Lapsen osallisuus esiopetuksessa:aikuisen rooli. Päiväkodin arjessa näkyviä lapsen osallisuutta edistäviä toimintoja

Tiivistelmä. Osallisuuden käsite on ollut esillä julkisuudessa viime vuosina. Etenkin lapsen osallisuus varhaiskasvatuksessa on noussut puheenaiheeksi. Aikuisen roolin on todettu olevan merkityksellinen lapsen osallisuuden toteutumisessa. Tämän tutkimuksen tehtävä on nostaa esille asioita, jotka edistävät lapsen osallisuutta varhaiskasvatuksen arjessa. Tutkimuskysymykset ovat: Miten aikuisen mahdollistama lapsen osallisuus näkyy esikoulun arjessa? Millainen rooli aikuisella on lapsen osallisuuden mahdollistajana? Teoreettiset lähtökohdat rakentuvat esiopetuksen ja osallisuuden käsitteistä. Osallisuus kietoutuu lopulta kokonaisvaltaisesti esiopetuksen arkeen. Tutkimus on toteutettu osana Oulun yliopiston Politics of belonging: Promoting children’s inclusion in educational settings across borders. NordForsk: No. 85644-tutkimushanketta. Aineisto koostuu kolmesta haastattelusta, johon osallistui yhden lapsiryhmän kolme aikuista. Tutkimus on laadullinen tutkimus, jossa analyysimenetelmänä on käytetty aineistolähtöistä sisällönanalyysiä. Ensimmäistä tutkimuskysymystä lähestytään aineistolähtöisesti ja toisen tutkimuskysymyksen analysoinnissa sovelletaan Kankaan ja Vennisen (2010) luomaa osallisuuden kulmakivimallia. Tutkimus osoitti, että lapsen osallisuutta voidaan tukea monella tavalla esiopetuksen arjessa. Lapsen osallisuuden toteutumiseen tarvitaan sitä tukeva ilmapiiri. Se muodostuu vastavuoroisesta aikuisen ja lapsen välisestä sekä lapsen ja lapsen välisestä vuorovaikutuksesta. Osallisuutta tukevassa ilmapiirissä aikuinen on aidosti läsnä arjessa, kuunnellen ja kulkien lasten kanssa “samaa polkua”. Kun aikuinen näkee lapsiryhmän moninaisuuden pedagogisena rikkautena ja monien mahdollisuuksien oppimisympäristönä, lapsen osallisuuden kokemus vahvistuu. Osallisuutta tukevan ilmapiirin lähtökohtana on myös kaikenlaisen lapsiin kohdistuvan syrjinnän vastustaminen ja inkluusion periaatteiden noudattaminen. Tulokset osoittavat myös sen, että toimiva ja toisiaan tukeva työyhteisö on tärkeä osa lapsen osallisuuden toteutumista päiväkodin toimintakulttuurissa

Gold Coating of Respiratory Cilia for Scanning Electron Microscopy

The optimal thickness of gold coating of cilia for scanning electron microscopy was studied using respiratory mucosa obtained from pigs. We tested 8 different coating times, from 10 seconds to 4 minutes, which resulted in gold layer thicknesses varying from 16 ± 1 nm to 100 ± 3 nm. The thickness of the gold layer with a coating time of 60 seconds and voltage of 2.5 kV was 43 ± 5 nm. This thickness of gold layer gave good image quality without causing any electric charging. With thinner gold films, the amount of electric charging increased. When the coating time was longer, the gold layer was thicker but image quality did not improve. The thicknesses of the gold layers were measured using transmission electron microscopy (TEM)

