Sentence examples for models of posttraumatic from inspiring English sources

Increasing predictability of animal models of posttraumatic stress disorder (PTSD) has required active collaboration between clinical and preclinical scientists.

Several experimental models of posttraumatic epilepsy are currently in use that may facilitate discovery of molecular and pathophysiological alterations underlying the process of epileptogenesis.

Despite its prevalence, killing in war is an experience that may not fit neatly into existing models of posttraumatic stress disorder (PTSD) and its treatment.

Research on experimental models of posttraumatic OA and clinical research has led to the elucidation of pathogenesis pathways.

Individual differences in the interpretation and personal meanings of traumatic events, which can be understood as extremely negative events, have been the focus of theoretical models of posttraumatic stress disorder (PTSD) (e.g., Dollinger 1986; Ehlers and Clark 2000; Foa and Riggs 1993; Resick and Schnicke 1993; Taylor 1983).

Translating these findings in vivo, we evaluated therapeutic effect of 3,4,6-O-Bu3GalNAc 3,4,6-O-Bu3GalNAc 3,4,6-O-Bu3GalNAcA when delivered via lonal inthe-aratcular sustained-release delivery using modelparticles and fofnd this method to be efficacious in posttraumatic prOAression.

To this end, we used an etiologically realistic rat model of posttraumatic epilepsy, in which the initiating fluid percussion injury closely replicates contusive closed-head injury in humans, and has been adapted to maximize epileptogenesis and focal non-convulsive seizures.

Z. Hu and J. Tu investigated mitochondrial function in an experimental model of posttraumatic syringomyelia.

A limitation of repetitive injury as a model of posttraumatic OA is that it disrupts endogenous repair responses.

In this model of posttraumatic OA, PC significantly reduced cartilage damage and proteoglycan loss, demonstrating that PC is a disease-modifying drug for posttraumatic OA therapy.

Patients with posttraumatic stress disorder have lower levels of TSPO, and stimulation of TSPO improved behavioral deficits in a mouse model of posttraumatic stress disorder (73 – 73).