396 research outputs found
Clinical impact of B-cell depletion with the anti-CD20 antibody rituximab in chronic fatigue syndrome: a preliminary case series
Bygningsinterne luftlekkasjer
Byggteknisk forskrift stiller i dag kun krav til lufttettheten til bygningers klimaskjerm og bygningsinterne luftlekkasjer blir dermed neglisjert. I denne oppgaven undersøkes hvilke konsekvenser bygningsinterne luftlekkasjer har og hvorvidt det bør stilles krav til disse luftlekkasjene. Det blir også undersøkt ulike utfordringer man møter på når man skal dokumentere lufttetthet der bygningsinterne luftlekkasjer inngår.
Gjennom syv intervjuer med personer som har erfaring med lufttetthet fra sitt arbeid konkluderer oppgaven med at konsekvensene av bygningsinterne luftlekkasjer er så alvorlige at de ikke bør ignoreres i forskriftene.
Lufttetthetsmålinger på to case-prosjekter er blitt gjennomført; et laboratorium på NMBU og en boligblokk i Finstad Park i Ski. På laboratoriet ble endeseksjonens lufttetthet målt ved hjelp av støttetrykksmålinger og målingene viser at laboratoriet er svært utett. I Finstad Park ble samtlige 14 leiligheter i en oppgang trykktestet og ni interne leilighetsskillende veggers lufttetthet ble målt ved bruk av støttetrykksmålinger. I tillegg ble hele oppgangen trykktestet.
Eksemplifisert gjennom disse case-prosjektene tar denne oppgaven for seg ulike utfordringer knyttet til gjennomføring og dokumentasjon ved delmåling av lufttetthet. En stor utfordring ved en slik dokumentering er å få målt et utvalg som er representativt for bygningen. Gjennom resultater fra case-prosjektet i Finstad Park presenterer oppgaven hvordan utvalget man gjør kan påvirke måleresultatene. En konkretisering av utvalgskriterier som ikke åpner for like stor grad av tolkning vil kunne hindre både forsøk på og spekulasjoner om manipulasjon av måleresultater. En av erfaringene fra arbeidet med case-prosjektene er at støttetrykksmålinger er en egnet metode for kvantifisering av bygningsinterne luftlekkasjer, men så ressurskrevende at det i praksis ikke er fornuftig å benytte til dokumentasjon av forskriftskrav. Ved å stille samme krav til interne overflater som til klimaskjermen, kan man gjennomføre delmålinger uten støttetrykk der man likevel tar hensyn til de interne luftlekkasjene. Ved bruk av en slik metode vil ikke dagens normaliseringsmetode av lekkasjeluftmengdene være tilstrekkelig og kravene bør bli evaluert der det tas hensyn til overflateareal-volum-forholdet i området som testes.
Norway’s regulation of buildings has the same requirements for energy performance in buildings as the EU implementation by Energy Performance of Buildings Directive of 2010, despite Norway not being a member of EU. In the EPBD, airtightness requirements are set only for airtightness of the building envelope, not internal building leakages, and therefore internal leakages are ignored. This thesis examines which consequences internal building air leakages have and whether the Norwegian building regulation should set requirements for these air leakages. The European standard EN ISO 13829 allows separate measurements on individual parts of the building, which is necessary when documenting internal air leakages. The separate measurement method raises a series of challenges linked to interpretation of the results, which is presented in this thesis.
By conducting seven interviews with persons experienced in the field of airtightness, the thesis states that the consequences of the internal air leakages may be so severe that it should not be ignored by the building regulation.
Airtightness measurements have been conducted in two case projects; a laboratory on the University of Life Sciences (NMBU) and an apartment building in Finstad Park, Ski. The laboratory’s end section’s airtightness was measured, as well as the airtightness of the adjoining wall between two laboratories by inducing pressure in the adjoining section. The result shows significant air leakages both out of the building envelope and through to the adjoining section. In Finstad Park, the airtightness was measured separately for 14 apartments connecting to the same common area and for the whole common area combined with all the apartments. The adjoining walls between the apartments on the same floor were also measured by inducing pressure in one of the adjoining apartments at a time.
