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1.
Med Sci Monit ; 26: e926142, 2020 Dec 25.
Article in English | MEDLINE | ID: mdl-33361735

ABSTRACT

BACKGROUND This study aimed to investigate the safety and clinical efficacy of 3 different surgical methods for treating spinal tuberculosis (ST) in children. MATERIAL AND METHODS We reviewed the cases of 62 children with ST who were treated in our hospital from January 2010 to December 2014. In this study, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) level, Frankel classification of neurological function, pain visual analog scale (VAS) score, and kyphosis Cobb (k-Cobb) angle were dynamically monitored to evaluate the efficacy of different surgical methods. Complications in the patients were evaluated at 3 time points: before surgery (T1), after surgery (T2), and during final follow-up (T3). The average follow-up was 27.4 months. Twenty-two patients underwent simple anterior debridement alone or combined with internal fixation (Method A), 13 patients underwent posterior debridement alone (Method B), and 27 patients received anteroposterior debridement and bone graft fusion together with internal fixation (Method C). RESULTS In all 3 groups after surgery, ESR, CRP levels, VAS scores, and k-Cobb angles significantly decreased. However, compared with patients who received Methods B and C, patients who received Method A had a significant rebound in k-Cobb angle and a higher incidence of complications at the T3 time point. The overall reoperation rate during follow-up was 37.10%. Fourteen patients (22.58%) had kyphosis, 2 patients (3.23%) had tuberculosis recurrence combined with kyphosis, and other complications were reported in 5 patients (8.06%). CONCLUSIONS Considering the incidence of complications and level of postoperative biochemical indicators, we concluded that caution should be exercised in using an anterior approach to treat pediatric ST.


Subject(s)
Debridement , Tuberculosis, Spinal/surgery , Adolescent , Blood Sedimentation , C-Reactive Protein/metabolism , Child , Child, Preschool , Female , Follow-Up Studies , Humans , Infant , Male , Postoperative Complications/etiology , Treatment Outcome , Tuberculosis, Spinal/blood , Tuberculosis, Spinal/physiopathology , Visual Analog Scale
2.
Biosci Rep ; 39(12)2019 12 20.
Article in English | MEDLINE | ID: mdl-31763668

ABSTRACT

Spinal cord injury (SCI) often occurs in young and middle-aged population. The present study aimed to clarify the function of Galectin-3 (Gal-3) in neuroinflammation of SCI. Sprague-Dawley (SD) rat models with SCI were established in vivo. PC12 cell model in vitro was induced by lipopolysaccharide (LPS). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Gene chip were used to analyze the expression levels of genes in the signaling pathway. Histological assessment, ELISA and Western blotting were conducted to evaluate the effects of Gal-3 upon the SCI model. In the in vivo SD rat model, Gal-3 expression level was up-regulated. The inhibition of Gal-3 attenuated the neuroinflammation in SCI model. The inhibition of Gal-3 could also mitigate the neuroinflammation and reactive oxygen species (ROS) in in vitro model. ROS reduced the effect of Gal-3 on oxidative stress in in vitro model. Down-regulating the content of TXNIP decreased the effect of Gal-3 on neuroinflammation in in vitro model. Suppressing the level of NLRP3 could weaken the effect of Gal-3 on neuroinflammation in in vitro model. Our data highlight that the Gal-3 plays a vital role in regulating the severity of neuroinflammation of SCI by enhancing the activation of ROS/TXNIP/NLRP3 signaling pathway. In addition, inflammasome/IL-1ß production probably acts as the therapeutic target in SCI.


Subject(s)
Cell Cycle Proteins/genetics , Galectin 3/genetics , Inflammation/genetics , NLR Family, Pyrin Domain-Containing 3 Protein/genetics , Spinal Cord Injuries/genetics , Animals , Biomarkers/metabolism , Disease Models, Animal , Galectin 3/antagonists & inhibitors , Galectin 3/deficiency , Humans , Inflammasomes/genetics , Inflammation/chemically induced , Inflammation/drug therapy , Inflammation/pathology , Lipopolysaccharides/toxicity , Oxidative Stress/drug effects , PC12 Cells , Rats , Reactive Oxygen Species , Signal Transduction/genetics , Spinal Cord Injuries/drug therapy , Spinal Cord Injuries/pathology
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