58 research outputs found
Глобальне інформаційне суспільство: поняття, структура, комунікації
Розглядаються базові поняття, структура та соціальні комунікації глобального інформаційного суспільства.Рассматриваются базовые понятия, структура и социальные коммуникации глобального информационного общества.The basic terms, structures and social communications of global information society are considered
Chronic pain, depression and cardiovascular disease linked through a shared genetic predisposition:Analysis of a family-based cohort and twin study
BACKGROUND: Depression and chronic pain are the two most important causes of disability (Global Burden of Disease Study 2013). They occur together more frequently than expected and both conditions have been shown to be co-morbid with cardiovascular disease. Although shared socio-demographic risk factors (e.g. gender, deprivation) might explain the co-morbidity of these three conditions, we hypothesised that these three long-term, highly prevalent conditions co-occur and may be due to shared familial risk, and/or genetic factors. METHODS AND FINDINGS: We employed three different study designs in two independent cohorts, namely Generation Scotland and TwinsUK, having standardised, validated questionnaire data on the three traits of interest. First, we estimated the prevalence and co-occurrence of chronic pain, depression and angina among 24,024 participants of a population-based cohort of extended families (Generation Scotland: Scottish Family Health Study), adjusting for age, gender, education, smoking status, and deprivation. Secondly, we compared the odds of co-morbidity in sibling-pairs with the odds in unrelated individuals for the three conditions in the same cohort. Lastly, examination of similar traits in a sample of female twins (TwinsUK, n = 2,902), adjusting for age and BMI, allowed independent replication of the findings and exploration of the influence of additive genetic (A) factors and shared (C) and non-shared (E) environmental factors predisposing to co-occurring chronic widespread pain (CWP) and cardiovascular disease (hypertension, angina, stroke, heart attack, elevated cholesterol, angioplasty or bypass surgery). In the Generation Scotland cohort, individuals with depression were more than twice as likely to have chronic pain as those without depression (adjusted OR 2·64 [95% CI 2·34-2·97]); those with angina were four times more likely to have chronic pain (OR 4·19 [3·64-4·82]); those with depression were twice as likely to have angina (OR 2·20 [1·90-2·54]). Similar odds were obtained when the outcomes and predictors were reversed and similar effects seen among sibling pairs; depression in one sibling predicted chronic pain in the other (OR 1·34 [1·05-1·71]), angina predicted chronic pain in the other (OR 2·19 [1·63-2·95]), and depression, angina (OR 1·98 [1·49-2·65]). Individuals with chronic pain and angina showed almost four-fold greater odds of depression compared with those manifesting neither trait (OR 3·78 [2·99-4·78]); angina showed seven-fold increased odds in the presence of chronic pain and depression (OR 7·76 [6·05-9·95]) and chronic pain nine-fold in the presence of depression and angina (OR 9·43 [6·85-12·98]). In TwinsUK, the relationship between CWP and depression has been published (R = 0.34, p<0.01). Considering the CWP-cardiovascular relationship, the most suitable model to describe the observed data was a combination of A, C and E, with a small but significant genetic predisposition, shared between the two traits (2·2% [95% CI 0·06-0·23]). CONCLUSION: We found an increased co-occurrence of chronic pain, depression and cardiovascular disease in two independent cohorts (general population-based cohort, twins cohort) suggesting a shared genetic contribution. Adjustment for known environmental influences, particularly those relating to socio-economic status (Generation Scotland: age, gender, deprivation, smoking, education; Twins UK: age,BMI) did not explain the relationship observed between chronic pain, depression and cardiovascular disease. Our findings from two independent cohorts challenge the concept of traditional disease boundaries and warrant further investigation of shared biological mechanisms
A low cortisol response to stress is associated with musculoskeletal pain combined with increased pain sensitivity in young adults: A longitudinal cohort study
