Computer-mediated communication and time pressure induce higher cardiovascular responses in the preparatory and execution phases of cooperative tasks / La comunicación mediada por ordenador y la presión temporal inducen mayores respuestas cardiovasculares durante la preparación y la ejecución de tareas cooperativas

The cardiovascular (CV) response to social challenge and stress is associated with the etiology of cardiovascular diseases. New ways of communication, time pressure and different types of information are common in our society. In this study, the cardiovascular response to two different tasks (open vs. closed information) was examined employing different communication channels (computer-mediated vs. face-to-face) and with different pace control (self vs. external). Our results indicate that there was a higher CV response in the computer-mediated condition, on the closed information task and in the externally paced condition. These role of these factors should be considered when studying the consequences of social stress and their underlying mechanisms(AU)

Las respuestas cardiovasculares (CV) en situaciones de estrés y reto han sido asociadas a diversos trastornos cardiovasculares, de alta prevalencia en las sociedades actuales. El empleo de nuevos canales de comunicación, el ritmo acelerado y el tipo de información manejada son potenciales factores moduladores de la respuesta psicofisiológica a situaciones comunes en nuestra sociedad, como la cooperación en grupos de trabajo. En este estudio se ha analizado la respuesta cardiovascular ante dos tareas (con información abierta vs cerrada), realizadas mediante distintos canales de comunicación (mediado por ordenador vs cara a cara) y con o sin presión temporal. Los datos muestran mayor frecuencia cardíaca y presión arterial sistólica en la condición mediada por ordenador, con información cerrada y con presión temporal. Estos factores deberán tenerse en cuenta en el estudio de las consecuencias del estrés social y de los mecanismos subyacentes(AU)

Estructura factorial y consistencia interna de la versión española del Parenting Stress Index-Short Form / Factor structure and internal consistency of the Spanish version of the Parenting Stress Index-Short Form

El objetivo de este estudio fue analizar las propiedades psicométricas de la versión española del Parenting Stress Index-Short Form. Después de traducir el instrumento utilizando el procedimiento de traducción (inglés-español) y retrotraducción (español-inglés), se administró a una muestra de 129 madres de niños entre 10 y 39 meses de edad. El análisis factorial exploratorio identificó dos factores: Estrés derivado del Cuidado del Niño y Malestar Personal, que explicaron el 48,77% de la varianza. La consistencia interna de dichos factores fue elevada (Estrés derivado del Cuidado del Niño: 0,90; Malestar Personal: 0,87). Se discuten las implicaciones de estos hallazgos y se dan sugerencias para futuras investigaciones(AU)

The aim of this study was to analyze the psychometric properties of the Spanish version of Parenting Stress Index-Short Form. After translating the instrument from English into Spanish using the forward-backward translation method, it was administered to a sample of 129 mothers of children aged between 10 and 39 months olds. The exploratory factor analysis identified two factors: Childrearing Stress and Personal Distress, which accounted for 48.77% of the variance. The internal consistency of these factors was high (Childrearing Stress: .90 and Personal Distress: .87). Implications of these findings and suggestions for future research are discussed(AU)

Estructura familiar, acontecimientos vitales estresantes y psicopatología en la adolescencia / Family structure, stressful life events and psychopathology in the teenager

El presente trabajo plantea estudiar el impacto de la experiencia de acontecimientos vitales estresantes y las manifestaciones clínicas de la población de adolescentes y jóvenes atendida en los Servicios de Salud Mental de Parla (Madrid, Área 10). Explorar cuáles son las variables de personalidad que determinan una respuesta diferencial ante los acontecimientos vitales estresantes, nos ayuda a comprender mejor los factores que hacen que los adolescentes resistan las adversidades de la vida, cuáles son los déficits de aquellos que sucumben y qué factores han de ponerse en marcha para lograr intervenciones eficaces (AU)

The aim of this research is the analysis of the impact of the stressful life experiences lived through the teenager clinic cases in the Parla mental health services (Area 10, Madrid). Scanning which personality variables carry out gap responses due to stressful vital events, it allow us to understand better the reasons how teenager can hold up the life adversities, which deficits are associated to who have failed, and which measures have to be set up to reach effective intervention (AU)

