925 resultados para post-traumatic stress


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Cold-drawn steel rods and wires retain significant residual stresses as a consequence of the manufacturing process. These residual stresses are known to be detrimental for the mechanical properties of the wires and their durability in aggressive environments. Steel makers are aware of the problem and have developed post-drawing processes to try and reduce the residual stresses on the wires. The present authors have studied this problem for a number of years and have performed a detailed characterization of the residual stress state inside cold-drawn rods, including both experimental and numerical techniques. High-energy synchrotron sources have been particularly useful for this research. The results have shown how residual stresses evolve as a consequence of cold-drawing and how they change with subsequent post-drawing treatments. The authors have been able to measure for the first time a complete residual strain profile along the diameter in both phases (ferrite and cementite) of a cold-drawn steel rod.

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Polarized growth in yeast requires cooperation between the polarized actin cytoskeleton and delivery of post-Golgi secretory vesicles. We have previously reported that loss of the major tropomyosin isoform, Tpm1p, results in cells sensitive to perturbations in cell polarity. To identify components that bridge these processes, we sought mutations with both a conditional defect in secretion and a partial defect in polarity. Thus, we set up a genetic screen for mutations that conferred a conditional growth defect, showed synthetic lethality with tpm1Δ, and simultaneously became denser at the restrictive temperature, a hallmark of secretion-defective cells. Of the 10 complementation groups recovered, the group with the largest number of independent isolates was functionally null alleles of RAS2. Consistent with this, ras2Δ and tpm1Δ are synthetically lethal at 35°C. We show that ras2Δ confers temperature-sensitive growth and temperature-dependent depolarization of the actin cytoskeleton. Furthermore, we show that at elevated temperatures ras2Δ cells are partially defective in endocytosis and show a delocalization of two key polarity markers, Myo2p and Cdc42p. However, the conditional enhanced density phenotype of ras2Δ cells is not a defect in secretion. All the phenotypes of ras2Δ cells can be fully suppressed by expression of yeast RAS1 or RAS2 genes, human Ha-ras, or the double disruption of the stress response genes msn2Δmsn4Δ. Although the best characterized pathway of Ras function in yeast involves activation of the cAMP-dependent protein kinase A pathway, activation of the protein kinase A pathway does not fully suppress the actin polarity defects, suggesting that there is an additional pathway from Ras2p to Msn2/4p. Thus, Ras2p regulates cytoskeletal polarity in yeast under conditions of mild temperature stress through the stress response pathway.

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As an essential nutrient and a potential toxin, iron poses an exquisite regulatory problem in biology and medicine. At the cellular level, the basic molecular framework for the regulation of iron uptake, storage, and utilization has been defined. Two cytoplasmic RNA-binding proteins, iron-regulatory protein-1 (IRP-1) and IRP-2, respond to changes in cellular iron availability and coordinate the expression of mRNAs that harbor IRP-binding sites, iron-responsive elements (IREs). Nitric oxide (NO) and oxidative stress in the form of H2O2 also signal to IRPs and thereby influence cellular iron metabolism. The recent discovery of two IRE-regulated mRNAs encoding enzymes of the mitochondrial citric acid cycle may represent the beginnings of elucidating regulatory coupling between iron and energy metabolism. In addition to providing insights into the regulation of iron metabolism and its connections with other cellular pathways, the IRE/IRP system has emerged as a prime example for the understanding of translational regulation and mRNA stability control. Finally, IRP-1 has highlighted an unexpected role for iron sulfur clusters as post-translational regulatory switches.

