Background
Near‐infrared (NIR) fluorescence imaging has recently been introduced to the sentinel lymph node (SLN) mapping because of the benefits of the SLN biopsy, such as providing real‐time and high‐resolution optical guidance. Methylene blue is available and less expensive as an SLN mapping tracer. Our study aims to identify SLN through the NIR fluorescence imaging system mediated by blue dye.
Methods
Early‐stage breast cancer patients were prospectively enrolled. All participants received a subareolar or peritumoral injection of 1 mL methylene blue (MB) before surgery. The MB fluorescence system was set immediately after injection. SLNs were searched and removed under the guidance of fluorescence and blue dye.
Results
We identified SLN adequately with the help of real‐time lymphography and blue dye. Symbolic lymphatic drainage patterns were also observed.
Conclusion
NIR fluorescence imaging mediated by blue dye has benefits on the identification of lymph vessels, the location of SLN, and the patterns of breast lymphatic flow.
Purpose: Neuroinflammation often initiates iron overload in the pathogenesis of neurological disorders. Chemokine-driven neuroinflammation is required for central sensitization and chronic allodynia following fractures, but specific molecular modulations are elusive. This present study explored whether hydrogen-rich saline, as one potent anti-inflammatory pharmaceutical, could alleviate fracture-caused allodynia by suppressing chemokine CXCL1 expression and iron overload. Methods: A mouse model of tibial fracture with intramedullary pinning was employed for establishing chronic allodynia. Three applications of hydrogen-rich saline (1, 5 or 10 mL/kg) were administrated intraperitoneally on a daily basis from days 4 to 6 following fractures. Spinal CXCL1 and its receptor CXCR2 levels, transferrin receptor 1 (TfR1) expression and iron concentration were examined. Recombinant CXCL1, a selective CXCR2 antagonist and an iron chelator were used for verification of mechanisms. Results: Repetitive injections of hydrogen-rich saline (5 and 10 mL/kg but not 1 mL/kg) prevent fracture-caused mechanical allodynia and cold allodynia in a dose-dependent manner. Single exposure to hydrogen-rich saline (10 mL/kg) on day 14 after orthopedic surgeries controls the established persistent fracture allodynia. Furthermore, hydrogen-rich saline therapy reduces spinal CXCL1/CXCR2 over-expression and TfR1-mediated iron accumulation in fracture mice. Spinal CXCR2 antagonism impairs allodynia and iron overload following fracture surgery. Intrathecal delivery of recombinant CXCL1 induces acute allodynia and spinal iron overload, which is reversed by hydrogen-rich saline. Moreover, iron chelation alleviates exogenous CXCL1-induced acute pain behaviors. Conclusions: These findings identify that hydrogen-rich saline confers protection against fracture-caused chronic allodynia via spinal down-modulation of CXCL1-dependent TfR1-mediated iron accumulation in mice.
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