Dynamics of diurnal cortisol and alpha-amylase secretion and their associations with PTSD onset in recent interpersonal trauma survivors

Abstract Background Dysfunction in major stress response systems during the acute aftermath of trauma may contribute to risk for developing posttraumatic stress disorder (PTSD). The current study investigated how PTSD diagnosis and symptom severity, depressive symptoms, and childhood trauma uniquely relate to diurnal neuroendocrine secretion (cortisol and alpha-amylase rhythms) in women who recently experienced interpersonal trauma compared to non-traumatized controls (NTCs). Method Using a longitudinal design, we examined diurnal cortisol and alpha-amylase rhythms in 98 young women (n = 57 exposed to recent interpersonal trauma, n = 41 NTCs). Participants provided saliva samples and completed symptom measures at baseline and 1-, 3-, and 6-month follow-up. Results Multilevel models (MLMs) revealed lower waking cortisol predicted the development of PTSD in trauma survivors and distinguished at-risk women from NTCs. Women with greater childhood trauma exposure exhibited flatter diurnal cortisol slopes. Among trauma-exposed individuals, lower waking cortisol levels were associated with higher concurrent PTSD symptom severity. Regarding alpha-amylase, MLMs revealed women with greater childhood trauma exposure exhibited higher waking alpha-amylase and slower diurnal alpha-amylase increase. Conclusions Results suggest lower waking cortisol in the acute aftermath of trauma may be implicated in PTSD onset and maintenance. Findings also suggest childhood trauma may predict a different pattern of dysfunction in stress response systems following subsequent trauma exposure than the stress system dynamics associated with PTSD risk; childhood trauma appears to be associated with flattened diurnal cortisol and alpha-amylase slopes, as well as higher waking alpha-amylase.

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Cumulative childhood interpersonal trauma is associated with reduced cortical differentiation between threat and non-threat faces in posttraumatic stress disorder adults

Australian & New Zealand Journal of Psychiatry ◽

10.1177/0004867418761578 ◽

2018 ◽

Vol 53 (1) ◽

pp. 48-58 ◽

Cited By ~ 1

Author(s):

Denise A Chu ◽

Richard A Bryant ◽

Justine M Gatt ◽

Anthony WF Harris

Keyword(s):

Posttraumatic Stress Disorder ◽

Posttraumatic Stress ◽

Childhood Trauma ◽

Symptom Severity ◽

Stress Disorder ◽

Trauma Exposure ◽

Interpersonal Trauma ◽

Reward Processing ◽

Cumulative Exposure ◽

Neural Pathways

Objective: Posttraumatic stress disorder and childhood trauma frequently co-occur. Both are associated with abnormal neural responses to salient emotion stimuli. As childhood trauma is a risk factor for posttraumatic stress disorder, differentiating between their neurophysiological effects is necessary to elucidate the neural pathways by which childhood trauma exposure contributes to increased posttraumatic stress disorder risks. Methods: Face-specific N170 evoked response potentials for backward-masked (non-conscious) and conscious threat (fear, angry) and non-threat (happy) faces were measured in 77 adults (18–64 years old, 64% women, 78% right-handed) symptomatic for posttraumatic stress disorder. Differences in N170 peak amplitudes for fear-versus-happy and angry-versus-happy faces at bilateral temporo-occipital (T5, T6) sites were computed. The effect of cumulative exposure to childhood interpersonal trauma, other childhood trauma, adult trauma, depression and posttraumatic stress disorder symptom severity on the N170 response was assessed using hierarchical multiple regression analyses. Results: T5 N170 peak amplitudes for non-conscious fear-versus-happy faces were inversely related to cumulative childhood interpersonal trauma after accounting for socio-demographic, clinical symptom and other trauma factors. Posttraumatic stress disorder Avoidance was positively associated with N170 peak amplitudes for non-conscious fear-versus-happy faces, primarily due to reduced N170 responsivity to happy faces. Conclusion: Childhood interpersonal trauma exposure is associated with reduced discrimination between fear and happy faces, while avoidance symptom severity is associated with dampened responsivity to automatically processed happy faces in posttraumatic stress disorder adults. Results are discussed in terms of the likely contributions of impaired threat discrimination and deficient reward processing during neural processing of salient emotion stimuli, to increased risks of posttraumatic stress disorder onset and chronicity in childhood interpersonal trauma–exposed adults.

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Identification and optimization of PrsA in Bacillus subtilis for improved yield of amylase

Microbial Cell Factories ◽

10.1186/s12934-019-1203-0 ◽

2019 ◽

Vol 18 (1) ◽

Cited By ~ 6

Author(s):

Ane Quesada-Ganuza ◽

Minia Antelo-Varela ◽

Jeppe C. Mouritzen ◽

Jürgen Bartel ◽

Dörte Becher ◽

...

