No description available.

No description available.

No description available.

A comunicação entre sistema nervoso e imune contribui para a homeostasia. Em humanos, a convivência com portadores de doenças crônicas (\"caregiving\") é agente causador de alterações inclusive imunológicas. Modelos animais podem contribuir para a compreensão dos mecanismos aí envolvidos. Avaliamos aqui, em fêmeas sadias, as alterações decorrentes do convívio com parceira singenêica (C57/Bl6) portadora do melanoma B16F10. Os resultados mostraram que esta convivência, por 20 dias: 1) alterou o comportamento, sem modificar a concentração sérica de corticosterona; 2) aumentou a expressão de CD80 nas populações MHCII+CD11c+, no baço, mas não nos linfonodos; 3) diminuiu o percentual de células MHCII+CD80+ após cultura de medula óssea, por sete dias em meio com GM-CSF, IL-4 e LPS; 4) inibiu, parcialmente, a indução de uma reação de hipersensibilidade tardia; 5) não modificou o estabelecimento do melanoma. Assim, este modelo pode, com cautela, ser usado para o estudo das alterações imunes observadas em \"caregivers\". / The communication between the nervous and immune systems contributes to the homeostasis. In humans, living with chronic disease bearers (caregiving) is the causing agent of alterations including the immunological ones. Animal models can contribute for understanding the involved mechanisms. Herein, we evaluated, in healthy females, the alterations caused by cohabiting with a syngeneic (C57Bl/6) partner bearing the B16F10 melanoma. The results showed that such cohabitation for 20 days: 1) altered the behavior without modifying the corticosterone seric level; 2) increased the CD80 expression on MHC+CD11c+ cells at the spleen, but not those at the lymph node; 3) decreased the percentage of MHCII+CD80+ bone marrow cells cultured for 7 days in a GM-CSF, IL-4 and LPS medium. 4) partially inhibited the induction of a delayed type hypersensitivity; 5) did not modified the melanoma establishment. So forth, this model may cautiously be taken as a means for the study of immune alteration observed in caregivers.

Coronary heart disease is the leading cause of death in American women, accounting for one in six deaths in 2004. One third of women over the age of forty will develop coronary heart disease in their lifetime. The role of chronic and excessive inflammation and risk factors, such as smoking and high cholesterol, are now well-established factors contributing to coronary heart disease pathology. A knowledge gap exists in that little is known about the mechanisms by which psychosocial factors, such as anger, may be associated with pro-inflammatory processes that contribute to cardiovascular morbidity and mortality in women. The purpose of this study was to determine if there were differences in serum levels of the proinflammatory biomarker, C-reactive protein, in post-menopausal women who scored high on anger characteristics compared to those with low anger characteristics. Mean levels of C-reactive protein were not found to be different in a sample of 42 women with high trait anger or high anger expression compared to those with low trait anger or low anger expression. Significant relationships were found in C-reactive protein and some anger control characteristics (anger control-in) and might imply that certain anger expression styles may play a role in pro-inflammatory responses in post-menopausal women.

