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Search Results: 1 - 10 of 199 matches for " Terje Risberg "
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Curriculum factors influencing knowledge of communication skills among medical students
Anders Baerheim, Per Hjortdahl, Are Holen, Tor Anvik, Ole Fasmer, Hilde Grimstad, Tore Gude, Terje Risberg, Per Vaglum
BMC Medical Education , 2007, DOI: 10.1186/1472-6920-7-35
Abstract: The study design was a cross-sectional survey performed in the four Norwegian medical schools with different curricula, spring 2003. A self-administered questionnaire regarding knowledge of communication skills (an abridged version of van Dalen's paper-and-pencil test) was sent to all students attending the four medical schools. A total of 1801 (59%) students responded with complete questionnaires.At the end of the 1st year of study, the score on the knowledge test was higher in students at the two schools running communication courses and providing early patient contact (mean 81%) than in the other two medical schools (mean 69–75%, P ≤ 0.001), with students studying a traditional curriculum scoring the lowest. Their scores increased sharply towards the end of the 3rd year, during which they had been subjected to extensive patient contact and had participated in an intensive communication course (77% vs. 72% the previous year, P ≤ 0.01). All students scored generally lower in academic years in which there was no communication training. However, at the end of the final year the difference between the schools was only 5% (81% vs. 86%, P ≤ 0.001).The acquisition of knowledge regarding communication skills by medical students may be optimised when the training is given together with extensive supervised patient contact, especially if this teaching takes place in the initial years of the curriculum.Excellent communication skills are essential to medical professionalism [1]. Clinical communication is complex in nature, and both personal and curricular factors will influence how medical students master the relevant skills [2]. Basic or general communication skills are developed early in life. Theoretical knowledge about communication skills comes years later, and not through medical studies alone. Contrary to clinical procedural skills, communication skills appear to be an integral part of one's cognition [3].Communication training builds on the assumption that understandi
Assessing medical students' attitudes towards learning communication skills – which components of attitudes do we measure?
Tor Anvik, Tore Gude, Hilde Grimstad, Anders Baerheim, Ole B Fasmer, Per Hjortdahl, Are Holen, Terje Risberg, Per Vaglum
BMC Medical Education , 2007, DOI: 10.1186/1472-6920-7-4
Abstract: The CSAS questionnaire was mailed simultaneously to all students (n = 3055) of the four medical schools in Norway in the spring of 2003. Response from 1833 students (60.0%) were analysed by use of SPSS ver.12.A Principal component analysis yielded findings that differ in many respects from those of earlier papers. We found the CSAS to measure three factors. The first factor describes students' feelings about the way communication skills are taught, whereas the second factor describes more fundamental attitudes and values connected to the importance of having communication skills for doctors. The third factor explores whether students feel that good communication skills may help them respecting patients and colleagues.Our findings indicate that in this sample the CSAS measures broader aspects of attitudes towards learning communication skills than the formerly described two-factor model with PAS and NAS. This may turn out to be helpful for monitoring the effect of different teaching strategies on students' attitudes during medical school.Medical students' attitudes towards doctor-patient communication have for long been a concern among medical teachers, curriculum planners and policy makers [1,2] and have been addressed in many studies.Kaufmann [3] constructed the Attitudes Towards Medical Communication Scale with 41 items and used it in a cross-sectional study on 203 students in their first, second and fourth year respectively. This study, which was published in 2001, showed that female students had more positive attitudes than male students, and that first and second year students had more positive attitudes than fourth year students.In 2001 de Valck [4] presented a questionnaire measuring students' attitudes towards full disclosure versus non-disclosure in breaking bad news. Following one cohort of students for three years (53 students responded in all three years) they found that students became more in favour of non-disclosure as they progressed through medical
Low expression levels of ATM may substitute for CHEK2 /TP53 mutations predicting resistance towards anthracycline and mitomycin chemotherapy in breast cancer
Stian Knappskog, Ranjan Chrisanthar, Erik L?kkevik, Gun Anker, Bj?rn ?stenstad, Steinar Lundgren, Terje Risberg, Ingvil Mjaaland, Beryl Leirvaag, Hrvoje Miletic, Per E L?nning
Breast Cancer Research , 2012, DOI: 10.1186/bcr3147