Intervenções psicoeducativas para manejo de estresse ocupacional: um estudo comparativo / Psychoeducational interventions to occupational stress management: a comparative study

Este estudo implementou e avaliou um programa de manejo de estresse ocupacional em um grupo de 74 funcionários administrativos de uma universidade privada, dos quais 42 foram designados para uma Intervenção Multimodal de Manejo de Estresse (ME) e 32 foram designados para um Treino em Habilidades Sociais (HS). Foram conduzidas 12 sessões psicoeducativas, de 90 minutos, em grupo, durante o horário de trabalho. Medidas pré e pós-teste foram feitas em imunidade, pressão arterial e respostas verbais de estresse, habilidades sociais e coping a problemas no trabalho. Ao final do programa, os participantes de ambas as intervenções apresentaram níveis similares de sintomas de estresse, coping a problemas no trabalho, habilidades sociais e imunidade. Apenas diferiram em pressão arterial diastólica: os participantes da intervenção ME apresentaram médias mais baixas nesta variável. Os resultados obtidos não encontraram superioridade de um tipo de intervenção sobre outro(AU)

This study implemented and evaluated an occupational stress management program for a group of 74 non-academics from a private university in the state of Goiás, Brazil. Forty-two employees attended a multimodal intervention for stress management while the other 32 attended social skills training. Both were conducted in 12 group sessions of 60 minutes each, during working hours. Preand post-test measurements were taken for immunity, blood pressure, and verbal stress responses, social skills and coping with problems at work. Covariance analyses and analyses of variance with stratification has demonstrated that the participants in both interventions presented similar levels of stress symptoms, coping with problems at work, social skills and immunity. They only differed in terms of diastolic blood pressure: The participants from the stress management intervention showed lower mean results (F (3.73) = 15.69, p< .05) for this variable. The results did not indicate that one type of intervention was superior to the other(AU)

Malocclusion induces chronic stress.

We examined the effect of occlusal disharmony in senescence-accelerated (SAMP8) mice on plasma corticosterone levels, spatial learning in the water maze, fos induction, hippocampal neuron number, expression of glucocorticoid receptors (GR) and glucocorticoid receptor messenger ribonucleic acid (GRmRNA) in hippocampus and inhibitor of glucocorticoid (metyrapone). Bite-raised aged mice had significantly greater plasma corticosterone levels than age-matched control mice as well as impaired spatial memory and decreased Fos induction and a number of neurons in hippocampus. GR and GRmRNA expressions were significantly decreased in aged bite-raised mice compared with age-matched control mice. Pretreatment with metyrapone inhibited not only the bite-raised induced increase in plasma corticosterone levels, but also the reduction in the number of hippocampal neurons and impaired spatial learning. These datas suggest that the bite-raised condition may enhance the aging process in hippocampus, thereby leading to impairment of spatial memory by stress.

The Fourth National Institutes of Health Symposium on the Functional Genomics of Critical Injury: Surviving stress from organ systems to molecules.

Recent strides in computational biology and high-throughput technologies have generated considerable interest in understanding complex biological systems. The application of these technologies to critical illness and injury offers the potential to define adaptive and maladaptive programs of gene expression induced by infection, shock, trauma, or other inflammatory triggers, and to detect biomarkers and genetic polymorphisms linked to these responses and outcome. A systems biology approach is timely because despite substantial effort, treatment approaches directed at a single mediator or inflammatory pathway have met with little success in altering outcomes of critically ill or injured patients. Highlights from the Fourth National Institute of Health Functional Genomics of Critical Illness and Injury Symposium are described herein, in addition to deliverables for the field identified during panel discussions. Next steps for the community and suggestions for future research are presented.

Differences in ethanol drinking between mice selected for high and low swim stress-induced analgesia.

Alcoholism is a complex disorder, still not fully understood, in which environmental and inherited risk factors play essential roles. Of particular importance may be chronic exposure to stress thought to increase preference for ethanol in genetically susceptible individuals. Animal and human data suggest that the opioid system may be involved in the development of alcohol dependence. We studied the effects of chronic mild stress (CMS) on the voluntary intake of 8% ethanol in the mouse lines displaying high (HA) or low (LA) swim stress-induced analgesia. These lines differ in the activity of the endogenous opioid system. Normally, 8% ethanol is aversive to rodents. We found that LA mice with the low opioid system activity exposed to CMS manifested greater ethanol intake than under no stress conditions. No such effect of CMS on ethanol consumption was observed in HA mice that display the enhanced opioid system activity. We conclude that CMS imposed on individuals with a genetically determined low opioid activity may favor the development of ethanol abuse.

