Kuka kasvattaa, kuka opettaa? : Genealoginen tutkimus perheen ja koulun välisen kasvatusvastuun politiikasta

FAMILIES AND SCHOOLS AND THE POLITICS OF RESPONSIBILITIES - a genealogical study on family and school as carers and educators of the child population in modern society This study aims to uncover the politics behind such discourses in the media which have claimed the family to be totally responsible for children and which ignore the various responsibilities accorded to the state in matters concerning the child population. Using Max Weber s and Michael Mann s theorizing on the history of power relationships, feminist social history on patriarchy and Foucauldian power analytic concept of dispositif the study traces two competing child policies which have influenced the historical formation of modern generational order in Western societies. One of them is based on the interests of the hegemonic bourgeois elite and the other on the interests of the non-elite population, which were expressed during the phase of building the welfare state in Finland in the 1960 1980 s. The central strategies of the bourgeois child policy are 1) to construct the childhood years as a time for preparation and formation of the individual according to the interests of the elite, 2) to construct the family as the sole site of holistic care and responsibility of children in society, and 3) compulsory schooling of children of the non-elite population in state organized schools. To implement these strategies the elite uses strategically patriarchal cultural formations/dispositifs in modernized versions. The result has been the formation of a sexually divided and hierarchical order of care and education, where, on the one hand, there is the less important feminine care of children done by mothers at home and, on the other, the real education of the school, where children are made the object of authoritarian shaping and where the needs and the personal experiences of the child are ignored. The welfare order of care and education is based on the ethos of welfare society, where the state and the families are seen to share the responsibility for the child population. In this vein, families and schools are seen as partners who both have a caring attitude to children s welfare and learning. The study shows that discourses and terminology in the mainstream educational policy texts in Finland create a chaotic linguistic game which makes it difficult to have a rational discussion about the roles of family and school in the holistic care and education of children. This has opened the door to political discourses where familist interpretations of the question of responsibility are claimed to be based on law.

Dementiakuolleisuuden sosiaaliset determinantit - rekisteriaineistoon pohjautuva tutkimus dementiakuolleisuuteen vaikuttavista sosiodemografisista tekijöistä

