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BACKGROUND:Non-targeted metabolomic profiling is used to uncover metabolic changes and to identify relationships between metabolites and spinal cord injury,which contributes to further understanding the pathophysiological process and mechanisms of secondary spinal cord injury.OBJECTIVE:To detect and analyze the serum metabolite changes after complete spinal cord transaction in macaques,explore its relationship with the pathophysiological progress of spinal cord injury,and screen the potential biomarkers.METHODS:Five adult macaques were selected,in which the models of complete spinal cord transaction were established.The serum metabolic features were detected using a non-targeted metabolic profiling strategy based on gas chromatography time-of-flight mass spectrometry at 1 day before modeling,3 hours (superacute phase) and 3 days (acute phase) after modeling.After compared with the spectrometry profiling,recognizing the metabolites,searching for differential metabolites and the related metabolic pathways,the pathophysiological process and mechanisms were analyzed.RESULTS AND CONCLUSION:Three hundred and fifty-eight chromatographic peaks were obtained for subsequent data analysis.Fourteen metabolites,including low-molecular-weight organic acid,amino acids,fatty acid and carbohydrate,were identified as differential metabolites.To conclude,the acute phase of complete spinal cord transection is closely related to some metabolic pathways,such as amino acid metabolism,tricarboxylic acid cycle and pyruvate metabolism.
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<p><b>OBJECTIVE</b>To investigate the relationship between the changes of amino acids contents in hippocampus of rats and electromagnetic pulse (EMP) exposure.</p><p><b>METHODS</b>Rats were decapitated and hippocampus were removed after EMP (6 x 10(4) V/m, rise time 20 ns, pulse width 30 micro s, 5 pulses in 2 minutes) irradiation, and contents of amino acids were detected with high performance liquid chromatograpy (HPLC).</p><p><b>RESULTS</b>The contents of aspartic acid (Asp) and glutamic acid (Glu) increased significantly 0, 3, 6 h after irradiation. The peak values of Asp [(17.25 +/- 1.63) pmol/ micro l] and Glu [(13.67 +/- 0.95) pmol/ micro l] were higher than those of control [(10.56 +/- 1.50), (6.94 +/- 1.10) pmol/ micro l respectively, P < 0.05]. Then both decreased gradually and reached the normal level 24 - 48 h after irradiation. The contents of glycine (Gly), taurine (Tau) and gamma-aminobutyric acid (GABA) also rose after exposure, the peak value of them [(4.51 +/- 0.60), (29.85 +/- 2.70), (5.14 +/- 0.73) pmol/ micro l respectively] were higher than those of control group [(2.18 +/- 0.31), (9.88 +/- 1.47), (2.84 +/- 0.67) pmol/ micro l, P < 0.05], then recovered 48 h after irradiation. The value of Glu/GABA increased immediately after exposure (3.45 +/- 0.25, P < 0.05), then decreased 24 h (1.62 +/- 0.23, P < 0.05) and recovered 48 h after exposure.</p><p><b>CONCLUSION</b>The toxic effect of excess excitatory amino acids may be partly responsible for the early retardation (within 24 h) of learning of rats.</p>