Physicians, therapists, staff and patients who were employed or receiving care in a primary care practice were asked about their direct experience with the site. Using ethnographic research methods, informants' points of view were elicited through interviews and their comments were examined using domain analysis. Two physicians were interviewed on 5 occasions, 5 therapists between 2 to 4 times, 5 patients twice, an office manager on 3 occasions and 1 nurse twice for a total of 40 interviews. The interviews ranged between 30 to 75 minutes (50 minute average) and took place over an eighteen-month period. Six categorical themes were identified: Characteristics of the Environment; Characteristics of Therapists; The Referral Process; Characteristics of Collaboration; The Psychotherapy Process; and Social Considerations. This study, the first ethnographic investigation of Family Systems Medicine, generated 5 principal conclusions. First, several marked dissimilarities between Family Systems Medicine as depicted in the professional literature and by informants emerged. Second, although the bio-psycho-social model promotes innovative awareness of social issues in health care, informants demonstrated status-quo knowledge. Third, certain aspects of the physician-therapist relationship--which includes an employee-employer arrangement--likely impedes collaboration. Fourth, patients emphasized the relevance of several issues (e.g., central location and prestige by association) that have heretofore been casually discussed in the literature. And, fifth, several problems associated with the use of ethnographies in a for-profit setting were identified. Finally, based upon a review of the findings, 4 major theoretical assertions are proposed: (1) Central location significantly reduces underutilization of health care; (2) Clinical outcomes are significantly enhanced due to / therapists' direct association with physicians ("prestige by association"); (3) Family therapists are not ideally suited to provide biopsychosocial care; and (4) The employee-employer relationship between therapists and physicians impedes collaboration. / Source: Dissertation Abstracts International, Volume: 56-07, Section: B, page: 3674. / Major Professor: Thomas Edward Smith. / Thesis (Ph.D.)--The Florida State University, 1995.

<p> This study employed a quantitative correlational research design to determine the extent of the relationship between professionals' spirituality, stress, and different dimensions of burnout in the workplace. Instruments included the Daily Spiritual Experience Scale (DSES), the Perceived Stress Scale (PSS), and the Maslach Burnout Inventory &ndash; General Survey (MBI-GS) Burnout Inventory. The study was conducted among male and female full-time employees working in an office setting located in the United States of America (<i> N</i> = 92) using an internet-based questionnaire service. Results indicate that spirituality was positively correlated with the Exhaustion and Cynicism burnout dimensions, and negatively correlated with the professional efficacy burnout dimension. The findings suggest that spirituality is a crucial predictor of occupational stress and burnout in the workplace and could be used as a coping strategy.</p><p>

Manipulations of central cholinergic activity alter the female rodent sexual behavior, lordosis. Agents that enhance cholinergic function, such as the acetylcholinesterase inhibitor physostigmine, activate lordosis in intact cycling female rats during proestrus when endogenous estrogen levels are high and not during diestrus when endogenous estrogen levels are low. In the present experiments, intraventricular administration of physostigmine activated lordosis in intact female rats at Mid-diestrus or Diestrus II only when exogenous estrogen was administered the day before. The degree of activation of lordosis by physostigmine at Mid-diestrus or Diestrus II was related to the priming dose of estrogen. These results indicate that cholinergic mechanisms that regulate sexual receptivity depend upon sufficient estrogen priming. Serum progesterone titers measured in these females were higher at Mid-diestrus than Diestrus II. In the absence of cholinergic manipulations, females were more likely to exhibit lordosis at Mid-diestrus than at Diestrus II, possibly as a consequence of elevated progesterone levels at Mid-Diestrus. Despite dissimilar levels of circulating progesterone, physostigmine activated lordosis equally at Mid-diestrus and Diestrus II following estradiol priming. These results suggest that the level of progesterone did not influence the ability of the cholinergic system to activate lordosis. Muscarinic binding as determined by the muscarinic antagonist ($\sp3$H) QNB varied across the estrous cycle. When compared to muscarinic binding during diestrus, muscarinic binding during Proestrus-Estrus was increased in two brain regions traditionally associated with the activation of lordosis, the medio-basal hypothalamus and central gray, and decreased in a brain region traditionally associated with the inhibition of lordosis, the preoptic area. However, administration of estradiol on the day before decreased muscarinic binding in the septum, preoptic area, and central gray. Estradiol administration did not change muscarinic binding in the medio-basal hypothalamus. Because these changes in binding were complex and unpredicted, a relationship between the estrogen regulation of lordosis and muscarinic binding in these areas was not evident. These results do not support the hypothesis that changes in muscarinic binding in these brain regions are necessary for the cholinergic activation of lordosis / acase@tulane.edu