Abstract: We sequenced ATM and assessed gene expression levels in pre-treatment biopsies from 71 locally advanced breast cancers treated in the neoadjuvant setting with doxorubicin monotherapy or mitomycin combined with 5-fluorouracil. Findings were confirmed in a separate patient cohort treated with epirubicin monotherapy. Each tumor was previously analyzed for CHEK2 and TP53 mutation status.While ATM mutations were not associated with chemo-resistance, low ATM expression levels predicted chemo-resistance among patients with tumors wild-type for TP53 and CHEK2 (P = 0.028). Analyzing the ATM-chk2-p53 cascade, low ATM levels (defined as the lower 5 to 50% percentiles) or mutations inactivating TP53 or CHEK2 robustly predicted anthracycline resistance (P-values varying between 0.001 and 0.027 depending on the percentile used to define "low" ATM levels). These results were confirmed in an independent cohort of 109 patients treated with epirubicin monotherapy. In contrast, ATM-levels were not suppressed in resistant tumors harboring TP53 or CHEK2 mutations (P > 0.5).Our data indicate loss of function of the ATM-Chk2-p53 cascade to be strongly associated with resistance to anthracycline/mitomycin-containing chemotherapy in breast cancer.Despite significant improvements in cancer therapy over the last decades, resistance towards chemotherapy remains the main obstacle to cure among patients suffering from solid tumors [1].The molecular mechanisms causing chemo-resistance in breast cancer, as for most other cancer forms, are poorly understood. While Topoisomerase-II amplified tumors on average reveal enhanced anthracycline sensitivity compared to non-amplified tumors [2-5], lack of Topoisomerase-II expression may not explain anthracycline resistance.p53, the tumor suppressor protein encoded by the TP53 gene, plays a key role with respect to apoptosis but also senescence, growth arrest and DNA repair [6,7]. Our group has previously linked mutations in TP53, (in particular those affect
The Influence of Optimistic Expectations and Negative Life Events on Somatic Symptoms among Adolescents: A One-Year Prospective Study  [PDF]
Terje Arnfinn Murberg
Psychology (PSYCH) , 2012, DOI: 10.4236/psych.2012.32018
Abstract: This study prospectively examined the main effect of optimism on subsequent somatic symptomatology as well as optimism as moderating factors in the link between negative life events and somatic symptoms in a sample of 198 (111 females, 87 males) students in a Norwegian senior high school. Results from the longitudinal multivariate analyses, indicated that the scores for optimism and negative life events were significantly associated with scores of somatic symptoms at time-point two (T2). Moreover, a significant Optimism × Negative life events interaction was found in predicting somatic symptoms. Implications of these findings are discussed.
CHEK2 Mutations Affecting Kinase Activity Together With Mutations in TP53 Indicate a Functional Pathway Associated with Resistance to Epirubicin in Primary Breast Cancer
Ranjan Chrisanthar, Stian Knappskog, Erik L?kkevik, Gun Anker, Bj?rn ?stenstad, Steinar Lundgren, Elisabet O. Berge, Terje Risberg, Ingvil Mjaaland, Lovise M?hle, Lars Fredrik Engebretsen, Johan Richard Lillehaug, Per Eystein L?nning
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0003062
Abstract: Background Chemoresistance is the main obstacle to cure in most malignant diseases. Anthracyclines are among the main drugs used for breast cancer therapy and in many other malignant conditions. Single parameter analysis or global gene expression profiles have failed to identify mechanisms causing in vivo resistance to anthracyclines. While we previously found TP53 mutations in the L2/L3 domains to be associated with drug resistance, some tumors harboring wild-type TP53 were also therapy resistant. The aim of this study was; 1) To explore alterations in the TP53 gene with respect to resistance to a regular dose epirubicin regimen (90 mg/m2 every 3 week) in patients with primary, locally advanced breast cancer; 2) Identify critical mechanisms activating p53 in response to DNA damage in breast cancer; 3) Evaluate in vitro function of Chk2 and p14 proteins corresponding to identified mutations in the CHEK2 and p14(ARF) genes; and 4) Explore potential CHEK2 or p14(ARF) germline mutations with respect to family cancer incidence. Methods and Findings Snap-frozen biopsies from 109 patients collected prior to epirubicin (as preoperative therapy were investigated for TP53, CHEK2 and p14(ARF) mutations by sequencing the coding region and p14(ARF) promoter methylations. TP53 mutastions were associated with chemoresistance, defined as progressive disease on therapy (p = 0.0358; p = 0.0136 for mutations affecting p53 loop domains L2/L3). Germline CHEK2 mutations (n = 3) were associated with therapy resistance (p = 0.0226). Combined, mutations affecting either CHEK2 or TP53 strongly predicted therapy resistance (p = 0.0101; TP53 mutations restricted to the L2/L3 domains: p = 0.0032). Two patients progressing on therapy harbored the CHEK2 mutation, Arg95Ter, completely abrogating Chk2 protein dimerization and kinase activity. One patient (Epi132) revealed family cancer occurrence resembling families harboring CHEK2 mutations in general, the other patient (epi203) was non-conclusive. No mutation or promoter hypermethylation in p14(ARF) were detected. Conclusion This study is the first reporting an association between CHEK2 mutations and therapy resistance in human cancers and to document mutations in two genes acting direct up/down-stream to each other to cause therapy failure, emphasizing the need to investigate functional cascades in future studies.
