Lapsen tunnesäätelytaitojen ilmeneminen ja tukeminen päiväkodissa

Tiivistelmä. Tutkielmassa oli tarkoituksena selvittää miten 3–6-vuotiaiden lasten tunteiden säätelytaidot ilmenevät ja kehittyvät päiväkodissa. Erityisesti selvitettiin millaisia tukemisen eri keinoja kasvattaja pystyy hyödyntämään lapsen tunteiden säätelyn kehittyessä. Tutkielman kysymykset nousivat aiheen ajankohtaisuudesta, sillä tunnekasvatus on korostunut päiväkodeissa. Tutkimusten perusteella yhä useammalla lapsella on hankaluuksia säädellä tunteitaan. Erityisesti hankaluudet näkyvät ulospäin suuntautuneena negatiivisena käyttäytymisenä, esimerkiksi raivokohtauksina. Koska päiväkodilla on merkittävä rooli lapsen tunnekasvattajana, on kasvattajalla tärkeää olla erilaisia tukikeinoja lapsen tukemiseen. Tutkielma toteutettiin systemaattisena kirjallisuuskatsauksena ja aineiston valinnassa painotettiin kehityspsykologista näkökulmaa ja tukemisen eri keinoissa korostettiin toiminnanohjauksen näkökulmaa. Tutkimuksessa korostettiin lapsen kehittyviä kykyjä säädellä emotioitaan ja käyttäytymistään. Tutkielma osoitti, että tunteiden säätelytaitojen kehitykseen vaikuttavat ulkoiset ja sisäiset tekijät. Lapsella on myötäsyntyinen tarve hallita ympäristöään ja sen tapahtumia. Tunteiden säätelyyn lapsi tarvitsee kuitenkin aikuisen tukea, sillä se ei ole synnynnäinen taito, vaan se opitaan. Ympäristön tulee turvata lapsen tunteiden varhainen säätely. Tulokset osoittivat, että tunteiden säätely vaikuttaa kaikkiin lapsen kehityksen osa-alueisiin. Yksilölliset kehitykselliset taidot vaikuttavat siihen, miten lapsi säätelee tunteitaan. Koska tunteiden säätely nivoutuu myös muihin itsesäätelyn osa-alueisiin, on tukemisen keinoissa otettava huomioon itsesäätelyyn kuuluvat käyttäytymisen säätely sekä kognitioiden säätely. Mahdolliset ongelmat tunteiden säätelyssä vaikuttavat lapsen käyttäytymiseen ja toimintaan päiväkodissa. Kun tunteiden säätelyä tuetaan oikealla tavalla, kykenee lapsi säätelemään tunteitaan onnistuneesti, jolloin häiriökäyttäytyminen vähenee tai katoaa kokonaan. Tukemisen keinoissa tärkeimmiksi alueiksi aineiston perusteella muodostui kasvattajan rooli lapsen kanssasäätelijänä sekä kasvattajan toiminnan johdonmukaisuus. Erityisesti vuorovaikutuksella ja sen laadulla on merkitystä tunteiden säätelyn kehittymisessä, sillä kasvattajan ja lapsen välisen vuorovaikutuksen laatu vaikuttaa siihen, millaiseksi lapsen käsitys omista mahdollisuuksista vaikuttaa ympäristöön ja omiin tunteisiin muodostuu

Lastentarhanopettajien pedagoginen taito huomata ja tulkita 5–6-vuotiaiden lasten riitatilanteita

Tiivistelmä. Riitatilanteet ovat arkipäiväinen osa lasten välisiä suhteita. Lapset ratkaisevat riitatilanteita eri tavoin ja tarvitsevat niiden ratkaisemiseen usein aikuisen apua. Riitatilanteiden selvittämistä harjoitellaan arjen eri tilanteissa, jossa lastentarhanopettaja on merkittävässä roolissa. Tutkimuksen tavoitteena on selvittää lastentarhanopettajien käsityksiä 5–6-vuotiaiden lasten välisistä riitatilanteista. Lisäksi tutkimuksessa halutaan selvittää millaisia käsityksiä lastentarhanopettajilla on omista keinoista tukea riitatilanteita. Tutkimus toteutettiin laadullisena, fenomenografisena tutkimuksena. Aineiston analyysissa on käytetty soveltuvin osin fenomenografista analyysimenetelmää. Aineisto kerättiin haastattelun avulla. Haastatteluun osallistui 4 lastentarhanopettajaa. Haastateltavilla lastentarhanopettajilla oli työkokemusta 1–30 vuoden väliltä. Haastateltavat olivat koulutustaustaltaan opistotaustaisia lastentarhanopettajia tai kasvatustieteen maistereita. Tutkimuksen teoreettinen viitekehys on rakentunut aiemmista aiheeseen liittyvistä tutkimuksista ja teorioista, jotka ovat olleet pääasiassa kehityspsykologisia. Analyysin tuloksena syntyi kaksi kuvauskategoriaa, jotka kuvaavat lastentarhanopettajien käsityksiä lasten riitatilanteista ja omista keinoista tukea niitä. Nämä kuvauskategoriat olivat: lasten sosiaaliset taidot ja lastentarhanopettajan ammattitaito. Lastentarhanopettajat käsittivät lasten riitatilanteet tavallisina, vertaissuhteessa tapahtuvana ilmiönä, joiden syntymiseen vaikuttaa lapsen sosiaalisten taitojen kehittyneisyys. Lastentarhanopettajan ammattitaito ja sensitiivisyys koettiin tärkeimpinä tekijöinä lasten riitatilanteiden tukemisessa