These case projects exemplify different challenges encountered when conducting and documenting partial measurements. One of the challenges by doing separate individual measurements is finding an appropriate sampling method that is representative for the whole building. Chapter 4 presents how different sampling methods can affect the end result of separate measurements. By making a more specific sampling method one could reduce the interpretation of the standard and decrease variation in the end results.
The case projects has led to the conclusion that doing measurements with pressure in adjoining spaces is an optimal method of quantifying building internal leakages, but because of practical limitations it is not an appropriate way of documenting. By setting the same requirements for internal surfaces as for surfaces in the building envelope it enables the possibility of doing partial measurements without pressurizing the adjoining spaces and still acknowledging the internal air leakages. In the context of such a method, the air change rate n50 does not attain enough information about the surface’s quality and therefore such requirements should be evaluated in relation to the surface-area-to-volume ratio
Storms, insurance, and climate change - An exploratory study of property damage, compensation, and climate adaptation
This thesis is structured around four research questions that explore different aspects of storms
and how they affect the insurance sector. Due to climate change, extreme weather events, such as
storms, are expected to occur more frequently and more intensely than before. This is quite
costly in terms of compensation payouts for the insurance companies.
The purpose of this thesis is to provide insight into the occurrence of storms, to what extent they
cause damage, at what speeds they cause damage, and evaluate to what extent the insurance
sector is able to incorporate this increased climate risk in their policies.
Data from the Norwegian Natural Perils Pool and SSB have been used to explore which counties
in Norway that have been hardest affected by storm-related damages over the years. As they vary
considerably in size, the number of damages per building has been included to neutralize the
importance of the area of a county and determine which areas that have been most affected by
winds per building. Furthermore, data on wind measurements from different weather stations has
been downloaded from the Norwegian Meteorological Institute and compared to the damage
observations to determine what wind speeds that cause damage. At last, the non-life insurance
contribution criteria from the EU Taxonomy have been validated against the current operation of
the Norwegian Natural Perils Pool to identify the most apparent weaknesses of the scheme from
a climate perspective.
To answer the research questions, we have assessed a considerable amount of literature and
discussed it in light of the observations from our data. Regarding the probability of wind damage
for different wind strengths, we have used a practical approach and modeled the results in R.
In sum, the research has shown that the occurrence of storms is highly challenging to predict but
that certain areas are more prone to storms than others due to various climatic conditions.
Despite the complexity, simple methods have often provided high accuracy and relatively good
predictions on the wind strengths that cause damage. Nevertheless, the increased climate risk
seems hard to incorporate into the insurance sector due to large uncertainties.nhhma
Storms, insurance, and climate change - An exploratory study of property damage, compensation, and climate adaptation
This thesis is structured around four research questions that explore different aspects of storms
and how they affect the insurance sector. Due to climate change, extreme weather events, such as
storms, are expected to occur more frequently and more intensely than before. This is quite
costly in terms of compensation payouts for the insurance companies.
The purpose of this thesis is to provide insight into the occurrence of storms, to what extent they
cause damage, at what speeds they cause damage, and evaluate to what extent the insurance
sector is able to incorporate this increased climate risk in their policies.
Data from the Norwegian Natural Perils Pool and SSB have been used to explore which counties
in Norway that have been hardest affected by storm-related damages over the years. As they vary
considerably in size, the number of damages per building has been included to neutralize the
importance of the area of a county and determine which areas that have been most affected by
winds per building. Furthermore, data on wind measurements from different weather stations has
been downloaded from the Norwegian Meteorological Institute and compared to the damage
observations to determine what wind speeds that cause damage. At last, the non-life insurance
contribution criteria from the EU Taxonomy have been validated against the current operation of
the Norwegian Natural Perils Pool to identify the most apparent weaknesses of the scheme from
a climate perspective.
To answer the research questions, we have assessed a considerable amount of literature and
discussed it in light of the observations from our data. Regarding the probability of wind damage
for different wind strengths, we have used a practical approach and modeled the results in R.
In sum, the research has shown that the occurrence of storms is highly challenging to predict but
that certain areas are more prone to storms than others due to various climatic conditions.