Predictive and Prognostic Impact of TP53 Mutations and MDM2 Promoter Genotype in Primary Breast Cancer Patients Treated with Epirubicin or Paclitaxel
Ranjan Chrisanthar,Stian Knappskog,Erik L?kkevik,Gun Anker,Bj?rn ?stenstad,Steinar Lundgren,Terje Risberg,Ingvil Mjaaland,Gudbrand Skj?nsberg,Turid Aas,Ellen Schlichting,Hans E. Fj?sne,Arne Nysted,Johan Richard Lillehaug,Per Eystein L?nning
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0019249
Abstract: 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 wild-type 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.
Persistence of disseminated tumor cells after neoadjuvant treatment for locally advanced breast cancer predicts poor survival
Randi R Mathiesen, Elin Borgen, Anne Renolen, Erik L?kkevik, Jahn M Nesland, Gun Anker, Bj?rn ?stenstad, Steinar Lundgren, Terje Risberg, Ingvil Mjaaland, Gunnar Kvalheim, Per Eystein L?nning, Bj?rn Naume
Breast Cancer Research , 2012, DOI: 10.1186/bcr3242
Abstract: Bone marrow and peripheral blood were collected before NACT (BM1: n = 231/PB1: n = 219), at surgery (BM2: n = 69/PB2: n = 71), and after 12 months from start of NACT (BM3: n = 162/PB3: n = 141). Patients were included from 1997 to 2003 and followed until 2009 (or ten years follow-up). DTC- and CTC-status were determined by morphological evaluation of immunocytochemically detected cytokeratin-positive cells. The prognostic significance of DTCs/CTCs was assessed by univariate and multivariate Cox-regression analyses.Before NACT, DTCs and CTCs were detected in 21.2% and 4.9% of the patients, respectively. At surgery, 15.9% and 1.4% had DTC- and CTC-presence, compared to 26.5% and 4.3% at 12 months from start of NACT. Of patients for whom DTC results both before NACT and at 12 months were available, concordant results were observed in 68%, and 14 out of 65 had positive DTC-status at both time points. Presence of ≥ 1 DTC 12 months from start of NACT, but not at other time points, predicted reduced disease-free survival (DFS; HR 2.3, p = 0.003), breast cancer-specific survival (BCSS; HR 3.0, p < 0.001) and overall survival (OS; HR 2.8, p < 0.001). Before NACT, presence of ≥ 3 DTCs was also associated with unfavorable outcome, and reduced BCSS was observed for CTC-positive patients (HR 2.2, p = 0.046). In multivariate analysis, DTC status (
The alpha-2A adrenoceptor agonist guanfacine improves sustained attention and reduces overactivity and impulsiveness in an animal model of Attention-Deficit/Hyperactivity Disorder (ADHD)
Terje Sagvolden
Behavioral and Brain Functions , 2006, DOI: 10.1186/1744-9081-2-41
Abstract: The present study tested behavioral effects of guanfacine at doses of 0.075, 0.15, 0.30 and 0.60 mg base/kg i.p. in both male SHRs and their controls, the Wistar Kyoto rat (WKY). ADHD-like behavior was tested with a visual discrimination task measuring overactivity, impulsiveness and inattentiveness.The striking impulsiveness, overactivity, and reduced sustained attention during baseline conditions in the SHR improved by treatment with guanfacine. The most pronounced improvement in SHR behavior was seen following the two highest doses (0.3 and 0.6 mg/kg) of guanfacine when SHR behaviors virtually normalized. The positive effects of the drug were most marked towards the end of the session.The results indicate that guanfacine improved poor noradrenergic modulation of neuronal circuits that involve the frontal lobes in an animal model of ADHD. The present results support the beneficial effects of guanfacine on ADHD behavior reported clinically and experimentally in primate models of frontal function. It is likely that guanfacine improved prefrontal functions in the SHR. It cannot be concluded, however, that the effects of the drug are mediated solely by norepinephrine.Attention-deficit/hyperactivity disorder (ADHD) is currently defined as a cognitive developmental disorder where all clinical criteria are behavioral [1]. Overactivity, impulsiveness, and inattentiveness are presently regarded as the main clinical symptoms.There have been many attempts to explain the origins of ADHD symptoms. A dual-process model [2-5] suggests that less efficient reinforcement processes and deficient extinction of previously reinforced behavior are fundamental to the problems described as response inhibition [6] and poor executive functions [7].ADHD is highly heritable and the genetic and neurobiological causes are likely to reside in brain catecholaminergic systems (for a review see [4]). Most likely, ADHD symptoms are associated with dysregulation of dopaminergic and noradrenergic modu
