909 resultados para Stress, Psychological
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First published online: 30 October 2015
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Objective: To review the literature on the association between breastfeeding and postpartum depression. Sources: A review of literature found on MEDLINE/ PubMed database. Summary of findings: The literature consistently shows that breastfeeding provides a wide range of benefits for both the child and the mother. The psychological benefits for the mother are still in need of further research. Some studies point out that pregnancy depression is one of the factors that may contribute to breastfeeding failure. Others studies also suggest an association between breastfeeding and postpartum depression; the direction of this association is still unclear. Breastfeeding can promote hormonal processes that protect mothers against postpartum depression by attenuating cortisol response to stress. It can also reduce the risk of postpartum depression, by helping the regulation of sleep and wake patterns for mother and child, improving mothers self efficacy and her emotional involvement with the child, reducing the childs temperamental difficulties, and promoting a better interaction between mother and child. Conclusions: Studies demonstrate that breastfeeding can protect mothers from postpartum depression, and are starting to clarify which biological and psychological processes may explain this protection. However, there are still equivocal results in the literature that may be explained by the methodological limitations presented by some studies.
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Past research has demonstrated that divorced adults show more health problems and psychological distress than married adults. Considering the high prevalence rates of divorce among Western countries, new and robust measures should be developed to measure psychological distress after this specific transition in adulthood. The aim of this study was to adapt and validate a Portuguese version of the Psychological Adjustment to Separation Test-Part A (PAST-A; Sweeper and Halford in J Family Psychol 20(4):632640, 2006). PAST-A is a self-report measure that assesses two key dimensions of separation adjustment problems: lonely-negativity and former partner attachment. Psychometric properties of the Portuguese version of PAST-A were assessed in terms of factor structure, internal consistency, and convergent and divergent validity, in an online convenience sample with divorced adults (N = 460). The PAST-A two-factor structure was confirmed by exploratory and confirmatory factor analyses, with each factor demonstrating very satisfactory internal consistency and good convergence. In terms of discriminant validity, the Portuguese PAST-A reveals a distinct factor from psychological growth after divorce. The results provided support for the use of the Portuguese PAST-A with divorced adults and also suggested that the explicative factors of the psychological adjustment to divorce may be cross-cultural stable. The non-existence of validated divorce-related well-being measures and its implications for divorce research are also discussed.
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The aim of this study was to develop and validate a Portuguese version of the Short Form of the Posttraumatic Growth Inventory (PTGI-SF). Using an online convenience sample of Portuguese divorced adults (N = 482), we confirmed the oblique five-factor structure of the PTGI-SF by confirmatory factor analysis. The results demonstrated the measurement invariance across divorce initiator status groups. Total score and factors of PTGI-SF showed good internal consistency, with the exception of the New Possibilities factor, which revealed an acceptable reliability. The Portuguese PTGI-SF showed a satisfactory convergent validity. In terms of discriminant validity, posttraumatic growth assessed by the Portuguese PTGI-SF was a distinct factor from posttraumatic psychological adjustment. These preliminary findings suggest the cultural adaptation and also psychometric properties of the present Portuguese PTGI-SF to measure posttraumatic growth after personal crisis.
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Objective: To review the literature on the effects of parental divorce over the psychological maladjustment and physical health problems in children of divorced parents, thus contributing to the integration of existing scientific knowledge based on the biopsychosocial model of the impact of divorce on childrens physical health as proposed by Troxel and Matthews (2004). Sources: Review of the literature using MEDLINE and PsycInfo (1980-2007) databases, selecting the most representative articles on the subject. Special attention was paid to contributions by internationally renowned investigators on the subject. Summary of the findings: Divorce may be responsible for a decline of physical and psychological health in children. The developmental maladjustment of children is not triggered by divorce itself, but rather by other risk factors associated with it, such as interparental conflict, parental psychopathology, decline in socio-economic level, inconsistency in parenting styles, a parallel and conflicting co-parenting relationship between parents and low levels of social support. Such risk factors trigger maladjusted developmental pathways, marked by psychopathological symptoms, poor academic performance, worst levels of physical health, risk behavior, exacerbated psychophysiological responses to stress and weakening of the immune system. Conclusions: Clear links were observed between experiencing parental divorce and facing problems of physical and psychological maladjustment in children. Divorce is a stressor that should be considered by health professionals as potentially responsible for maladjusted neuropsychobiological responses and for decline in childrens physical health.
