Gjenreisningsbyen Bodø. Ein omstridt byplan sosialdemokratiet gjorde til sin

Dette er publiserte versjonen av artikkelen Aas, S. (2015). Gjenreisningsbyen Bodø. Ein omstridt byplan sosialdemokratiet gjorde til sin. Årbok / Fortidsminneforeningen: Brann og bypanlegging, 165-184. http://www.fortidsminneforeningen.no/ny/fortidsminneforeningens-arbo

Finst det byar i Nord-Noreg?

Finst det byar i Nord-Noreg? Finst det byar i Nord-Noreg?Steinar AasDet var spørsmålet Einar-Arne Drivenes ville ha meg til å svare på. Spørsmålet vart også stilt i Nord-Norsk kulturhistorie på byrjinga av 1990-talet, og den gong svarte Astri Andresen på det, med å svare som i dag; - Ja, det finst byar i Nord-Noreg. Så då skulle vel oppdraget vere utført. Men det er sjølvsagt forventa meir av ein som har arbeidd med nordnorsk byhistorie. Eg skal derfor bruke mine 20 minutt tilmålte tid og reise nokre moment som skulle vore drøfta når vi behandlar eit slikt tema.For temaet kjem ikkje ut av ingenting. Byane nordpå er truleg meir perifere, spreidde og mindre enn mange andre stader i landet, noko som sjølvsagt gjør at landsdelens byar har eit mindre omland og kanskje ein meir smålåten framtoning enn mange andre stader i landet vårt. Ikkje minst har dei utvikla seg på eit seinare stadium enn sørpå. Har denne særeigne regionale urbaniseringa så noka å seie for dagens regionale utfordringar, er eit viktig spørsmål.Finst det byar i Nord-Noreg?publishedVersio

Gjenreisningsbyen Bodø. Ein omstridt byplan sosialdemokratiet gjorde til sin

Dette er publiserte versjonen av artikkelen Aas, S. (2015). Gjenreisningsbyen Bodø. Ein omstridt byplan sosialdemokratiet gjorde til sin. Årbok / Fortidsminneforeningen: Brann og bypanlegging, 165-184. http://www.fortidsminneforeningen.no/ny/fortidsminneforeningens-arbo

Johan Medby – From the Sulitjelma affair to Lillestrøm

publishedVersio

Patterns of childhood adverse events are associated with clinical characteristics of bipolar disorder

Background Previous studies in bipolar disorder investigating childhood trauma and clinical presentations of the illness have mainly focused on physical and sexual abuse. Our aim was to explore further the relationship between childhood trauma and disease characteristics in bipolar disorder to determine which clinical characteristics were most strongly associated with childhood trauma total score, as well as subtypes of adverse childhood events, including physical, sexual, emotional abuse and neglect. Methods 141 Patients with bipolar disorder were consecutively recruited, and disease history and clinical characteristics were assessed. History of childhood abuse was obtained using the Childhood Trauma Questionnaire (CTQ). Statistical methods used were factor analysis, Poisson and linear regression, and generalized additive modeling (GAM). Results The factor analysis of CTQ identified three factors: emotional abuse/neglect, sexual abuse and physical abuse. There were significant associations between CTQ total score and earlier onset of illness, reduced level of psychosocial functioning (GAF; Global Assessment of Functioning) and decreased number of hospitalization, which mainly were due to the factor emotional abuse/neglect. Physical abuse was significantly associated with lower GAF scores, and increased number of mood episodes, as well as self-harm. Sexual abuse was significantly associated with increased number of mood episodes. For mood episodes and self-harm the associations were characterized by great variance and fluctuations. Conclusions Our results suggest that childhood trauma is associated with a more severe course of bipolar illness. Further, childhood abuse (physical and sexual), as well as emotional abuse and neglect were significantly associated with accelerating staging process of bipolar disorder. By using specific trauma factors (physical abuse, sexual abuse and emotional abuse/neglect) the associations become both more precise, and diverse

Predictive and Prognostic Impact of TP53 Mutations and MDM2 Promoter Genotype in Primary Breast Cancer Patients Treated with Epirubicin or Paclitaxel