Yhteiset lukuhetket tukemassa lapsen kielellistä kehitystä

Tiivistelmä. Lapselle lukeminen on ollut säännöllisin väliajoin sekä median että tutkijoiden mielenkiinnon kohteena. Yhdessä lukemista onkin tarkasteltu kautta aikojen monesta eri näkökulmasta. Tässä kandidaatin tutkielmassa selvitetään aikuisen ja lapsen yhteisten lukuhetkien yhteyttä lapsen kielelliseen kehitykseen. Tutkielman tavoitteena on pohtia, kuinka yhdessä lukeminen tukee lapsen kielellistä kehitystä sekä tarkastella erilaisten lukuhetkiin yhteydessä olevien tekijöiden vaikutusta lapsen kielelliseen kehitykseen. Tutkimus on rajattu koskemaan alle kouluikäisiä lapsia. Tutkielma on toteutettu kuvailevana kirjallisuuskatsauksena. Tiedonhaussa on hyödynnetty sekä kotimaisia että kansainvälisiä tietokantoja. Käytettäväksi tutkimusaineistoksi on pyritty valitsemaan mahdollisimman relevantteja ja ajantasaisia lähteitä sekä tutkimusaihetta käsitteleviä klassikkotutkimuksia, joihin vertaisarvioiduissa artikkeleissa viitataan vielä tänäkin päivänä yleisesti. Kirjallisuuden ja aihetta koskevien tutkimusten perusteella yhteisten lukuhetkien voidaan sanoa tukevan lasten kielellisiä taitoja monipuolisesti. Yhdessä lukemisen on havaittu muun muassa rikastuttavan lapsen sanavarastoa, tukevan kielellisen tietoisuuden ja kuullun ymmärtämisen taitojen kehittymistä sekä edistävän lapsen lukutaitoon liittyviä valmiuksia (mm. Bus, van Ijzendoorn & Pellegrini, 1995; Lerkkanen, 2006). Tutkimusten mukaan tiettyjen tekijöiden, kuten lukutyylin sekä kodin ja varhaiskasvatuksen lukuympäristöjen huomioiminen voi auttaa aikuista tukemaan lasten kielellistä kehitystä yhteisillä lukuhetkillä (Laakso, Poikkeus & Torppa, 2011; Merisuo-Storm, 2010). Yhteisten lukuhetkien on huomattu edistävän myös lapsen kiinnostusta lukemista kohtaan (Nurmilaakso & Välimäki, 2011). Parhaimmillaan yhteisen lukemisen tilanne onkin vuorovaikutusta, joka sisältää yhteistä pohdintaa ja keskustelua aikuisen ja lapsen välillä

Exome sequencing identifies FANCM as a susceptibility gene for triple-negative breast cancer

Peer reviewe

Preconditioning of mesenchymal stromal cells with low-intensity ultrasound: influence on chondrogenesis and directed SOX9 signaling pathways

Background: Continuous low-intensity ultrasound (cLIUS) facilitates the chondrogenic differentiation of human mesenchymal stromal cells (MSCs) in the absence of exogenously added transforming growth factor-beta (TGFβ) by upregulating the expression of transcription factor SOX9, a master regulator of chondrogenesis. The present study evaluated the molecular events associated with the signaling pathways impacting SOX9 gene and protein expression under cLIUS. Methods: Human bone marrow-derived MSCs were exposed to cLIUS stimulation at 14 kPa (5 MHz, 2.5 Vpp) for 5 min. The gene and protein expression of SOX9 was evaluated. The specificity of SOX9 upregulation under cLIUS was determined by treating the MSCs with small molecule inhibitors of select signaling molecules, followed by cLIUS treatment. Signaling events regulating SOX9 expression under cLIUS were analyzed by gene expression, immunofluorescence staining, and western blotting. Results: cLIUS upregulated the gene expression of SOX9 and enhanced the nuclear localization of SOX9 protein when compared to non-cLIUS-stimulated control. cLIUS was noted to enhance the phosphorylation of the signaling molecule ERK1/2. Inhibition of MEK/ERK1/2 by PD98059 resulted in the effective abrogation of cLIUS-induced SOX9 expression, indicating that cLIUS-induced SOX9 upregulation was dependent on the phosphorylation of ERK1/2. Inhibition of integrin and TRPV4, the upstream cell-surface effectors of ERK1/2, did not inhibit the phosphorylation of ERK1/2 and therefore did not abrogate cLIUS-induced SOX9 expression, thereby suggesting the involvement of other mechanoreceptors. Consequently, the effect of cLIUS on the actin cytoskeleton, a mechanosensitive receptor regulating SOX9, was evaluated. Diffused and disrupted actin fibers observed in MSCs under cLIUS closely resembled actin disruption by treatment with cytoskeletal drug Y27632, which is known to increase the gene expression of SOX9. The upregulation of SOX9 under cLIUS was, therefore, related to cLIUS-induced actin reorganization. SOX9 upregulation induced by actin reorganization was also found to be dependent on the phosphorylation of ERK1/2. Conclusions: Collectively, preconditioning of MSCs by cLIUS resulted in the nuclear localization of SOX9, phosphorylation of ERK1/2 and disruption of actin filaments, and the expression of SOX9 was dependent on the phosphorylation of ERK1/2 under cLIUS

