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Background: In this controlled postdiagnosis study, the authors examined various aspects of body image of breast cancer survivors in cross-sectional and longitudinal designs., Methods: In 2004 and 2007 the Body Image Scale (BIS) was completed by the same 248 disease-free women who had been treated for stage II and III breast cancer between 1998 and 2002. "Poorer" body image was defined as greater than the 70th percentile (N=76 women) of the BIS scores in contrast to "better" body image (N=172 women). Breast cancer survivors were examined clinically in 2004, and their BIS scores were compared with the scores from an age-matched group of women from the general population., Results: In this cross-sectional study, poorer body image in 2004 was associated significantly with modified radical mastectomy, undergoing or planning to undergo breast-reconstructive surgery, a change in clothing, poor physical and mental health, chronic fatigue, and reduced quality of life (QoL). In univariate analyses, most of these factors and manually planned radiotherapy were significant predictors of poorer body image in 2007. In multivariate analyses, manually planned radiotherapy, poor physical QoL and high BIS score in 2004 remained independent predictors of a poorer body image in 2007. Body image ratings were relatively stable from 2004 to 2007. Twenty-one percent of breast cancer survivors reported body image dissatisfaction, similar to the proportion of dissatisfaction in controls., Conclusions: In this cross-sectional analysis, body image in breast cancer survivors was associated with the types of surgery and radiotherapy and with mental distress, reduced health, and impaired QoL. Body image ratings were relatively stable over time, and the antecedent body image score was a strong predictor of body image at follow-up. Body image in breast cancer survivors differed very little from that in controls., (Copyright (c) 2010 American Cancer Society.)

Fatigue is a common symptom and includes both physical and mental components. It can be associated with a variety of different syndromes and diseases, but in many cases is not associated with other comorbid conditions. Most humans have experienced acute fatigue in relation to different stressors. Acute fatigue typically decreases as the effect of the triggering factor is reduced and a normal homeostatic balance is restored. Fatigue that persists for 6 months or more is termed chronic fatigue. Chronic fatigue (CF) in combination with a minimum of 4 of 8 symptoms and the absence of diseases that could explain these symptoms, constitute the case definition for chronic fatigue syndrome. In spite of its prevalence, the biology of fatigue is relatively poorly understood and biological markers have not yet been identified. This literature search was performed in PubMed to identify research on the genetics and epigenetics of fatigue. Publications were included if fatigue was a major topic and the topic was combined with genetic and/or epigenetic measurements in adult humans. A total of 40 publications were identified. Although altered functioning in the hypothalamic-pituitary-adrenal axis, the serotonergic system, and associations with infectious agents have been identified, the search for genetic or epigenetic markers of fatigue, either in the context of CF or chronic fatigue syndrome (CFS) has been relatively unproductive or, in the case of epigenetics, nonexistent. Although several studies, both hypothesis-testing and hypothesis-generating, have been performed to search for biomarkers, they have mostly been underpowered, restricted by the heterogeneity of the phenotype, or limited by an unsystematic study design. To be able to confirm the hypothesis that risk for, or levels of, fatigue are influenced by the genetic or epigenetic background of an individual, studies need to be based on larger sample sizes with a more clearly defined phenotype. Studies need to focus not only on the influence of a single aspect such as single nucleotide polymorphisms (SNPs) or differential gene expression on disease risk or state, but also on the systems biology behind the disease in combination with information on environmental influences and validation of findings in functional studies., (Copyright (c) 2010 American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved.)

Purpose: A possible association between thyroid diseases (TD) and breast cancer (BC) has been debated. We examined prevalence and development of TD in women after multimodal treatment for Stage II/III BC compared with women from a general population. Secondarily, we explored the impact of two different radiotherapy (RT) techniques (standardized field arrangements vs. computed tomography [CT]-based dose planning) on TD in BC patients examined 35-120 months after primary BC treatment., Methods and Materials: A total of 403 BC patients completed a questionnaire about TD and had blood samples taken for analyses of thyroid function. All had undergone postoperative RT with or without (2%) adjuvant systemic treatment. The results in the BC patients were compared with a cancer-free, age-matched control group from a general population (CGr)., Results: There was higher prevalence of self-reported hypothyroidism in the BC patients as compared with the CGr (18% vs. 6%, p < 0.001). The raised prevalence was predominantly due to a substantial increase in the development of hypothyroidism after BC diagnosis, whereas the prevalence of hypothyroidism before BC diagnosis was similar to that observed in the CGr. Patients treated with CT-based RT showed a trend for increased post-BC development of hypothyroidism as compared with those treated with standardized field arrangements (p = 0.08)., Conclusions: Hypothyroidism is significantly increased in women after multimodal treatment for Stage II/III BC. Radiation to the thyroid gland may be a contributing factor. BC patients should be routinely screened for hypothyroidism.

Fatigue is one of the most frequent complaints among breast cancer survivors. However, mechanisms underlying persisting fatigue after end of treatment are poorly understood. To explore whether biological processes underlying persistent fatigue can affect gene expression of blood cells, genome-wide expression analyses were performed on whole blood samples from breast cancer survivors classified as chronic fatigued 2-6 years after diagnosis. Non-fatigued survivors served as controls. Several gene sets involved in plasma- and B-cell pathways differed between the chronic fatigued and the non-fatigued, suggesting that a dysregulation in these pathways is associated with chronic fatigue and that a B-cell-mediated inflammatory process might underlie fatigue. The chronic fatigued also had a higher level of leucocytes, lymphocytes and neutrophiles compared with the non-fatigued, thus further indicating that an activation of the immune system plays a role in the biology of chronic fatigue in breast cancer survivors.

This study is based on data on autopsies performed at the Institute of Forensic Medicine, National Hospital, Oslo, in 1989. Solitary men and women were compared with non-solitary men and women with respect to causes of death and manner of death. Solitary men died more often from potentially curable diseases, especially pneumonia. These individuals had often suffered from chronic alcoholism and had lived in central Oslo. Among women there were no differences in the causes of death of solitary and non-solitary individuals.

Sodium-linked and sodium-independent HCO3-/Cl- antiport was measured under different conditions in a number of cell lines. Transport of HCO3- was estimated from its effect on intracellular pH (pHi) measured with the fluorescent probe 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein. The associated ion fluxes were estimated from the transport of 36Cl- and 22Na+. Na+-dependent and Na+-independent HCO3-/Cl- antiport were found in many, but not in all cell lines tested. The Na+-independent HCO3-/Cl- antiport was found to be highly pHi-dependent in a number of cell lines, whereas in others this was not the case. Some cell lines were found to have both Na+-dependent and Na+-independent HCO3-/Cl- antiport, whereas in others we could detect only one of these mechanisms. Na+/H+ antiport, which is quantitatively the most important H+-extruding mechanism, was found in all cell lines tested, but the activity varied strongly. Possible reasons for the qualitative and quantitative differences in antiport activity are discussed.