Background: TP53 mutations have been associated with resistance to anthracyclines but not to taxanes in breast cancer patients. The MDM2 promoter single nucleotide polymorphism (SNP) T309G increases MDM2 activity and may reduce wildtype p53 protein activity. Here, we explored the predictive and prognostic value of TP53 and CHEK2 mutation status together with MDM2 SNP309 genotype in stage III breast cancer patients receiving paclitaxel or epirubicin monotherapy. Experimental Design: Each patient was randomly assigned to treatment with epirubicin 90 mg/m2 (n= 109) or paclitaxel 200 mg/m2 (n = 114) every 3rd week as monotherapy for 4–6 cycles. Patients obtaining a suboptimal response on first-line treatment requiring further chemotherapy received the opposite regimen. Time from last patient inclusion to follow-up censoring was 69 months. Each patient had snap-frozen tumor tissue specimens collected prior to commencing chemotherapy. Principal Findings: While TP53 and CHEK2 mutations predicted resistance to epirubicin, MDM2 status did not. Neither TP53/ CHEK2 mutations nor MDM2 status was associated with paclitaxel response. Remarkably, TP53 mutations (p = 0.007) but also MDM2 309TG/GG genotype status (p = 0.012) were associated with a poor disease-specific survival among patients having paclitaxel but not patients having epirubicin first-line. The effect of MDM2 status was observed among individuals harbouring wild-type TP53 (p = 0.039) but not among individuals with TP53 mutated tumors (p.0.5). Conclusion: TP53 and CHEK2 mutations were associated with lack of response to epirubicin monotherapy. In contrast, TP53 mutations and MDM2 309G allele status conferred poor disease-specific survival among patients treated with primary paclitaxel but not epirubicin monotherapy

Olaparib monotherapy as primary treatment in unselected triple negative breast cancer

Background - The antitumor efficacy of PARP inhibitors (PARPi) for breast cancer patients harboring germline BRCA1/2 (gBRCA1/2) mutations is well established. While PARPi monotherapy was ineffective in patients with metastatic triple negative breast cancer (TNBC) wild type for BRCA1/2, we hypothesized that PARPi may be effective in primary TNBCs without previous chemotherapy exposure. Patients and methods - In the phase II PETREMAC trial, patients with primary TNBC >2 cm received olaparib for up to 10 weeks before chemotherapy. Tumor biopsies collected before and after olaparib underwent targeted DNA sequencing (360 genes) and BRCA1 methylation analyses. In addition, BRCAness (multiplex ligation-dependent probe amplification), PAM50 gene expression, RAD51 foci, tumor-infiltrating lymphocytes (TILs) and PD-L1 analyses were performed on pretreatment samples. Results - The median pretreatment tumor diameter was 60 mm (range 25-112 mm). Eighteen out of 32 patients obtained an objective response (OR) to olaparib (56.3%). Somatic or germline mutations affecting homologous recombination (HR) were observed in 10/18 responders [OR 55.6%, 95% confidence interval (CI) 33.7-75.4] contrasting 1/14 non-responders (OR 7.1%; CI 1.3-31.5, P = 0.008). Among tumors without HR mutations, 6/8 responders versus 3/13 non-responders revealed BRCA1 hypermethylation (P = 0.03). Thus, 16/18 responders (88.9%, CI 67.2-96.9), in contrast to 4/14 non-responders (28.6%, CI 11.7-54.7, P = 0.0008), carried HR mutations and/or BRCA1 methylation. Excluding one gPALB2 and four gBRCA1/2 mutation carriers, 12/14 responders (85.7%, CI 60.1-96.0) versus 3/13 non-responders (23.1%, CI 8.2-50.3, P = 0.002) carried somatic HR mutations and/or BRCA1 methylation. In contrast to BRCAness signature or basal-like subtype, low RAD51 scores, high TIL or high PD-L1 expression all correlated to olaparib response. Conclusion - Olaparib yielded a high clinical response rate in treatment-naïve TNBCs revealing HR deficiency, beyond germline HR mutations