975 resultados para Self injury


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The effects of stress at work are estimated to cost Canadian employers more than 20 billion dollars annually through absenteeism, sick leave and decreased productivity. Over the past two decades, Canadians have reported higher stress levels, increased work hours and more work performed outside of normal business hours. This work-life imbalance has far-reaching repercussions–affecting an employee’s performance as well as their health. Chronic exposure to these high levels of stress can also lead to burnout. The primary purpose of this study was to determine the magnitude in which burnout symptoms influence the relationship between work-life balance and self-rated health. The secondary purpose of this study was to determine if gender and age interactions exist in the relationship between burnout, work-life balance, and self-rated health. This cross-sectional study involved secondary analysis of 220 managers, workers and human service professionals who completed an Occupational Health Clinics for Ontario Workers’ Mental Injury Toolkit (MIT) survey for the launch of the MIT. The MIT survey is a modified form of the short version of the Copenhagen Psychosocial Questionnaire and includes expanded questioning around burnout, stress, sleep troubles, cognitive, and somatic symptoms. There were no significant differences in self-rated health based on a respondent’s gender or age, indicating that no interaction of gender and age would be required. Respondents with low self-rated health reported significantly higher burnout and work-life imbalance compared to those with high self-rated health. The regression analysis demonstrated that the magnitude in which burnout mediates the relationship between work-life balance and self-rated health was 96%. These findings support previous studies that associate high levels of work-life imbalance or burnout with poor self-rated health or health outcomes. In this study, the shared variance between work-life balance and burnout also supports recent efforts to redefine the context and causes of burnout to include non-work factors. Based on our findings, the potential exists for the development of workplace health promotion strategies that address maintaining a balance between work and home as they may improve employee health and reduce burnout.

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Characterization of cognitive and behavioral complaints is explored in Post-traumatic stress disorder (PTSD) and mild traumatic brain injury (MTBI) samples according to the severity of PTSD, depression and general anxiety conditions. Self-reported questionnaires on cognitive and behavioral changes are administered to PTSD, MTBI, MTBI/PTSD and control groups. Confounding variables are controlled. All groups report more complaints since the traumatic event. PTSD and MTBI/PTSD groups report more anxiety symptoms, depression and complaints compared to the MTBI group. Relatives of the PTSD group confirm most of the behavioral changes reported. Results suggest the utility of self-reported questionnaires to personalize cognitive and behavioral interventions in PTSD and MTBI to cope with the impacts of the traumatic event.

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We show that the prion protein (PrP) is expressed on the surface of bone marrow cell populations enriched in long-term repopulating hematopoietic stem cells. Affinity purification of the PrP-positive and PrP-negative fractions from these populations, followed by competitive reconstitution assays, show that all long-term repopulating hematopoietic stem cells express PrP. Hematopoietic stem cells from PrP null bone marrow exhibit impaired self-renewal in serial competitive transplantation experiments, and premature exhaustion when exposed to cell cycle-specific myelotoxic injury. Therefore, PrP is a novel marker for hematopoietic stem cells and regulates their self-renewal.

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Ischemia reperfusion injury (IRI) is a potential contributor for the development of chronic allograft nephropathy. T cells are important mediators of injury, even in the absence of alloantigens. We performed a depletion of TCD4(+)CTLA4(+)Foxp3(+) cells with anti-CD25(PC61), a treatment with anti-GITR (DTA-1) and rat-IgG, followed by 45 min of ischemia and 24/72 h of reperfusion, and then analyzed blood urea, kidney histopathology and gene expression in kidneys by QReal Time PCR. After 24 h of reperfusion, depletion of TCD4(+)CTLA4(+)Foxp3(+) cells reached 30.3%(spleen) and 67.8%(lymph nodes). 72 h after reperfusion depletion reached 43.1%(spleen) and 90.22%(lymph nodes) and depleted animals presented with significantly poorer renal function, while DTA-1 (anti-GITR)-treated ones showed a significant protection, all compared to serum urea from control group (IgG: 150.10 +/- 50.04; PC61: 187.23 +/- 31.38; DTA-1: 64.53 +/- 25.65, mg/dL, p<0.05). These data were corroborated by histopathology. We observed an increase of HO-1 expression in animals treated with DTA-1 at 72 h of reperfusion with significant differences. Thus, our results suggest that PC61 (anti-CD25) mAb treatment is deleterious, while DTA-1 (anti-GITR) mAb treatment presents a protective role in the renal IRI, indicating that some regulatory populations of T cells might have a role in IRI. (C) 2009 Elsevier B.V. All rights reserved.

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Increasing evidence suggests that the basic foundations of the self lie in the brain systems that represent the body. Specific sensorimotor stimulation has been shown to alter the bodily self. However, little is known about how disconnection of the brain from the body affects the phenomenological sense of the body and the self. Spinal cord injury (SCI) patients who exhibit massively reduced somatomotor processes below the lesion in the absence of brain damage are suitable for testing the influence of body signals on two important components of the self-the sense of disembodiment and body ownership. We recruited 30 SCI patients and 16 healthy participants, and evaluated the following parameters: (i) depersonalization symptoms, using the Cambridge Depersonalization Scale (CDS), and (ii) measures of body ownership, as quantified by the rubber hand illusion (RHI) paradigm. We found higher CDS scores in SCI patients, which show increased detachment from their body and internal bodily sensations and decreasing global body ownership with higher lesion level. The RHI paradigm reveals no alterations in the illusory ownership of the hand between SCI patients and controls. Yet, there was no typical proprioceptive drift in SCI patients with intact tactile sensation on the hand, which might be related to cortical reorganization in these patients. These results suggest that disconnection of somatomotor inputs to the brain due to spinal cord lesions resulted in a disturbed sense of an embodied self. Furthermore, plasticity-related cortical changes might influence the dynamics of the bodily self.

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STUDY DESIGN: Open label study to determine drug dose for a randomized double-blind placebo-controlled parallel study. OBJECTIVES: To assess the efficacy and side effects of oral Delta(9)-tetrahydrocannabinol (THC) and rectal THC-hemisuccinate (THC-HS) in SCI patients. SETTING: REHAB Basel, Switzerland. METHOD: Twenty-five patients with SCI were included in this three-phase study with individual dose adjustment, each consisting of 6 weeks. Twenty-two participants received oral THC open label starting with a single dose of 10 mg (Phase 1, completed by 15 patients). Eight subjects received rectal THC-HS (Phase 2, completed by seven patients). In Phase 3, six patients were treated with oral THC and seven with placebo. Major outcome parameters were the spasticity sum score (SSS) using the Modified Ashworth Scale (MAS) and self-ratings of spasticity. RESULTS: Mean daily doses were 31 mg with THC and 43 mg with THC-HS. Mean SSS for THC decreased significantly from 16.72 (+/-7.60) at baseline to 8.92 (+/-7.14) on day 43. Similar improvement was seen with THC-HS. We observed a significant improvement of SSS with active drug (P=0.001) in the seven subjects who received oral THC in Phase 1 and placebo in Phase 3. Major reasons for drop out were increase of pain and psychological side effects. CONCLUSION: THC is an effective and safe drug in the treatment of spasticity. At least 15-20 mg per day were needed to achieve a therapeutic effect.

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The expression pattern of angiotensin AT2 receptors with predominance during fetal life and upregulation under pathological conditions during tissue injury/repair process suggests that AT2 receptors may exert an important action in injury/repair adaptive mechanisms. Less is known about AT2 receptors in acute ischemia-induced cardiac injury. We aimed here to elucidate the role of AT2 receptors after acute myocardial infarction. Double immunofluorescence staining showed that cardiac AT2 receptors were mainly detected in clusters of small c-kit+ cells accumulating in peri-infarct zone and c-kit+AT2+ cells increased in response to acute cardiac injury. Further, we isolated cardiac c-kit+AT2+ cell population by modified magnetic activated cell sorting and fluorescence activated cell sorting. These cardiac c-kit+AT2+ cells, represented approximately 0.19% of total cardiac cells in infarcted heart, were characterized by upregulated transcription factors implicated in cardiogenic differentiation (Gata-4, Notch-2, Nkx-2.5) and genes required for self-renewal (Tbx-3, c-Myc, Akt). When adult cardiomyocytes and cardiac c-kit+AT2+ cells isolated from infarcted rat hearts were cocultured, AT2 receptor stimulation in vitro inhibited apoptosis of these cocultured cardiomyocytes. Moreover, in vivo AT2 receptor stimulation led to an increased c-kit+AT2+ cell population in the infarcted myocardium and reduced apoptosis of cardiomyocytes in rats with acute myocardial infarction. These data suggest that cardiac c-kit+AT2+ cell population exists and increases after acute ischemic injury. AT2 receptor activation supports performance of cardiomyocytes, thus contributing to cardioprotection via cardiac c-kit+AT2+ cell population.

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BACKGROUND Bodily sensations are an important component of corporeal awareness. Spinal cord injury can leave affected body parts insentient and unmoving, leading to specific disturbances in the mental representation of one's own body and the sense of self. OBJECTIVE Here, we explored how illusions induced by multisensory stimulation influence immediate sensory signals and tactile awareness in patients with spinal cord injuries. METHODS The rubber hand illusion paradigm was applied to 2 patients with chronic and complete spinal cord injury of the sixth cervical spine, with severe somatosensory impairments in 2 of 5 fingers. RESULTS Both patients experienced a strong illusion of ownership of the rubber hand during synchronous, but not asynchronous, stroking. They also, spontaneously reported basic tactile sensations in their previously numb fingers. Tactile awareness from seeing the rubber hand was enhanced by progressively increasing the stimulation duration. CONCLUSIONS Multisensory illusions directly and specifically modulate the reemergence of sensory memories and enhance tactile sensation, despite (or as a result of) prior deafferentation. When sensory inputs are lost, and are later illusorily regained, the brain updates a coherent body image even several years after the body has become permanently unable to feel. This particular example of neural plasticity represents a significant opportunity to strengthen the sense of the self and the feelings of embodiment in patients with spinal cord injury.

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Post-traumatic sleep-wake disturbances are common after acute traumatic brain injury. Increased sleep need per 24 h and excessive daytime sleepiness are among the most prevalent post-traumatic sleep disorders and impair quality of life of trauma patients. Nevertheless, the relation between traumatic brain injury and sleep outcome, but also the link between post-traumatic sleep problems and clinical measures in the acute phase after traumatic brain injury has so far not been addressed in a controlled and prospective approach. We therefore performed a prospective controlled clinical study to examine (i) sleep-wake outcome after traumatic brain injury; and (ii) to screen for clinical and laboratory predictors of poor sleep-wake outcome after acute traumatic brain injury. Forty-two of 60 included patients with first-ever traumatic brain injury were available for follow-up examinations. Six months after trauma, the average sleep need per 24 h as assessed by actigraphy was markedly increased in patients as compared to controls (8.3 ± 1.1 h versus 7.1 ± 0.8 h, P < 0.0001). Objective daytime sleepiness was found in 57% of trauma patients and 19% of healthy subjects, and the average sleep latency in patients was reduced to 8.7 ± 4.6 min (12.1 ± 4.7 min in controls, P = 0.0009). Patients, but not controls, markedly underestimated both excessive sleep need and excessive daytime sleepiness when assessed only by subjective means, emphasizing the unreliability of self-assessment of increased sleep propensity in traumatic brain injury patients. At polysomnography, slow wave sleep after traumatic brain injury was more consolidated. The most important risk factor for developing increased sleep need after traumatic brain injury was the presence of an intracranial haemorrhage. In conclusion, we provide controlled and objective evidence for a direct relation between sleep-wake disturbances and traumatic brain injury, and for clinically significant underestimation of post-traumatic sleep-wake disturbances by trauma patients.

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The purpose of this study was to exam the relationship between internet use and depression among a population of individuals who have sustained spinal cord injury. This was cross-sectional survey design conducted among spinal cord injury (SCI) patients in the Model Spinal Cord Injury System. We included a total of 1,011 SCI-patients who were interviewed face-to-face or by telephone interview over approximately a three year time period (2004–2006). All data were collected through a telephone survey which included the Patient Health Questionnaire-9 (PHQ-9) to assess depression. We examined various scales of this survey, included a reduced 3-item scale (items 1, 2 and 6) to avoid the presence of somatic symptoms among SCI patients from influencing classification of depression. The frequency of internet usage was grouped as daily/weekly/monthly/non user. Covariates examined as possible confounders included demographic characteristics, occupational status, educational level, injury type, daily function of living, pain level, self-perceived health status and satisfaction with life. We observed a negative association between the frequency of internet use and the level of depression. Daily use of internet was associated with lower PHQ-9 score and depression; however this association did not reach statistical significance after for the mentioned covariates. In conclusion, the factors related to lower depression in SCI patients who use the internet are complicated. Daily internet usage was associated with lower levels of depression. The accuracy of 3-item scale needs further validation and investigation. Further study of internet usage pattern in SCI patient is recommended. ^