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The mechanisms by which stress and anti-depressants exert opposite effects on the course of clinical depression are not known. However, potential candidates might include neurotrophic factors that regulate the development, plasticity, and survival of neurons. To explore this hypothesis, we examined the effects of stress and antidepressants on neurotrophin expression in the locus coeruleus (LC), which modulates many of the behavioral and physiological responses to stress and has been implicated in mood disorders. Using in situ hybridization, we demonstrate that neurotrophin 3 (NT-3) is expressed in noradrenergic neurons of the LC. Recurrent, but not acute, immobilization stress increased NT-3 mRNA levels in the LC. In contrast, chronic treatment with antidepressants decreased NT-3 mRNA levels. The effect occurred in response to antidepressants that blocked norepinephrine uptake, whereas serotonin-specific reuptake inhibitors did not alter NT-3 levels. Electroconvulsive seizures also decreased NT-3 expression in the LC as well as the hippocampus. Ntrk3 (neurotrophic tyrosine kinase receptor type 3; formerly TrkC), the receptor for NT-3, is expressed in the LC, but its mRNA levels did not change with stress or antidepressant treatments. Because, NT-3 is known to be trophic for LC neurons, our results raise the possibility that some of the effects of stress and antidepressants on LC function and plasticity could be mediated through NT-3. Moreover, the coexpression of NT-3 and its receptor in the LC suggests the potential for autocrine mechanisms of action.

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The last two decades have been marked by a growing public awareness of family violence. Research by social scientists has suggested that family violence is widespread (Gelles and Straus, 1988). It is estimated that every year 1.8 to 4 million women are physically abused by their partners (Novello, 1992). In fact, more women are abused by their husbands or boyfriends than are injured in car accidents, muggings, or rapes (Jaffe, Wolfe, and Wilson, 1990). A recent prevalence study by Fantuzzo, Boruch, Beriama, Atkins, and Marcus (1997) found that children were disproportionately present in households where there was a substantial incident of adult female assault. Experts estimate that 3.3 to 10 million children are exposed to marital violence each year (Carlson, 1984; Straus, 1991). Until recently, most researchers did not consider the impact of parental conflict on the children who witness this violence. The early literature in this field primarily focused on the incidence of violence against women and the inadequate response of community agencies (Jaffe et al, 1990). The needs of children were rarely considered. However, researchers have become increasingly aware that children exposed to marital violence are victims of a range of psychological maltreatment (e.g., terrorizing, isolation;Hart, Brassared & Karlson, 1996) and are at serious risk for the development of psychological problems (Fantuzzo, DePaola, Lambert, Martino, Anderson, and Sutton, 1991). Jouriles, Murphy and O'Leary (1989) found that children of battered women were four times more likely to exhibit psychopathology as were children living in non-violent homes. Further, researchers have found associations between childhood exposure to parental violence and the expression of violence in adulthood (Carlson, 1990). Existing research suggests that children who have witnessed marital violence manifest numerous emotional, social, and behavioral problems (Sternberg et al., 1993; Fantuzzo et al., 1991; Jaffe et al, 1990). Studies have found that children of battered women exhibit more internalizing and externalizing behavior problems than non-witnesschildren (Hughes and Fantuzzo, 1994; McCloskey, Figueredo, and Koss, 1995). In addition, children exposed to marital violence have been found to exhibit difficulties with social problem-solving, and have lower levels of social competence than nonwitnesses (Rosenberg, 1987; Moore, Pepler, Weinberg, Hammond, Waddell, & Weiser, 1990). Other reported difficulties include low self esteem (Hughes, 1988), poor school performance (Moore et al., 1990) and problems with aggression (Holden & Ritchie, 1991; Jaffe, Wolfe, Wilson, & Zak, 1986). Further, within the last decade, researchers have found that some children are traumatized by the witnessing experience, showing elevated levels of posttraumatic stress symptoms (Devoe & Graham-Bermann, 1997; Rossman, Bingham, & Emde, 1996; Kilpatrick, Litt, & Williams, 1997). These findings corroborate clinical reports that describe many exposed children as experiencing trauma reactions. It appears that the negative effects of witnessing marital violence are numerous and varied, ranging from mild emotional and behavioral problems to clinically significant levels of posttraumatic stress symptoms. These incidence figures and research findings indicate that children's exposure to violence is a significant problem in our nation today and has serious implications for the future.