Tutkimuksessa tarkastellaan dementiakuolleisuutta sekä siihen vaikuttavia sosiaalisia tekijöitä. Dementia on oireyhtymä, jota pääasiassa sairastavat yli 65 -vuotiaat henkilöt. Väestön ikääntyessä sekä elinajanodotteen kasvaessa on odotettavissa, että dementiaa sairastavien määrä tulee kasvamaan merkittävästi lähivuosina. On viitteitä siitä, että dementiaan sairastumisen riskiin vaikuttavat erilaiset sosiaaliset tekijät kuten koulutus, mutta varsinkin dementiakuolleisuudesta tiedetään vähän. Tutkielman aineistona käytettiin Tilastokeskuksen muodostamaa Elinolot ja kuolinsyyt -rekisteriaineistoa, joka koostuu väestölaskentatiedoista sekä työssäkäyntitilaston pitkittäisaineistosta, johon on liitetty kuolinsyytietoja. Peruskuolinsyyn lisäksi aineistossa oli tieto korkeintaan kolmesta myötävaikuttavasta syystä. Dementiakuolleisuuden on esitetty aliarvioituvan peruskuolinsyynä, joten dementiakuolleisuuden määrittelyssä käytettiin myös tietoa myötävaikuttavista syistä. Rajausten jälkeen aineistossa on 317 944 henkilöä, joista 128 562 on miehiä ja 189 382 naisia. Pääanalyysimenetelmänä on käytetty elinaikamalleihin kuuluvaa Coxin regressiota. Dementiakuolleisuudessa oli vaihtelua kaikkien tutkimuksessa käytettyjen muuttujien, eli koulutuksen, sosiaaliluokan, tulojen, siviilisäädyn sekä perhemuodon mukaan. Koulutuksen vaikutus välittyi osin ammattiasemaan perustuvan sosiaaliluokan kautta. Suurimpia ryhmien väliset suhteelliset erot olivat nuoremmissa ikäryhmissä sekä sosiaaliluokan ja siviilisäädyn kohdalla. Eronneilla ja naimattomilla oli selvästi kohonnut riski suhteessa naimisissa oleviin. Myös työntekijöillä havaittiin kohonnut riski suhteessa ylempiin toimihenkilöihin. Siviilisääty vaikutti olevan merkittävä tekijä siinä mielessä, että koulutuksen, sosiaaliluokan ja tulojen tuominen malliin ei juuri vaikuttanut siviilisäätyryhmien välillä havaittuun vaihteluun. Dementiakuolleisuudessa havaitut ryhmien väliset suhteelliset erot olivat hieman pienempiä kuin muissa syissä, mutta kuitenkin hyvin samaa suuruusluokkaa. Tulosten perusteella on identifioitavissa tekijöitä, jotka suojaavat dementialta. Erityisesti avioliitto, korkea koulutus sekä ylemmät toimihenkilöammatit vaikuttavat olevan dementialta suojaavia tekijöitä. Avioliiton suojaavan vaikutuksen voidaan tulkita liittyvän sosiaaliseen kanssakäymiseen sekä puolison tukeen ja läsnäoloon. Korkea koulutus sekä toimihenkilöammatit indikoivat virikkeellisempää työympäristöä, mutta niiden vaikutus voi myös kulkea ylipäänsä aktiivisemman ja kognitiivisesti virikkeellisemmän elämäntavan kautta. Aktiivisen ja kognitiivisesti haastavan elämäntavan on esitetty suojaavan dementiaan sairastumiselta. Tuloksia voidaan tulkita elämänkaarinäkökulman kautta. Jo nuoruudessa vaikuttavilla tekijöillä, kuten koulutuksella, on vaikutusta. Tämän lisäksi elämänkaaren aikana myöhemmin vaikuttavat tekijät ovat merkityksellisiä. Näiden tekijöiden on esitetty vaikuttavan aivojen hermoverkostoon ja -yhteyksiin ja luovan kognitiivista reserviä, minkä on esitetty ehkäisevän tai lykkäävän dementiaan sairastumista.

Poststroke survival and ischemic stroke recurrence : the cerebral small-vessel disease perspective

The aim of the present study was to investigate the influence of different manifestations of cerebral SVD on poststroke survival and ischemic stroke recurrence in long-term follow-up. The core imaging features of small-vessel disease (SVD) are confluent and extensive white matter changes (WMC) and lacunar infarcts. These are associated with minor motor deficits but a major negative influence on cognition, mood, and functioning in daily life, resulting from small-vessel lesions in the fronto-subcortical brain network. These sub-studies were conducted as part of the Helsinki Stroke Aging Memory (SAM) study. The SAM cohort consisted of 486 consecutive patients aged 55 to 85 years who were admitted to Helsinki University Central Hospital with acute ischemic stroke. The study included comprehensive clinical, neuropsychological, psychiatric and radiological assessment three months poststroke. The patients were followed up up for 12 years using extensive national registers. The effect of different manifestations of cerebral SVD on poststroke survival and stroke recurrence was analyzed controlling for factors such as age, education, and cardiovascular risk factors. Poststroke dementia and cognitive impairment relate to poor long-term survival. In particular, deficits in executive functions as well as visuospatial and constructional abilities predict poor outcome. The predictive value of cognitive deficits is further underlined by the finding that depression-executive dysfunction syndrome (DES), but not depression in itself, is associated with poor poststroke survival. Delirium is not independently associated with increased risk for long-term poststroke mortality, although it is associated with poststroke dementia. Furthermore, acute index stroke attributable to SVD is associated with poorer long-term survival and a higher risk for cardiac death than other stroke subtypes. Severe WMC, a surrogate of SVD, is independently related to an increased risk of stroke recurrence at five years. In summary, cognitive poststroke outcomes reflecting changes in the executive network brain, and the presence of cerebral SVD are important determinants of poststroke mortality and ischemic stroke recurrence, regardless of whether SVD is the cause of the index stroke or a condition concurrent to some other etiology.

