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Search Results: 1 - 10 of 818 matches for " Morten Vatn "
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Improvement in Stress, General Self-Efficacy, and Health Related Quality of Life following Patient Education for Patients with Neuroendocrine Tumors: A Pilot Study
Trude Haugland,Marijke Veenstra,Morten H. Vatn,Astrid K. Wahl
Nursing Research and Practice , 2013, DOI: 10.1155/2013/695820
Abstract: The purpose of the study was to evaluate changes in general self-efficacy, health related quality of life (HRQoL), and stress among patients with neuroendocrine tumors (NET) following a multidisciplinary educational intervention. Forty-one patients were enrolled in this exploratory pilot study. A total of 37 patients completed the full 26-week intervention based on the principles of self-efficacy. General self-efficacy was measured by the General Self-Efficacy Scale, HRQoL was measured with the SF-36, and stress was measured with the Impact of Event Scale. Mixed effect models were used to evaluate changes in general self-efficacy, mental and physical components of HRQoL, and stress adjusting for demographic and clinical variables. Results showed significant improvements in patients’ general self-efficacy ( = 0.71; ), physical component scores of HRQoL ( = 3.09; ), and stress ( , ). Findings suggest that patients with NET have the capacity to improve their ability to cope with their disease, problem-solve, improve their physical status, and reduce their stress following an educational intervention based on the principles of self-efficacy. These preliminary data provide a basis for future randomized controlled trials to test interventions to improve HRQoL for patients with NET. 1. Introduction The incidence of the relatively slow growing and rare types of neuroendocrine tumors (NET) is 5.3/100,000, and the prevalence is 35/100,000 [1]. Neuroendocrine cells are distributed widely throughout the body, including the nervous and endocrine systems. Neuroendocrine tumors produce and secrete regulatory hormones, giving rise to symptoms including fatigue, flushing, diarrhea, food intolerance, restlessness, dyspnea, fluctuations in mood [2], and pain [3]. Symptoms vary widely and may occur late in the course of the disease, depending on the type of hormone affected and the rate of secretion and localization, thus making diagnosis challenging. In the majority of cases, a definitive diagnosis is not made until after the tumor has metastasized [4]. Thus, NET represents a clinical challenge in diagnosis, treatment, and care. Palliative treatment includes biological agents, such as somatostatin analogues, interferon, and embolization of liver metastases, and frequently gives rise to side effects that may be similar to the symptoms of NET [5, 6]. Stress is a common reaction to cancer [7–11] and may influence patients’ adaptation to the disease [5]. Consequently, stress can have a sustained impact on patients’ ability to function, which in turn may increase the risk of
Fatty Acids in Habitual Diet, Plasma Phospholipids, and Tumour and Normal Colonic Biopsies in Young Colorectal Cancer Patients
Paula Berstad,Espen Thiis-Evensen,Morten H. Vatn,Kari Almendingen
Journal of Oncology , 2012, DOI: 10.1155/2012/254801
Abstract:
Fatty Acids in Habitual Diet, Plasma Phospholipids, and Tumour and Normal Colonic Biopsies in Young Colorectal Cancer Patients
Paula Berstad,Espen Thiis-Evensen,Morten H. Vatn,Kari Almendingen
Journal of Oncology , 2012, DOI: 10.1155/2012/254801
Abstract: Fatty acid metabolism is altered in colorectal cancer (CRC). We aimed to investigate incorporation of dietary -6 and -3 polyunsaturated fatty acids (PUFAs) into plasma phospholipids (PLs), tumour tissue, and normal mucosa in young CRC patients. We also aimed to study differences in PUFA composition between tumour and normal mucosa, and PUFA status associated with cancer stage. Sixty-five CRC patients younger than 55 years were included in a multicenter study. We assessed dietary fatty acid composition by food-frequency questionnaire. Fatty acid composition in plasma PL ( ) and tumour and normal colonic biopsies ( ) were analysed by gas chromatography. We observed a significant correlation for docosahexaenoic acid (DHA) between dietary intake and concentration in plasma PL (weight%) ( ; ), but not for any -6 PUFA. Tissue concentrations of arachidonic acid, eicosapentaenoic acid, and DHA (weight%) were 1.7–2.5 times higher in tumour than normal mucosa ( ). Concentrations of -3 and -6 PUFA in plasma PL and tissues were not related to Duke's stage, although patients with more severe cancer stage reported higher intake of -3 PUFA. In conclusion, we found accumulation of the long-chained -3 and -6 PUFA in tumour tissue in young CRC patients. 