Cohort study of Iraq and Afghanistan veterans in VHA (N = 181,620) with a PTSD diagnosis and ≥1 psychotherapy-coded outpatient visit from 2001 to 2014.
The present study investigated whether angiotensin (Ang) II-elicited hypertensive response is sensitized in a model of PTSD and whether inhibition of angiotensin-converting enzyme (ACE) or tumor necrosis factor (TNF)-α prior to PTSD blocks this sensitization of Ang II hypertension.
Our results show that CaN/NFATc4 pathway were involved in the development of PTSD model, which suggested that the changes of CaN/NFATc4 pathway may be one of the pathological molecular mechanism in the dysfunction of hippocampus in PTSD.
Ten genes (C5orf24, RBAK, CREBZF, CD69, PMAIP1, AGL, ZNF644, ANKRD13C, ESCO1, and ZCCHC10) were upregulated in participants with PTSD and high intrusion symptoms at baseline and downregulated in participants with improved PTSD symptoms following treatment.
However, a significant interaction effect between GHRL rs696217 and HCRTR1rs2271933 was found to predict the PTSD Checklist (PCL-5) total score (P = 0.007).
183 veterans with DSM-IV PTSD and SUD at two VA Medical Centers were randomized to one of two psychotherapies during which Motivational Enhancement Therapy [MET] for SUD and Prolonged Exposure [PE] for PTSD were either phased or integrated throughout treatment.
HLA-B*58:01 (p = 0.035), HLA-C*07:01 (p = 0.035), HLA-DQA1*01:01 (p = 0.003), HLA-DQB1*05:01 (p = 0.009) and HLA-DPB1*17:01 (p = 0.017) were more common in PTSD cases, while HLA-A*02:01 (p = 0.026), HLA-DQA1*05:05 (p = 0.011) and HLA-DRB1*11:01 (p < 0.001) were more frequent in controls.
The primary outcome measure was severity of PTSD-symptoms (Harvard Trauma Questionnaire (HTQ)) and secondary outcome measures were depression and anxiety symptoms (Hopkins Symptom Checklist-25 (HSCL-25), Hamilton Depression and Anxiety rating scales (HAM-D, HAM-A)), somatisation (somatisation items of SCL-90 (SI-SCL-90)), quality of life (WHO-5-Well-being Index (WHO-5)) and functioning (Sheehan Disability Scale (SDS), Global Assessment of Functioning (GAF-F, GAF-S)).
HLA-B*58:01 (p = 0.035), HLA-C*07:01 (p = 0.035), HLA-DQA1*01:01 (p = 0.003), HLA-DQB1*05:01 (p = 0.009) and HLA-DPB1*17:01 (p = 0.017) were more common in PTSD cases, while HLA-A*02:01 (p = 0.026), HLA-DQA1*05:05 (p = 0.011) and HLA-DRB1*11:01 (p < 0.001) were more frequent in controls.
However, the results of MBPrs12458282 within the patients with lifetime PTSD may point to a possible correlation of the major allele (T) with elevated CAPS scores.
We conducted systematic searches in five databases (Medline, Embase, PyscINFO, CINAHL, ERIC, Sociological Abstracts) from database inception to October 17, 2017 using index terms and keywords for CSA, disclosure, and PTSD.
This study aimed to assess and compare drug use patterns and the presence of childhood sexual abuse (CSA) experiences among ecstasy and LSD users with and without Posttraumatic Stress Disorder (PTSD).
Mostly as a complementary treatment, however, for some disorders already with a 1a evidence level, e.g., depression, dementia or MCI but also post-traumatic stress disorder.
Given that stress is a critical component in PTSD, we next assessed the impact of stress and stress-enhanced fear learning (SEFL) on mir-598-3p levels, finding the miRNA is elevated in the BLA of male, but not female, mice susceptible to the effects of stress in SEFL.
In summary, GRg2 alleviated the PTSD-associated behavioral deficits with biosynthesis of neurosteroids, normalization of serotonergic system and HPA axis dysfunction.
Successful treatment of PTSD was accompanied by significant changes in DNA methylation at 12 differentially methylated regions (DMRs) in the genes: APOB, MUC4, EDN2, ZFP57, GPX6, CFAP45, AFF3, TP73, UBCLP1, RPL13P, and two intergenic regions (p values < 0.0001 were confirmed using permutation and sensitivity analyses).
SET-Q total score was positively correlated with HTQ Part IV Post-Traumatic Stress Disorder (PTSD) and Self-Perception of Functioning scales (SPFS) while the number of stressful experiences with the local population was positively related to BDI-II depression symptoms.
Our results uncover a physiological and partly sex-dependent function for TIA1 in fear memory and may provide molecular insight into stress-related psychiatric conditions, such as post-traumatic stress disorder (PTSD) and anxiety.
However, the students with PTSD had significantly lower levels of glucose, insulin and homeostasis model assessment of insulin resistance (HOMA-IR) than the students without PTSD in the C allele carriers of GHSRrs495225 after the adjustment for age, gender and body mass index (BMI), but higher levels of TG and TG/HDL-C in the TT homozygotes.