Fra reformasjonen til mellomkrigstiden. Framveksten av det norske utdanningssystemet.

Avhandlingen er, etter eksisterende faginndelinger, både en studie i historisk utdanningssosiologi og i komparativ pedagogikk. Den sentrale problemstillingen er hvilke vilkår og prosesser som førte til framveksten av det norske utdanningssystemet, når dette oppstod, og om det var et sentralisert eller desentralisert system. Arbeidet anvender, vurderer og modifiserer (reparerer) Margaret Archers morfogenetiske teori om den historiske framveksten av europeiske statlige utdanningssystemer fremsatt i Social Origins of Educational Systems ([1979] 2013). I etterprøvingen av Archers teori går avhandlingen helt tilbake til reformasjonen på 1500-tallet. Archer hevder at reformasjonen i Danmark ikke medførte endringer i kirkens skoledominans, men avhandlingen underbygger at skolen etter reformasjonen ble dominert både av kirken og staten. Skolen var dualt integrert med kirke og stat, ikke monointegrert med kirken, slik Archer hevder. Dermed er det identifisert en ny type morfogenetisk syklus i skolens utvikling som ikke er teoretisert av Archer. Avhandlingen analyserer skoleutviklingen i Danmark-Norge på 1600-, 1700- og 1800-tallet i lys av tesen om dual integrasjon. I en videreføring av analysen til å omfatte skoleutviklingen i Norge etter 1814 konkluderes det med at det norske utdanningssystemet oppstod etter lovvedtaket av 1896 om høyere almendannende skoler og at systemet utviklet seg til et sentralisert system i perioden fra 1896 til midten av 1930-årene. Det empiriske grunnlaget for arbeidet omfatter foreliggende kirkehistoriske, politisk historiske og utdanningshistoriske studier. Avhandlingen bidrar til kunnskapsutviklingen med en videreutvikling og en modifikasjon (reparasjon) av Archers teori: i) videreutviklingen av teorien omfatter teoretiseringen av en morfogenetisk syklus betinget i skolens duale integrasjon (fase 1) som også er en alternativ teori om skolens utvikling i Danmark etter reformasjonen fram til 1814, og ii) en modifikasjon av den overordnede teorien om framveksten av utdanningssystemene, som åpner for at skolens utvikling fra integrasjonen med kirken i europeisk middelalder til framveksten av utdanningssystemene kan ha omfattet mer enn én morfogenetisk syklus.This thesis can be categorized both as a study on the historical sociology of education and as a study in comparative education. It applies, extends and repairs Margaret Archer’s morphogenetic theory of the emergence of state educational systems to enable it to account for the emergence of the Norwegian educational system. The questions generated by Archer’s theory are: When did the Norwegian educational system emerge? Was the system centralized or decentralized? And, what kind of processes led to the emergence of the system? Starting at the time of the Lutheran reformation in Denmark-Norway, Archer’s account of educational development in Denmark until 1814, based on the assumption of mono-integration between education and the church, is evaluated against an alternative assumption of education being integrated with both the church and the state. Further analysis of educational development in Norway from 1814 till the mid 1930ies concludes with the finding that the Norwegian educational system emerged after the passing of the law on higher education in 1896 and that the system evolved into a centralized system during the period from 1896 to 1936.The study is based on previous research on Danish and Norwegian church history, educational history and political history. The theoretical contribution of the study is an extension and modification of Margaret Archer's theory of the emergence of educational systems, which include theoretical elaborations at two theoretical levels: i) the development of a theory of a morphogenetic cycle that started with the dual integration of education with the state and the church and 2) the development of the general theory of the emergence of educational system to potentially include more than one morphogenetic cycle

Et dypdykk i Tromsøs musikkmiljø med fokus på undergrunnen - trengs det en musikkbransje i byen

Hovedtema i denne oppgaven er forholdet mellom musikk og identitet slik en del bandmedlemmer i Tromsø, som representerer ulike sjangere, tenker om dette. Identitet kan handle om klassetilhørighet, etnisitet, geografisk og politisk tilhørighet. Det kan også handle om personlig identitet. Musikk kan være politisk, den kan formidle politisk identitet, og være et redskap innenfor politiske bevegelser for å styrke fellesskapet og formidle viktige budskap. I ulike historiske faser kan musikken være mer eller mindre viklet inn i politiske kamper og motsetninger. Et undertema i dette arbeidet er forholdet til språket, og om norsk språk og dialekt fungerer bedre enn engelsk når man skal skrive og formidle låter. Hvorfor velger noen å bruke norsk, mens andre velger engelsk som uttrykksform, når de skal formidle identitet av forskjellig slag og gi hverdagsskildringer fra lokalmiljøet

