Publications by authors named "Chaoqin Wu"

JOURNAL/nrgr/04.03/01300535-202419110-00030/figure1/v/2024-03-08T184507Z/r/image-tiff The inflammatory microenvironment and neurotoxicity can hinder neuronal regeneration and functional recovery after spinal cord injury. Ruxolitinib, a JAK-STAT inhibitor, exhibits effectiveness in autoimmune diseases, arthritis, and managing inflammatory cytokine storms.

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The current study aims to ascertain the anatomical feasibility of transferring the contralateral S1 ventral root (VR) to the ipsilateral L5 VR for treating unilateral spastic lower limb paralysis. Six formalin-fixed (three males and three females) cadavers were used. The VR of the contralateral S1 was transferred to the VR of the ipsilateral L5.

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Study Design: Eight cadavers were included in this anatomical study.

Objective: This study aimed to confirm the anatomical feasibility of extradural transfer of the contralateral T11 ventral root (VR) to the ipsilateral L2 level and the contralateral L1 VR to the ipsilateral L3 level to restore lower limb function in cases of paraplegia.

Summary Of Background Data: Motor dysfunction due to hemiplegia significantly affects the daily life of patients.

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Osteoporotic vertebral compression fracture (OVCF) has become a major public health issue that becomes more pressing with increasing global aging. Percutaneous kyphoplasty (PKP) is an effective treatment for OVCF. Robot-assisted PKP has been utilized in recent years to improve accuracy and reduce complications.

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Article Synopsis
  • Excessive inflammation after spinal cord injury activates microglia, contributing to long-term neurological problems, and the exact mechanisms behind this activation are not well understood.
  • Ruxolitinib (RUX), a drug that inhibits certain inflammatory pathways, was tested on microglia and in a mouse model of spinal cord injury, showing that it reduced pro-inflammatory markers and microglial proliferation.
  • The study suggests that RUX limits neuroinflammation by blocking the interferon-γ/JAK/STAT signaling pathway, leading to improved neuromotor function and less damage to nerve fibers post-injury.
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