The moderating effect of personal mastery and the relations between stress and Plasminogen Activator Inhibitor-1 (PAI-1) antigen

OBJECTIVE: This study tested whether feelings of personal control over one's life circumstances (i.e., personal mastery) would attenuate the relations between stress (i.e., negative life events and caregiving distress) and Plasminogen Activator Inhibitor (PAI)-1 antigen, an inhibitor of fibrinolysis implicated in the development of cardiovascular disease. DESIGN: Seventy-one spousal dementia caregivers were assessed for plasma levels of PAI-1 antigen, negative life events, caregiver distress, and feelings of personal mastery. Regression analysis was used to determine if personal mastery moderated the relations between stress (i.e., life stress and caregiving distress) and PAI-1 antigen levels. MAIN OUTCOME MEASURE: Plasminogen activator inhibitor (PAI)-1 antigen in plasma. RESULTS: After controlling for other factors associated with PAI-1 antigen levels, negative life events were positively associated with plasma PAI-1 antigen concentrations in participants low in personal mastery (beta = .31; p = .050) but not in individuals high in personal mastery (beta = .22; p = .184). The moderating effect of mastery on the relations between caregiving distress and PAI-1 antigen did not reach statistical significance (p = .091). CONCLUSIONS: These data suggest that mastery may protect individuals from some of the alterations in hemostatic factors that have been linked to cardiovascular risk.

The association between beliefs about low back pain and work presenteeism

OBJECTIVE: To examine the influence of beliefs about low back pain (LBP) on reduced productivity at work ("presenteeism") caused by LBP. METHODS: Two thousand five hundred seven individuals completed the Back Beliefs Questionnaire, the Fear Avoidance Beliefs questionnaire (FABQ), and questions about LBP-related work-absence, reduced work-productivity, pain, comorbidity, and demographics. RESULTS: Six hundred seventy (25%) individuals were of working age, employed and reported current LBP. Univariate models showed beliefs were more "negative" in individuals with work-absence and reduced productivity (P = 0.0001). In multivariable analysis, controlling for confounders, "FABQwork" was a unique predictor of both absenteeism and presenteeism (each, P = 0.0001), though with small effect sizes. CONCLUSIONS: Negative beliefs about LBP are associated with both work absence and reduced work-productivity. Further investigations should examine their potential as a target for educational interventions when considering initiatives to reduce the socioeconomic costs of LBP.

The effect of natural habituation on coagulation responses to acute mental stress and recovery in men

Blood coagulation activation might be one mechanism linking acute mental stress with coronary events. We investigated the natural habituation of coagulation responses and recovery to short-term mental stress. Three times with one-week intervals, 24 men (mean age 47 +/- 7 years) underwent the same 13-min stressor (preparation, job interview, mental arithmetic). During each visit venous blood was obtained four times (baseline, immediately post-stress, 45 min of recovery, 105 min of recovery). Eight blood coagulation parameters were measured at weeks one and three. Acute stress provoked increases in von Willebrand factor antigen, fibrinogen, clotting factor FVII activity (FVII:C), FVIII:C, FXII:C (p's < or = 0.019), and D-dimer (N.S.). All coagulation parameters experienced full recovery except FVIII:C (p = 0.022). Stress did not significantly affect activated partial thromboplastin time and prothrombin time. At all time points FVIII:C and FXII:C levels were significantly higher at week one compared to week three (p's < or = 0.041). Before catheter insertion, systolic blood pressure (p = 0.001) and heart rate (p = 0.026) were relatively higher at week one. Unlike the magnitude of systolic blood pressure response to stress (p = 0.007) and of cortisol recovery from stress (p = 0.002), the magnitude of all coagulation responses to stress and the recovery from stress were similar in week one and week three. Sympathetic activation with anticipatory stress best explained increased baseline activity in FVIII and FXII at week one. An incapacity of the coagulation system to adapt to stress repeats is perhaps a consequence of evolution, but might also contribute to increased coronary risk in some individuals, particularly in those with cardiovascular diseases.