1. Introduction The association between dietary fat and risk of cancer has been extensively investigated, and the composition of polyunsaturated fatty acids (PUFA) in diet seems to be of particular importance [1]. However, the effects of single dietary -3 and -6 PUFA, and the ratio -3/ -6 PUFA are not completely clear. The majority of case-control studies seem to support a protective role of dietary -3 PUFA and -3/ -6 PUFA ratio [2–4], but these associations have been confirmed by only one cohort study [5], and have been contradicted or not found by several cohort studies [6–8]. Studies on serum and erythrocyte membrane fatty acid composition, regarded as biomarkers for fatty acid intake, mainly support a protective role for the very long-chained -3 PUFA docosahexaenoic acid (DHA) [8–11]. Abnormalities in plasma PUFA composition may also be interpreted as metabolic changes in CRC patients [12]. Dietary and biomarker studies have not established the role of -6 PUFA in CRC. Based on changes in -3 and -6 PUFA expression in colorectal tumours, compared to normal mucosal tissue [13, 14], also found at early stages of adenomas [13], it seems obvious that patients with CRC have an altered PUFA metabolism. Literature on CRC tumour PUFA pattern is sparse, and previous studies have not concluded on which particular PUFAs are
Dominant Fecal Microbiota in Newly Diagnosed Untreated Inflammatory Bowel Disease Patients
Lill Therese Thorkildsen,Felix Chinweije Nwosu,Ekaterina Avershina,Petr Ricanek,G?ri Perminow,Stephan Brackmann,Morten H. Vatn,Knut Rudi
Gastroenterology Research and Practice , 2013, DOI: 10.1155/2013/636785
Abstract: Our knowledge about the microbiota associated with the onset of IBD is limited. The aim of our study was to investigate the correlation between IBD and the fecal microbiota for early diagnosed untreated patients. The fecal samples used were a part of the Inflammatory Bowel South-Eastern Norway II (IBSEN II) study and were collected from CD patients ( ), UC patients ( ), unclassified IBD (IBDU) patients ( ), and from a control group ( ). The bacteria associated with the fecal samples were analyzed using a direct 16S?rRNA gene-sequencing approach combined with a multivariate curve resolution (MCR) analysis. In addition, a 16S?rRNA gene clone library was prepared for the construction of bacteria-specific gene-targeted single nucleotide primer extension (SNuPE) probes. The MCR analysis resulted in the recovery of five pure components of the dominant bacteria present: Escherichia/Shigella, Faecalibacterium, Bacteroides, and two components of unclassified Clostridiales. Escherichia/Shigella was found to be significantly increased in CD patients compared to control subjects, and Faecalibacterium was found to be significantly reduced in CD patients compared to both UC patients and control subjects. Furthermore, a SNuPE probe specific for Escherichia/Shigella showed a significant overrepresentation of Escherichia/Shigella in CD patients compared to control subjects. In conclusion, samples from CD patients exhibited an increase in Escherichia/Shigella and a decrease in Faecalibacterium indicating that the onset of the disease is associated with an increase in proinflammatory and a decrease in anti-inflammatory bacteria. 1. Introduction The gut microbiota has the potential to exert both pro- and anti-inflammatory responses [1–3]. The gut microbiota is also supposed to be an epigenetic factor modifying the pathogenesis of extraintestinal disorders, including type I diabetes [4], obesity [5], atopic disorders such as asthma and eczema [6], and a contributing factor in the pathogenesis of inflammatory bowels disease (IBD) [7]. Knowledge of the composition of the intestinal microbiota, therefore, is vital to our understanding of which groups of bacteria are of importance in maintaining gut health or promoting disease. The two major forms of IBD are ulcerative colitis (UC) and Crohn’s disease (CD) [8, 9]. The etiology of IBD is complex and the causes are not yet fully understood. The pathogenesis of IBD involves interactions between the intestinal microbiota, the immune system, and epithelial cells. In addition, genetic and environmental factors modify this interplay