Keyword(s):

Bacillus Subtilis ◽

Stress Response ◽

Alpha Amylase ◽

Amylase Secretion ◽

Secretion Stress ◽

Final Yield ◽

Alpha Amylases

Abstract Background PrsA is an extracytoplasmic folding catalyst essential in Bacillus subtilis. Overexpression of the native PrsA from B. subtilis has repeatedly lead to increased amylase yields. Nevertheless, little is known about how the overexpression of heterologous PrsAs can affect amylase secretion. Results In this study, the final yield of five extracellular alpha-amylases was increased by heterologous PrsA co-expression up to 2.5 fold. The effect of the overexpression of heterologous PrsAs on alpha-amylase secretion is specific to the co-expressed alpha-amylase. Co-expression of a heterologous PrsA can significantly reduce the secretion stress response. Engineering of the B. licheniformis PrsA lead to a further increase in amylase secretion and reduced secretion stress. Conclusions In this work we show how heterologous PrsA overexpression can give a better result on heterologous amylase secretion than the native PrsA, and that PrsA homologs show a variety of specificity towards different alpha-amylases. We also demonstrate that on top of increasing amylase yield, a good PrsA–amylase pairing can lower the secretion stress response of B. subtilis. Finally, we present a new recombinant PrsA variant with increased performance in both supporting amylase secretion and lowering secretion stress.

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Dynamics and determinants of cortisol and alpha-amylase responses to repeated stressors in recent interpersonal trauma survivors

Psychoneuroendocrinology ◽

10.1016/j.psyneuen.2020.104899 ◽

2020 ◽

Vol 122 ◽

pp. 104899

Author(s):

Matthew C. Morris ◽

Brooklynn Bailey ◽

Natalie Hellman ◽

Amber Williams ◽

Edward W. Lannon ◽

...

Keyword(s):

Interpersonal Trauma ◽

Alpha Amylase ◽

Trauma Survivors

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Stress Hormones: How Do They Measure Up?

Biological Research For Nursing ◽

10.1177/1099800402238334 ◽

2002 ◽

Vol 4 (2) ◽

pp. 92-103 ◽

Cited By ~ 57

Author(s):

Shirley L. King ◽

Kathy M. Hegadoren

Keyword(s):

Stress Response ◽

Health Outcomes ◽

Stress Reduction ◽

Symptom Severity ◽

Stress Hormones ◽

Stress Disorders ◽

Biological Mechanisms ◽

Response Systems ◽

Negative Health Outcomes ◽

Adequate Data

Stress as a stimulus is integral to dynamic homeostatic functioning. However, evidence of its potentially deleterious effects on health is mounting. The impetus to understand the mechanisms that underlie stress-related negative health outcomes and prevent the development of stress-related disorders has never been greater. Symptom severity and subjective levels of stress, although frequently assessed in studies of stress in nursing research, may not provide adequate data to fully understand the pervasive effects of chronic or overwhelming stress associated with stress disorders. The measurement of stress hormones such as cortisol can help identify bodily changes that are stressor specific, people at risk for development of stress-related disorders, and the efficacy of interventions aimed at stress reduction. Cortisol, as the peripheral output of one of the major stress response systems, possesses several properties that make its measurement highly useful for investigations of stress. This article discusses some of the biological mechanisms involved in the stress response, why cortisol is commonly measured, and issues and approaches in cortisol measurement.

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Neuroanatomical Risk Factors for Post Traumatic Stress Disorder (PTSD) in Recent Trauma Survivors

10.1101/721134 ◽

2019 ◽

Author(s):

Ziv Ben-Zion ◽

Moran Artzi ◽

Dana Niry ◽

Nimrod Jackob Keynan ◽

Yoav Zeevi ◽

...

Keyword(s):

Risk Factors ◽

Post Traumatic Stress Disorder ◽

Traumatic Stress ◽

Symptom Severity ◽

Stress Disorder ◽

Trauma Exposure ◽

Hippocampal Volume ◽

Trauma Survivors ◽

Post Traumatic Stress ◽

Post Traumatic

AbstractBackgroundLow hippocampal volume could serve as an early risk factor for Post-traumatic Stress Disorder (PTSD) in interaction with other brain anomalies of developmental origin. One such anomaly may well be a presence of large Cavum Septum Pellucidum (CSP), which has been loosely associated with PTSD. Here, we performed a longitudinal prospective study of recent trauma survivors. We hypothesized that at one-month after trauma exposure, the relation between hippocampal volume and PTSD symptom severity will be moderated by CSP volume, and that this early interaction will account for persistent PTSD symptoms at subsequent time-points.Methods171 adults (87 females, average age=34.22, range=18-65) admitted to a general hospital’s emergency department following a traumatic event, underwent clinical assessment and structural MRI within one-month after trauma. Follow-up clinical evaluations were conducted at six (n=97) and fourteen (n=78) months after trauma. Hippocampus and CSP volumes were measured automatically by FreeSurfer software and verified manually by a neuroradiologist.ResultsAt one-month following trauma, CSP volume significantly moderated the relation between hippocampal volume and PTSD severity (p=0.026), and this interaction further predicted symptom severity at fourteen months post-trauma (p=0.018). Specifically, individuals with smaller hippocampus and larger CSP at one-month post-trauma, showed more severe symptoms at one-and fourteen months following trauma exposure.ConclusionsOur study provides evidence for an early neuroanatomical risk factors for PTSD, which could also predict the progression of the disorder in the year following trauma exposure. Such a simple-to-acquire neuroanatomical signature for PTSD could guide early management, as well as long-term monitoring.Trial RegistrationNeurobehavioral Moderators of Post-traumatic Disease Trajectories. ClinicalTrials.gov registration:NCT03756545.https://clinicaltrials.gov/ct2/show/NCT03756545

