Theraplay terapian vaikuttavuus vanhempi-lapsi suhteeseen ja lapsen psykiatriseen oireiluun: pilottitutkimus

BSTRACT Theraplay® is a short-term parent–child interaction therapy combining structured, attachment-based, joyful and adult-led playful sessions with reflective guidance work with the parents. This pilot study evaluates the impact of Theraplay® therapy in improving the quality of parent–child interaction and decreasing the internalizing and externalizing symptoms of children diagnosed with emotional and/or behavioral disorders. Participants were eighteen 4–8 year-old children (M = 4.42, SD = 1.54) from two outpatient child psychiatric clinics whose mothers, and in 13 of those cases fathers also participated in the Theraplay® therapy together with the child. Pre- and post- treatment measures included videotaped observations of parent–child interaction quality, and child psychiatric symptoms (CBCL). The results showed improvements in parent–child interaction quality as well as decreases in children’s internalizing and externalizing symptoms. The results of this pilot study indicate that Theraplay® therapy may be an effective treatment among children diagnosed with emotional and/or behavioral psychiatric disorders.Theraplay® is a short-term parent–child interaction therapy combining structured, attachment-based, joyful and adult-led playful sessions with reflective guidance work with the parents. This pilot study evaluates the impact of Theraplay® therapy in improving the quality of parent–child interaction and decreasing the internalizing and externalizing symptoms of children diagnosed with emotional and/or behavioral disorders. Participants were eighteen 4–8 year-old children (M = 4.42, SD = 1.54) from two outpatient child psychiatric clinics whose mothers, and in 13 of those cases fathers also participated in the Theraplay® therapy together with the child. Pre- and post-treatment measures included videotaped observations of parent–child interaction quality, and child psychiatric symptoms (CBCL). The results showed improvements in parent–child interaction quality as well as decreases in children's internalizing and externalizing symptoms. The results of this pilot study indicate that Theraplay® therapy may be an effective treatment among children diagnosed with emotional and/or behavioral psychiatric disorders.Peer reviewe

Suomi seuraavan sukupolven kasvuympäristönä : Seuranta Suomessa vuonna 1997 syntyneistä lapsista, joilla on ulkomailla syntynyt vanhempi

Tässä raportissa tarkastellaan Suomessa vuonna 1997 syntynyttä ikäluokkaa ja erityisesti niitä lapsia, joiden vanhemmista toinen tai molemmat ovat syntyneet ulkomailla. Kyseessä on ensimmäinen yleiskatsaus näiden lasten kehityksestä ja kasvuympäristöistä. Tutkimuskohteina olivat lasten perhetaustat, koulutus, terveys, lastensuojelu ja rikollisuus. Lisäksi tutkittiin lasten asuinpaikkojen alueellista jakautumista ja heidän asuinalueidensa piirteitä. Tutkimustulosten mukaan suurin osa ikäluokan lapsista voi hyvin riippumatta siitä, ovatko heidän vanhempansa syntyneet Suomessa vai ulkomailla. Eroja lasten hyvinvoinnissa ja palveluiden käytössä havaittiin kuitenkin sen mukaan, onko vanhemmista toinen vai molemmat syntyneet ulkomailla, sekä sen mukaan, missä maassa vanhemmat ovat syntyneet. Eroja oli muun muassa perheiden taloudellisessa tilanteessa, lasten koulutuksessa sekä sosiaali- ja terveyspalveluiden käytössä. Raportti tuo kaivattua tietoa hyvinvointipolitiikan haasteista, ongelmista ja kehittämiskohteista. Se on suunnattu päätöksentekijöille, asiantuntijoille ja tutkijoille, jotka toimivat sosiaali-, terveys-, koulutus-, työllisyys-, alue-, asunto- ja kotoutumispolitiikan sekä -palveluiden parissa

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies

The genomics of heart failure: design and rationale of the HERMES consortium

AIMS: The HERMES (HEart failure Molecular Epidemiology for Therapeutic targetS) consortium aims to identify the genomic and molecular basis of heart failure. METHODS AND RESULTS: The consortium currently includes 51 studies from 11 countries, including 68 157 heart failure cases and 949 888 controls, with data on heart failure events and prognosis. All studies collected biological samples and performed genome-wide genotyping of common genetic variants. The enrolment of subjects into participating studies ranged from 1948 to the present day, and the median follow-up following heart failure diagnosis ranged from 2 to 116 months. Forty-nine of 51 individual studies enrolled participants of both sexes; in these studies, participants with heart failure were predominantly male (34–90%). The mean age at diagnosis or ascertainment across all studies ranged from 54 to 84 years. Based on the aggregate sample, we estimated 80% power to genetic variant associations with risk of heart failure with an odds ratio of ≥1.10 for common variants (allele frequency ≥ 0.05) and ≥1.20 for low-frequency variants (allele frequency 0.01–0.05) at P < 5 × 10^{-8} under an additive genetic model. CONCLUSIONS: HERMES is a global collaboration aiming to (i) identify the genetic determinants of heart failure; (ii) generate insights into the causal pathways leading to heart failure and enable genetic approaches to target prioritization; and (iii) develop genomic tools for disease stratification and risk prediction