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Le cancer de l’ovaire (COv) est le cancer gynécologique le plus létal chez la femme et les traitements existants, chirurgie et chimiothérapie, ont peu évolué au cours des dernières décennies. Nous proposons que la compréhension des différents destins cellulaires tels que la sénescence que peuvent choisir les cellules du cancer de l’ovaire en réponse à la chimiothérapie pourrait conduire à de nouvelles opportunités thérapeutiques. La sénescence cellulaire a été largement associée à l’activité de la protéine TP53, qui est mutée dans plus de 90% des cas de cancer de l’ovaire séreux de haut grade (COv-SHG), la forme la plus commune de la maladie. Dans nos travaux, à partir d’échantillons dérivés de patientes, nous montrons que les cultures primaires du cancer de l’ovaire séreux de haut grade exposées au stress ou à des drogues utilisées en chimiothérapie entrent en senescence grâce à l’activité d’un isoforme du gène CDKN2A (p16INK4A). Dans ces cellules, nous avons évalué les caractéristiques fondamentales de la sénescence cellulaire tels que les altérations morphologiques, l’activité béta galactosidase associée à la sénescence, les dommages à l’ADN, l’arrêt du cycle cellulaire et le phénotype sécrétoire associé à la sénescence. En utilisant des micromatrices tissulaires construites à partir d’échantillons humains de COv-SHG pré- et post-chimiothérapie, accompagnées de leurs données cliniques, nous avons quantifié des marqueurs de sénescence incluant une diminution de la prolifération cellulaire quelques semaines après chimiothérapie. De façon intéressante, l’expression de p16INK4A dans les échantillons de COv-SHG prétraitement corrèle avec une survie prolongée des patientes suite au traitement. Ceci suggère ainsi pour la première fois un impact biologique bénéfique pour la présence de cellules cancéreuses qui sont capable d’activer la sénescence, particulièrement pour le traitement du cancer de l’ovaire. Dans le but de complémenter les thérapies actuelles avec des approches de manipulation pharmacologique de la sénescence, nos résultats suggèrent qu’il serait important de déterminer l’impact positif ou négatif de la sénescence induite par la thérapie sur la progression de la maladie et la survie, pour chaque type de cancer de façon indépendante.

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L’acceptabilité d’un décès lors d’une simulation médicale reste débattue mais il existe peu de données sur la perspective des apprenants. Des médecins résidents ont effectué une pratique de code et ont rempli un questionnaire pré et post-simulation. Ils ont été exposés à deux scénarios où un bébé naissait sans signe de vie: 1. Nouveau-né ne répondant pas aux manœuvres de réanimation (DCD); 2. Nouveau-né s’améliorant avec une réanimation adéquate (REA). Les performances étaient évaluées à l’aide de la grille standardisée du Programme de Réanimation Néonatale. Le stress objectif (cortisol salivaire) et subjectif a été mesuré après le code. La rétroaction («feedback»), individuelle et en groupe, fut analysée à l’aide de méthodologies qualitatives. 59/62 apprenants ont répondu au questionnaire et 42 ont participé à la simulation. Tous les résidents trouvent les simulations bénéfiques et souhaitent y être exposés davantage. Le type et l’ordre des scénarios n’ont pas eu d’impact sur la performance. Un seul résident a interrompu les manœuvres de réanimation après 10 minutes d’asystolie, tel que recommandé, et 31% ont poursuivi après 20 minutes. Les participants trouvaient le scénario DCD plus stressant. Les niveaux de cortisol salivaire ont augmenté après les simulations (p<0.001) et ce, pour les deux scénarios. Cette augmentation était indépendante du scénario (p=0.06) et n’était pas associée à la performance. Les réponses à la question « Comment a été votre expérience? », ont permis d’identifier deux thèmes: 1. Le mannequin ne meurt pas en simulation médicale; 2. Le décès lors de la simulation signifie une réanimation inadéquate. Le décès lors d’une pratique de code est stressant, mais n’interfère pas avec la performance des soignants. Les apprenants trouvent cet exercice acceptable et bénéfique à leur pratique future.