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Endometriosis is a chronic condition affecting 10 to15% of women in childbearing age. Understanding the impact of this disease on womens well-being is still a challenge, namely to intervene. Pain is the most current and troublesome symptom. Although medical treatments for pain relief are effective, recurrence rate remains significant, calling for a better understanding and development of new approaches for pain management. A group Cognitive Behavioral Therapy (CBT) for management of associated co-morbidities is suggested, paying special attention to Chronic Pelvic Pain (CPP). CBT design can be grounded on information collected from focus groups and a one-group exploratory trial. Evaluation of therapy effectiveness is possible to be performed by comparing group CBT to Usual Care (UC) and Support Group (SG) in a randomized controlled trial. Research in this area could represent an important step in providing a solution to the management of endometriosis and, to the best of our knowledge, the first national psychological approach for its understanding and treatment.
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OBJECTIVE: To determine the influence of stress on teaching medical emergencies in an Advanced Cardiac Life Support (ACLS) course and to verify this influence on learning, and the efficiency of emergency care training. METHODS: Seventeen physicians signed up for an ACLS course. Their pulses were taken and blood pressure (BP) verified on the first day, before the beginning of the course, and on the second day, during the theoretical and practical test (TPT). Variations in pulse rates and BP were compared with students' test grades. Then, students answered a questionnaire of variables (QV) about the amount of sleep they had during the course, the quantity of study material and the time spent studying for the course, and a stress scale graphic. RESULTS: Seven students had a pulse variation less than 10% between the 2 periods and 10 had a 10% or more variation. Grades on TPT were, respectively, 91.4±2.4 and 87.3±5.2 (p<0.05). Six students had a BP variation less than 20 mmHg, and in 11 it varied more than 21 mmHg. Grades on the TPT were 92.3±3.3 and 86.2± 8.1, respectively (p<0.05). The QV dates did not significantly influence grades. CONCLUSION: Stress, as an isolated variable, had a negative influence on the learning process and on the efficiency of emergency training in this situation.
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El objetivo principal de este proyecto es estudiar los mecanismos neurobiolgicos involucrados en el proceso de sensibilizacin emocional inducido por la abstinencia a drogas de abuso o por la exposicin a un estmulo estresante de caracteristicas incontrolables. El modelo animal de sensibilizacin a utilizar en este proyecto es la facilitacin en la formacin de memoria de miedo producida por dichos tratamientos. Nuestra hiptesis sugiere que este proceso es el resultado de un mecanismo desinhibitorio de las interneuronas GABArgicas del complejo basolateral de la amigdala. Por lo tanto se proponen los siguientes experimentos: 1) El estudio del curso temporal del efecto facilitador sobre la formacin de una nueva memoria de miedo luego de la abstinencia a drogas o la exposicin a un estmulo estresante (inmovilizacin). 2) La evaluacin de la liberacin"in vivo" de dopamina del complejo basolateral de la amigdala durante la adquisicin y la expresin de la memoria de miedo en animales previamente expuestos a la abstinencia o al estres. 3) El estudio de la infusin local de antagonistas de receptores dopaminrgicos en el complejo basolateral de la amgdala (BLA) o en el nucleo central de la amgdala (CeA) antes del estrs sobre la adquisicin y la expresin de una memoria de miedo. 4) La determinacin de la actividad de ERK 1/2 y CREB en el complejo basolateral de la amigdala o en el nucleo central de la amgdala durante la adquisicin y la expresin de una memoria de miedo en animales abstinentes o estresados. 5)El estudio de la infusin local de inhibidores de la MEK 1/2 en el complejo basolateral de la amigdala o en el nucleo central de la amgdala antes del estrs sobre la adquisicin y la expresin de una memoria de miedo. La facilitacin para generar memorias de miedo podra ser un componente crtico del sndrome de abstinencia al etanol responsable de las altas tasas de recurrencia asociadas con el alcoholismo. Por lo tanto se investigar el efecto de la evocacin de la memoria de miedo sobre la autoadministracin de etanol utilizando un paradigma de libre eleccin entre agua y soluciones de concentracin creciente de etanol en animales en abstinencia al etanol. Con el objeto de investigar si las propiedades reforzantes del etanol estn involucradas en el potencial aumento de la ingesta de etanol inducido por la evocacin de una memoria de miedo, se evaluar el efecto reforzante de etanol utilizando el paradigma de preferencia por un contexto asociado al etanol.