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies

The genomics of heart failure: design and rationale of the HERMES consortium

Aims The HERMES (HEart failure Molecular Epidemiology for Therapeutic targets) consortium aims to identify the genomic and molecular basis of heart failure.Methods and results The consortium currently includes 51 studies from 11 countries, including 68 157 heart failure cases and 949 888 controls, with data on heart failure events and prognosis. All studies collected biological samples and performed genome-wide genotyping of common genetic variants. The enrolment of subjects into participating studies ranged from 1948 to the present day, and the median follow-up following heart failure diagnosis ranged from 2 to 116 months. Forty-nine of 51 individual studies enrolled participants of both sexes; in these studies, participants with heart failure were predominantly male (34-90%). The mean age at diagnosis or ascertainment across all studies ranged from 54 to 84 years. Based on the aggregate sample, we estimated 80% power to genetic variant associations with risk of heart failure with an odds ratio of >1.10 for common variants (allele frequency > 0.05) and >1.20 for low-frequency variants (allele frequency 0.01-0.05) at P < 5 x 10(-8) under an additive genetic model.Conclusions HERMES is a global collaboration aiming to (i) identify the genetic determinants of heart failure; (ii) generate insights into the causal pathways leading to heart failure and enable genetic approaches to target prioritization; and (iii) develop genomic tools for disease stratification and risk prediction.Cardiolog

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies

The genomics of heart failure: design and rationale of the HERMES consortium

Aims The HERMES (HEart failure Molecular Epidemiology for Therapeutic targets) consortium aims to identify the genomic and molecular basis of heart failure.Methods and results The consortium currently includes 51 studies from 11 countries, including 68 157 heart failure cases and 949 888 controls, with data on heart failure events and prognosis. All studies collected biological samples and performed genome-wide genotyping of common genetic variants. The enrolment of subjects into participating studies ranged from 1948 to the present day, and the median follow-up following heart failure diagnosis ranged from 2 to 116 months. Forty-nine of 51 individual studies enrolled participants of both sexes; in these studies, participants with heart failure were predominantly male (34-90%). The mean age at diagnosis or ascertainment across all studies ranged from 54 to 84 years. Based on the aggregate sample, we estimated 80% power to genetic variant associations with risk of heart failure with an odds ratio of >1.10 for common variants (allele frequency > 0.05) and >1.20 for low-frequency variants (allele frequency 0.01-0.05) at P Conclusions HERMES is a global collaboration aiming to (i) identify the genetic determinants of heart failure; (ii) generate insights into the causal pathways leading to heart failure and enable genetic approaches to target prioritization; and (iii) develop genomic tools for disease stratification and risk prediction.</p

The genomics of heart failure: design and rationale of the HERMES consortium

Aims: The HERMES (HEart failure Molecular Epidemiology for Therapeutic targetS) consortium aims to identify the genomic and molecular basis of heart failure. Methods and results: The consortium currently includes 51 studies from 11 countries, including 68 157 heart failure cases and 949 888 controls, with data on heart failure events and prognosis. All studies collected biological samples and performed genome‐wide genotyping of common genetic variants. The enrolment of subjects into participating studies ranged from 1948 to the present day, and the median follow‐up following heart failure diagnosis ranged from 2 to 116 months. Forty‐nine of 51 individual studies enrolled participants of both sexes; in these studies, participants with heart failure were predominantly male (34–90%). The mean age at diagnosis or ascertainment across all studies ranged from 54 to 84 years. Based on the aggregate sample, we estimated 80% power to genetic variant associations with risk of heart failure with an odds ratio of ≥1.10 for common variants (allele frequency ≥ 0.05) and ≥1.20 for low‐frequency variants (allele frequency 0.01–0.05) at P &lt; 5 × 10−8 under an additive genetic model. Conclusions: HERMES is a global collaboration aiming to (i) identify the genetic determinants of heart failure; (ii) generate insights into the causal pathways leading to heart failure and enable genetic approaches to target prioritization; and (iii) develop genomic tools for disease stratification and risk prediction