Fit, Interplay, and Scale: A Diagnosis
Arild Vatn,Paul Vedeld
Ecology and Society , 2012, DOI: 10.5751/es-05022-170412
Abstract: Developing institutions to handle human-environment interactions well is important. In relation to that, the theory of resource regimes, and the themes of fit, interplay, and scale--as originating not least in the work of Oran Young--are core. His work is very impressive. At the same time we observe two sets of issues where we think further development is needed. The first relates to the ontological underpinning of Young's conceptual framework. The second set of issues concerns the definitions of and the relationships between the concepts of fit, interplay, and scale. Regarding the former, we emphasize issues related to "marrying" different theories about human action. Regarding the latter, we note that while the three concepts have a lot of practical appeal, there are still some important challenges surfacing, not least when using them in empirical research. We analyze three challenges: the definitions of the concepts; their internal overlap; and finally, the way environmental regimes are defined and understood as opposed to the wider institutional context of the economy. Our paper offers some direction for how to move forward on the issues specified.
Distinct high resolution genome profiles of early onset and late onset colorectal cancer integrated with gene expression data identify candidate susceptibility loci
Marianne Berg, Trude H ?gesen, Espen Thiis-Evensen, [the INFAC-study group], Marianne A Merok, Manuel R Teixeira, Morten H Vatn, Arild Nesbakken, Rolf I Skotheim, Ragnhild A Lothe
Molecular Cancer , 2010, DOI: 10.1186/1476-4598-9-100
Abstract: The total fraction of the genome with aberrant copy number, the overall genomic profile and the TP53 mutation spectrum were similar between the two age groups. However, both the number of chromosomal aberrations and the number of breakpoints differed significantly between the groups. Gains of 2q35, 10q21.3-22.1, 10q22.3 and 19q13.2-13.31 and losses from 1p31.3, 1q21.1, 2q21.2, 4p16.1-q28.3, 10p11.1 and 19p12, positions that in total contain more than 500 genes, were found significantly more often in the early onset group as compared to the late onset group. Integration analysis revealed a covariation of DNA copy number at these sites and mRNA expression for 107 of the genes. Seven of these genes, CLC, EIF4E, LTBP4, PLA2G12A, PPAT, RG9MTD2, and ZNF574, had significantly different mRNA expression comparing median expression levels across the transcriptome between the two groups.Ten genomic loci, containing more than 500 protein coding genes, are identified as more often altered in tumors from early onset versus late onset CRC. Integration of genome and transcriptome data identifies seven novel candidate genes with the potential to identify an increased risk for CRC.Less than five percent of all patients diagnosed with colorectal cancers (CRC) carry known genetic germline alterations that predispose to the disease [1]. However, it has been estimated that up to 30% of all CRC patients may carry a genetic risk as suggested by young age at onset, multiple tumors in the same patient, and an excess of individuals with CRC within a family [2,3]. Many studies have tried to identify some of these genetic risk factors, and several recent genome-wide association studies (GWAS) have pinpointed SNP loci on chromosome arms 8q, 10p, 11q, 14q, 15q, 16q, 18q, 19q, and 20p to be associated with CRC [4-10]. Furthermore, a study by Mourra et al. [11] showed that microsatellite loci within chromosome arm 14q, known to be deleted in about 30% of all colorectal cancers, were more frequently
Gene methylation profiles of normal mucosa, and benign and malignant colorectal tumors identify early onset markers
