Accepted

Chronic pain involves communication between neural and immune systems. Recent data suggest localization of glial (brain immune cells) activation to the sensorimotor regions of the brain cortex (S1/M1) in chronic […]

The most common peripheral neuronal feature of pain is a lowered stimulation threshold or hypersensitivity of terminal nerves from the dorsal root ganglia (DRG). One proposed cause of this hypersensitivity […]

Evaluation of neurovascular compression-related trigeminal neuralgia (NVC-TN) and its resolution through microvascular decompression are demonstrable by MRI and intraoperatively [Leal . (Atrophic changes in the trigeminal nerves of patients with […]

Neuropathic pain is caused by nerve injury and involves brain areas such as the central nucleus of the amygdala (CeA). We developed the first 3-D agent-based model (ABM) of neuropathic […]

Opioid use during pregnancy can lead to negative infant health outcomes, including neonatal opioid withdrawal syndrome(NOWS). NOWS comprises gastrointestinal, autonomic nervous system, and neurological dysfunction that manifest during spontaneous withdrawal. […]

It is well established that dopamine neurons of the ventral tegmental area (VTA) play a critical role in reward and aversion as well as pathologies including drug dependence and addiction. […]

Chronic pain and depression share common neural mechanisms, but their impacts on empathy are different. It is unclear how comorbid depressive symptoms affect empathy-related brain function in patients with chronic […]

This study introduces a novel approach of repetitive modeling to simulate the pathological process of recurrent gout attacks in humans. This methodology addresses the instability issues present in rat models […]

Mitochondrial dysfunction is associated with inflammatory bowel diseases (IBDs). To understand how microbial-metabolic circuits contribute to intestinal injury, we disrupt mitochondrial function in the epithelium by deleting the mitochondrial chaperone, […]

The data to support chronic automated red cell exchange (RCE) in sickle cell disease (SCD) outside of stroke prevention, is limited, especially in adults.