Gene networks specific for innate immunity define post-traumatic stress disorder.

The molecular factors involved in the development of Post-Traumatic Stress Disorder (PTSD) remain poorly understood. Previous transcriptomic studies investigating the mechanisms of PTSD apply targeted approaches to identify individual genes under a cross-sectional framework lack a holistic view of the behaviours and properties of these genes at the system-level. Here we sought to apply an unsupervised gene-network based approach to a prospective experimental design using whole-transcriptome RNA-Seq gene expression from peripheral blood leukocytes of U.S. Marines (N=188), obtained both pre- and post-deployment to conflict zones. We identified discrete groups of co-regulated genes (i.e., co-expression modules) and tested them for association to PTSD. We identified one module at both pre- and post-deployment containing putative causal signatures for PTSD development displaying an over-expression of genes enriched for functions of innate-immune response and interferon signalling (Type-I and Type-II). Importantly, these results were replicated in a second non-overlapping independent dataset of U.S. Marines (N=96), further outlining the role of innate immune and interferon signalling genes within co-expression modules to explain at least part of the causal pathophysiology for PTSD development. A second module, consequential of trauma exposure, contained PTSD resiliency signatures and an over-expression of genes involved in hemostasis and wound responsiveness suggesting that chronic levels of stress impair proper wound healing during/after exposure to the battlefield while highlighting the role of the hemostatic system as a clinical indicator of chronic-based stress. These findings provide novel insights for early preventative measures and advanced PTSD detection, which may lead to interventions that delay or perhaps abrogate the development of PTSD.

Effects of myofascial release leg pull and sagittal plane isometric contract-relax techniques on passive straight-leg raise angle.

Experimental evidence does not currently exist to support the claims of clinical effectiveness for myofascial release techniques. This presents an obvious need to document the effects of myofascial release. The purpose of this study was to compare the effects of two techniques, sagittal plane isometric contract-relax and myofascial release leg pull for increasing hip flexion range of motion (ROM) as measured by the angle of passive straight-leg raise. Seventy-five nondisabled, female subjects 18-29 years of age were randomly assigned to contract-relax, leg pull, or control groups. Pretest hip flexion ROM was measured for each subject's right hip with a passive straight-leg raise test using a fluid-filled goniometer. Subjects in the treatment groups received either contract-relax or leg pull treatment applied to the right lower extremity; subjects in the control group remained supine quietly for 5 minutes. Following treatment, posttest straight-leg raise measurements were performed. A one-way analysis of variance followed by a Newman-Keuls post hoc comparison of mean gain scores showed that subjects receiving contract-relax treatment increased their ROM significantly more than those who received leg pull treatment, and the increase in ROM of subjects in both treatment groups was significantly higher than those of the control group. The results suggest that while both contract-relax and leg pull techniques can significantly increase hip flexion ROM in normal subjects, contract-relax treatment may be more effective and efficient than leg pull treatment.