Terje Ahlquist, Guro E Lind, Vera L Costa, Gunn I Meling, Morten Vatn, Geir S Hoff, Torleiv O Rognum, Rolf I Skotheim, Espen Thiis-Evensen, Ragnhild A Lothe
Molecular Cancer , 2008, DOI: 10.1186/1476-4598-7-94
Abstract: The methylation status of eleven genes (ADAMTS1, CDKN2A, CRABP1, HOXA9, MAL, MGMT, MLH1, NR3C1, PTEN, RUNX3, and SCGB3A1) was determined in 154 tissue samples including normal mucosa, adenomas, and carcinomas of the colorectum. The gene-specific and widespread methylation status among the carcinomas was related to patient gender and age, and microsatellite instability status. Possible CIMP tumors were identified by comparing the methylation profile with microsatellite instability (MSI), BRAF-, KRAS-, and TP53 mutation status.The mean number of methylated genes per sample was 0.4 in normal colon mucosa from tumor-free individuals, 1.2 in mucosa from cancerous bowels, 2.2 in adenomas, and 3.9 in carcinomas. Widespread methylation was found in both adenomas and carcinomas. The promoters of ADAMTS1, MAL, and MGMT were frequently methylated in benign samples as well as in malignant tumors, independent of microsatellite instability. In contrast, normal mucosa samples taken from bowels without tumor were rarely methylated for the same genes. Hypermethylated CRABP1, MLH1, NR3C1, RUNX3, and SCGB3A1 were shown to be identifiers of carcinomas with microsatellite instability. In agreement with the CIMP concept, MSI and mutated BRAF were associated with samples harboring hypermethylation of several target genes.Methylated ADAMTS1, MGMT, and MAL are suitable as markers for early tumor detection.Most cases of colorectal cancer (CRC) originate from adenomas. The malignant potential of adenomas increases with size, grade of dysplasia, and degree of villous components,[1] along with the number and order of genetic and epigenetic aberrations.[2] The majority (~85%) of the sporadic carcinomas are characterized by chromosomal aberrations, referred to as a chromosomal unstable (CIN) phenotype, whereas the smaller group (~15%) typically show microsatellite instability (MSI) caused by defect DNA mismatch repair.[2] Most CIN tumors are microsatellite stable (MSS). A third molecular phenotyp
DNA Sequence Profiles of the Colorectal Cancer Critical Gene Set KRAS-BRAF-PIK3CA-PTEN-TP53 Related to Age at Disease Onset
Marianne Berg,Stine A. Danielsen,Terje Ahlquist,Marianne A. Merok,Trude H. ?gesen,Morten H. Vatn,Tom Mala,Ole H. Sjo,Arne Bakka,Ingvild Moberg,Torunn Fetveit,?ystein Mathisen,Anders Husby,Oddvar Sandvik,Arild Nesbakken,Espen Thiis-Evensen,Ragnhild A. Lothe
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0013978
Abstract: The incidence of colorectal cancer (CRC) increases with age and early onset indicates an increased likelihood for genetic predisposition for this disease. The somatic genetics of tumor development in relation to patient age remains mostly unknown. We have examined the mutation status of five known cancer critical genes in relation to age at diagnosis, and compared the genomic complexity of tumors from young patients without known CRC syndromes with those from elderly patients. Among 181 CRC patients, stratified by microsatellite instability status, DNA sequence changes were identified in KRAS (32%), BRAF (16%), PIK3CA (4%), PTEN (14%) and TP53 (51%). In patients younger than 50 years (n = 45), PIK3CA mutations were not observed and TP53 mutations were more frequent than in the older age groups. The total gene mutation index was lowest in tumors from the youngest patients. In contrast, the genome complexity, assessed as copy number aberrations, was highest in tumors from the youngest patients. A comparable number of tumors from young (<50 years) and old patients (>70 years) was quadruple negative for the four predictive gene markers (KRAS-BRAF-PIK3CA-PTEN); however, 16% of young versus only 1% of the old patients had tumor mutations in PTEN/PIK3CA exclusively. This implies that mutation testing for prediction of EGFR treatment response may be restricted to KRAS and BRAF in elderly (>70 years) patients. Distinct genetic differences found in tumors from young and elderly patients, whom are comparable for known clinical and pathological variables, indicate that young patients have a different genetic risk profile for CRC development than older patients.
