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      Neuropsychiatric Disease and Treatment (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on all aspects of neuropsychiatric and neurological disorders. Sign up for email alerts here.

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      Is Open Access

      Atrial natriuretic peptide and posterior pituitary neurohormone changes in patients with acute schizophrenia

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          Abstract

          Objectives

          Interactions between neuropeptides and psychiatric disorders have been investigated for many years. The aim of this study was to evaluate oxytocin (OXT), arginine-vasopressin (AVP), and atrial natriuretic peptide (ANP) and assess their interactions with each other, as well as investigate these changes with the manifestations of schizophrenia.

          Participants and methods

          Thirty-four individuals having acute schizophrenia and 24 healthy individuals as the control group were included in the study. Positive and Negative Syndrome Scales, Global Assessment of Functionality score, and Clinical Global Impression (CGI) scores were measured. Serum hormone levels were analyzed using enzyme-linked immunosorbent assay and were compared with the clinical findings.

          Results

          OXT levels were significantly lower and AVP levels were significantly higher in patients having acute schizophrenia than the control group. OXT was negatively correlated with Positive and Negative Syndrome Scales positive score and CGI score, while it was positively correlated with Global Assessment of Functionality score. AVP was negatively correlated with CGI score. ANP levels of the patients having schizophrenia were lower than the control group; however, there was no significant correlation with clinical findings.

          Conclusion

          The obtained data indicate that the AVP level was higher, but OXT and ANP levels were lower in the patients having acute schizophrenia. Specifically OXT is related with reduced disease severity and increased functionality.

          Most cited references25

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          The positive and negative syndrome scale (PANSS) for schizophrenia.

          The variable results of positive-negative research with schizophrenics underscore the importance of well-characterized, standardized measurement techniques. We report on the development and initial standardization of the Positive and Negative Syndrome Scale (PANSS) for typological and dimensional assessment. Based on two established psychiatric rating systems, the 30-item PANSS was conceived as an operationalized, drug-sensitive instrument that provides balanced representation of positive and negative symptoms and gauges their relationship to one another and to global psychopathology. It thus constitutes four scales measuring positive and negative syndromes, their differential, and general severity of illness. Study of 101 schizophrenics found the four scales to be normally distributed and supported their reliability and stability. Positive and negative scores were inversely correlated once their common association with general psychopathology was extracted, suggesting that they represent mutually exclusive constructs. Review of five studies involving the PANSS provided evidence of its criterion-related validity with antecedent, genealogical, and concurrent measures, its predictive validity, its drug sensitivity, and its utility for both typological and dimensional assessment.
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            When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders.

            Previous theories have emphasized the role of excessive glucocorticoid activity in the pathology of chronic stress. Nevertheless, insufficient glucocorticoid signaling (resulting from decreased hormone bioavailability or reduced hormone sensitivity) may have equally devastating effects on bodily function. Such effects may be related in part to the role of glucocorticoids in restraining activation of the immune system and other components of the stress response, including the sympathetic nervous system (SNS) and corticotropin-releasing hormone (CRH). The literature on neuroendocrine function and glucocorticoid-relevant pathologies in stress-related neuropsychiatric disorders, including posttraumatic stress disorder and major depression, was reviewed. Although not occurring together, both hypocortisolism and reduced responsiveness to glucocorticoids (as determined by dexamethasone challenge tests) were reliably found. Stress-related neuropsychiatric disorders were also associated with immune system activation/inflammation, high SNS tone, and CRH hypersecretion, which are all consistent with insufficient glucocorticoid-mediated regulation of stress hyperresponsiveness. Finally, antidepressants, a mainstay in the treatment of stress-related disorders, were regularly associated with evidence of enhanced glucocorticoid signaling. Neuroendocrine data provide evidence of insufficient glucocorticoid signaling in stress-related neuropsychiatric disorders. Impaired feedback regulation of relevant stress responses, especially immune activation/inflammation, may, in turn, contribute to stress-related pathology, including alterations in behavior, insulin sensitivity, bone metabolism, and acquired immune responses. From an evolutionary perspective, reduced glucocorticoid signaling, whether achieved at the level of the hormone or its receptor, may foster immune readiness and increase arousal. Emphasis on insufficient glucocorticoid signaling in stress-related pathology encourages development of therapeutic strategies to enhance glucocorticoid signaling pathways.
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              Modulating social behavior with oxytocin: how does it work? What does it mean?

              Among its many roles in body and brain, oxytocin influences social behavior. Understanding the precise nature of this influence is crucial, both within the broader theoretical context of neurobiology, social neuroscience and brain evolution, but also within a clinical context of disorders such as anxiety, schizophrenia, and autism. Research exploring oxytocin's role in human social behavior is difficult owing to its release in both body and brain and its interactive effects with other hormones and neuromodulators. Additional difficulties are due to the intricacies of the blood-brain barrier and oxytocin's instability, which creates measurement issues. Questions concerning how to interpret behavioral results of human experiments manipulating oxytocin are thus made all the more pressing. The current paper discusses several such questions. We highlight unresolved fundamental issues about what exactly happens when oxytocin is administered intranasally, whether such oxytocin does in fact reach appropriate receptors in brain, and whether central or peripheral influences account for the observed behavioral effects. We also highlight the deeper conceptual issue of whether the human data should be narrowly interpreted as implicating a specific role for oxytocin in complex social cognition, such a generosity, trust, or mentalizing, or more broadly interpreted as implicating a lower-level general effect on general states and dispositions, such as anxiety and social motivation. Using several influential studies, we show how seemingly specific, higher-level social-cognitive effects can emerge via a process by which oxytocin's broad influence is channeled into a specific social behavior in a context of an appropriate social and research setting. This article is part of a Special Issue entitled Oxytocin, Vasopressin, and Social Behavior. Copyright © 2011 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Neuropsychiatr Dis Treat
                Neuropsychiatr Dis Treat
                Neuropsychiatric Disease and Treatment
                Neuropsychiatric Disease and Treatment
                Dove Medical Press
                1176-6328
                1178-2021
                2018
                16 July 2018
                : 14
                : 1855-1860
                Affiliations
                [1 ]Department of Physiology, School of Medicine, Sakarya University, Sakarya, Turkey
                [2 ]Department of Psychiatry, School of Medicine, Sakarya University, Sakarya, Turkey, a.bulentyaz@ 123456gmail.com
                Author notes
                Correspondence: Ahmet Bulent Yazici, Department of Psychiatry, Sakarya University, Medical Faculty, Korucuk Street, Sakarya 54290, Turkey, Tel +90 532 599 4988, Fax +90 264 255 2105, Email a.bulentyaz@ 123456gmail.com
                Article
                ndt-14-1855
                10.2147/NDT.S169619
                6052919
                56ff5d47-d324-4da0-9f17-21ad8fb5dc99
                © 2018 Guzel et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Neurology
                schizophrenia,oxytocin,pans,gaf,cgi,avp
                Neurology
                schizophrenia, oxytocin, pans, gaf, cgi, avp

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