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The Novelty P300 as an Index of Symptom Severity in Trauma Survivors

PsycEXTRA Dataset ◽

10.1037/e517302011-324 ◽

2008 ◽

Author(s):

Matthew Kimble ◽

Molly Bowman ◽

Yanik Bababekov ◽

Libby Marks

Keyword(s):

Symptom Severity ◽

Trauma Survivors

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Childhood trauma moderates morphometric associations between orbitofrontal cortex and amygdala: implications for pathological personality traits

Psychological Medicine ◽

10.1017/s0033291720004468 ◽

2020 ◽

pp. 1-10

Author(s):

Nadia Bounoua ◽

Rickie Miglin ◽

Jeffrey M. Spielberg ◽

Curtis L. Johnson ◽

Naomi Sadeh

Keyword(s):

Personality Traits ◽

Childhood Trauma ◽

Orbitofrontal Cortex ◽

Functional Neuroimaging ◽

Trauma Exposure ◽

Diagnostic Interview ◽

Emotional Dysregulation ◽

Self Report ◽

Traumatic Experiences ◽

Pathological Personality Traits

Abstract Background Research has demonstrated that chronic stress exposure early in development can lead to detrimental alterations in the orbitofrontal cortex (OFC)–amygdala circuit. However, the majority of this research uses functional neuroimaging methods, and thus the extent to which childhood trauma corresponds to morphometric alterations in this limbic-cortical network has not yet been investigated. This study had two primary objectives: (i) to test whether anatomical associations between OFC–amygdala differed between adults as a function of exposure to chronic childhood assaultive trauma and (ii) to test how these environment-by-neurobiological effects relate to pathological personality traits. Methods Participants were 137 ethnically diverse adults (48.1% female) recruited from the community who completed a clinical diagnostic interview, a self-report measure of pathological personality traits, and anatomical MRI scans. Results Findings revealed that childhood trauma moderated bilateral OFC–amygdala volumetric associations. Specifically, adults with childhood trauma exposure showed a positive association between medial OFC volume and amygdalar volume, whereas adults with no childhood exposure showed the negative OFC–amygdala structural association observed in prior research with healthy samples. Examination of the translational relevance of trauma-related alterations in OFC–amygdala volumetric associations for disordered personality traits revealed that trauma exposure moderated the association of OFC volume with antagonistic and disinhibited phenotypes, traits characteristic of Cluster B personality disorders. Conclusions The OFC–amygdala circuit is a potential anatomical pathway through which early traumatic experiences perpetuate emotional dysregulation into adulthood and confer risk for personality pathology. Results provide novel evidence of divergent neuroanatomical pathways to similar personality phenotypes depending on early trauma exposure.

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Endocrine secretion of alpha-amylase by the pancreas

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1981.241.2.g170 ◽

1981 ◽

Vol 241 (2) ◽

pp. G170-G175 ◽

Cited By ~ 1

Author(s):

K. Miyasaka ◽

S. S. Rothman

Keyword(s):

Acinar Cell ◽

Digestive Enzyme ◽

Alpha Amylase ◽

Gastrointestinal Hormone ◽

Amylase Secretion ◽

Amylase Release ◽

Applied Dose ◽

Rabbit Pancreas ◽

Order Of Magnitude ◽

Endocrine Secretion

The effect of the gastrointestinal hormone, cholecystokinin-pancreozymin (CCK-PZ), on the flux of alpha-amylase across the basolateral surface of the pancreas into interstitial fluid was measured by following its appearance in the medium bathing whole rabbit pancreas in organ culture. CCK-PZ increased the rate of amylase release by about an order of magnitude for the maximum applied dose. The response was only observed at concentrations of CCK-PZ that were supramaximal for ductal enzyme secretion (320 pmol/l to 10 nmol/l). Over this range, amylase secretion into the bath varied widely with dose, whereas that into the duct remained relatively unchanged. These observations, in conjunction with others, suggest that the acinar cell, and not the duct system, is the direct source of this amylase and that there is a natural secretion of digestive enzyme from the acinar cell in the endocrine direction that is augmented by CCK-PZ or a homologous peptide.

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