477 research outputs found

    Cognitive Appraisals, Coping and Depressive Symptoms in Breast Cancer Patients

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    Depression in breast cancer patients and survivors is related to negative disease outcomes and worse quality of life. Factors that explain this depression can serve as targets of intervention. This study, guided by the Transactional Theory of Stress, examined the relationship between cognitive appraisals, coping strategies and depressive symptoms in a group of women with mostly advanced-stage breast cancer (N = 65), who scored mostly within the normal range for depressive symptoms. Path analysis was used to determine the relationships among variables, measured with the Cognitive Appraisals of Illness Scale, the Ways of Coping Questionnaire and the Center for Epidemiological Studies Depression Scale. The results of the path analysis showed that higher appraisals of harm/loss and greater use of escape–avoidance coping predicted higher depressive symptoms. These findings enhance the prediction of depression among breast cancer patients and suggest the need to examine cognitive appraisals when attempting to understand depressive symptoms

    Depression in Husbands of Breast Cancer Patients: Relationships to Coping and Social Support

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    PURPOSE: The purpose of the present study was to examine depression in husbands of women with breast cancer, as depression is typically as high in husbands as in patients, and impacts functioning in both. METHODS: We compared husbands of patients to husbands of women without chronic illness on depressive symptoms with the Center for Epidemiological Studies Depression Scale, social support with the Interpersonal Support Evaluation List, and coping with the Ways of Coping Questionnaire. Using the stress and coping model, we examined whether coping mediated social support and depression differently by group, as has been found in the literature. RESULTS: Husbands of patients reported higher scores on the measure of depression and lower use of problem-focused coping, while groups reported equivalent social support. Escape-avoidance coping emerged as a full mediator between social support and depression in husbands of patients, but only a partial mediator in comparison husbands. Accepting responsibility coping partially mediated social support and depression in both groups. Low social support appears particularly detrimental in husbands of patients as it is associated with ineffective coping and depression. CONCLUSIONS: Findings suggest that among husbands of patients, social support relates to depression only through its relationship with coping, indicating healthcare providers should direct attention and intervention to the coping strategies employed by husbands with low social support

    Acceptance and commitment therapy for symptom interference in metastatic breast cancer patients: a pilot randomized trial

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    PURPOSE: Breast cancer is the leading cause of cancer mortality in women worldwide. With medical advances, metastatic breast cancer (MBC) patients often live for years with many symptoms that interfere with activities. However, there is a paucity of efficacious interventions to address symptom-related suffering and functional interference. Thus, this study examined the feasibility and preliminary efficacy of telephone-based acceptance and commitment therapy (ACT) for symptom interference with functioning in MBC patients. METHODS: Symptomatic MBC patients (N = 47) were randomly assigned to six telephone sessions of ACT or six telephone sessions of education/support. Patients completed measures of symptom interference and measures assessing the severity of pain, fatigue, sleep disturbance, depressive symptoms, and anxiety. RESULTS: The eligibility screening rate (64%) and high retention (83% at 8 weeks post-baseline) demonstrated feasibility. When examining within-group change, ACT participants showed decreases in symptom interference (i.e., fatigue interference and sleep-related impairment; Cohen's d range = - 0.23 to - 0.31) at 8 and 12 weeks post-baseline, whereas education/support participants showed minimal change in these outcomes (d range = - 0.03 to 0.07). Additionally, at 12 weeks post-baseline, ACT participants showed moderate decreases in fatigue and sleep disturbance (both ds = - 0.43), whereas education/support participants showed small decreases in these outcomes (ds = - 0.24 and - 0.18 for fatigue and sleep disturbance, respectively). Both the ACT and education/support groups showed reductions in depressive symptoms (ds = - 0.27 and - 0.28) at 12 weeks post-baseline. Group differences in all outcomes were not statistically significant. CONCLUSIONS: ACT shows feasibility and promise in improving fatigue and sleep-related outcomes in MBC patients and warrants further investigation

    Predicting fear of breast cancer recurrence and self-efficacy in survivors by age at diagnosis

