BackgroundTraumatic spinal cord injury (SCI) causes severe motor dysfunction and persistent central neuropathic pain (Nep), which has not yet been effectively cured. Programmed cell death ligand-1 (PD-L1) is typically produced by cancer cells and contributes to the immune-suppressive in tumor microenvironment. However, the role of PD-L1 in regulating inflammatory response and Nep after SCI remains unclear. A growing amount of researches have begun to investigate the effect of PD-L1 on macrophages and microglia in recent years. Considering the pivotal role of macrophages/microglia in the inflammatory response after SCI, we proposed the hypothesis that PD-L1 improved the recovery of locomotor and sensory functions after SCI through regulating macrophages and microglia.MethodsThe mice SCI model was established to determine the changes in expression patterns of PD-L1. Meanwhile, we constructed PD-L1 knockout mice to observe differences in functional recovery and phenotypes of macrophages/microglia post-SCI.ResultsIn present study, PD-L1 was significantly upregulated after SCI and highly expressed on macrophages/microglia at the injury epicenter. PD-L1 knockout (KO) mice showed worse locomotor recovery and more serious pathological pain compared with wild-type (WT) mice. Furthermore, deletion of PD-L1 significantly increased the polarization of M1-like macrophages/microglia. Mechanistic analysis revealed that PD-L1 may improve functional outcomes following SCI by inhibiting phosphorylation of p38 and ERK1/2.ConclusionsOur observations implicate the involvement of PD-L1 in recovery of SCI and provide a new treatment strategy for the prevention and treatment of this traumatic condition.
Background: Various factors have been reported to affect the obliteration of brain arteriovenous malformations (AVM) following stereotactic radiosurgery (SRS). This meta-analysis was conducted to identify the factors potentially associated with AVM obliteration after SRS. Methods: We comprehensively searched databases and included studies that evaluated predictors of AVM obliteration after SRS using Cox proportional hazard regression analysis. Hazard ratios (HRs) with 95% confidence intervals (CIs) were utilized as effect estimates. Results: Twelve studies, involving 4415 AVM cases, were included. According to combined estimates on univariate (UV) and multivariate (MV) analysis, age, gender and prior haemorrhage did not affect the closure probability. The following factors showed a significant and independent association with increased AVM obliteration: smaller AVMs maximal diameter (MV, HR: 1.32), smaller AVM volume (MV, HR: 1.05), AVM volume <10-15 cc (MV, HR: 1.55), higher margin dose (MV, HR: 1.05), margin dose ≥17-18 Gy (MV, HR: 3.71) and early treatment period (MV, HR: 1.78). Previous embolization and deep-seated AVM were independently negative predictors of obliteration whereas deep venous drainage was a positive predictor. Prior surgery, compactness of nidus, lower grading scores and higher SRS maximum dose were associated factors subject to confounding factors. Conclusion: Multiple factors associated with obliteration should be taken into consideration for selection of candidates with AVMs for SRS. AVM volume and radiation dose are the most prominent factor in assessing obliteration after SRS. Age, gender and prior haemorrhage may not affect the consideration of SRS treatment. Cautious use of SRS is needed for previously embolized AVM patients. * Two sets of data were extracted for presentation, namely data for AVMs treated by GK alone (81 patients) and data for AVMs with post-GK embolization (17 patients). † Two sets of data in different treatment periods were extracted.
Purpose: To investigate the effect of anti-cold induced RNA binding protein (CIRP) antibody on inflammation, tumor formation and abdominal aortic aneurysm in rats.Methods: Thirty healthy male Wistar rats were assigned to pseudo-operation, abdominal aortic aneurysm model, and anti-CIRP groups, with 10 in each group. The levels of CIRP, TNF- α, monocyte giant cytokine chemokine-1 (MCP-1), Toll-like receptor 4 (TLR4)) and nuclear factor kappaB (NF- κB)were determined compared among the groups.Results: At both 2 and 4 weeks, the expression of CIRP protein in the model group was significantly higher than that in the sham operation group (p < 0.05). At these two time-points, tumor formation and maximum diameter were higher in anti-CIRP and model control rats than in pseudo-operation rats. After 4 weeks of treatment, the protein expressions of TNF- α, MCP-1, TLR4 and NF-κB were higher in anti-CIRP and model control rats than in pseudo-operation rats, but were lower than model control values (p < 0.05).Conclusion: CIRP expression is significantly increased in abdominal aortic aneurysm tissue and serum, and is involved in the onset and progress of abdominal aortic aneurysm. Anti-CIRP antibody therapy effectively suppresses tumorigenesis, and inhibits tumor wall inflammatory reaction viaTLR4/NF-κB pathway. This finding provides a clue and new strategy for the clinical management of abdominal aortic aneurysm. Keywords: CIRP, Abdominal aortic tumor wall, Inflammatory reaction, Protein expression, Tumor body
Background: Spinal injuries is with high frequency in the modern wars and some patients with severe spinal injures have to accept the emergency spinal surgery. Nutrient foramen is easy to identify intraoperatively. The purpose of this study was to investigate the feasibility and reliability of using the nutrient foramen to guide the pedicle screw placement.Methods: Nine dried human vertebral bone were involved in this study. The anatomical association to the pedicles and bony landmarks were measured in the vertebrae for C6-T6. We also determined the frequency with which the nutrient foramina were present in 86 cadaveric vertebrae. We identified the pedicle location, base of the superior articular process, base of inferior articular process, base of transverse process, and the posterior median line with respect to the nutrient foramenResults: The overall presence of the nutrient foramina was 63% in the specimens. The nutrient foramina located cranially and laterally on the lamina, and the nutrient foramen was located near to the pedicle. Conclusion: The location of nutrient foramen can be used for identifying the entry point for pedicle screws in the cervicothoracic junction. The nutrient foramen is easy to identify during operation and with a high frequency of occurrence. Therefore, the nutrient foramen could be used as a reliable landmark to guide the entry point localization in emergency spinal surgeries in the battlefield.
Background Traumatic spinal cord injury (SCI) causes severe motor dysfunction and persistent central neuropathic pain (Nep) that remains uncured yet. Programmed cell death ligand-1 (PD-L1) is typically produced by cancer cells and contributes to the immune-suppressive in tumor microenvironment, and the role of PD-L1 in regulating inflammatory response and Nep after SCI remains unclear. A growing amount of research has begun to investigate the effect of PD-L1 on macrophages and microglia. Considering the pivotal role of macrophages/microglia in the inflammatory response after SCI, we tested the hypothesis that PD-L1 improved the recovery of locomotor and sensory functions after SCI through macrophages and microglia. Methods The mice SCI model was employed to determine the changes in expression patterns of PD-L1. Meanwhile, we constructed PD-L1 knockout mice to observe differences in functional recovery and phenotypes of macrophages/microglia post-SCI. Results In present study, PD-L1 was significantly upregulated after SCI and highly expressed on macrophages/microglia. PD-L1 knockout (KO) mice showed poor locomotor recovery and serious pathological pain compared with wild-type (WT) mice. Furthermore, deletion of PD-L1 significantly increased the polarization of M1-like macrophages/microglia. Mechanistic analysis revealed that PD-L1 may improve functional outcomes following SCI by inhibiting phosphorylation of p38 and ERK1/2. Conclusions Our observations implicate the involvement of PD-L1 in recovery of SCI and provide a new treatment strategy for prevention and treatment of this traumatic condition.
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