Extracellular heat-shock proteins (eHsp) such as those belonging to the 70-kDa family of Hsp (eg, Hsp72) have been hypothesized to act as a \"danger signal\" to immune cells, promote immune responses, and improve host defense. The current study tested this hypothesis. Adult male F344 rats were exposed to an acute laboratory stressor (100, 5-second, 1.6-mA inescapable tail shocks) and challenged with Escherichia coli. The number of colony-forming units (CFU) of bacteria at the site of injection, the levels of eHsp72, the immune response to eHsp72 and E. coli-derived lipopolysaccharide (LPS), and the amount of time required to recover from in vivo bacterial challenge were measured. CFUs were reduced 2, 4, and 6 hours after injection of E. coli in rats exposed to stress. Rats exposed to stress had elevated eHsp72 that was elevated rapidly (25 minutes) and remained elevated in the circulation and at the inflammatory site (2 hours after stressor termination). Both stressor exposure and eHsp72 administration in the absence of stress resulted in a facilitated pattern of recovery after bacterial inflammation induced by subcutaneous E. coli injection. Rats exposed to acute restraint (100 minutes) did not demonstrate elevated circulating eHsp72 or a facilitated pattern of recovery after bacterial challenge. In vitro stimulation of rat splenocytes and macrophages with eHsp72 elevated nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6, and this effect was specific to eHsp72 because it was not diminished by polymyxin B and was reduced by earlier heat-denature treatment. Stimulation of cells with eHsp72 combined with LPS resulted in a greater NO and cytokine response than that observed after stimulation with eHsp72 or LPS alone. In vivo, at the inflammatory site, the bacterial-induced NO response was potentiated by stress, and NO inhibition (L-NIO) reduced the stress-induced facilitation but had no effect on the control kinetics of bacterial inflammation recovery. Thus, these results lend support to the hypothesis that intense stressor exposure increases eHsp72, which acts as a danger signal to potentiate the NO response to bacterial challenge and facilitate recovery from bacterial inflammation.

Stress-induced extracellular hsp72 is a functionally significant danger signal to the immune system

Venipuncture training is an integral part of healthcare educational programs. Despite its extensive use, no previous studies have evaluated the psychobiological impact of this procedure among health-care students. Participants were 26 healthy students, practicing venipuncture on each other as part of their curricular activity. Self reported pencil and paper questionnaires aimed at assessing depression, anxiety and mood states were administered before and after venipuncture and saliva sample collection. Anti heat shock protein (Hsp) 70 and cortisol levels in blood and saliva were collected from the participants. A reduction in anxiety, anger and confusion mood states took place after venipuncture. All participants had high levels of cortisol and anti-Hsp 70 in the serum and saliva. Anti-Hsp 70 and cortisol evaluated in the serum were correlated with some of the mood variables. Routine educational practices such as venipuncture elicit significant psychological stress. If confirmed by additional studies it will have a significant implication on health-care educational practices.

/pdf/undergoing-venipuncture-in-healthcare-education-the-psycho-3y4c0byhze.pdf

Undergoing Venipuncture in Healthcare Education: The Psycho-Biological Effect on Students

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Undergoing Venipuncture in Healthcare Education: The Psycho-Biological Effect on Students

HSD79 Physicians’ Experience and Perceptions of Tetrabenazine for the Treatment of Tardive Dyskinesia

HSD102 Physicians’ Experience and Perceptions of Tetrabenazine for the Treatment of Huntington Disease-Related Chorea

EE654 Occupational Impact of Tardive Dyskinesia: A Cross-Sectional, International Survey Assessing the Perceptions and Experiences of Patients With TD and Physicians Who Treat TD