Effects of group stability on aggression, stress and injuries in breeding rabbits

On Swiss rabbit breeding farms, group-housed does are usually kept singly for 12 days around parturition to avoid pseudograviclity, double litters and deleterious fighting for nests. After this isolation phase there is usually an integration of new group members. Here we studied whether keeping the group composition stable would reduce agonistic interactions, stress levels and injuries when regrouping after the isolation phase. Does were kept in 12 pens containing 8 rabbits each. In two trials, with a total of 24 groups, the group composition before and after the 12 days isolation period remained the same (treatment: stable, S) in 12 groups. In the other 12 groups two or three does were replaced after the isolation phase by unfamiliar does (treatment: mixed, M). Does of S-groups had been housed together for one reproduction cycle. One day before and on days 2, 4 and 6 after regrouping, data on lesions, stress levels (faecal corticosterone metabolites, FCM) and agonistic interactions were collected and statistically analysed using mixed effects models. Lesion scores and the frequency of agonistic interactions were highest on day 2 after regrouping and thereafter decrease in both groups. There was a trend towards more lesions in M-groups compared to S-groups. After regrouping FCM levels were increased in M-groups, but not in S-groups. Furthermore, there was a significant interaction of treatment and experimental day on agonistic interactions. Thus, the frequency of biting and boxing increased more in M-groups than in S-groups. These findings indicate that group stability had an effect on agonistic interactions, stress and lesions. (C) 2012 Elsevier B.V. All rights reserved.

Oxidative-nitrosative stress and systemic vascular function in highlanders with and without exaggerated hypoxemia

BACKGROUND Acute exposure to high altitude stimulates free radical formation in lowlanders, yet whether this persists during chronic exposure in healthy, well-adapted and maladapted highlanders suffering from chronic mountain sickness (CMS) remains to be established. METHODS Oxidative-nitrosative stress (as determined by the presence of the biomarkers ascorbate radical [A •- ], via electron paramagnetic resonance spectroscopy, and nitrite [NO 2 2 ], via ozone-based chemiluminescence) was assessed in venous blood of 25 male highlanders in Bolivia living at 3,600 m with CMS (n 5 13, CMS 1 ) and without CMS (n 5 12, CMS 2 ). Twelve age- and activity-matched, healthy, male lowlanders were examined at sea level and during acute hypoxia. We also measured fl ow-mediated dilatation (FMD), arterial stiffness defined by augmentation index normalized for a heart rate of 75 beats/min (AIx-75), and carotid intima-media thickness (IMT). RESULTS Compared with normoxic lowlanders, oxidative-nitrosative stress was moderately increased in the CMS 2 group ( P , .05), as indicated by elevated A •- (3,191 457 arbitrary units [AU] vs 2,640 445 AU) and lower NO 2 2 (206 55 nM vs 420 128 nM), whereas vascular function remained preserved. This was comparable to that observed during acute hypoxia in lowlanders in whom vascular dysfunction is typically observed. In contrast, this response was markedly exaggerated in CMS 1 group (A •- , 3,765 429 AU; NO 2 2 , 148 50 nM) compared with both the CMS 2 group and lowlanders ( P , .05). This was associated with systemic vascular dysfunction as indicated by lower ( P , .05 vs CMS 2 ) FMD (4.2% 0.7% vs 7.6% 1.7%) and increased AIx-75 (23% 8% vs 12% 7%) and carotid IMT (714 127 m M vs 588 94 m M). CONCLUSIONS Healthy highlanders display a moderate, sustained elevation in oxidative-nitrosative stress that, unlike the equivalent increase evoked by acute hypoxia in healthy lowlanders, failed to affect vascular function. Its more marked elevation in patients with CMS may contribute to systemic vascular dysfunction.

Stress and hemostasis: an update

Numerous naturalistic, experimental, and mechanistic studies strongly support the notion that-as part of fight-or-flight response-hemostatic responses to acute psychosocial stress result in net hypercoagulability, which would protect a healthy organism from bleeding in case of injury. Sociodemographic factors, mental states, and comorbidities are important modulators of the acute prothrombotic stress response. In patients with atherosclerosis, exaggerated and prolonged stress-hypercoagulability might accelerate coronary thrombus growth following plaque rupture. Against a background risk from acquired prothrombotic conditions and inherited thrombophilia, acute stress also might trigger venous thromboembolic events. Chronic stressors such as job strain, dementia caregiving, and posttraumatic stress disorder as well as psychological distress from depressive and anxiety symptoms elicit a chronic low-grade hypercoagulable state that is no longer viewed as physiological but might impair vascular health. Through activation of the sympathetic nervous system, higher order cognitive processes and corticolimbic brain areas shape the acute prothrombotic stress response. Hypothalamic-pituitary-adrenal axis and autonomic dysfunction, including vagal withdrawal, are important regulators of hemostatic activity with longer lasting stress. Randomized placebo-controlled trials suggest that several cardiovascular drugs attenuate the acute prothrombotic stress response. Behavioral interventions and psychotropic medications might mitigate chronic low-grade hypercoagulability in stressed individuals, but further studies are clearly needed. Restoring normal hemostatic function with biobehavioral interventions bears the potential to ultimately decrease the risk of thrombotic diseases.