Cerebrospinal fluid markers in Creutzfeldt-Jakob disease

<p>Abstract</p> <p>Background</p> <p>The objective was to assess the utility of total tau protein (tTau), the ratio of (tTau)/181 phosphorylated tau protein (P-Tau) and 14-3-3 protein, as diagnostic markers in cerebrospinal fluid (CSF) for Creutzfeldt-Jakob disease (CJD).</p> <p>Methods</p> <p>CSF samples received from Norwegian hospitals between August 2005 and August 2007 were retrospectively selected from consecutive patients with tTau values > 1200 ng/L (n = 38). The samples from patients clinically diagnosed with CJD (n = 12) were compared to those from patients with other degenerative neurological diseases: Alzheimer's/vascular dementia (AD/VaD, n = 21), other neurological diseases (OND, n = 5). Total Tau, P-Tau, and β-Amyloid (Aβ₄₂) were measured with commercial kits. Additionally, 14-3-3 protein was measured semi-quantitatively by immunoblot.</p> <p>Results</p> <p>The minimum cut-off limits for diagnosis of CJD were chosen from the test results. For tTau the lower limit was fixed at 3000 ng/L, for the tTau/P-Tau ratio it was 60, and for 14-3-3 protein it was 0.75 arbitrary units. For tTau and tTau/P-Tau ratio, all but three CJD patients had levels above the minimum, whereas almost all of the other patients were below. For the 14-3-3 protein, two CJD patients were below the minimum and five were above. Only one of the other patients was higher than the limit. The sensitivities, specificities and diagnostic efficiencies were: tTau 75%, 92%, and 87%; tTau/P-Tau 75%, 96%, and 89%; and 14-3-3 protein 80%, 96%, and 91%.</p> <p>Conclusion</p> <p>The results suggest that 14-3-3 protein may be the better marker for CJD, tTau/P-Tau ratio and tTau are also efficient markers, but showed slightly inferior diagnostic properties in this study, with tTau/P-Tau marginally better than tTau.</p

The anatomical landmarks effective in the localisation of the median nerve during orthopaedic procedures

Background: The aim of this study was to create a safe zone for surgeons who perform procedures in the wrist to avoid iatrogenic damage to the median nerve (MN) by identifying anatomical landmarks using ultrasound (USG).Materials and methods: We measured the distances between the MN and two easily identifiable anatomical landmarks at the level of the proximal border of carpal ligament using USG.Results: A total of 57 volunteers (n = 114 upper limbs) were included in this study. Our main findings revealed that the distance from the flexor carpi radialis tendon to MN (FCR-MN) was 7.87 mm (95% confidence interval 7.37–8.37) and the distance from flexor carpi ulnaris tendon to MN (FCU-MN) was 19.09 mm (95% confidence interval 18.51–19.67).Conclusions: The tendons of FCR and FCU are easily identifiable landmarks that can be distinguished using simple palpation. Based on our USG findings, the area around FCR should be carefully navigated to avoid iatrogenic injury to the MN during surgical procedures around the carpal tunnel

Large prospective validation and cultural adaptation of the Polish version of the Swiss Spinal Stenosis Questionnaire for patients with lumbar spinal stenosis

Objective The aim of this prospective cohort study was to translate, validate and perform a cultural adaptation of the Polish version of the Swiss Spinal Stenosis Questionnaire (P-SSSQ), a disease-specific questionnaire for assessing symptom severity, physical function and satisfaction with treatment in patients with lumbar spinal stenosis (LSS). Material and methods Patients were prospectively recruited at two orthopedic centres in Krakow, Poland, between January 2011 – October 2016. During the interview, each patient completed the P-SSSQ, SF-36 Health Survey, and a demographic data questionnaire. After translation, cross-cultural adaptation, and pilot testing, assessment was made of the internal consistency, test–retest reliability, construct validity, and responsiveness of the P-SSSQ subscales. Results Finally, 171 consecutive patients were included in the study. Cronbach’s alpha and ICC values were above 0.8 for all three subscales of the P-SSSQ. The symptom severity domain was highly negatively correlated with physical functioning and bodily pain of SF-36, with Pearson correlation coefficients of -0.68 and -0.63, respectively. The physical function domain was highly negatively correlated with physical functioning (r = -0.62). The satisfaction subscale was also highly negatively correlated with the change in the symptom severity (r = −0.61) and physical function scale (r = −0.65). Conclusions The proposed version of the P-SSSQ showed excellent measurement properties and can be considered validated for use in Polish. It is easy to understand, quick to complete, and the psychometric properties of the original version are maintained

