and it was inhibited by p38 MAPK inhibitors SB202190 and BIRB 796. Stimulation with cytokine mixture or LPS enhanced also DUSP1 expression. Down-regulation of DUSP1 by siRNA increased p38 MAPK phosphorylation and iNOS expression in A549 and J774 cells. In addition, LPS-induced iNOS expression was enhanced in BMMs from DUSP1(−/−) mice as compared to that in BMMs from wild-type mice. The results indicate that DUSP1 suppresses iNOS expression by limiting p38 MAPK activity in human and mouse cells. Compounds that enhance DUSP1 expression or modulate its function may be beneficial in diseases complicated with increased iNOS-mediated NO production

Down-regulation of protein kinase Cdelta inhibits inducible nitric oxide synthase expression through IRF1

Peer reviewe

Discovery of potential causative mutations in human coding and noncoding genome with the interactive software BasePlayer

Next-generation sequencing (NGS) is routinely applied in life sciences and clinical practice, but interpretation of the massive quantities of genomic data produced has become a critical challenge. The genome-wide mutation analyses enabled by NGS have had a revolutionary impact in revealing the predisposing and driving DNA alterations behind a multitude of disorders. The workflow to identify causative mutations from NGS data, for example in cancer and rare diseases, commonly involves phases such as quality filtering, case-control comparison, genome annotation, and visual validation, which require multiple processing steps and usage of various tools and scripts. To this end, we have introduced an interactive and user-friendly multi-platform-compatible software, BasePlayer, which allows scientists, regardless of bioinformatics training, to carry out variant analysis in disease genetics settings. A genome-wide scan of regulatory regions for mutation clusters can be carried out with a desktop computer in -10 min with a dataset of 3 million somatic variants in 200 whole-genome-sequenced (WGS) cancers.Peer reviewe