Background: In this study, we investigated whether an abnormal hypothalamic-pituitary-adrenal (HPA) axis response to psychosocial stress at 18 years of age is associated with musculoskeletal (MS) pain alone and MS pain combined with increased pain sensitivity at 22 years of age. Methods: The study sample included 805 participants from the Western Australian Pregnancy Cohort (Raine) Study who participated in the Trier Social Stress Test (TSST) at age 18 years. Number of pain sites, pain duration, pain intensity and pain frequency were assessed at age 22 to measure severity of MS pain. Cold and pressure pain thresholds were determined at age 22. Group-based trajectory modeling was applied to establish cortisol response patterns based on the TSST. Logistic regression was used to study the association of TSST patterns with MS pain alone and MS pain combined with increased cold or pressure pain sensitivity, adjusted for relevant confounding factors. All analyses were stratified by sex. Results: The mean (standard deviation) age during the TSST was 18.3 (0.3) years, and during MS pain assessment it was 22.2 (0.6). Forty-five percent of the participants were female. Three cortisol response patterns were identified, with cluster 1 (34 % of females, 21 % of males) reflecting hyporesponse, cluster 2 (47 %, 54 %) reflecting intermediate response and cluster 3 (18 %, 24 %) reflecting hyperresponse of the HPA axis. MS pain was reported by 42 % of females and 33 % of males at age 22 years. Compared with females in cluster 2, females in cluster 1 had an increased likelihood of having any MS pain (odds ratio 2.3, 95 % confidence interval 1.0-5.0) and more severe MS pain (2.8, 1.1-6.8) if their cold pain threshold was above the median. In addition, females in cluster 1 had an increased likelihood (3.5, 1.3-9.7) of having more severe MS pain if their pressure pain threshold was below the median. No statistically significant associations were observed in males. Conclusions: This study suggests that a hyporesponsive HPA axis at age 18 years is associated with MS pain at 22 years in young females with increased pain sensitivity
The brain-derived neurotrophic factor pathway, life stress, and chronic multi-site musculoskeletal pain
Stress-related psychiatric disorders across the life spa
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Biological stress systems, adverse life events and the onset of chronic multisite musculoskeletal pain : a six-year cohort study
Background Dysregulated biological stress systems and adverse life events, both independently and in interaction, have been hypothesized to initiate chronic pain. Objectives We examine whether (i) function of biological stress systems, (ii) adverse life events, and (iii) their combination predict the onset of chronic multi-site musculoskeletal pain. Methods Subjects (n=2039) of the Netherlands Study of Depression and Anxiety, free from chronic multi-site musculoskeletal pain at baseline, were identified using the Chronic Pain Grade Questionnaire and followed-up for the onset of chronic multi-site musculoskeletal pain over 6 years. Baseline assessment of biological stress systems comprised function of the hypothalamic-pituitary-adrenal (HPA)-axis (1-h cortisol awakening response, evening levels, post-dexamethasone levels), the immune system (IMS; basal and lipopolysaccharide-stimulated inflammation) and the autonomic nervous system (ANS; heart rate, pre-ejection period, standard deviation of the normal-to-normal interval, respiratory sinus arrhythmia). The number of recent adverse life events were assessed at baseline using the List of Threatening Events Questionnaire. Results HPA-axis, IMS and ANS functioning was not associated with onset of chronic multi-site musculoskeletal pain, either by itself or in interaction with adverse life events. Adverse life events did predict onset of chronic multi-site musculoskeletal pain
Biological stress systems, adverse life events and the onset of chronic multisite musculoskeletal pain : a six-year cohort study
Background Dysregulated biological stress systems and adverse life events, both independently and in interaction, have been hypothesized to initiate chronic pain. Objectives We examine whether (i) function of biological stress systems, (ii) adverse life events, and (iii) their combination predict the onset of chronic multi-site musculoskeletal pain. Methods Subjects (n=2039) of the Netherlands Study of Depression and Anxiety, free from chronic multi-site musculoskeletal pain at baseline, were identified using the Chronic Pain Grade Questionnaire and followed-up for the onset of chronic multi-site musculoskeletal pain over 6 years. Baseline assessment of biological stress systems comprised function of the hypothalamic-pituitary-adrenal (HPA)-axis (1-h cortisol awakening response, evening levels, post-dexamethasone levels), the immune system (IMS; basal and lipopolysaccharide-stimulated inflammation) and the autonomic nervous system (ANS; heart rate, pre-ejection period, standard deviation of the normal-to-normal interval, respiratory sinus arrhythmia). The number of recent adverse life events were assessed at baseline using the List of Threatening Events Questionnaire. Results HPA-axis, IMS and ANS functioning was not associated with onset of chronic multi-site musculoskeletal pain, either by itself or in interaction with adverse life events. Adverse life events did predict onset of chronic multi-site musculoskeletal pain
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