CHEK2 c.1100delC mutation is associated with an increased risk for male breast cancer in Finnish patient population

Background: Several susceptibility genes have been established for female breast cancer, of which mutations in BRCA1 and especially in BRCA2 are also known risk factors for male breast cancer (MBC). The role of other breast cancer genes in MBC is less well understood.Methods: In this study, we have genotyped 68 MBC patients for the known breast or ovarian cancer associated mutations in the Finnish population in CHEK2, PALB2, RAD51C, RAD51D, and FANCM genes.Results: CHEK2 c.1100delC mutation was found in 4 patients (5.9%), which is significantly more frequent than in the control population (OR: 4.47, 95% CI 1.51-13.18, p = 0.019). Four CHEK2 I157T variants were also detected, but the frequency did not significantly differ from population controls (p = 0.781). No RAD51C, RAD51D, PALB2, or FANCM mutations were found.Conclusions: These data suggest that the CHEK2 c.1100delC mutation is associated with an increased risk for MBC in the Finnish population

RAD51C Germline Mutations in Breast and Ovarian Cancer Cases from High-Risk Families

BRCA1 and BRCA2 are the most well-known breast cancer susceptibility genes. Additional genes involved in DNA repair have been identified as predisposing to breast cancer. One such gene, RAD51C, is essential for homologous recombination repair. Several likely pathogenic RAD51C mutations have been identified in BRCA1- and BRCA2-negative breast and ovarian cancer families. We performed complete sequencing of RAD51C in germline DNA of 286 female breast and/or ovarian cancer cases with a family history of breast and ovarian cancers, who had previously tested negative for mutations in BRCA1 and BRCA2. We screened 133 breast cancer cases, 119 ovarian cancer cases, and 34 with both breast and ovarian cancers. Fifteen DNA sequence variants were identified; including four intronic, one 5′ UTR, one promoter, three synonymous, and six non-synonymous variants. None were truncating. The in-silico SIFT and Polyphen programs were used to predict possible pathogenicity of the six non-synonomous variants based on sequence conservation. G153D and T287A were predicted to be likely pathogenic. Two additional variants, A126T and R214C alter amino acids in important domains of the protein such that they could be pathogenic. Two-hybrid screening and immunoblot analyses were performed to assess the functionality of these four non-synonomous variants in yeast. The RAD51C-G153D protein displayed no detectable interaction with either XRCC3 or RAD51B, and RAD51C-R214C displayed significantly decreased interaction with both XRCC3 and RAD51B (p<0.001). Immunoblots of RAD51C-Gal4 activation domain fusion peptides showed protein levels of RAD51C-G153D and RAD51C-R214C that were 50% and 60% of the wild-type, respectively. Based on these data, the RAD51C-G153D variant is likely to be pathogenic, while the RAD51C- R214C variant is hypomorphic of uncertain pathogenicity. These results provide further support that RAD51C is a rare breast and ovarian cancer susceptibility gene

BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers

Background: The K3326X variant in BRCA2 (BRCA2*c.9976A&gt;T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed. Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations