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Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) srt2:(2010-2014);srt2:(2011);mspu:(conferencepaper)"

Sökning: AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) > (2010-2014) > (2011) > Konferensbidrag

  • Resultat 1-10 av 27
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1.
  • Öhlén, Joakim, 1958, et al. (författare)
  • A Clinical Intervention Model for Communication and Information Focusing on Existential Uncertainty – A Participatory Action Research Project Informed by Qualitative Outcome Analysis
  • 2011
  • Ingår i: Supportive Care in Cancer. ; 19:Suppl 2
  • Konferensbidrag (refereegranskat)abstract
    • Objectives. The aim was to develop a team oriented intervention model for palliative cancer care focusing on communicating changes in goals of care. Methods. A participatory action research project was designed by means of qualitative outcome analysis. Initially, bimonthly focus groups with one palliative care team at an oncology outpatient unit were performed during one and a half year. Previous major results, from qualitative studies into patients’ knowledge seeking and experiences of communication and information in palliative cancer care, were used as facilitators for discussion and reflection on the team’s professional experiences. Collaboratively, the researchers and the team worked on developing an intervention model for communication and information. Group discussion data were analyzed concurrently. A preliminary clinical intervention model was developed and refined by means of focus groups with additional palliative care teams and patients respectively. Results. A model of communication and information in palliative cancer care aimed for clinical intervention will be presented, including main concepts, strategies and outcomes. The focus of the model is communication of changes in patients’ goals of care in relation to progress of disease as well as patients’ existential uncertainty (conceptualized as certainty–uncertainty). Conclusions. The model is found to have clinical fit, thanks of the collaborative development by clinicians and researchers. The next step is to further evaluate it clinically.
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2.
  • Y Banaem, Hossein, et al. (författare)
  • Brain tumor modeling : glioma growth and interaction with chemotherapy
  • 2011
  • Ingår i: International Conference on Graphic and Image Processing (ICGIP 2011). - : SPIE. ; 8285
  • Konferensbidrag (refereegranskat)abstract
    • In last decade increasingly mathematical models of tumor growths have been studied, particularly on solid tumors which growth mainly caused by cellular proliferation. In this paper we propose a modified model to simulate the growth of gliomas in different stages. Glioma growth is modeled by a reaction-advection-diffusion. We begin with a model of untreated gliomas and continue with models of polyclonal glioma following chemotherapy. From relatively simple assumptions involving homogeneous brain tissue bounded by a few gross anatomical landmarks (ventricles and skull) the models have been expanded to include heterogeneous brain tissue with different motilities of glioma cells in grey and white matter. Tumor growth is characterized by a dangerous change in the control mechanisms, which normally maintain a balance between the rate of proliferation and the rate of apoptosis (controlled cell death). Result shows that this model closes to clinical finding and can simulate brain tumor behavior properly.
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3.
  • Edlinger, M., et al. (författare)
  • Metabolic syndrome and risk of brain tumour in a large population-based cohort study
  • 2011
  • Ingår i: IEA World Congress of Epidemiology, 7–11 August 2011, Edinburgh International Conference Centre, Edinburgh, Scotland. - : BMJ.
  • Konferensbidrag (refereegranskat)abstract
    • Background: There are few established determinants of brain tumour. We assessed among adults the risk of brain tumour in relation to metabolic syndrome factors. Methods: 580 000 subjects from Sweden, Austria, and Norway were followed for a median of 10 years (Me-Can). Brain tumour information was obtained from national cancer registries. The factors of metabolic syndrome, body mass index, blood pressure, and blood levels of glucose, cholesterol, and triglycerides, were analysed in quintiles and for transformed z-scores (mean of 0 and SD of 1). Cox proportional hazards regression models were applied, stratified by cohort and corrected for measurement error. Results: In total 1312 primary brain tumours were diagnosed during follow-up, predominantly high-grade glioma (n=436) and meningioma (n=348). For meningioma, the HR was increased for systolic blood pressure (HR=1.27 per unit SD, 95% CI 1.03 to 1.57), for diastolic blood pressure (HR=1.29, 95% CI 1.04 to 1.58), and for the combined metabolic syndrome score (HR=1.31, 95% CI 1.11 to 1.54). For high-grade glioma the risk was increased for diastolic blood pressure (HR=1.23, 95% CI 1.01 to 1.50) and triglycerides (HR=1.35, 95% CI 1.05 to 1.72). For both meningioma and high-grade glioma, the risk was more than doubled in the fifth quintiles of diastolic blood pressure compared to the first quintile. For systolic blood pressure the meningioma risk was even larger. Conclusion: Increased blood pressure was related to risk of brain tumour, particularly of meningiomas.
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  • Mehrara, Esmaeil, 1971, et al. (författare)
  • Assessment of tumour response to therapy
  • 2011
  • Ingår i: European Association of Nuclear Medicine Congress. Birmingham. ; 2011
  • Konferensbidrag (refereegranskat)
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