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El Estrs de Retculo Endoplsmico (RE) es inducido por la acumulacin de protenas sin plegar en el lumen de la organela. Esto se puede observar en diversas situaciones fisio-patolgicas como durante una infeccin viral o en proceso isqumico. Adems, contribuye a la base molecular de numerosas enfermedades ya sea ndole metablico (Fibrosis qustica o Diabetes Miellitus) o neurodegenerativas como mal de Alzheimer o Parkinson (Mutat Res, 2005, 569). Para restablecer la homeostasis en la organela se activa una seal de transduccin (UPR), cuya respuesta inmediata es la atenuacin de la sntesis de protena debido a la fosforilacin de subunidad alpha del factor eucaritico de iniciacin de translacin (eIF2) va PERK. Esta es una protena de membrana de RE que detecta estrs. Bajo condiciones normales, PERK est inactiva debido a la asociacin de su dominio luminar con la chaperona BIP (Nat Cell Biol, 2000, 2: 326). Frente a una situacin de estrs, la chaperona se disocia causando desinhibicin. Recientemente, (Plos One 5: e11925) se observ, bajo condiciones de estrs, un aumento de Ca2+ citoslico y un rpido incremento de la expresin de calcineurina (CN), una fosfatasa citoslica dependiente de calcio, heterodimrica formada por una subunidad cataltica (CN-A) y una regulatoria (CN-B). Adems, CN interacciona, sin intermediarios, con el dominio citoslico de PERK favoreciendo su trans-autofosforilacin. Resultados preliminares indican que, astrocitos CNA-/- exhibieron, en condiciones basales, un mayor nmero de clulas muertas y de niveles de eIF2 fosforilado que los astrocitos CNA-/-. Hiptesis: CNA/B interacciona con PERK cuando el Ca2+ citoslico esta incrementado luego de haberse inducido Estrs de RE, lo cual promueve dimerizacin y auto-fosforilacin de la quinasa, acentundose as la fosforilacin de eIF2 e inhibicin de la sntesis de protenas. Esta activacin citoslica de PERK colaborara con la ya descrita, desinhibicin luminal llevada cabo por BIP. Cuando el Ca2+ citoslico retorna a los niveles basales, PERK fosforila a CN, reduciendo su afinidad de unin y disocindose el complejo CN/PERK. Objetivo general: Definir las condiciones por las cuales CN interacciona con PERK y regula la fosforilacin de eIF2 e inhibicin de la sntesis de protena. Objetivos especficos: I-Estudiar la diferencia de afinidades y dependencia de Ca2+, de las dos isoformas de CN ( y ) en su asociacin con PERK. Adems verificar la posible participacin de la subunidad B de CN en esta interaccin. II-Determinar si la auto-fosforilacin de PERK es diferencialmente regulada por las dos isoformas de CN. III-Discernir la relacin del estado de fosforilacin de CN con su unin a PERK. IV-Determinar efectos fisiolgicos de la interaccin de CN-PERK durante la respuesta de Estrs de RE. Para llevar a cabo este proyecto se realizarn experimentos de biologa molecular, interaccin protena-protena, ensayos de fosforilacin in