Sex-specific programming of offspring emotionality after stress early in pregnancy.

Prenatal stress is associated with an increased vulnerability to neurodevelopmental disorders, including autism and schizophrenia. To determine the critical time window when fetal antecedents may induce a disease predisposition, we examined behavioral responses in offspring exposed to stress during early, mid, and late gestation. We found that male offspring exposed to stress early in gestation displayed maladaptive behavioral stress responsivity, anhedonia, and an increased sensitivity to selective serotonin reuptake inhibitor treatment. Long-term alterations in central corticotropin-releasing factor (CRF) and glucocorticoid receptor (GR) expression, as well as increased hypothalamic-pituitary-adrenal (HPA) axis responsivity, were present in these mice and likely contributed to an elevated stress sensitivity. Changes in CRF and GR gene methylation correlated with altered gene expression, providing important evidence of epigenetic programming during early prenatal stress. In addition, we found the core mechanism underlying male vulnerability may involve sex-specific placenta responsivity, where stress early in pregnancy significantly increased expression of PPARalpha (peroxisome proliferator-activated receptor alpha), IGFBP-1 (insulin-like growth factor binding protein 1), HIF3alpha (hypoxia-inducible factor 3a), and GLUT4 (glucose transporter 4) in male placentas but not females. Examination of placental epigenetic machinery revealed basal sex differences, providing further evidence that sex-specific programming begins very early in pregnancy, and may contribute to the timing and vulnerability of the developing fetus to maternal perturbations. Overall, these results indicate that stress experience early in pregnancy may contribute to male neurodevelopmental disorders through impacts on placental function and fetal development.

Salivary cortisol concentrations, stress and quality of life in women with endometriosis and chronic pelvic pain.

The objective of this study was to evaluate the perceived stress index, quality of life, and hypothalamus-pituitary-adrenal axis activity in women with endometriosis and chronic pelvic pain. For the study, 93 women with endometriosis and 82 healthy women volunteered. The visual analogue scale (VAS) (0=no pain; 10=severe pain) was used to determine pain intensity; the perceived stress questionnaire (PSQ) defined stress index, and the health-related quality-of-life (HRQOL)-SF-36 questionnaire was used to evaluate quality of life. Salivary cortisol was measured at 0800, 1600, and 2000 h and the awakening cortisol response was assessed to evaluate the hypothalamus-pituitary-adrenal axis activity. The results show that women with endometriosis and chronic pelvic pain of moderate intensity (4.1+/-0.58, mean+/-SEM) have higher levels of perceived stress (0.55+/-0.01 versus 0.42+/-0.01, p<0.05), a poorer quality of life expressed as lower scores for all items of the inventory and hypocortisolism. Lower levels of salivary cortisol were observed in all three samples collected, as well as in the awakening cortisol response, for women with endometriosis (0.19+/-0.09 microg/dl) when compared with controls (0.78+/-0.08 microg/dl, p<0.05 l), and it was independent of pain intensity and Mental health (MH) scores in SF-36. We concluded that women with endometriosis and chronic pelvic pain show low concentrations of salivary cortisol and a high level of perceived stress, associated with a poor quality of life. Whether the hypocortisolism was an adaptive response to the aversive symptoms of the disorder or a feature related to the etiology of endometriosis remains to be elucidated.

Do early-life insults contribute to the late-life development of Parkinson and Alzheimer diseases?

How early-life events "set the stage" for adult disease has emerged as a research focus. Historically, the epidemiology of disease risk factors has centered on adult life, with little scrutiny of early-life events. Here we review the concept that events in early life may contribute to late-life neurodegenerative disease development, with a focus on Parkinson disease (PD) and Alzheimer disease (AD). Suspect events in early life include infections, stress, poor nutrition, and environmental factors such as chemical and pesticide exposure. Adiposity appears to contribute to both PD and AD; and because early-life events contribute to the development of obesity, linkages may exist between early determinants of obesity and the subsequent development of these neurologic diseases. Many now suggest a life-course approach for determining the relative contributions of genetic and environmental factors in any chronic disease. This requires determining when during the life course that a given exposure has its greatest effect and how exposures may accumulate over the life span. The data for PD and AD suggest that a number of insults occurring early in life may lead or contribute to these diseases. More definitive knowledge of the key risk factors involved will be needed to implement intervention and preventative strategies early in life to dampen or prevent any adverse late-life outcomes.

Immobilization stress inhibits intimal fibromuscular proliferation in the process of arterial remodeling in rats.

We investigated role of beta-endorphin (END), which is released by immobilization stress, on intimal fibromuscular proliferation in a rat model of arterial remodeling after intimal injury. The endothelium of the abdominal aorta of Wistar-Kyoto rats was denuded, and the rats were subjected to immobilization stress (6 h/d), which raised the serum concentration of END, and intraperitoneal administration of either END (20 ng/kg/d) or naltrexone (NAL: 4 mg/kg/d). The proliferative activity (PA) of medial smooth muscle cells (SMCs) and the intima/media area ratio (R) were determined at 3 and 14 d after denudation, respectively. PA and R were significantly reduced by immobilization (PA: 64.8%, R: 34.6%), and NAL treatment completely reversed the decreases in PA and R. On the other hand, END reduced both PA and R (PA: 21.7% and R: 24.9%), and NAL also reversed the decreases in PA and R. END (20 pg/mL) inhibited both the proliferation (79% at 96 h) and migration (26%) of SMCs cultured with 5% fetal bovine serum in vitro, and NAL (100 microg/mL) reversed the inhibition of both activities. Our results suggest that immobilization stress stimulates the release of endogenous END, which then prevents both proliferation and migration of medial SMCs after intimal injury.

Monitoring changes in rugby league players' perceived stress and recovery during intensified training.

This study assessed whether the Recovery-Stress Questionnaire for Athletes (RESTQ-Sport) could be used to monitor changes in perceived stress and recovery during intensified training of rugby league players. 20 semiprofessional rugby league players were divided into two equal groups randomly assigned to complete 6 wk. of Normal Training or Intensified Training, each followed with a 7-day taper. Multistage Fitness Test performance and RESTQ-Sport measures were taken at the beginning, at 2-wk. intervals, and at the end of the training period. Endurance significantly decreased with Intensified Training and returned to baseline levels following the taper, while remaining unchanged in the Normal Training group. The RESTQ-Sport scores with training were positively related to stress subscale scores (Fatigue, Disturbed Breaks, and General Stress) and recovery subscale measures (Success, Physical Recovery, Being in Shape, Self-efficacy, Social Relaxation, General Well-being, and Sleep Quality) decreasing in the Intensified Training group and then normalising following the taper (Stress subscales: Fatigue and General Stress, and Recovery subscales: Physical Recovery and General Well-being). The RESTQ-Sport is a practical psychometric tool for monitoring responses to training in team-sport athletes.

A cell stress signaling model of fetal hemoglobin induction: what doesn't kill red blood cells may make them stronger.

A major goal of hemoglobinopathy research is to develop treatments that correct the underlying molecular defects responsible for sickle cell disease and beta-thalassemia. One approach to achieving this goal is the pharmacologic induction of fetal hemoglobin (HbF). This strategy is capable of inhibiting the polymerization of sickle hemoglobin and correcting the globin chain imbalance of beta-thalassemia. Despite this promise, none of the currently available HbF-inducing agents exhibit the combination of efficacy, safety, and convenience of use that would make them applicable to most patients. The recent success of targeted drug therapies for malignant diseases suggests that this approach could be effective for developing optimal HbF-inducing agents. A first step in applying this approach is the identification of specific molecular targets. However, while >70 HbF-inducing agents have been described, neither molecular mechanisms nor target molecules have been definitively verified for any of these compounds. To help focus investigation in this area, we have reviewed known HbF-inducing agents and their proposed mechanisms of action. We find that in many cases, current models inadequately explain key experimental results. By integrating features of the erythropoietic stress model of HbF induction with data from recent intracellular signaling experiments, we have developed a new model that has the potential to explain several findings that are inconsistent with previous models and to unify most HbF-inducing agents under a common mechanism: cell stress signaling. If correct, this or related models could lead to new opportunities for development of targeted therapies for the beta-hemoglobinopathies.