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Thesis (Ph.D.)--University of Washington, 2016-06

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Identifying inequities in access to health care requires critical scrutiny of the patterns and processes of care decisions. This paper describes a conceptual model. derived from social problems theory. which is proposed as a useful framework for explaining patterns of post-acute care referral and in particular, individual variations in referral to rehabilitation after traumatic brain injury (TBI). The model is based on three main components: (1) characteristics of the individual with TBI, (2) activities of health care professionals and the processes of referral. and (3) the contexts of care. The central argument is that access to rehabilitation following TBI is a dynamic phenomenon concerning the interpretations and negotiations of health care professionals. which in turn are shaped by the organisational and broader health care contexts. The model developed in this paper provides opportunity to develop a complex analysis of post-acute care referral based on patient factors, contextual factors and decision-making processes. It is anticipated that this framework will have utility in other areas examining and understanding patterns of access to health care. (C) 2002 Elsevier Science Ltd. All rights reserved.

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In this study we examined three aspects pertaining to adrenocortical responsiveness in free-ranging Australian freshwater crocodiles (Crocodylus johnstoni). First, we examined the ability of freshwater crocodiles to produce corticosterone in response to a typical capture-stress protocol. A second objective addressed the relationship between capture stress, plasma glucose and corticosterone. Next we examined if variation in basal and capture-stress-induced levels of plasma corticosterone was linked to ecological or demographic factors for individuals in this free-ranging population. Blood samples obtained on three field trips were taken from a cross-sectional sample of the population. Crocodiles were bled once during four time categories at 0, 0. 5, 6, and 10 h post-capture. Plasma corticosterone increased significantly with time post-capture. Plasma glucose also significantly increased with duration of capture-stress and exhibited a positive and significant relationship with plasma corticosterone. Significant variation in basal or stress induced levels of corticosterone in crocodiles was not associated with any ecological or demographic factors including sex, age class or the year of capture that the crocodiles were sampled from. However, three immature males had basal levels of plasma corticosterone greater than 2 standard deviations above the mean. While crocodiles exhibited a pronounced, adrenocortical and hyperglycaemic response to capture stress, limited variation in adrenocortical responsiveness due to ecological and demographic factors was not evident. This feature could arise in part because this population was sampled during a period of environmental benigness. (C) 2003 Elsevier Science (USA). All rights reserved.

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We investigated the gene expression profiles of different members of the 1-aminocyclopropane-1-carboxilic acid (ACC) synthase (EC 4.4.1.14) gene family in broccoli (Brassica oleracea L. var. italica) during the post-harvest-induced senescence process. Using RT-PCR, three different cDNAs coding for ACC synthase (BROCACS1, BROCACS2 and BROCACS3) were amplified from floret tissue at the start of the senescence process. The three genes share relatively little homology, but have highly homologous sequences in Arabidopsis thaliana, and could be functionally related to these counterparts. Southern analyses suggest that BROCACS1 and BROCACS3 are present as single copy genes, while there are probably two copies of BROCACS2. All three genes showed different expression patterns: BROCACS1 is likely to be either wound - or mechanical stress-induced showing high transcript levels after harvesting, but no detectable expression afterwards. BROCACS2 shows steady expression throughout senescence, increasing at the latest stages, and BROCACS3 is almost undetectable until the final stages. Our results suggest that BROCACS1 could be required to initiate the senescence process, while BROCACS2 would be the main ACC synthase gene involved throughout the post-harvest-induced senescence. BROCACS3's expression pattern indicates that it is not directly involved in the initial stages of senescence, but in the final remobilization of cellular resources.

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Purpose : The purpose of this article is to critically review the literature to examine factors that are most consistently related to employment outcome following traumatic brain injury (TBI), with a particular focus on metacognitive skills. It also aims to develop a conceptual model of factors related to employment outcome. Method : The first stage of the review considered 85 studies published between 1980 and December 2003 which investigated factors associated with employment outcome following TBI. English-language studies were identified through searches of Medline and PsycINFO, as well as manual searches of journals and reference lists. The studies were evaluated and rated by two independent raters (Kappa = 0.835) according to the quality of their methodology based upon nine criteria. Fifty studies met the criteria for inclusion in the second stage of the review, which examined the relationship between a broad range of variables and employment outcome. Results : The factors most consistently associated with employment outcome included pre-injury occupational status, functional status at discharge, global cognitive functioning, perceptual ability, executive functioning, involvement in vocational rehabilitation services and emotional status. Conclusions : A conceptual model is presented which emphasises the importance of metacognitive, emotional and social environment factors for improving employment outcome.