vitro y un perfil de polisoma con astrocitos CNA-/- , CNA-/- y astrocitos controles. Se espera encontrar una mayor afinidad de unin a PERK de la isoforma de CN y en condiciones donde la concentracin de Ca2+ sea del orden micromolar e imite niveles del in durante un estrs. Con respecto al estado de fosforilacin de CN, debido a los resultados preliminares, donde solo se la encontr fosforilada en condiciones basales, se piensa que CN podra interactuar con mayor afinidad con PERK cuando CN se encuentre desfosforilada. Por ltimo, se espera encontrar un aumento de eIF2 fosforilado y una acentuacin de la atenuacin de la sntesis de protena como consecuencia de la mayor activacin de PERK por su asociacin con la isoforma de CN en astrocitos donde el Estrs de RE se indujo por privacin de oxigeno y glucosa. Estos experimentos permitirn avanzar en el estudio de una nueva funcin citoprotectora de CN recientemente descrita por nuestro grupo de trabajo y sus implicancias en un modelo de isquemia. The accumulation of unfolded proteins into the Endoplasmic Reticulum (ER) activates a signal transduction cascade called Unfolding Protein Response (UPR), which attempts to restore homeostasis in the organelle. (PKR)-like-ER kinase (PERK) is an early stress response transmembrane protein that is generally inactive due to its association with the chaperone BIP. During ER stress, BIP is tritrated by the unfolded protein, leading PERK activation and phosphorylation of eukaryotic initiation factor-2 alpha (eIF2alpha), which attenuates protein sntesis. If ER damage is too great and homeostasis is not restored within a certain period of time, an apoptotic response is elicited. We recently demonstrated a cytosolic Ca2+ increase in Xenopus oocytes after induce ER stress. Moreover, calcineurin A/B, a an heterotrimeric Ca2+ dependent phosphatases (CN-A/B), associates with PERK increasing its auto-phosphorylation and significantly enhancing cell viability. Preliminary results suggest that, CN-A-/- knockout astrocytes exhibit a significant higher eIF2 phosphorylated level compared to CN-A-/- astrocytes. Our working hypothesis establishes that: CN binds to PERK when cytosolic Ca2+ is initially increased by ER stress, promoting dimerization and autophosphorylation, which leads to phosphorylation of elF2 and subsequently attenuation of protein translation. When cytosolic Ca2+ returns to resting levels, PERK phosphorylates CN, reducing its binding affinity so that the CN/PERK complex dissociates. The goal of this project is to determine the conditions by which CN binding to PERK attenuates protein translation during the ER stress response and subsequently, to determine how the interaction of CN with PERK is terminated when stress is removed. To perform this project is planed to do molecular biology experiments, pull down assays, in vitro phosphorylations and assess overall mRNA translation efficiency doing a polisome profile.