Toxic Stress and Child Hunger Over the Life Course: Three Case Studies

The causes and contexts of food insecurity among children in the U.S. are poorly understood because the prevalence of food insecurity at the child level is low compared to the prevalence of household food insecurity. In addition, caregivers may be reluctant to admit their children may not be getting enough food due to shame or fear they might lose custody of their children. Based on our ongoing qualitative research with mothers of young children, we suggest that food security among children is related to adverse childhood experiences of caregivers. This translates into poor mental and physical health in adolescence and adulthood, which can lead to inability to secure and maintain meaningful employment that pays a living wage. In this paper we propose that researchers shift the framework for understanding food insecurity in the United States to adopt a life course approach. This demands we pay greater attention to the lifelong consequences of exposure to trauma or toxic stress—exposure to violence, rape, abuse and neglect, and housing, food, and other forms of deprivation—during childhood. We then describe three case studies of women from our ongoing study to describe a variety of toxic stress exposures and how they have an impact on a woman’s earning potential, her mental health, and attitudes toward raising children. Each woman describes her exposure to violence and deprivation as a child and adolescent, describes experiences with child hunger, and explains how her experiences have shaped her ability to nourish her children. We describe ways in which we can shift the nature of research investigations on food insecurity, and provide recommendations for policy-oriented solutions regarding income support programs, early intervention programs, child and adult mental health services, and violence prevention programs.

Attitudes, stress and use of force in selected areas of Texas law enforcement

This research aimed to explore the extent to which police use of force was related to attitudes towards violence, agency type, and racism. Previous studies have found a culture of honor in the psychology of violence in the Southern United States. Were similar attitudes measurable among Texas professional line officers? Are there predictors of use of force?^ A self reported anonymous survey was administered to Texas patrol officers in the cities of Austin and Houston, and the Counties of Harris and Travis. A total of seventy-four questionnaires were used in the statistical analyses. Scales were developed measuring use of force, attitudes towards violence, and feelings on racism. Their relationship was examined.^ A regression model shows a strong and significant relationship between the officers' attitudes towards violence and the self-reported use of force. Further, agency type, municipal versus sheriff, also predicts use of force. Attitudes regarding race or racism, as measured by this study, were not predictive of use of force. ^

Oxidative Stress and Ca2+ Release Events in Mouse Cardiomyocytes

Cellular oxidative stress, associated with a variety of common cardiac diseases, is well recognized to affect the function of several key proteins involved in Ca2+ signaling and excitation-contraction coupling, which are known to be exquisitely sensitive to reactive oxygen species. These include the Ca2+ release channels of the sarcoplasmic reticulum (ryanodine receptors or RyR2s) and the Ca2+/calmodulin-dependent protein kinase II (CaMKII). Oxidation of RyR2s was found to increase the open probability of the channel, whereas CaMKII can be activated independent of Ca2+ through oxidation. Here, we investigated how oxidative stress affects RyR2 function and SR Ca2+ signaling in situ, by analyzing Ca2+ sparks in permeabilized mouse cardiomyocytes under a broad range of oxidative conditions. The results show that with increasing oxidative stress Ca2+ spark duration is prolonged. In addition, long and very long-lasting (up to hundreds of milliseconds) localized Ca2+ release events started to appear, eventually leading to sarcoplasmic reticulum (SR) Ca2+ depletion. These changes of release duration could be prevented by the CaMKII inhibitor KN93 and did not occur in mice lacking the CaMKII-specific S2814 phosphorylation site on RyR2. The appearance of long-lasting Ca2+ release events was paralleled by an increase of RyR2 oxidation, but also by RyR-S2814 phosphorylation, and by CaMKII oxidation. Our results suggest that in a strongly oxidative environment oxidation-dependent activation of CaMKII leads to RyR2 phosphorylation and thereby contributes to the massive prolongation of SR Ca2+ release events.