22 research outputs found

    Impact of group care living.

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    This study was designed to analyze and research the impact of group care placements on the child's development in the specific areas of educational development, relationship development, social skills development, and safety. Participants consisted of 33 (N= 33) alumni from two participating group homes in the state of Oklahoma. Requirements were that participants were 18 years or older and had been a resident at one of the participating group homes for at least one year of their childhood. A questionnaire consisting of 26 questions was completed by all participants. Respondents were asked questions regarding their perception of their educational development before and during their stay at the group home, their relationship development, their social skills development and their overall opinion of the level of safety they felt while in the group home. A correlation matrix was performed in SPSS to analyze the degree of association among variables. Significant correlations were found between many of the variables. The strongest correlation was found between the following variables: Feeling of Encouragement and Formed Positive Relationships (r= .804). In order to compare the means of the independent samples, a t-test was performed using the SPSS program. The following variables had obtained significance values; Enjoyed School (.025), Grades Improved (.006), Good Grades before Group Home (.006), Recommend Group Home (.024), Friends outside Group Home (.043), and Participated in activities outside group home (.007)

    The Effects of Health Promotion on Heart Disease in a Law Enforcement Agency

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    This paper demonstrates the validity or health promotion programs in the work place in the areas or health risk factors and health status. It concentrated on the effect that health promotion programs have on heart disease. The Surgeon General suggests that institutions (e.g., schools, medical settings, and workplaces should provide the time, physical facilities, and behavioral programs that lead to increased participation at low levels or physical activity and to more vigorous exercise activity. Some indicators that would be useful in convincing corporate managements to commit resources to health promotional projects would be reduction in absenteeism, improvements in staff members moral, and increased productivity, as well as improvements in risk factors and health status. A health screening test was given at a Police Department to determine which officers had risk factors that lead to heart disease. A series or physical and written examinations were given. The results indicated that most were in no danger, but some were prime candidates for heart disease

    Reduced orexin system function underlies resilience to repeated social defeat stress

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    Exposure to stress increases the risk of developing affective disorders such as depression and post-traumatic stress disorder (PTSD). However, these disorders occur in only a subset of individuals, those that are more vulnerable to the effects of stress, whereas others remain resilient. The coping style adopted to deal with the stressor, either passive or active coping, is related to vulnerability or resilience, respectively. Important neural substrates that mediate responses to a stressor are the orexins. These neuropeptides are altered in the cerebrospinal fluid of patients with stress-related illnesses such as depression and PTSD. The present experi- ments used a rodent social defeat model that generates actively coping rats and passively coping rats, which we have previously shown exhibit resilient and vulnerable profiles, respectively, to examine if orexins play a role in these stress-induced phenotypes. In situ radiolabeling and qPCR revealed that actively coping rats expressed significantly lower prepro-orexin mRNA compared with passively coping rats. This led to the hypothesis that lower levels of orexins contribute to resilience to repeated social stress. To test this hypothesis, rats first underwent 5 d of social defeat to establish active and passive coping phenotypes. Then, orexin neurons were inhibited before each social defeat for three additional days using designer receptors exclusively activated by designer drugs (DREADDs). Inhibition of orexins increased social interaction behavior and decreased depressive-like behavior in the vulnerable population of rats. Indeed, these data suggest that lowering orexins promoted resilience to social defeat and may be an important target for treatment of stress-related disorders

    Reduced orexin system function underlies resilience to repeated social defeat stress

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    Exposure to stress increases the risk of developing affective disorders such as depression and post-traumatic stress disorder (PTSD). However, these disorders occur in only a subset of individuals, those that are more vulnerable to the effects of stress, whereas others remain resilient. The coping style adopted to deal with the stressor, either passive or active coping, is related to vulnerability or resilience, respectively. Important neural substrates that mediate responses to a stressor are the orexins. These neuropeptides are altered in the cerebrospinal fluid of patients with stress-related illnesses such as depression and PTSD. The present experi- ments used a rodent social defeat model that generates actively coping rats and passively coping rats, which we have previously shown exhibit resilient and vulnerable profiles, respectively, to examine if orexins play a role in these stress-induced phenotypes. In situ radiolabeling and qPCR revealed that actively coping rats expressed significantly lower prepro-orexin mRNA compared with passively coping rats. This led to the hypothesis that lower levels of orexins contribute to resilience to repeated social stress. To test this hypothesis, rats first underwent 5 d of social defeat to establish active and passive coping phenotypes. Then, orexin neurons were inhibited before each social defeat for three additional days using designer receptors exclusively activated by designer drugs (DREADDs). Inhibition of orexins increased social interaction behavior and decreased depressive-like behavior in the vulnerable population of rats. Indeed, these data suggest that lowering orexins promoted resilience to social defeat and may be an important target for treatment of stress-related disorders

    Orexin 2 receptor regulation of the hypothalamic–pituitary–adrenal (HPA) response to acute and repeated stress

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    Orexins are hypothalamic neuropeptides that have a documented role in mediating the acute stress response. However, their role in habituation to repeated stress, and the role of orexin receptors (OX1R and OX2R) in the stress response, has yet to be defined. Orexin neuronal activation and levels in the cerebrospinal fluid were found to be stimulated with acute restraint, but were significantly reduced by day five of repeated restraint. As certain disease states such as panic disorder are associated with increased central orexin levels and failure to habituate to repeated stress, the effect of activating orexin signaling via Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) on the hypothalamic-pituitary-adrenal (HPA) response was evaluated after repeated restraint. While vehicle-treated rats displayed habituation of Adrenocorticotropic Hormone (ACTH) from day 1 to day 5 of restraint, stimulating orexins did not further increase ACTH beyond vehicle levels for either acute or repeated restraint. We delineated the roles of orexin receptors in acute and repeated stress by using a selective OX2R antagonist (MK-1064). Pretreatment with MK-1064 reduced day 1 ACTH levels, but did not allow further habituation on day 5 compared with vehicle-treated rats, indicating that endogenous OX2R activity plays a role in acute stress, but not in habituation to repeated stress. However, in restrained rats with further stimulated orexins by DREADDs, MK-1064 decreased ACTH levels on day 5. Collectively, these results indicate that the OX2R plays a role in acute stress, and can prevent habituation to repeated stress under conditions of high orexin release

    Orexin 2 receptor regulation of the hypothalamic–pituitary–adrenal (HPA) response to acute and repeated stress

    Get PDF
    Orexins are hypothalamic neuropeptides that have a documented role in mediating the acute stress response. However, their role in habituation to repeated stress, and the role of orexin receptors (OX1R and OX2R) in the stress response, has yet to be defined. Orexin neuronal activation and levels in the cerebrospinal fluid were found to be stimulated with acute restraint, but were significantly reduced by day five of repeated restraint. As certain disease states such as panic disorder are associated with increased central orexin levels and failure to habituate to repeated stress, the effect of activating orexin signaling via Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) on the hypothalamic-pituitary-adrenal (HPA) response was evaluated after repeated restraint. While vehicle-treated rats displayed habituation of Adrenocorticotropic Hormone (ACTH) from day 1 to day 5 of restraint, stimulating orexins did not further increase ACTH beyond vehicle levels for either acute or repeated restraint. We delineated the roles of orexin receptors in acute and repeated stress by using a selective OX2R antagonist (MK-1064). Pretreatment with MK-1064 reduced day 1 ACTH levels, but did not allow further habituation on day 5 compared with vehicle-treated rats, indicating that endogenous OX2R activity plays a role in acute stress, but not in habituation to repeated stress. However, in restrained rats with further stimulated orexins by DREADDs, MK-1064 decreased ACTH levels on day 5. Collectively, these results indicate that the OX2R plays a role in acute stress, and can prevent habituation to repeated stress under conditions of high orexin release

    Orexin signaling during social defeat stress influences subsequent social interaction behaviour and recognition memory

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    Orexins are neuropeptides synthesized in the lateral hypothalamus that influence arousal, feeding, reward pathways, and the response to stress. However, the role of orexins in repeated stress is not fully characterized. Here, we examined how orexins and their receptors contribute to the coping response during repeated social defeat and subsequent anxiety-like and memory-related behaviors. Specifically, we used Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) to stimulate orexins prior to each of five consecutive days of social defeat stress in adult male rats. Additionally, we determined the role of the orexin 2 receptor in these behaviors by using a selective orexin 2 receptor antagonist (MK-1064) administered prior to each social defeat. Following the 5 day social defeat conditioning period, rats were evaluated in social interaction and novel object recognition paradigms to assess anxiety-like behavior and recognition memory, respectively. Activation of orexin neurons by DREADDs prior to each social defeat decreased the average latency to become defeated across 5 days, indicative of a passive coping strategy that we have previously linked to a stress vulnerable phenotype. Moreover, stimulation of orexin signaling during defeat conditioning decreased subsequent social interaction and performance in the novel object recognition test indicating increased subsequent anxiety-like behavior and reduced working memory. Blocking the orexin 2 receptor during repeated defeat did not alter these effects. Together, our results suggest that orexin neuron activation produces a passive coping phenotype during social defeat leading to subsequent anxiety-like behaviors and memory deficits

    Bidirectional Relationship Between Opioids And Disrupted Sleep

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    The opioid epidemic has generated massive societal, economic, and medical consequences over the last 20 years. Opioids, like most drugs of abuse disrupt sleep, and conversely, poor sleep can be a risk factor for opioid use. However, the precise nature of the relationship between opioids and disrupted sleep is not well known. The research presented here serves to further our knowledge of the neurobiological underpinnings of this pathophysiological feedback cycle between opioids and disrupted sleep. First, we model chronic short sleep in mice and use innovative open-source tools to noninvasively and automatically generate data relating to sleep and morphine reward. We then use electroencephalography to show that morphine disrupts sleep during the dark cycle (active period) after 11 days of morphine. We then look to Mu Opioid Receptors (MORs) in the Paraventricular Nucleus of the Thalamus (PVT) as the locus of morphine-induced sleep disturbance. Manipulating PVT MOR expressing neurons transiently blocked morphine-induced wakefulness in the drug group but not general wakefulness in controls. Finally, using the same morphine administration paradigm, we examine the negative affect associated with protracted withdrawal from morphine. We find that the major cellular energy sensor in the brain, Adenosine Monophosphate-Activated Protein Kinase (AMPK) mediates certain behaviors during protracted withdrawal from morphine. This body of work contributes to our understanding of the intersection between sleep and opioids and demonstrates the importance of considering sleep in the treatment of substance use disorders
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