Articles: function.
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Critical care medicine · Nov 2024
ICU-Electroencephalogram Unit Improves Outcome in Status Epilepticus Patients: A Retrospective Before-After Study.
Continuous electroencephalogram (cEEG) monitoring is recommended for status epilepticus (SE) management in ICU but is still underused due to resource limitations and inconclusive evidence regarding its impact on outcome. Furthermore, the term "continuous monitoring" often implies continuous recording with variable intermittent review. The establishment of a dedicated ICU-electroencephalogram unit may fill this gap, allowing cEEG with nearly real-time review and multidisciplinary management collaboration. This study aimed to evaluate the effect of ICU-electroencephalogram unit establishing on SE outcome and management. ⋯ Integrating neurology expertise in the ICU setting through the establishment of an ICU-electroencephalogram unit with nearly real-time cEEG review, shortened SE duration, and increased likelihood of returning to premorbid neurologic function, with an increased number of antiseizure medications used. Further studies are warranted to validate these findings and assess long-term prognosis.
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Visceral hypersensitivity is considered the core pathophysiological mechanism that causes abdominal pain in patients with irritable bowel syndrome (IBS). Fungal dysbiosis has been proved to contribute to visceral hypersensitivity in IBS patients. However, the underlying mechanisms for Dectin-1, a major fungal recognition receptor, in visceral hypersensitivity are poorly understood. This study aimed to explore the role of Dectin-1 in visceral hypersensitivity and elucidate the impact of Dectin-1 activity on the function of transient receptor potential vanilloid type 1 (TRPV1). ⋯ This work provides direct evidence for the functional regulation of TRPV1 channel by Dectin-1 activity, proposing a new mechanism underlying TRPV1 sensitization. Control of intestinal fungi might be beneficial for the treatment of refractory abdominal pain in patients with IBS or IBD in remission.
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Myofascial trigger points (MTrPs) are the primary etiological characteristics of chronic myofascial pain syndrome. Receptor tyrosine kinases (RTKs) are associated with signal transduction in the central mechanisms of chronic pain, but the role of RTKs in the peripheral mechanisms of MTrPs remains unclear. The current study aimed to identify RTKs expression in MTrPs and elucidate the molecular mechanisms through which platelet-derived growth factor receptor-α (PDGFR-α) induces contraction knots and inflammatory pain-like behavior in a rat model of myofascial trigger points. ⋯ COL1A1-induced phosphorylation of PDGFR-α and the subsequent activation of the JAK2/STAT3 pathway may induce dysfunctional muscle contraction and increased nociception at MTrPs.
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As a mechanosensitive cation channel and key regulator of vascular barrier function, endothelial transient receptor potential vanilloid type 4 (TRPV4) contributes critically to ventilator-induced lung injury and edema formation. Ca2+ influx via TRPV4 can activate Ca2+-activated potassium (KCa) channels, categorized into small (SK1-3), intermediate (IK1), and big (BK) KCa, which may in turn amplify Ca2+ influx by increasing the electrochemical Ca2+ gradient and thus promote lung injury. The authors therefore hypothesized that endothelial KCa channels may contribute to the progression of TRPV4-mediated ventilator-induced lung injury. ⋯ KCa channels, specifically IK1, act as amplifiers of TRPV4-mediated Ca2+ influx and establish a detrimental feedback that promotes barrier failure and drives the progression of ventilator-induced lung injury.