Tyr-W-MIF-1 (Tyr-Pro-Trp-Gly-NH$\sb2$) is an endogenous brain peptide that was recently isolated from human cortex and bovine hypothalamus. In the absence of a gene or specific antibody for this small tetrapeptide, a detailed plan of investigation was developed to: (1) characterize the spinal mechanism of analgesic induction following intrathecal (IT) injection of Tyr-W-MIF-1; (2) characterize the supraspinal mechanism of analgesic induction following the intracerebroventricular (ICV) administration of Tyr-W-MIF-1; (3) determine the in vivo analgesic efficacy of Tyr-W-MIF-1 at the $\mu\sb1$ and $\mu\sb2$ subtypes of $\mu$ opioid receptors; and (4) investigate the functional localization of the peptide in brain using immunocytochemical detection of the fos proto-oncogene protein (FOS) after ICV administration of an analgesic dose of Tyr-W-MIF-1 Spinal administration of Tyr-W-MIF-1 produced a potent, naloxone-reversible analgesic response in mice. The analgesia induced by IT Tyr-W-MIF-1 was significantly attenuated by the $\mu$ opioid receptor-selective antagonist $\beta$-funaltrexamine but not by the $\mu\sb1$ opioid receptor-selective antagonist naloxonazine, indicating the response is mediated through the $\mu\sb2$ subtype of $\mu$ opioid receptors. Pretreatment with desipramine, an inhibitor of norepinephrine reuptake, potentiated the analgesic response of IT Tyr-W-MIF-1 whereas coadministration of IT yohimbine, an $\alpha\sb2$-adrenoceptor antagonist, attenuated the analgesic response of IT Tyr-W-MIF-1 alone. Thus, spinal administration of Tyr-W-MIF-1 induces analgesia that is mediated by $\mu\sb2$ opioid receptors and modulated by norepinephrine Supraspinal administration of Tyr-W-MIF-1 induced an analgesic response in mice that was about 75-fold less potent than IT Tyr-W-MIF-1 and about 15-fold less potent than ICV morphine. The analgesic response was antagonized by $\beta$-funaltrexamine but not by naloxonazine, indicating the response is mediated by $\mu\sb2$ opioid receptors. Although the response was antagonized by ICV naloxone, IT naloxone was nearly 40-fold more potent than ICV naloxone at antagonizing the analgesic response. Coadministration of ICV Tyr-W-MIF-1 with ICV morphine significantly antagonized the analgesic response of ICV morphine alone. These results indicate that Tyr-W-MIF-1 functions as a mixed $\mu\sb2$ opioid receptor agonist/$\mu\sb1$ opioid receptor antagonist after ICV administration in mice Immunocytochemical detection of FOS 3 h after ICV administration of an analgesic dose of Tyr-W-MIF-1 revealed an activation of neurons in brain areas associated with conditioning and reward processes, hypothalamic and neuroendocrine functioning and autonomic responses, but not analgesic induction. The pattern of FOS expression induced by ICV Tyr-W-MIF-1 was largely confined to the dopaminergic limbic forebrain and associated nuclei. The densest immunoreactivity, however, was detected in the nucleus of the solitary tract of animals administered Tyr-W-MIF-1 / acase@tulane.edu

The goal of the present study was to assess in middle-aged rats the effects of long-term ovarian hormone deprivation on the ability of subsequent estradiol treatment to influence levels of molecular markers in hippocampus and prefrontal cortex and performance on a prefrontal cortex sensitive attention task. In initial experiments to assess estradiol effects in young adults, 2-month-old rats were ovariectomized and implanted with capsules containing cholesterol or estradiol. One set of rats was sacrificed 10 days after treatment initiation and protein levels of choline acetyltransferase (ChAT), estrogen receptors alpha (ERalpha) and beta (ERbeta), and steroid receptor coactivator-1 (SRC-1) were measured using western blotting. Another set of animals was tested on the prefrontal cortex dependent 5-choice serial reaction time task (5-CSRTT). In a second set of experiments, middle-aged rats, 10 to 12 months of age, were ovariectomized and received either cholesterol control treatment, estradiol treatment initiated immediately following ovariectomy, or estradiol treatment initiated following 5 months of ovarian hormone deprivation. ChAT, ERalpha, ERbeta and SRC-1 protein levels were assessed in one set of animals, and 5-CSRTT performance was assessed in the second set. In young animals, estradiol treatment increased levels of ChAT and ERalpha in hippocampus, and ERalpha in prefrontal cortex relative to controls. In middle-aged animals, immediate estradiol treatment significantly increased ChAT and ERalpha in hippocampus, but not prefrontal cortex. However, delayed estradiol treatment failed to significantly increase ChAT and ERalpha protein levels in hippocampus, but did so in prefrontal cortex. Levels of ERbeta and SRC-1 were unaffected by estradiol treatment in either brain area in either age group. On the 5-CSRTT, young estradiol-treated rats outperformed controls when behavior was challenged by shortening the intertrial interval (Short ITI). In the same Short ITI condition, middle-aged rats receiving immediate estradiol treatment beginning at the age of 17 months, but not 12 months, outperformed controls as well as animals receiving delayed estradiol treatment. These data indicate that prolonged ovarian hormone deprivation alters the ability of subsequent estradiol treatment to regulate ChAT and ERalpha in brain areas important for cognition, and attenuates the ability of estradiol to enhance prefrontal cortex dependent cognitive performance / acase@tulane.edu

