19 research outputs found
Optimization of stochastic control processes with respect to probability on entering a target manifold
Optimization of stochastic control processes with respect to probability of entering target manifold in specific time interva
Linking Symptom Inventories using Semantic Textual Similarity
An extensive library of symptom inventories has been developed over time to
measure clinical symptoms, but this variety has led to several long standing
issues. Most notably, results drawn from different settings and studies are not
comparable, which limits reproducibility. Here, we present an artificial
intelligence (AI) approach using semantic textual similarity (STS) to link
symptoms and scores across previously incongruous symptom inventories. We
tested the ability of four pre-trained STS models to screen thousands of
symptom description pairs for related content - a challenging task typically
requiring expert panels. Models were tasked to predict symptom severity across
four different inventories for 6,607 participants drawn from 16 international
data sources. The STS approach achieved 74.8% accuracy across five tasks,
outperforming other models tested. This work suggests that incorporating
contextual, semantic information can assist expert decision-making processes,
yielding gains for both general and disease-specific clinical assessment
The Role of Brain Interleukin-1 in Stress-Enhanced Fear Learning
Posttraumatic stress disorder (PTSD) has been shown to be associated with pro-inflammatory markers, including elevated plasma levels of interleukin-1β (IL-1β). However, the precise role of neuroinflammation and central immune signaling on the development of this debilitating psychological disorder is not known. Here, we used stress-enhanced fear learning (SEFL), an animal model of the disorder, to examine the role of central IL-1β in PTSD. The results show that the severe stressor in SEFL induces a time-dependent increase in IL-1β immunoreactivity and mRNA expression within the dentate gyrus of the dorsal hippocampus (DH). There was no increase in IL-1β in the basolateral amygdala or the perirhinal cortex. Moreover, blocking the action of IL-1β following the severe stressor with IL-1 receptor antagonist (10 μg, intracerebroventricular (i.c.v.), 24 and 48 h after the stressor) prevented the development of SEFL. To provide further support for the role of IL-1β in the development of SEFL, we show that systemic morphine, a treatment which is known to reduce both PTSD and SEFL, also reduces IL-1β expression in the DH induced by the severe stressor. These studies provide the first evidence that IL-1 is involved SEFL and suggest that IL-1 signaling in the brain may have a critical role in the development of PTSD