Publications by authors named "Omar Yaipen"

Article Synopsis
  • The study investigates how the central nervous system, specifically the M1 muscarinic acetylcholine receptor (M1AChR), affects inflammation during sepsis in mice, particularly after an induced model of sepsis called cecal ligation and puncture (CLP).
  • Results showed that M1AChR activity decreases during sepsis, leading to increased inflammation as indicated by higher levels of inflammatory cytokines and changes in immune cell populations.
  • Treatment with xanomeline, an M1AChR agonist, was found to restore some cholinergic activity and reduce inflammation markers, suggesting that targeting M1AChR could be a potential therapeutic strategy in managing sepsis.
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Article Synopsis
  • The study investigates the role of the central nervous system in sepsis, specifically how the activity of M1/M4 muscarinic acetylcholine receptors (AChRs) affects inflammation in mice following sepsis induced by cecal ligation and puncture (CLP).
  • It was found that the activity of certain brain cells (ChAT-expressing neurons) significantly decreased after CLP, leading to increased levels of pro-inflammatory cytokines and changes in immune cell populations.
  • Treatment with xanomeline, which stimulates M1AChRs, restored neuronal activity and reduced serum levels of some inflammatory markers, suggesting that enhancing cholinergic activity may help mitigate the inflammatory response in sepsis.
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Interfaces between the nervous and immune systems have been shown essential for the coordination and regulation of immune responses. Non-invasive ultrasound stimulation targeted to the spleen has recently been shown capable of activating one such interface, the splenic cholinergic anti-inflammatory pathway (CAP). Over the past decade, CAP and other neuroimmune pathways have been activated using implanted nerve stimulators and tested to prevent cytokine release and inflammation.

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LPS challenge is used to model inflammation-induced organ dysfunction. The effects of T cell activation on LPS-mediated organ dysfunction and immune responses are unknown. We studied these interactions through in vivo administration of anti-CD3ε (CD3) T cell activating antibody and LPS.

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We describe the case of a 50-year-old man with history of remote splenectomy who underwent routine lung cancer screening chest computed tomography and was incidentally found to have a liver lesion. Dedicated liver protocol computed tomography demonstrated "archiform" enhancement pattern in the arterial phase and homogenous filling-in enhancement on portal venous and delayed phases. Multiple other smaller enhancing intraperitoneal lesions were also found.

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