Stress and heart rate variability in surgeons during a 24-hour shift.

OBJECTIVE: To determine the specific effects of working long hours in surgery and potential cardiac stress in the individual surgeon by measuring heart rate variability (HRV). DESIGN, SETTING, AND PARTICIPANTS: This prospective study measured HRV before, during, and after a 24-hour shift in a standardized resting period of 10 minutes. Measurements were repeated over 10 shifts for each participant. Eight surgeons from a high-volume inner-city surgery department took part in the study. MAIN OUTCOME MEASURES: Time and frequency domain parameters of HRV as parameters of cardiac stress and correlations with perceived stress and fatigue on a visual analog scale. RESULTS: Perceived fatigue increased over 24 hours (P < .001), whereas stress levels decreased slightly (P = .06). Time domain parameters of HRV increased from before the shift to after the shift (standard deviation of normal to normal intervals, square root of the mean normal to normal interval, and percentage of adjacent pairs of normal to normal intervals differing by more than 50 milliseconds: all P < .01), denoting more cardiac relaxation. Both the low- and high-frequency components increased (P = .04 and P < .001, respectively), showing a heightened activity of the autonomic nervous system. CONCLUSIONS: Measurements of HRV during a 24-hour surgical shift did not show an increase in cardiac stress concerning time domain parameters despite intense workloads for a median of 20 hours. Frequency components increased in parallel, though, suggesting alterations in sympathovagal balance. Perceived stress levels correlated with HRV, whereas fatigue did not. Further studies on occupational stress and its cardiac effects in surgeons are needed.

The U-shaped response of initial mortality in Caenorhabditis elegans to mild heat shock: does it explain recent trends in human mortality?

U-shaped dose-response relationships (hormesis) have been documented in numerous biological, toxicological, and pharmacological investigations. For example, in response to a mild 35 degrees C heat shock, the longevity of Caenorhabditis elegans exhibits an inverted U-shaped dose-response. By applying the demographic concept of heterogeneity, we find that this U-shaped curve for longevity response is driven by a U-shaped dose-response of initial mortality. When worms are subjected to mild heat shock, the initial mortality decreases compared to the control. This initial mortality benefit increases with moderate increases in the length of heat shock, peaking at a point that coincides with the induction of damage to the worms. The dose of heat shock that coincided with this benefit in initial mortality did not affect the rate of increase in mortality.

Molecular mechanisms of stress-induced prefrontal cortical impairment: implications for mental illness.

The symptoms of mental illness often involve weakened regulation of thought, emotion, and behavior by the prefrontal cortex. Exposure to stress exacerbates symptoms of mental illness and causes marked prefrontal cortical dysfunction. Studies in animals have revealed the intracellular signaling pathways activated by stress exposure that induce profound prefrontal cortical impairment: Excessive dopamine stimulation of D1 receptors impairs prefrontal function via cAMP intracellular signaling, leading to disconnection of prefrontal networks, while excessive norepinephrine stimulation of alpha1 receptors impairs prefrontal function via phosphatidylinositol-protein kinase C intracellular signaling. Genetic studies indicate that the genes disrupted in serious mental illness (bipolar disorder and schizophrenia) often encode for the intracellular proteins that serve as brakes on the intracellular stress pathways. For example, disrupted in schizophrenia 1 (DISC1) normally regulates cAMP levels, while regulator of G protein signaling 4 (RGS4) and diacylglycerol kinase (DGKH)-the molecule most associated with bipolar disorder- normally serve to inhibit phosphatidylinositol-protein kinase C intracellular signaling. Patients with mutations resulting in loss of adequate function of these genes likely have weaker endogenous regulation of these stress pathways. This may account for the vulnerability to stress and the severe loss of PFC regulation of behavior, thought, and affect in these illnesses. This review highlights the signaling pathways onto which genetic vulnerability and stress converge to impair PFC function and induce debilitating symptoms such as thought disorder, disinhibition, and impaired working memory.

Chronic maternal stress affects growth, behaviour and hypothalamo-pituitary-adrenal function in juvenile offspring.