Lack of association of the CIITA -168A→G promoter SNP with myasthenia gravis and its role in autoimmunity

<p>Abstract</p> <p>Background</p> <p>The major histocompatibility complex class II transactivator (CIITA) regulates MHC class II gene expression. A promoter SNP -168A→G (rs3087456) has previously been shown to be associated with susceptibility to several immune mediated disorders, including rheumatoid arthritis (RA), multiple sclerosis (MS) and myocardial infarction (MI). Myasthenia gravis (MG) is an autoimmune disorder which has previously been shown to be associated with polymorphisms of several autoimmune predisposing genes, including <it>IL-1</it>, <it>PTPN22</it>, <it>TNF-α </it>and the <it>MHC</it>. In order to determine if allelic variants of rs3087456 increase predisposition to MG, we analyzed this SNP in our Swedish cohort of 446 MG patients and 1866 controls.</p> <p>Results</p> <p>No significant association of the SNP with MG was detected, neither in the patient group as a whole, nor in any clinical subgroup. The vast majority of previous replication studies have also not found an association of the SNP with autoimmune disorders.</p> <p>Conclusions</p> <p>We thus conclude that previous findings with regard to the role of the <it>CIITA </it>-168A→G SNP in autoimmunity may have to be reconsidered.</p

Transforming growth factor-β-regulated miR-24 promotes skeletal muscle differentiation

MicroRNAs (miRNAs) have recently been proposed as a versatile class of molecules involved in regulation of a variety of biological processes. However, the role of miRNAs in TGF-β-regulated biological processes is poorly addressed. In this study, we found that miR-24 was upregulated during myoblast differentiation and could be inhibited by TGF-β1. Using both a reporter assay and Northern blot analysis, we showed that TGF-β1 repressed miR-24 transcription which was dependent on the presence of Smad3 and a Smads binding site in the promoter region of miR-24. TGF-β1 was unable to inhibit miR-24 expression in Smad3-deficient myoblasts, which exhibited accelerated myogenesis. Knockdown of miR-24 led to reduced expression of myogenic differentiation markers in C2C12 cells, while ectopic expression of miR-24 enhanced differentiation, and partially rescued inhibited myogenesis by TGF-β1. This is the first study demonstrating a critical role for miRNAs in modulating TGF-β-dependent inhibition of myogenesis, and provides a novel mechanism of the genetic regulation of TGF-β signaling during skeletal muscle differentiation

A luteinizing hormone receptor intronic variant is significantly associated with decreased risk of Alzheimer's disease in males carrying an apolipoprotein E ε4 allele

Genetic and biochemical studies support the apolipoprotein E (APOE) ε4 allele as a major risk factor for late-onset Alzheimer's disease (AD), though ~50% of AD patients do not carry the allele. APOE transports cholesterol for luteinizing hormone (LH)-regulated steroidogenesis, and both LH and neurosteroids have been implicated in the etiology of AD. Since polymorphisms of LH beta-subunit (LHB) and its receptor (LHCGR) have not been tested for their association with AD, we scored AD and age-matched control samples for APOE genotype and 14 polymorphisms of LHB and LHCGR. Thirteen gene-gene interactions between the loci of LHB, LHCGR, and APOE were associated with AD. The most strongly supported of these interactions was between an LHCGR intronic polymorphism (rs4073366; lhcgr2) and APOE in males, which was detected using all three interaction analyses: linkage disequilibrium, multi-dimensionality reduction, and logistic regression. While the APOE ε4 allele carried significant risk of AD in males [p = 0.007, odds ratio (OR) = 3.08(95%confidence interval: 1.37, 6.91)], ε4-positive males carrying 1 or 2 C-alleles at lhcgr2 exhibited significantly decreased risk of AD [OR = 0.06(0.01, 0.38); p = 0.003]. This suggests that the lhcgr2 C-allele or a closely linked locus greatly reduces the risk of AD in males carrying an APOE ε4 allele. The reversal of risk embodied in this interaction powerfully supports the importance of considering the role gene-gene interactions play in the etiology of complex biological diseases and demonstrates the importance of using multiple analytic methods to detect well-supported gene-gene interactions

Late Onset Myasthenia Gravis Is Associated with HLA DRB1*15:01 in the Norwegian Population