This study examines the relation between trauma, HPA-Axis dysregulation and PTSD symptoms as moderated by exposure to chronic life stress and parental stress. Sixty-three children and their parents participated in the study. Participants ranged in age from 7 to 14 years and were predominantly African-American. It was hypothesized (1) that there would be a significant positive relation between the number of traumatic events experienced and PTSD symptoms, and that this relationship would be moderated by both chronic stress and parental stress, such that as stress increased so would PTSD symptoms; and (2) that there would be a significant relation between exposure to trauma and HPA-Axis dysregulation, as measured by cortisol level, such that cortisol levels would show greater dysregulation under conditions of high trauma exposure than under conditions of low trauma exposure, and that this relationship would be moderated by both chronic stress and parental stress. Results revealed that children in the present sample endorsed high exposure to trauma and generally low cortisol levels, although trauma was not directly related to cortisol levels. Chronic stress moderated the relation between trauma and PTSD symptoms, such that as chronic stress increased, so did PTSD symptoms. Parental stress moderated the relation between trauma and PM cortisol, such that as parental stress increased, PM cortisol decreased. Additionally, chronic stress by parental stress moderated the relation between trauma and PTSD symptoms, as well as the relation between trauma and PM cortisol. Findings are interpreted within a psychobiological framework and suggest distinct biological processes for traumatic stress versus stress / acase@tulane.edu

The hypothesis that uric acid induces hyperactivity by interacting with adenosine receptors in a manner analagous to caffeine was investigated. First, the extent to which uric acid and caffeine compete with the binding of the adenosine agonist ($\sp3$H) N$\sp6$-cyclohexyladenosine ($\sp3$H)CHA was examined in vitro. Only caffeine was found to inhibit ($\sp3$H) CHA binding in rat forebrain membranes in vitro. Second, possible developmental modification of adenosine receptors was examined by administering the uricase inhibitor allantoxanamide, which produces hyperuricemia, caffeine, or a control vehicle to young rats on Days 4 through 27 after birth. A significant increase in the number of binding sites for ($\sp3$H) CHA in the cortex of caffeine treated animals was observed. Non-significant increases in ($\sp3$H) CHA binding were observed in the striatum and thalamus. Chronic allantoxanamide, however, produced a non-significant decrease in ($\sp3$H) CHA binding. Fourteen days after withdrawal from treatment there were small non-significant increases in ($\sp3$H) CHA binding in both chronic caffeine and hyperuricemic rats. The results suggest that the mechanism by which uric acid induces hyperactivity is not through caffeine-sensitive adenosine receptors. Chronic caffeine administration in young rats results in an increase in the number of ($\sp3$H) CHA binding sites which does not appear to be permanent. Although a number of studies have suggested that uric acid acts like caffeine to increase activity, the present study clearly shows that the mode of action of uric acid is not like that of caffeine, at least as regards adenosine receptors / acase@tulane.edu

The cumulative results of the present experiments show that CREB is essential for long-term memory formation in both the hippocampus and striatum. First, CREB activation was shown to be selective to brain regions specialized for different forms of memory processing. Increased phosphorylated CREB levels were sustained in the hippocampus of rats choosing a hippocampal-dependent place strategy whereas increased phosphorylated CREB levels were sustained in the striatum of rats choosing a striatal-dependent response strategy. Second, basal hippocampal CREB levels were shown to be decreased in a rat model system of hippocampal dysfunction and long-term memory impairment. Third, blocking CREB function in either the hippocampus or striatum suppressed long-term memory formation in a hippocampal- or striatal-dependent task, respectively. Fourth, increasing levels of CREB in the hippocampus facilitated long-term memory in a hippocampal-dependent task. Finally, the results shown here reveal that enhancing or blocking CREB function is only successful in altering memory formation if CREB is manipulated in the brain region that supports the type of memory being measured. Taken together, the results support the hypothesis that the hippocampus and striatum are central structures of two independent memory systems that simultaneously acquire information from the environment. The behavior that is produced is mediated by the brain system most congruent with the incoming stimuli / acase@tulane.edu

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