Maternal stress during pregnancy, particularly that combined with low socioeconomic status (SES), has been linked to an increased risk for impaired behavioural and emotional development and affective disorders in children. In animal models, acute periods of prenatal stress have profound effects on hypothalamo-pituitary-adrenal (HPA) function and behaviour. However, few studies have determined the impact of chronic exposure to stress in animal models. The objective of this study was to determine the effects of chronic maternal stress (CMS) during the 2nd half of pregnancy and nursing on growth, locomotor behaviour and HPA axis function in juvenile guinea pig offspring. Pregnant guinea pigs were exposed to a random combination of variable stressors every other day over the 2nd half of gestation and from postnatal day (pnd) 1 until weaning (pnd25). CMS mothers displayed increased basal salivary cortisol levels in the later stages of pregnancy compared to control mothers (p<0.05). The male offspring of CMS mothers had a lower bodyweight, which was maintained to weaning (p<0.01). In open-field testing, CMS male offspring showed a decrease in activity compared to controls (p<0.05). There was no effect of CMS on bodyweight or activity in female offspring. In contrast, both male and female offspring born to CMS mothers displayed increased (p<0.05) basal salivary cortisol at pnd25, but a blunted adrenocortical response to exposure to the novel open-field enclosure. In conclusion, CMS leads to modification of growth trajectory, locomotor activity and adrenocortical responses to stress in juvenile offspring. Further, males appear considerably more vulnerable to these effects than females.

Effect of bacterial lipopolysaccharide on the reproductive axis of prepubertal and peripubertal female rats. Ontogenic changes in the immune-neuroendocrine interactions.

The immune, endocrine and nervous systems are closely interrelated, which allows the organism to respond to different types of stress such as infection. Chronic infectious and inflammatory conditions are often accompanied by an impaired reproductive function. Leptin, a hormone produced by adipose tissue, exerts a regulatory function on the reproductive axis. It has homology with other proinflammatory cytokines and could be modified by lipopolysaccharide (LPS). Therefore, these studies were designed to investigate the effect of LPS administration on the neuroendocrine mechanisms involved in the regulation of the reproductive axis during sexual maturation. Fifteen- and 30-day-old female rats were injected with a single dose of LPS 250 microg/kg (i.p.) and then nitric oxide synthase (NOS) activity, hypothalamic excitatory/inhibitory amino acids and Gn-RH content, serum LH and leptin concentration were studied. In 15-day-old female rats LPS treatment did not modify hypothalamic inducible (iNOS) and constitutive (cNOS) NOS activity, Gn-RH, glutamate (GLU) and GABA content. Also serum LH and leptin levels were not modified. In 30-day-old rats LPS increased iNOS and cNOS activity (p < 0.001) and hypothalamic Gn-RH content (p < 0.001). At this age hypothalamic GABA content was significantly decreased (p < 0.001) without changes in GLU content, and serum LH (p < 0.001) and leptin (p < 0.0001) decreased significantly. In summary, current studies have demonstrated that LPS administration to 15- and 30-day-old female rats results in a different response of the hypothalamus-pituitary-gonadal axis and of the adipose tissue, demonstrating an ontogenic response of the immune-neuroendocrine system to LPS administration.

The role of the glutamatergic system in posttraumatic stress disorder.

Antiglutamatergic agents, such as lamotrigine, have been used successfully for the treatment of posttraumatic stress disorder (PTSD). They could be potentially acting through the stabilization of the corticotropin-releasing factor (CRF) systems. Glutamate mediates CRF release in various brain regions involved in the pathophysiology of PTSD, antiglutamatergic agents could stabilize the CRF system and, thereby, improve the symptom complex of PTSD (reexperiencing, hyperarousal, and avoidance). The role of glutamate and CRF in PTSD and other anxiety disorders are still being elucidated. However, it is clear that the glutamatergic systems play a role in the pathophysiology of PTSD.

Mind-body medicine and cancer.

Mind-body medicine, grounded in a respectful, therapeutic partnership, should be a central element in the care of every person diagnosed with cancer. This article reviews some of the physiologic foundations of mind-body medicine, the introduction of mind-body approaches to cancer care in the 1970s, the specific mind-body approaches that have been used, and the evidence that supports their use. The importance of group support for enhancing the effectiveness of these approaches is discussed. Guidelines are offered for integrating mind-body approaches and perspectives in the care of people who have cancer.