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El lser de baja y media energa y la magnetoterapia son utilizados en desrdenes osteomioarticulares por sus efectos analgsico, antiinflamatorio y trfico, entre los ms destacados. Sin embargo, son insuficientes las investigaciones sobre su mecanismo de accin y antecedentes cientficos que avalen sus efectos. Es por ello, que la determinacin de acontecimientos celulares y moleculares que ocurren durante la interaccin de estos tipos de energa con el sistema muscular, sera relevante para el conocimiento y optimizacin de tales terapias en las ciencias biomdicas. En las miopatas inflamatorias idiopticas, se encuentra afectada la estructura, morfologa y bioqumica del tejido muscular. La energa que ste requiere para el normal funcionamiento es generada en la mitocondria. Esta organela tambin es la responsable de la generacin de especies oxidantes provocando estrs oxidativo y el inicio de los procesos de apoptosis. Por lo antes dicho, consideramos que la determinacin de los biomarcadores inflamatorios asociados a estrs oxidativo, realizando el anlisis histomorfomtrico ultraestructural y valorando la actividad de los complejos enzimticos mitocondriales, permitira una evaluacin de la accin teraputica del lser y la magnetoterapia en un modelo experimental de miopata. Para ello se propone evaluar el efecto de la magnetoterapia y del lser de baja energa (He-Ne y As.Ga) en miopata experimental determinando indicadores inflamatorios asociados a estrs oxidativo, anlisis histomorfomtrico y valoracin de la actividad enzimtica mitocondrial. Especficamente: -Determinar indicadores inflamatorios y de estrs oxidativo: Oxido Ntrico, Grupos carbonilos, L-citrulina, Fibringeno, Superxido dismutasa, Glutation peroxidasa y Catalasa por espectrofotometra. -Identificar los cambios anatomopatolgicos del msculo esqueltico por microscopa ptica (MO): cuantificacin del infiltrado inflamatorio; MO de alta resolucin (MOAR) y por microscopa electrnica: histomorfometra de la ultraestructura miofibrilar y mitocondrial. -Valorar las actividades enzimticas de la citrato sintasa y de los complejos: I (NADH-ubiquinona reductasa), II (succinato-ubiquinona-reductasa) III (ubiquinona-citocromo c-reductasa) y IV (citocromo c-oxidasa); en mitocondrias de tejido muscular por espectrofotometra. -Evaluar la actividad apopttica en las fibras musculares de los diferentes grupos por tnica de T.U.N.E.L. Las mediciones mitocondriales (por ME) y de infiltrado inflamatorio (por MO) se realizarn en un total de 5 fotos de aumentos similares en forma aleatoria por grupo estudiado (n=10). Los cambios estructurales observados se analizarn en el programa Axiovision 4.8, para cuantificar el rea total ocupada, nmero total y grado de alteracin de las mitocondrias y el porcentaje de infiltrado inflamatorio determinando el grado de inflamacin. Los resultados de los datos cuantitativos se analizarn aplicando ANAVA (test de Fisher para comparaciones mltiples); y para los datos categricos se utilizar Chi cuadrado (test de Pearson), establecindose un nivel de significacin de p < 0.05 para todos los casos. Importancia del Proyecto: La salud y el bienestar del hombre son los logros perseguidos por las ciencias de la salud. La obtencin de terapias curativas o paliativas con un mnimo de efectos colaterales para el enfermo se incluye en estos logros. Por esto y todo lo anteriormente expuesto es que consideramos de gran importancia poder esclarecer desde las ciencias bsicas los efectos celulares y moleculares en modelos experimentales la accin de la terapia con lser y magnetoterapia para una aplicacin clnica con base cientfica en todas las reas de las Ciencias Mdicas. In the idiopathic inflammatory myopathies, is affected the structure, morphology and biochemistry of muscle tissue. The mitochondria is responsible for the generation of oxidizing species leading to oxidative stress and the beginning of the process of apoptosis. As said before, we consider the determination of inflammatory biomarkers related to oxidative stress, by ultrastructural morphometric analysis and assessing the activity of mitochondrial enzyme complexes, permit an evaluation of the therapeutic action of laser and magnetic therapy in an experimental model myopathy. We propose to evaluate the effect of the treatment identifying indicators in experimental inflammatory myopathy associated with oxidative stress, histomorphometric analysis and assessment of mitochondrial enzyme activity. Specifically -determining: Nitric oxide, carbonyl groups, L-citrulline, fibrinogen, superoxide dismutase, glutathione peroxidase and catalase by spectrophotometry. -Identify the pathological changes in skeletal muscle by optical microscopy (OM): quantification of the inflammatory infiltrate, OM high resolution (MOAR) and electron microscopy, histomorphometry of myofibrillar and mitochondrial ultrastructure. -Evaluate the enzymatic activity of citrate synthase and complexes: I, II, III and IV in mitochondria muscle tissue by spectrophotometry. -Evaluate apoptotic activity in muscle fibers by TUNEL technique of Mitochondrial measurements and inflammatory infiltration (by OM) was performed in a total of 5 photos of similar increases in random by the study group (n = 10). The structural changes observed are discussed in the program Axiovision 4.8, to quantify number, degree of alteration of mitochondria and the percentage of inflammatory infiltrate determining the degree of inflammation. The results of the quantitative data were analyzed using ANOVA (Fisher test), and categorical data with Chi-square (Pearson test), establishing a significance level of p <0.05.