Despite the complexity, simple methods have often provided high accuracy and relatively good
predictions on the wind strengths that cause damage. Nevertheless, the increased climate risk
seems hard to incorporate into the insurance sector due to large uncertainties.nhhma
Treatment approach and survival from glioblastoma: results from a population-based retrospective cohort study from Western Norway
Objectives
To evaluate treatment and survival from glioblastoma in a real-world setting.
Design and settings
A population-based retrospective cohort study from Western Norway.
Participants
363 patients aged 18 years or older diagnosed with glioblastoma between 1 January 2007 and 31 December 2014.
Primary and secondary outcome measures
Overall survival and survival rates determined by Kaplan-Meier method, groups compared by log-rank test. Associations between clinical characteristics and treatment approach assessed by logistic regression. Associations between treatment approach and outcome analysed by Cox regression.
Results
Median overall survival was 10.2 months (95% CI 9.1 to 11.3). Resection was performed in 221 patients (60.9%), and was inversely associated with age over 70 years, higher comorbidity burden, deep-seated tumour localisation and multifocality. Median survival was 13.7 months (95% CI 12.1 to 15.4) in patients undergoing tumour resection, 8.3 months (95% CI 6.6 to 9.9) in patients undergoing biopsy and 4.5 months (95% CI 4.0 to 5.1) in patients where no surgical intervention was performed. Chemoradiotherapy according to the Stupp protocol was given to 157 patients (43%). Age over 70 years, higher comorbidity burden and cognitive impairment were associated with less intensive chemoradiotherapy. Median survival was 16.3 months (95% CI 14.1 to 18.5), 7.9 months (95% CI 6.7 to 9.0) and 2.0 months (95% CI 0.9 to 3.2) in patients treated according to the Stupp protocol, with less intensive chemoradiotherapy and with best supportive care, respectively. Surgical resection (HR 0.61 (95% CI 0.47 to 0.79)) and chemoradiotherapy according to the Stupp protocol (HR 0.09 (95% CI 0.06 to 0.15)) were strongly associated with favourable overall survival, when adjusted for clinical variables.
Conclusions
In a real-world setting, less than half of the patients received full-course chemoradiotherapy, with a median survival comparable to results from clinical trials. Survival was considerably worse in patients receiving less intensive treatment. Our results point out a substantial risk of undertreating glioblastoma, especially in elderly patients.publishedVersio
Anti-neutrophil cytoplasmatic antibodies and lung disease in cystic fibrosis
AbstractBackground: Bactericidal-permeability-increasing protein (BPI) is a potent anti-microbial protein produced by neutrophil granulocytes. Anti-neutrophil cytoplasmatic antibodies (ANCA) directed against BPI have been detected in up to 91% in patients with cystic fibrosis (CF). We aimed to evaluate the prevalence of BPI-ANCA in our CF patients and to determine whether presence of BPI-ANCA is correlated with organ damage. Methods: Twenty-four patients performed respiratory function testing and pulmonary high-resolution computed tomography (HRCT). HRCT was scored by using a modified Bhalla method. Serum samples were analysed by direct binding enzyme-linked immunosorbent assay for BPI-ANCA. Results: The prevalence of anti-BPI-IgG was 71% and anti-BPI-IgA 33%. Twenty-nine percent of our patients were positive for both BPI-ANCA isotypes. Mean HRCT score was 8.0 ranging from 0 to 22, bronchiectasis presented the most common finding (79%). There was a significant correlation between BPI-ANCA and both HRCT score and FEV1 (p<0.01). High levels of BPI-ANCA were correlated to chronic Pseudomonas aeruginosa lung infection (p<0.01). Conclusions: BPI-ANCA was common in our study group. Highly significant correlations between BPI-ANCA and parameters to evaluate lung disease in CF may be a consequence of the inflammation process, or it may indicate a pathogenic role of BPI-ANCA levels in the development of lung disease. More research is needed and the clinical significance of our findings needs further evaluation
Inverse correlation between PDGFC expression and lymphocyte infiltration in human papillary thyroid carcinoma
