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1.
Rozhl Chir ; 99(5): 212-218, 2020.
Article in English | MEDLINE | ID: mdl-32545972

ABSTRACT

INTRODUCTION: The authors analyzed a series of ankylosing spondylitis patients with cervical spine fracture undergoing posterior stabilization using spinal navigation based on intraoperative CT imaging. The purpose of this study was to evaluate the accuracy and safety of navigated posterior stabilization and to analyze the adequacy of this method for treatment of fractures in ankylosed cervical spine. METHODS: Prospectively collected clinical data, together with radiological documentation of a series of 8 consecutive patients with 9 cervical spine fracture were included in the analysis. The evaluation of screw insertion accuracy based on postoperative CT imaging, description of instrumentation-related complications and evaluation of morphological and clinical results were the subjects of interest. RESULTS: Of the 66 implants inserted in all cervical levels and in upper thoracic spine, only 3 screws (4.5%) did not meet the criteria of anatomically correct insertion. Neither screw malposition nor any other intraoperative events were complicated by any neural, vascular or visceral injury. Thus we did not find a reason to change implant position intraoperatively or during the postoperative period. The quality of intraoperative CT imaging in our group of patients was sufficient for reliable trajectory planning and implant insertion in all segments, irrespective of the habitus, positioning method and comorbidities. In addition to stabilization of the fracture, the posterior approach also allows reducing preoperative kyphotic position of the cervical spine. In all patients, we achieved a stable situation with complete bone fusion of the anterior part of the spinal column and lateral masses at one year follow-up. CONCLUSION: Spinal navigation based on intraoperative CT imaging has proven to be a reliable and safe method of stabilizing cervical spine with ankylosing spondylitis. The strategy of posterior stabilization seems to be a suitable method providing high primary stability and the conditions for a subsequent high fusion rate.


Subject(s)
Fractures, Bone , Spinal Fractures/surgery , Spondylitis, Ankylosing/complications , Spondylitis, Ankylosing/diagnostic imaging , Spondylitis, Ankylosing/surgery , Cervical Vertebrae/injuries , Humans , Tomography, X-Ray Computed
2.
Nature ; 496(7444): 238-42, 2013 Apr 11.
Article in English | MEDLINE | ID: mdl-23535595

ABSTRACT

Macrophages activated by the Gram-negative bacterial product lipopolysaccharide switch their core metabolism from oxidative phosphorylation to glycolysis. Here we show that inhibition of glycolysis with 2-deoxyglucose suppresses lipopolysaccharide-induced interleukin-1ß but not tumour-necrosis factor-α in mouse macrophages. A comprehensive metabolic map of lipopolysaccharide-activated macrophages shows upregulation of glycolytic and downregulation of mitochondrial genes, which correlates directly with the expression profiles of altered metabolites. Lipopolysaccharide strongly increases the levels of the tricarboxylic-acid cycle intermediate succinate. Glutamine-dependent anerplerosis is the principal source of succinate, although the 'GABA (γ-aminobutyric acid) shunt' pathway also has a role. Lipopolysaccharide-induced succinate stabilizes hypoxia-inducible factor-1α, an effect that is inhibited by 2-deoxyglucose, with interleukin-1ß as an important target. Lipopolysaccharide also increases succinylation of several proteins. We therefore identify succinate as a metabolite in innate immune signalling, which enhances interleukin-1ß production during inflammation.


Subject(s)
Hypoxia-Inducible Factor 1, alpha Subunit/metabolism , Interleukin-1beta/biosynthesis , Signal Transduction , Succinic Acid/metabolism , Animals , Bone Marrow Cells/cytology , Citric Acid Cycle/drug effects , Deoxyglucose/pharmacology , Down-Regulation/drug effects , Genes, Mitochondrial/drug effects , Genes, Mitochondrial/genetics , Glutamine/metabolism , Glycolysis/drug effects , Glycolysis/genetics , Humans , Immunity, Innate/drug effects , Inflammation/metabolism , Interleukin-1beta/genetics , Lipopolysaccharides/pharmacology , Macrophages/cytology , Macrophages/drug effects , Macrophages/metabolism , Mice , Up-Regulation/drug effects , gamma-Aminobutyric Acid/metabolism
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