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    PURPOSE/OBJECTIVES: To determine the effect that age at diagnosis has on fear of breast cancer recurrence and to identify the predictors of fear of recurrence using self-efficacy as a mediator. DESIGN: Cross-sectional survey. SETTING: Two university cancer centers and one cooperative group in the midwestern United States. SAMPLE: 1,128 long-term survivors. METHODS: Survivors were eligible if they were aged 18-45 years (younger group) or 55-70 years (older group) at cancer diagnosis, had received chemotherapy, and were three to eight years postdiagnosis. Fear of recurrence was compared between younger and older groups. Multiple regression analyses were used to test variables' prediction of fear of recurrence and breast cancer survivor self-efficacy, as well as breast cancer survivor self-efficacy mediation effects. MAIN RESEARCH VARIABLES: Fear of recurrence, breast cancer survivor self-efficacy, and age at diagnosis. FINDINGS: Survivors diagnosed at a younger age had significantly higher fear of recurrence, as well as health, role, womanhood, death, and parenting worries. Perceived risk of recurrence, trait anxiety, and breast cancer reminders explained significant variance in fear of recurrence and breast cancer survivor self-efficacy. Breast cancer survivor self-efficacy partially mediated the effects of variables on fear of recurrence. CONCLUSIONS: The findings suggest that breast cancer survivor self-efficacy may have a protective effect for survivors who are younger at diagnosis and have higher perceived risk of recurrence, higher trait anxiety, and more breast cancer reminders. Oncology nurses already use the skills required to support self-efficacy. Additional research is needed to define and test breast cancer survivor self-efficacy interventions. IMPLICATIONS FOR NURSING: Oncology nurses are in a key role to assess fear of recurrence and provide self-efficacy interventions to reduce it in breast cancer survivors. Strategies to efficiently address fear of recurrence to reduce psychological distress in survivorship follow-up care are warranted

    Ariel - Volume 4 Number 3

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    Editors David A. Jacoby Eugenia Miller Tom Williams Associate Editors Paul Bialas Terry Burt Michael Leo Gail Tenikat Editor Emeritus and Business Manager Richard J. Bonnano Movie Editor Robert Breckenridge Staff Richard Blutstein Mary F. Buechler Steve Glinks Len Grasman Alice M. Johnson J.D. Kanofsky Tom Lehman Dave Mayer Bernie Odd

    Galaxy Star Formation as a Function of Environment in the Early Data Release of the Sloan Digital Sky Survey

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    We present in this paper a detailed analysis of the effect of environment on the star formation activity of galaxies within the Early Data Release (EDR) of the Sloan Digital Sky Survey (SDSS). We have used the Halpha emission line to derive the star formation rate (SFR) for each galaxy within a volume-limited sample of 8598 galaxies with 0.05 less than or equal to z less than or equal to 0.095 and M (r*) less than or equal to 20.45. We find that the SFR of galaxies is strongly correlated with the local ( projected) galaxy density, and thus we present here a density-SFR relation that is analogous to the density-morphology relation. The effect of density on the SFR of galaxies is seen in three ways. First, the overall distribution of SFRs is shifted to lower values in dense environments compared with the field population. Second, the effect is most noticeable for the strongly star-forming galaxies (Halpha EW > 5 Angstrom) in the 75th percentile of the SFR distribution. Third, there is a break ( or characteristic density) in the density-SFR relation at a local galaxy density of similar to1 h(75)(-2) Mpc(-2). To understand this break further, we have studied the SFR of galaxies as a function of clustercentric radius from 17 clusters and groups objectively selected from the SDSS EDR data. The distribution of SFRs of cluster galaxies begins to change, compared with the field population, at a clustercentric radius of 3-4 virial radii (at the >1sigma statistical significance), which is consistent with the characteristic break in density that we observe in the density-SFR relation. This effect with clustercentric radius is again most noticeable for the most strongly star-forming galaxies. Our tests suggest that the density-morphology relation alone is unlikely to explain the density-SFR relation we observe. For example, we have used the ( inverse) concentration index of SDSS galaxies to classify late-type galaxies and show that the distribution of the star-forming (EW Halpha > 5Angstrom) late-type galaxies is different in dense regions ( within 2 virial radii) compared with similar galaxies in the field. However, at present, we are unable to make definitive statements about the independence of the density-morphology and density-SFR relation. We have tested our work against potential systematic uncertainties including stellar absorption, reddening, SDSS survey strategy, SDSS analysis pipelines, and aperture bias. Our observations are in qualitative agreement with recent simulations of hierarchical galaxy formation that predict a decrease in the SFR of galaxies within the virial radius. Our results are in agreement with recent 2dF Galaxy Redshift Survey results as well as consistent with previous observations of a decrease in the SFR of galaxies in the cores of distant clusters. Taken together, these works demonstrate that the decrease in SFR of galaxies in dense environments is a universal phenomenon over a wide range in density (from 0.08 to 10 h(75)(-2) Mpc(-2)) and redshift (out to z similar or equal to 0.5)

