3 T magnetic resonance diffusion tensor imaging and fibre tracking in cervical myelopathy.

AIM: To analyse the characterization of diffusion tensor imaging (DTI) with 3 T magnetic resonance imaging (MRI) in cervical myelopathy. METHODS: A total of 21 healthy controls and 84 patients with cervical myelopathy underwent T2-weighted imaging and DTI. The patients were divided into four groups based on the degree of cord compression and MRI signal intensity of the compressed cord as seen on T2-weighted images. The values of apparent diffusion coefficient (ADC), fractional anisotropy (FA), and eigenvalues (lambda(i)) were analysed, and fibre tracking (FT) was performed. RESULTS: For healthy controls, the mean values from the DTI of the cervical spinal cord were ADC=0.784+/-0.083x10(-3)mm(2)/s, FA=0.721+/-0.027, lambda(1), lambda(2), and lambda(3)=1.509+/-0.145x10(-3), 0.416+/-0.094x10(-3), and 0.411+/-0.102x10(-3)mm(2)/s, respectively. Only values for lambda(2) and lambda(3) differed significantly between the control and A groups (p<0.05). The mean values of lambda(2) and lambda(3) of group A were 0.516+/-0.105x10(-3) and 0.525+/-0.129x10(-3)mm(2)/s, respectively. ADC, FA, lambda(1), lambda(2) and lambda(3) differed significantly between the control and B, C, D groups (p<0.01). The FT map for group A showed a normal spinal cord, but that for groups B, C, and D showed a distorted spinal cord at the sites of compression. CONCLUSION: The values of ADC, FA, and lambda(i) obtained with DTI could assess subtle structural damage and changes of anisotropy in the cord of cervical myelopathy. Fibre tracking was useful in verifying changes in the compressed cord.

Early activation of pulmonary nuclear factor kappaB and nuclear factor interleukin-6 in polymicrobial sepsis.

BACKGROUND: Transcription factor activation may be a pivotal step in the pathophysiology of sepsis syndrome and adult respiratory distress syndrome. This study investigated the activation of lung nuclear factor kappaB (NFkappaB) and nuclear factor interleukin-6 (NF-IL6) and how they correlate to proinflammatory cytokine expression and mortality in a murine model of cecal ligation and puncture (CLP). METHODS: Polymicrobial sepsis was induced by CLP. Transcription factor activation was assessed at 0, 1, 2, 3, 4, 5, 6, 8, and 24 hours after CLP by the electrophoretic mobility-shift assay. Lung cytokine mRNA levels were established by reverse transcriptase-polymerase chain reaction. RESULTS: CLP induced pulmonary NFkappaB activation at 3, 4, and 8 hours (p < 0.05). Lung NFkappaB activation peaked at 3 hours (533% vs. no surgery, 2,900% vs. sham treatment) after CLP. Supershift analysis revealed a predominance of p50 subunits in the lung nuclear extracts of septic mice 3 hours after CLP, indicating the presence of p50 homodimer. In contrast, liver nuclear extracts from septic mice indicated the presence of both p65 and p50 subunits at 3 hours. Lung NF-IL6 activation (p < 0.05) was observed at 4 hours (649% vs. no surgery, 296% vs. sham treatment) and 6 hours after CLP. Lung tumor necrosis factor-alpha mRNA levels were increased (p < 0.05) at all time intervals after CLP. Lung IL-6 mRNA levels were increased at 3, 6, and 8 hours after CLP. CONCLUSION: Early activation of lung NFkappaB and NF-IL6 and lung cytokine mRNA expression correlated with mortality in polymicrobial sepsis. Although IL-6 mRNA levels correlated with NFkappaB and NF-IL6 activation, tumor necrosis factor-alpha mRNA levels did not, in that they preceded transcription factor activation. These data suggest a potential role for NFkappaB and NF-IL6 activation in the initiation and propagation of acute lung injury.