Introduction: Mucosal human papillomavirus (HPV) infection is the most common sexually transmitted infection (STI) and is associated with genitals warts, anogenital cancers, and oropharyngeal cancers. Most sexually active persons will become infected with HPV at some point in their lives, however few will develop HPV-related diseases such as warts, lesions, or cancer as a result of the infection. It is unclear why a minority of individuals fail to clear HPV infection and develop clinical disease. Due to initial associations with cervical lesions, much research has focused on women. Th1 type immune responses have been associated with successful response to HPV infection. Factors such as psychological stress and sleep have been associated with immune function. Stress has been associated with cervical lesions, however no study has evaluated effects of stress or sleep on HPV infection. This research sought to examine the associations between perceived stress and sleep problems with HPV prevalence, incidence, and clearance among men. Methods: Men were tested for 37 individual HPV genotypes every 6 months as part of a large natural history study. A total of 426 men were followed over 1 to 4 visits. Perceived stress was measured with a modified 4-item Perceived Stress Scale (PSS-4) assessing stress in the past six months and was dichotomized into high (scores in the 4th quartile) and low perceived stress. Self-reported sleep problems were measured by seven likert-scale items and categorized as high (4th quartile of sleep problems scores), moderate (second and third quartiles; reference group), and low (first quartile). Three HPV classifications were examined; men were categorized as positive for 'Any HPV' if they tested positive for any of the 37 HPV genotypes in the study protocol, men were categorized as positive for 'Oncogenic HPV' if they tested positive for any oncogenic HPV type, and men were categorized as positive for 'Non-oncogenic HPV' if they tested positive for any non-oncogenic HPV genotype. In the prevalence analysis, men who had no detectable HPV infection with any of the 37 types were the reference group in all analyses. Prevalence ratios and 95% confidence intervals (95% CI) were calculated using Poisson regression with robust variance. For HPV clearance and incidence, Cox regression with the robust sandwich estimator was used to calculated hazard ratios and 95% confidence intervals. Results: A total of 424 men had genotyping results available for the prevalence analysis. High perceived stress was significantly associated with higher prevalence of any HPV infection [PR =1.33 (95% CI: 1.06-1.68)] and oncogenic HPV infection [PR=1.53 (95% CI: 1.06-2.20)], adjusting for demographics, sexual behavior, and sleep problems. High self-reported sleep problems was significantly associated with higher prevalence of oncogenic HPV infection [PR=1.50 (95% CI:1.01-2.13)], adjusting for demographics, sexual behavior, and perceived stress. Perceived stress and self-reported sleep problems were not associated with incidence of HPV infection. Perceived stress was not significantly associated with clearance of HPV infection overall. Among men 50 and older however, men with high stress were significantly less likely to clear any HPV infection than those with low stress adjusting for demographics, HR=0.09 (95% CI: 0.02-0.49). Compared to men with moderate sleep problems, those with high sleep problems were significantly less likely to clear an infection with any HPV type, HR=0.68 (95% CI: 0.49-0.94), or an oncogenic HPV type, HR=0.51 (95% CI: 0.28-0.94), after adjustment for demographics and perceived stress. Discussion: This is the first study to examine associations between HPV infection with perceived stress and self-reported sleep problems. It is also the largest study to examine associations between these exposures and an infection outcome. Results suggest that perceived stress and self-reported sleep problems have independent effects on HPV. Evaluation of perceived stress, biological indicators of stress, objective measures of sleep, and measurement of immune parameters may aid in further elucidating how stress and sleep disturbance are related to HPV infection. Determination of modifiable factors that can influence HPV infection may aid in the prevention of adverse disease outcomes related to infection with this virus. Examining the impact of factors such as perceived stress and sleep problems on HPV infection may aid in risk stratification of patients and allow more targeted interventions among those most at risk for developing disease.

The current dissertation tested a model based on a systems perspective, where inflammation was hypothesized to mediate the influence of diet and physical condition on quality of life (base model) in a nationally representative U.S. dataset (NHANES). Three additional hypotheses, regarding social support (The Buffering Hypothesis), early microbial exposure (The Hygiene Hypothesis) and life history theory (The Tradeoff Hypothesis) were tested utilizing the base model. All analysis utilized a structural equation model. This study focused on objective measurements for dietary behavior and physical activity utilizing blood serum values of nutrients and metabolic markers and anthropometric data as well as blood serum concentrations of CRP and white blood cell count. Quality of life was assessed with the number of limitations in daily living, the number of days that were affected by mental, emotional and physical limitations and the self-reported general health condition. The hypothesized model fit well to the data and the results revealed that lower intake of healthy nutrients and reduced physical condition both predicted decreased quality of life, as mediated by inflammation and explained 31.9 % of the variation in quality of life (R² = .319, p<.001). Social support further predicted quality of life directly (β = .417, p<.001) and indirectly through dietary behavior and inflammation (β = -.106, p<.001), microbial exposure significantly moderated the relation between inflammation and quality of life (β = -.127, p<.001) and higher reproductive effort predicted lower intake of vital nutrients (β = .316, p<.001), physical condition (β = .352, p<.001) and subsequent inflammation. Reproductive effort also directly predicted reduced quality of life (β = .278, p<.001). These analyses indicated that inflammation can be considered a strong mediator between lifestyle factors and resulting quality of life and that social support, microbial exposure and reproductive effort each added unique predictive value to this model.

No abstract available / ix, 115 leaves : ill. (some col.) ; 29 cm.

Thesis (Ph.D. (Psychiatry))--University of Pretoria, 2003. / Summary in English and Afrikaans. Includes bibliographical references.

Thesis (Ph. D.)--Ohio State University, 2007. / Title from first page of PDF file. Includes bibliographical references (p. 75-89).