Impulsiveness, overactivity, and poorer sustained attention improve by chronic treatment with low doses of l-amphetamine in an animal model of Attention-Deficit/Hyperactivity Disorder (ADHD)
Terje Sagvolden
Behavioral and Brain Functions , 2011, DOI: 10.1186/1744-9081-7-6
Abstract: The present study tested the behavioral effects of 0.75 and 2.2 mg l-amphetamine base/kg i.p. in male SHRs and their controls, the Wistar Kyoto rat (WKY). ADHD-like behavior was tested with a visual discrimination task measuring overactivity, impulsiveness and inattentiveness.The striking impulsiveness, overactivity, and poorer sustained attention seen during baseline conditions in the SHR were improved by chronic treatment with l-amphetamine. The dose-response curves were, however, different for the different behaviors. Most significantly, the 0.75 mg/kg dose of l-amphetamine improved sustained attention without reducing overactivity and impulsiveness. The 2.2 mg/kg dose improved sustained attention as well as reduced SHR overactivity and impulsiveness.The effects of l-amphetamine to reduce the behavioral symptoms of ADHD in the SHR were maintained over the 14 days of daily dosing with no evidence of tolerance developing.Attention-deficit/hyperactivity disorder (ADHD) is currently defined as a cognitive developmental disorder where all clinical criteria are behavioral [1]. Overactivity, impulsiveness, and inattentiveness are presently regarded as the main clinical symptoms.There have been many attempts to explain the origins of ADHD symptoms. A dual-process theory [2-5] suggests that less efficient reinforcement processes and deficient extinction of previously reinforced behavior may explain behavioral changes often described as response disinhibition [6] or poor executive functioning [7].ADHD is highly heritable and the genetic and neurobiological causes are likely to reside in brain catecholamines (for a review see [4]). Most likely, ADHD symptoms are associated with reduced post-synaptic efficacy of dopaminergic and noradrenergic modulation of neuronal circuits that involve the frontal lobes [8,9]. Imaging of striatal neuronal networks indicates reduced dopamine efficacy in ADHD [10]. Further, noradrenergic systems are involved in attention processes and prime p
Behavioral and Brain Functions. A new journal
Terje Sagvolden
Behavioral and Brain Functions , 2005, DOI: 10.1186/1744-9081-1-1
Abstract: Behavioral and Brain Functions (BBF) is an Open Access, peer-reviewed, online journal considering original research, review, and modeling articles in all aspects of neurobiology or behavior, favoring research that relates to both domains. BBF is published by BioMed Central.The greatest challenge for empirical science is to understand human behavior, how human behavior arises from the myriad functions such as attention, language, memory and emotion, how these functions are reflected in the human brain, and how brain functions and behavior are altered in disease. Behavioral and cognitive neuroscience investigates the psychological, computational, and neuroscientific bases of normal and abnormal behavior. It is a field that receives a lot of attention through the Brain Awareness Week in March every year. The "Decade of the Brain" (1990–2000) was also important for promoting the field. The interdisciplinary nature of the field covers developments in human and animal behavioral science, neuroscience, neuropsychology, cognitive psychology, neurobiology, linguistics, computer science, and philosophy.Behavioral and Brain Functions is the first Open Access journal for basic research covering the entire area of behavioral and cognitive neuroscience – an area where animal studies traditionally play a prominent role. Behavioral and Brain Functions is published online, allowing unlimited space for figures, extensive datasets to allow readers to study the data for themselves, and moving pictures, which are important qualities assisting communication in modern science.Behavioral and Brain Functions' Open Access policy changes the way in which articles are published. First, all articles become freely and universally accessible online, and so an author's work can be read by anyone at no cost. Second, the authors hold copyright for their work and grant anyone the right to reproduce and disseminate the article, provided that it is correctly cited and no errors are introduced [1]. Thir
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