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BACKGROUND & AIMS The liver performs a panoply of complex activities coordinating metabolic, immunologic and detoxification processes. Despite the liver's robustness and unique self-regeneration capacity, viral infection, autoimmune disorders, fatty liver disease, alcohol abuse and drug-induced hepatotoxicity contribute to the increasing prevalence of liver failure. Liver injuries impair the clearance of bile acids from the hepatic portal vein which leads to their spill over into the peripheral circulation where they activate the G-protein-coupled bile acid receptor TGR5 to initiate a variety of hepatoprotective processes. METHODS By functionally linking activation of ectopically expressed TGR5 to an artificial promoter controlling transcription of the hepatocyte growth factor (HGF), we created a closed-loop synthetic signalling network that coordinated liver injury-associated serum bile acid levels to expression of HGF in a self-sufficient, reversible and dose-dependent manner. RESULTS After implantation of genetically engineered human cells inside auto-vascularizing, immunoprotective and clinically validated alginate-poly-(L-lysine)-alginate beads into mice, the liver-protection device detected pathologic serum bile acid levels and produced therapeutic HGF levels that protected the animals from acute drug-induced liver failure. CONCLUSIONS Genetically engineered cells containing theranostic gene circuits that dynamically interface with host metabolism may provide novel opportunities for preventive, acute and chronic healthcare. LAY SUMMARY Liver diseases leading to organ failure may go unnoticed as they do not trigger any symptoms or significant discomfort. We have designed a synthetic gene circuit that senses excessive bile acid levels associated with liver injuries and automatically produces a therapeutic protein in response. When integrated into mammalian cells and implanted into mice, the circuit detects the onset of liver injuries and coordinates the production of a protein pharmaceutical which prevents liver damage.

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OBJECTIVE This study is a prospective, controlled clinical and electrophysiologic trial examining the chronic course of posttraumatic sleep-wake disturbances (SWD). METHODS We screened 140 patients with acute, first-ever traumatic brain injury of any severity and included 60 patients for prospective follow-up examinations. Patients with prior brain trauma, other neurologic or systemic disease, drug abuse, or psychiatric comorbidities were excluded. Eighteen months after trauma, we performed detailed sleep assessment in 31 participants. As a control group, we enrolled healthy individuals without prior brain trauma matched for age, sex, and sleep satiation. RESULTS In the chronic state after traumatic brain injury, sleep need per 24 hours was persistently increased in trauma patients (8.1 ± 0.5 hours) as compared to healthy controls (7.1 ± 0.7 hours). The prevalence of chronic objective excessive daytime sleepiness was 67% in patients with brain trauma compared to 19% in controls. Patients significantly underestimated excessive daytime sleepiness and sleep need, emphasizing the unreliability of self-assessments on SWD in trauma patients. CONCLUSIONS This study provides prospective, controlled, and objective evidence for chronic persistence of posttraumatic SWD, which remain underestimated by patients. These results have clinical and medicolegal implications given that SWD can exacerbate other outcomes of traumatic brain injury, impair quality of life, and are associated with public safety hazards.

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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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Primary objective: To describe a prospective memory rehabilitation programme based on a compensatory training approach and report the results of three case studies. Research design: Programme evaluation using pre-and post-intervention assessments and telephone follow-up. Methods and procedures: Three participants with traumatic brain injury completed 8 weeks of training with 1 - 2 hour individual sessions. Assessments were formal prospective memory assessment, self-report and measures of diary use. Experimental interventions: Intervention aimed to identify potential barriers, establish self-awareness of memory deficits, introduce a customized compensatory tool, a cueing system and organizational strategies. A significant other was involved in training to assist generalization. Main outcomes and results: All three participants improved on formal prospective memory assessment and demonstrated successful diary use after the programme. Self-report of prospective memory failure fluctuated and may reflect increased self-awareness. Conclusion: A compensatory approach may be useful in improving prospective memory performance following TBI.