    Transcriptional and phenotypic characterization of novel Spx-regulated genes in Streptococcus mutans

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    CAPES - COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIORFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOIn oral biofilms, two of the major environmental challenges encountered by the dental pathogen Streptococcus mutans are acid and oxidative stresses. Previously, we showed that the S. mutans transcriptional regulators SpxA1 and SpxA2 (formerly SpxA and SpxB, respectively) are involved in stress survival by activating the expression of classic oxidative stress genes such as dpr, nox, sodA and tpx. We reasoned that some of the uncharacterized genes under SpxA1/A2 control are potentially involved in oxidative stress management. Therefore, the goal of this study was to use Spx-regulated genes as a tool to identify novel oxidative stress genes in S. mutans. Quantitative real-time PCR was used to evaluate the responses of ten Spx-regulated genes during H2O2 stress in the parent and Delta spx strains. Transcription activation of the H2O2-induced genes (8 out of 10) was strongly dependent on SpxA1 and, to a lesser extent, SpxA2. In vitro transcription assays revealed that one or both Spx proteins directly regulate three of these genes. The gene encoding the FeoB ferrous permease was slightly repressed by H2O2 but constitutively induced in strains lacking SpxA1. Nine genes were selected for downstream mutational analysis but inactivation of smu127, encoding a subunit of the acetoin dehydrogenase was apparently lethal. In vitro and in vivo characterization of the viable mutants indicated that, in addition to the transcriptional activation of reducing and antioxidant pathways, Spx performs an important role in iron homeostasis by regulating the intracellular availability of free iron. In particular, inactivation of the genes encoding the Fe-S biogenesis SUF system and the previously characterized iron-binding protein Dpr resulted in impaired growth under different oxidative stress conditions, increased sensitivity to iron and lower infectivity in rats. These results serve as an entryway into the characterization of novel genes and pathways that allow S. mutans to cope with oxidative stress.In oral biofilms, two of the major environmental challenges encountered by the dental pathogen Streptococcus mutans are acid and oxidative stresses. Previously, we showed that the S. mutans transcriptional regulators SpxA1 and SpxA2 (formerly SpxA and SpxB, respectively) are involved in stress survival by activating the expression of classic oxidative stress genes such as dpr, nox, sodA and tpx. We reasoned that some of the uncharacterized genes under SpxA1/A2 control are potentially involved in oxidative stress management. Therefore, the goal of this study was to use Spx-regulated genes as a tool to identify novel oxidative stress genes in S. mutans. Quantitative real-time PCR was used to evaluate the responses of ten Spx-regulated genes during H2O2 stress in the parent and Delta spx strains. Transcription activation of the H2O2-induced genes (8 out of 10) was strongly dependent on SpxA1 and, to a lesser extent, SpxA2. In vitro transcription assays revealed that one or both Spx proteins directly regulate three of these genes. The gene encoding the FeoB ferrous permease was slightly repressed by H2O2 but constitutively induced in strains lacking SpxA1. Nine genes were selected for downstream mutational analysis but inactivation of smu127, encoding a subunit of the acetoin dehydrogenase was apparently lethal. In vitro and in vivo characterization of the viable mutants indicated that, in addition to the transcriptional activation of reducing and antioxidant pathways, Spx performs an important role in iron homeostasis by regulating the intracellular availability of free iron. In particular, inactivation of the genes encoding the Fe-S biogenesis SUF system and the previously characterized iron-binding protein Dpr resulted in impaired growth under different oxidative stress conditions, increased sensitivity to iron and lower infectivity in rats. These results serve as an entryway into the characterization of novel genes and pathways that allow S. mutans to cope with oxidative stress104CAPES - COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIORFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCAPES - COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIORFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCAPES [6849-12-1]FAPESP [2012/032278-3, 2014/03816-4]6849-12-12012/032278-3; 2014/03816-
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