A CLEC16A variant confers risk for juvenile idiopathic arthritis and anti-cyclic citrullinated peptide antibody negative rheumatoid arthritis

Objective Variants in CLEC16A have conferred susceptibility to autoimmune diseases in genome-wide association studies. The present work aimed to investigate the locus' involvements in juvenile idiopathic arthritis (JIA) and further explore the association with rheumatoid arthritis (RA), type 1 diabetes (T1D) and Addison's disease (AD) in the Norwegian population. Methods Three single nucleotide polymorphisms (SNPs) were genotyped in patients with RA (n=809), JIA (n=509), T1D (n=1211) and AD (n=414) and in healthy controls (n=2149). Results All diseases were associated with CLEC16A, but with different SNPs. The intron 22 SNP, rs6498169, was associated with RA (p=0.006) and JIA (p=0.016) and the intron 19 SNPs, rs12708716/rs12917716, with T1D (p=1×10−5) and AD (p=2×10−4). The RA association was confined to the anti-cyclic citrullinated peptide antibody (anti-CCP) negative subgroup (p=2×10−4). Conclusion This is the first report of a CLEC16A association with JIA and a split of the RA association according to anti-CCP status. Different causative variants underlie the rheumatic versus the organ specific diseases

Genome-wide copy number variation (CNV) in patients with autoimmune Addison's disease

<p>Abstract</p> <p>Background</p> <p>Addison's disease (AD) is caused by an autoimmune destruction of the adrenal cortex. The pathogenesis is multi-factorial, involving genetic components and hitherto unknown environmental factors. The aim of the present study was to investigate if gene dosage in the form of copy number variation (CNV) could add to the repertoire of genetic susceptibility to autoimmune AD.</p> <p>Methods</p> <p>A genome-wide study using the Affymetrix GeneChip^®Genome-Wide Human SNP Array 6.0 was conducted in 26 patients with AD. CNVs in selected genes were further investigated in a larger material of patients with autoimmune AD (n = 352) and healthy controls (n = 353) by duplex Taqman real-time polymerase chain reaction assays.</p> <p>Results</p> <p>We found that low copy number of <it>UGT2B28 </it>was significantly more frequent in AD patients compared to controls; conversely high copy number of <it>ADAM3A </it>was associated with AD.</p> <p>Conclusions</p> <p>We have identified two novel CNV associations to <it>ADAM3A </it>and <it>UGT2B28 </it>in AD. The mechanism by which this susceptibility is conferred is at present unclear, but may involve steroid inactivation (<it>UGT2B28</it>) and T cell maturation (<it>ADAM3A</it>). Characterization of these proteins may unravel novel information on the pathogenesis of autoimmunity.</p

Interaction Analysis between HLA-DRB1 Shared Epitope Alleles and MHC Class II Transactivator CIITA Gene with Regard to Risk of Rheumatoid Arthritis

HLA-DRB1 shared epitope (SE) alleles are the strongest genetic determinants for autoantibody positive rheumatoid arthritis (RA). One of the key regulators in expression of HLA class II receptors is MHC class II transactivator (CIITA). A variant of the CIITA gene has been found to associate with inflammatory diseases

Karyotypic polymorphism of the zebra finch Z chromosome

We describe a karyotypic polymorphism on the zebra finch Z chromosome. This polymorphism was discovered because of a difference in the position of the centromere and because it occurs at varying frequencies in domesticated colonies in the USA and Germany and among two zebra finch subspecies. Using DNA fluorescent in situ hybridization to map specific Z genes and measurements of DNA replication, we show that this polymorphism is the result of a large pericentric inversion involving the majority of the chromosome. We sequenced a likely breakpoint for the inversion and found many repetitive sequences. Around the breakpoint, there are numerous repetitive sequences and several copies of PAK3 (p21-activated kinase 3)-related sequences (PAK3Z) which showed testes-specific expression by RT-PCR. Our findings further suggest that the sequenced genome of the zebra finch may be derived from a male heterozygote for the Z chromosome polymorphism. This finding, in combination with regional differences in the frequency of the polymorphism, has important consequences for future studies using zebra finches