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Invited Article : State of the Science: Salivary Biomarker Utilization for Stress Research
( An Kyungeh ),( Starkweather Angela ),( Sturgill Jamie L ),( Kao Hsueh Fen S ),( Salyer Jeanne ) 서울대학교 간호과학연구소 2014 간호학의 지평 Vol.11 No.2
Purpose: The use of salivary biomarkers for stress research is increasing based on the convenience of collection, affordability and scientific merit. This short review provides an overview of the state of the science of salivary biomarkers utilized in research related to stress. Methods: An integrative review was conducted. Results: The trend of utilizing salivary biomarkers in stress research was reviewed, specifically, focusing on the use of endocrine and inflammatory biomarkers incorporated in previous stress research. Then, a review of sampling procedures for salivary biomarkers and the analytic methods is provided. Finally, a discussion on the strengths and areas for improvement in the use of salivary biomarkers in stress research is included. Conclusion: Salivary biomarkers as an alternative to blood biomarkers are increasingly being recognized as a legitimate source for analyzing the stress response in humans.
Park, Hyun-Jung,Shim, Hyun-Soo,An, Kyungeh,Starkweather, Angela,Kim, Kyung Soo,Shim, Insop Hindawi Publishing Corporation 2015 Mediators of inflammation Vol.2015 No.-
<P>It has been known that activation of the central innate immune system or exposure to stress can disrupt balance of anti-/proinflammatory cytokines. The aim of the present study was to investigate the role of pro- and anti-inflammatory cytokines in the modulation of depressive-like behaviors, the hormonal and neurotransmitter systems in rats. We investigated whether centrally administered IL-1<I>β</I> is associated with activation of CNS inflammatory pathways and behavioral changes and whether treatment with IL-4 could modulate IL-1<I>β</I>-induced depressive-like behaviors and central neurotransmitter systems. Infusion of IL-4 significantly decreased IL-1<I>β</I>-induced anhedonic responses and increased social exploration and total activity. Treatment with IL-4 markedly blocked IL-1<I>β</I>-induced increase in PGE<SUB>2</SUB> and CORT levels. Also, IL-4 reduced IL-1<I>β</I>-induced 5-HT levels by inhibiting tryptophan hydroxylase (TPH) mRNA and activating serotonin transporter (SERT) in the hippocampus, and levels of NE were increased by activating tyrosine hydroxylase (TH) mRNA expression. These results demonstrate that IL-4 may locally contribute to the regulation of noradrenergic and serotonergic neurotransmission and may inhibit IL-1<I>β</I>-induced behavioral and immunological changes. The present results suggest that IL-4 modulates IL-1<I>β</I>-induced depressive behavior by inhibiting IL-1<I>β</I>-induced central glial activation and neurotransmitter alterations. IL-4 reduced central and systemic mediatory inflammatory activation, as well as reversing the IL-1<I>β</I>-induced alterations in neurotransmitter levels. The present findings contribute a biochemical pathway regulated by IL-4 that may have therapeutic utility for treatment of IL-1<I>β</I>-induced depressive behavior and neuroinflammation which warrants further study.</P>