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East Germany, men, fertility, first births, event history analysis, problem-centered interviews, methodical integration, triangulation, social psychology, gender
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Background: Studies have demonstrated the diagnostic accuracy and prognostic value of physical stress echocardiography in coronary artery disease. However, the prediction of mortality and major cardiac events in patients with exercise test positive for myocardial ischemia is limited. Objective: To evaluate the effectiveness of physical stress echocardiography in the prediction of mortality and major cardiac events in patients with exercise test positive for myocardial ischemia. Methods: This is a retrospective cohort in which 866 consecutive patients with exercise test positive for myocardial ischemia, and who underwent physical stress echocardiography were studied. Patients were divided into two groups: with physical stress echocardiography negative (G1) or positive (G2) for myocardial ischemia. The endpoints analyzed were all-cause mortality and major cardiac events, defined as cardiac death and non-fatal acute myocardial infarction. Results: G2 comprised 205 patients (23.7%). During the mean 85.6 ± 15.0-month follow-up, there were 26 deaths, of which six were cardiac deaths, and 25 non-fatal myocardial infarction cases. The independent predictors of mortality were: age, diabetes mellitus, and positive physical stress echocardiography (hazard ratio: 2.69; 95% confidence interval: 1.20 - 6.01; p = 0.016). The independent predictors of major cardiac events were: age, previous coronary artery disease, positive physical stress echocardiography (hazard ratio: 2.75; 95% confidence interval: 1.15 - 6.53; p = 0.022) and absence of a 10% increase in ejection fraction. All-cause mortality and the incidence of major cardiac events were significantly higher in G2 (p < 0. 001 and p = 0.001, respectively). Conclusion: Physical stress echocardiography provides additional prognostic information in patients with exercise test positive for myocardial ischemia.
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Background: Stress is associated with cardiovascular diseases. Objective: This study aimed at assessing whether chronic stress induces vascular alterations, and whether these modulations are nitric oxide (NO) and Ca2+ dependent. Methods: Wistar rats, 30 days of age, were separated into 2 groups: control (C) and Stress (St). Chronic stress consisted of immobilization for 1 hour/day, 5 days/week, 15 weeks. Systolic blood pressure was assessed. Vascular studies on aortic rings were performed. Concentration-effect curves were built for noradrenaline, in the presence of L-NAME or prazosin, acetylcholine, sodium nitroprusside and KCl. In addition, Ca2+ flux was also evaluated. Results: Chronic stress induced hypertension, decreased the vascular response to KCl and to noradrenaline, and increased the vascular response to acetylcholine. L-NAME blunted the difference observed in noradrenaline curves. Furthermore, contractile response to Ca2+ was decreased in the aorta of stressed rats. Conclusion: Our data suggest that the vascular response to chronic stress is an adaptation to its deleterious effects, such as hypertension. In addition, this adaptation is NO- and Ca2+-dependent. These data help to clarify the contribution of stress to cardiovascular abnormalities. However, further studies are necessary to better elucidate the mechanisms involved in the cardiovascular dysfunction associated with stressors. (Arq Bras Cardiol. 2014; [online].ahead print, PP.0-0)
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Neural nitric oxide synthase, neuroendocrine stress response, forced swimming, nNOS KO mice, hypothalamus, adrenal gland
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Prenatal stress, rodent, limbic system, neuronal development, dendritic spines, sex difference