Blood Selenium Associated with Health and Fertility in Norwegian Dairy Herds
E Kommisrud, O ?ster?s, T Vatn
Acta Veterinaria Scandinavica , 2005, DOI: 10.1186/1751-0147-46-229
Abstract: Selenium (Se) is a micronutrient that is essential in several biological functions in the organism, particularly in protection of cell membranes. Se is known to be incorporated in the enzyme glutathione peroxidase performing the antioxidative defense of the body by eliminating hydrogen peroxides. Several selenoproteins have later been identified, with functions connected e.g. to the thyroid hormone metabolism, testes and sperm function and muscle metabolism [3]. In addition to glutathione peroxidase enzymes, thioredoxin reductase, iodothyronine deiodinase enzymes, selenoprotein P and selenoprotein W are well characterized selenoproteins concerning their biological functions [3]. Se-deficient diet is a well-known cause of nutritional muscular disease, and is also connected to ill-thrift, reduced growth rate, retained placenta, impaired fertility and mastitis in ruminants [26]. In cattle, fertility has been improved by supplemental administration of vitamin E and Se as shown by [2], while others have not found association between herd Se concentrations and fertility parameters [28,16]. The incidence of metritis and ovarian cysts has been shown to decline in animals treated with Se injections [13], and the incidence of retained placenta declined when Se was given alone [17] or in combination with vitamin E [13,18].The positive role of Se in the immune system is well documented, where it stimulates both humoral and cell-mediated immunity [20,7,22]. Many clinical and epidemiological studies have revealed a positive association between Se supplementation, either alone or in combination with vitamin E, and udder health [31,14,21]. Both the severity and duration of natural and induced infections as well as somatic cell count (SCC) have been shown to be associated with Se status of the animals [29,4-6,16].In Norway, as in other Nordic countries, the content of Se in soil is low [11]. Thus, the Se content in plants is low [9], and cultivated roughage cannot alone supply the a
Norwegian farmers' vigilance in reporting sheep showing scrapie-associated signs
Petter Hopp, Synn?ve Vatn, Jorun Jarp
BMC Veterinary Research , 2007, DOI: 10.1186/1746-6148-3-34
Abstract: Although the potential detection of a scrapie-positive animal would lead to the destruction of the sheep flock concerned, almost all the farmers (97 %) expressed their willingness to report scrapie suspects. This was most certainly dependent on the Government taking the economic responsibility for the control programme as nearly all the farmers responded that this was an important condition. Listeriosis is relatively common disease in Norwegian sheep and a differential diagnosis for scrapie. In a multinomial logistic regression the reporting behaviour for non-recovering listeriosis cases, used as a measurement of willingness to report scrapie, was examined. The reporting of non-recovering listeriosis cases increased as the knowledge of scrapie-associated signs increased, and the reporting behaviour was dependent on both economic and non-economic values.The results indicate that in 2002 almost all sheep farmers showed willingness to report any scrapie suspects. Nevertheless there is an underreporting of scrapie suspects and the farmers' awareness and hence their vigilance of scrapie could be improved. Furthermore, the results suggest that to ensure the farmers' compliance to control programmes for serious infectious diseases, the farmers' concerns of non-economic as well as economic values should be considered.Scrapie is a fatal neurodegenerative disease affecting sheep and goat. It belongs to the transmissible spongiform encephalopathies (TSE), and there are at least two types: classical and atypical scrapie [1]. From the 1960s, the Norwegian Government has considered scrapie a serious animal disease, and if it was detected attempts would be made to eradicate it [2]. During recent years there has been growing international concern about TSEs in sheep as sheep might have acquired bovine spongiform encephalopathy (BSE) from concentrated feeds contaminated with the BSE agent [3], and BSE and scrapie cannot be differentiated by clinical signs or histopathological findin
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