BACKGROUND: Acquired myasthenia gravis (MG) is a rare antibody-mediated autoimmune disease caused by impaired neuromuscular transmission, leading to abnormal muscle fatigability. The aetiology is complex, including genetic risk factors of the human leukocyte antigen (HLA) complex and unknown environmental factors. Although associations between the HLA complex and MG are well established, not all involved components of the HLA predisposition to this heterogeneous disease have been revealed. Well-powered and comprehensive HLA analyses of subgroups in MG are warranted, especially in late onset MG. METHODOLOGY/PRINCIPAL FINDINGS: This case-control association study is of a large population-based Norwegian cohort of 369 MG patients and 651 healthy controls. We performed comprehensive genotyping of four classical HLA loci (HLA-A, -B, -C and -DRB1) and showed that the DRB1*15:01 allele conferred the strongest risk in late onset MG (LOMG; onset ≥ 60 years) (OR 2.38, p(c)7.4 × 10(-5)). DRB1*13:01 was found to be a protective allele for both early onset MG (EOMG) and LOMG (OR 0.31, p(c) 4.71 × 10(-4)), a finding not previously described. No significant association was found to the DRB1*07:01 allele (p(nc) = 0.18) in a subset of nonthymomatous anti-titin antibody positive LOMG as reported by others. HLA-B*08 was mapped to give the strongest contribution to EOMG, supporting previous studies. CONCLUSION: The results from this study provide important new information concerning the susceptibility of HLA alleles in Caucasian MG, with highlights on DRB1*15:01 as being a major risk allele in LOMG

Genome-Wide Association Study of Late-Onset Myasthenia Gravis: Confirmation of TNFRSF11A and Identification of ZBTB10 and Three Distinct HLA Associations

To investigate the genetics of late-onset myasthenia gravis (LOMG), we conducted a genome-wide association study imputation of >6 million single nucleotide polymorphisms (SNPs) in 532 LOMG cases (anti-acetylcholine receptor [AChR] antibody positive; onset age ≥50 years) and 2,128 controls matched for sex and population substructure. The data confirm reported TNFRSF11A associations (rs4574025, P = 3.9 × 10−7, odds ratio [OR] 1.42) and identify a novel candidate gene, ZBTB10, achieving genome-wide significance (rs6998967, P = 8.9 × 10−10, OR 0.53). Several other SNPs showed suggestive significance including rs2476601 (P = 6.5 × 10−6, OR 1.62) encoding the PTPN22 R620W variant noted in early-onset myasthenia gravis (EOMG) and other autoimmune diseases. In contrast, EOMG-associated SNPs in TNIP1 showed no association in LOMG, nor did other loci suggested for EOMG. Many SNPs within the major histocompatibility complex (MHC) region showed strong associations in LOMG, but with smaller effect sizes than in EOMG (highest OR ∼2 versus ∼6 in EOMG). Moreover, the strongest associations were in opposite directions from EOMG, including an OR of 0.54 for DQA1*05:01 in LOMG (P = 5.9 × 10−12) versus 2.82 in EOMG (P = 3.86 × 10−45). Association and conditioning studies for the MHC region showed three distinct and largely independent association peaks for LOMG corresponding to (a) MHC class II (highest attenuation when conditioning on DQA1), (b) HLA-A and (c) MHC class III SNPs. Conditioning studies of human leukocyte antigen (HLA) amino acid residues also suggest potential functional correlates. Together, these findings emphasize the value of subgrouping myasthenia gravis patients for clinical and basic investigations and imply distinct predisposing mechanisms in LOMG

Optimising process conditions for multiple quality criteria in micro-injection moulding

This paper presents a statistical technique to optimise process conditions for multiple quality criteria in micro-injection moulding. A sample hierarchical component with micro-features was replicated where it was required to improve the process conditions for both complete mould filling and variability in mass. A design-of-experiments approach was used to investigate the effect of five processing parameters on both criteria. It was found that holding pressure, melt temperature and injection velocity were statistically significant for part mass, whereas injection velocity alone was significant for mass variation. Desirability functions were used to predict processing conditions that improved both requirements within pre-set conditions. The technique was validated by experiment and it was shown to be applicable for process parameters for multiple criteria

Genome-wide linkage disequilibrium from 100,000 SNPs in the East Finland founder population

Information about linkage disequilibrium (LD) is important in understanding the genome structure and has its applications in association studies. Here we present the first genome-wide LD study based on a founder population (East Finland). The LD data consist of 118 unrelated individuals and around 480,000 SNP pairs genotyped with the Affymetrix 100K genotyping assay. Using the minor allele frequency (MAF) limit of .05, the squared correlation coefficient between two loci (r(2)) was .48, .37, .28, and .20 for distances of 5, 10, 20, and 40 kb respectively. MAF had a significant effect on the mean r(2) so that the extent of useful LD (r(2) >.3) varied from 17 kb to 80 kb depending on the limit set for the MAF. For D' the effect of MAF was smaller but reflected the possible age of the mutation: SNPs with high MAF had lower D' than those with low MAF. The X chromosome showed higher D' values than autosomes and the extent of useful LD (r(2) >.3) was twice as long on the X chromosome than on the autosomes. Based on the results, LD varies across the genome and is correlated to local recombination rate between and within chromosomes. However, the recombination rate does not explain all the variation found in LD. We also report a number of long chromosomal regions where exceptionally high or low LD were detected