Background: Members of the PDGF family have been suggested as potential biomarkers for papillary thyroid carcinomas (PTC). However, it is known that both expression and stimulatory effect of PDGF ligands can be affected by inflammatory cytokines. We have performed a microarray study in a collection of PTCs, of which about half the biopsies contained tumour-infiltrating lymphocytes or thyroiditis. To investigate the expression level of PDGF ligands and receptors in PTC we measured the relative mRNA expression of all members of the PDGF family by qRT-PCR in 10 classical PTC, eight clinically aggressive PTC, and five non-neoplastic thyroid specimens, and integrated qRT-PCR data with microarray data to enable us to link PDGF-associated gene expression profiles into networks based on recognized interactions. Finally, we investigated potential influence on PDGF mRNA levels by the presence of tumour-infiltrating lymphocytes. Methods: qRT-PCR was performed on PDGFA, PDGFB, PDGFC, PDGFD, PDGFRA PDGFRB and a selection of lymphocyte specific mRNA transcripts. Semiquantitative assessment of tumourinfiltrating lymphocytes was performed on the adjacent part of the biopsy used for RNA extraction for all biopsies, while direct quantitation by qRT-PCR of lymphocyte-specific mRNA transcripts were performed on RNA also subjected to expression analysis. Relative expression values of PDGF family members were combined with a cDNA microarray dataset and analyzed based on clinical findings and PDGF expression patterns. Ingenuity Pathway Analysis (IPA) was used to elucidate potential molecular interactions and networks. Results: PDGF family members were differentially regulated at the mRNA level in PTC as compared to normal thyroid specimens. Expression of PDGFA (p = 0.003), PDGFB (p = 0.01) and PDGFC (p = 0.006) were significantly up-regulated in PTCs compared to non-neoplastic thyroid tissue. In addition, expression of PDGFC was significantly up-regulated in classical PTCs as compared to clinically aggressive PTCs (p = 0.006), and PDGFRB were significantly up-regulated in clinically aggressive PTCs (p = 0.01) as compared to non-neoplastic tissue. Semiquantitative assessment of lymphocytes correlated well with quantitation of lymphocyte-specific gene expression. Further more, by combining TaqMan and microarray data we found a strong inverse correlation between PDGFC expression and the expression of lymphocyte specific mRNAs. Conclusion: At the mRNA level, several members of the PDGF family are differentially expressed in PTCs as compared to normal thyroid tissue. Of these, only the PDGFC mRNA expression level initially seemed to distinguish classical PTCs from the more aggressive PTCs. However, further investigation showed that PDGFC expression level correlated inversely to the expression of several lymphocyte specific genes, and to the presence of lymphocytes in the biopsies. Thus, we find that PDGFC mRNA expression were down-regulated in biopsies containing infiltrated lymphocytes or thyroiditis. No other PDGF family member could be linked to lymphocyte specific gene expression in our collection of PTCs biopsies
Endothelial dysfunction in ME/CFS patients
Objective: A few earlier studies have found impaired endothelial function in patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). The present study investigated large-vessel and small-vessel endothelial function in patients with ME/CFS.
Study design: The study was a substudy of the RituxME trial, a national, multicenter, randomized, double-blind, placebo-controlled phase III study on the effect of rituximab vs. placebo in ME/CFS patients in Norway. Flow-mediated dilation (FMD) and post-occlusive reactive hyperemia (PORH) was measured at baseline and after 18 months of treatment in 39 patients and compared with healthy controls. Other outcome measures were symptom severity and various physical function measures.
Results: ME/CFS patients had markedly reduced FMD compared to healthy controls at baseline (5.1% vs. 8.2%, p< 0.0001, adjusted for arterial diameter and sex), and significantly lower microvascular regulation measured by PORH than healthy controls (1354 PU vs. 2208 PU, p = 0.002). There were no differences between the treatment and placebo groups in symptom changes or vascular measures. As a group, the ME/CSF patients experienced a slight, but significant improvement in clinical symptoms after 18 months. PORH, but not FMD, was similarly improved (1360 to 1834 PU, p = 0.028). There was no significant correlation between FMD and PORH. There were non-significant tendencies towards associations between symptom severity/physical function measures and lower FMD and PORH, and a significant correlation between PORH and steps per 24 hours at baseline.
Conclusions: ME/CFS patients had reduced macro- and microvascular endothelial function, indicating that vascular homeostasis may play a role in the clinical presentation of this disease.publishedVersio
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