Dissection of the genetic background of childhood onset progressive myoclonic epilepsies

The progressive myoclonic epilepsies (PMEs) are a clinically and etiologically heterogeneous group of symptomatic epilepsies characterized by myoclonus, tonic-clonic seizures, psychomotor regression and ataxia. Different disorders have been classified as PMEs. Of these, the group of neuronal ceroid lipofuscinoses (NCLs) comprise an entity that has onset in childhood, being the most common cause of neurodegeneration in children. The primary aim of this thesis was to dissect the molecular genetic background of patients with childhood onset PME by studying candidate genes and attempting to identify novel PME-associated genes. Another specific aim was to study the primary protein properties of the most recently identified member of the NCL-causing proteins, MFSD8. To dissect the genetic background of a cohort of Turkish patients with childhood onset PME, a screen of the NCL-associated genes PPT1, TPP1, CLN3, CLN5, CLN6, MFSD8, CLN8 and CTSD was performed. Altogether 49 novel mutations were identified, which together with 56 mutations found by collaborators raised the total number of known NCL mutations to 364. Fourteen of the novel mutations affect the recently identified MFSD8 gene, which had originally been identified in a subset of mainly Turkish patients as the underlying cause of CLN7 disease. To investigate the distribution of MFSD8 defects, a total of 211 patients of different ethnic origins were evaluated for mutations in the gene. Altogether 45 patients from nine different countries were provided with a CLN7 molecular diagnosis, denoting the wide geographical occurrence of MFSD8 defects. The mutations are private with only one having been established by a founder-effect in the Roma population from the former Czechoslovakia. All mutations identified except one are associated with the typical clinical picture of variant late-infantile NCL. To address the trafficking properties of MFSD8, lysosomal targeting of the protein was confirmed in both neuronal and non-neuronal cells. The major determinant for this lysosomal sorting was identified to be an N-terminal dileucine based signal (9-EQEPLL-14), recognized by heterotetrameric AP-1 adaptor proteins, suggesting that MFSD8 takes the direct trafficking pathway en route to the lysosomes. Expression studies revealed the neurons as the primary cell-type and the hippocampus and cerebellar granular cell layer as the predominant regions in which MFSD8 is expressed. To identify novel genes associated with childhood onset PME, a single nucleotide polymorphism (SNP) genomewide scan was performed in three small families and 18 sporadic patients followed by homozygosity mapping to determine the candidate loci. One of the families and a sporadic patient were positive for mutations in PLA2G6, a gene that had previously been shown to cause infantile neuroaxonal dystrophy. Application of next-generation sequencing of candidate regions in the remaining two families led to identification of a homozygous missense mutation in USP19 for the first and TXNDC6 for the second family. Analysis of the 18 sporadic cases mapped the best candidate interval in a 1.5 Mb region on chromosome 7q21. Screening of the positional candidate KCTD7 revealed six mutations in seven unrelated families. All patients with mutations in KCTD7 were reported to have early onset PME, rapid disease progression leading to dementia and no pathologic hallmarks. The identification of KCTD7 mutations in nine patients and the clinical delineation of their phenotype establish KCTD7 as a gene for early onset PME. The findings presented in this thesis denote MFSD8 and KCTD7 as genes commonly associated with childhood onset symptomatic epilepsy. The disease-associated role of TXNDC6 awaits verification through identification of additional mutations in patients with similar phenotypes. Completion of the genetic spectrum underlying childhood onset PMEs and understanding of the gene products functions will comprise important steps towards understanding the underlying pathogenetic mechanisms, and will possibly shed light on the general processes of neurodegeneration and nervous system regulation, facilitating the diagnosis, classification and possibly treatment of the affected cases.