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Aims Alpha-lipoic acid (ALA) is a thiol compound with antioxidant properties used in the treatment of diabetic polyneuropathy. ALA may also improve arterial function, but there have been scant human trials examining this notion. This project aimed to investigate the effects of oral and intra-arterial ALA on changes in systemic and regional haemodynamics, respectively. Methods In study 1, 16 healthy older men aged 58 +/- 7 years (mean +/- SD) received 600 mg of ALA or placebo, on two occasions 1 week apart, in a randomized cross-over design. Repeated measures of peripheral and central haemodynamics were then obtained for 90 min. Central blood pressure and indices of arterial stiffness [augmentation index (AIx) and estimated aortic pulse wave velocity] were recorded non-invasively using pulse wave analysis. Blood samples obtained pre- and post-treatments were analysed for erythrocyte antioxidant enzyme activity, plasma nitrite and malondialdehyde. In study 2 the effects of incremental cumulative doses (0.5, 1.0, 1.5 and 2.0 mg ml(-1) min(-1)) of intra-arterial ALA on forearm blood flow (FBF) were assessed in eight healthy subjects (aged 31 +/- 5 years) by conventional venous occlusion plethysmography. Results There were no significant changes on any of the central or peripheral haemodynamic measures after either oral or direct arterial administration of ALA. Plasma ALA was detected after oral supplementation (95% confidence intervals 463, 761 ng ml(-1)), but did not alter cellular or plasma measures of oxidative stress. Conclusions Neither oral nor intra-arterial ALA had any effect on regional and systemic haemodynamics or measures of oxidative stress in healthy men.

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Primary Objective: To document the clinical characteristics of acute dysphagia in a group of pediatric patients after traumatic brain injury (TBI). Research Design: Prospective group study. Methods: Fourteen subjects (7 males, 7 females), aged 4 years 1 month to 15 years, with moderate or severe TBI (Glasgow Coma Scale [GCS] < 12). Subjects were assessed via clinical bedside examination documenting cognitive status, oromotor function, feeding function, dietary recommendations, and an indication of overall feeding severity Results: A pattern of impaired cognition, altered behavior related to feeding, severe tonal and postural deficits, oromotor, respiratory, and laryngeal impairments, and oral sensitivity issues was revealed. Conclusions: Swallowing impairment was affected by multilevel deficits, which both individually and in combination had a negative impact on swallowing competence and safety. In light of deficits identified, which could not be observed on videofluoroscopic investigation alone, this study highlighted the importance of the clinical bedside examination in assessing dysphagia in pediatric patients post-TBI for identifying targets for intervention.

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Objective: To evaluate the effectiveness of continuous positive airway pressure (CPAP) therapy in the treatment of hypernasality following traumatic brain injury (17111). Design: An A-B-A experimental research design. Assessments were conducted prior to commencement of the program, midway, immediately posttreatment, and 1 month after completion of the CPAP therapy program. Participants: Three adults with dysarthria and moderate to severe hypernasality subsequent to TBI. Outcome Measures: Perceptual evaluation using the Frenchay Dysarthria Assessment, the Assessment of Intelligibility of Dysarthric Speech, and a speech sample analysis, and instrumental evaluation using the Nasometer. Results: Between assessment periods, varying degrees of improvement in hypernasality and sentence intelligibility were noted. At the 1-month post-CPAP assessment, all 3 participants demonstrated reduced nasalance values, and 2 exhibited increased sentence intelligibility. Conclusions: CPAP may be a valuable treatment of impaired velopharyngeal function in the TBI population.