Study on between magnetic resonance venography and digital subtraction angiography on the inferior vena cava obstructive interface morphology of Budd-Chiari syndrome / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To evaluate magnetic resonance venography (MRV) in diagnosing obstructive interface morphology of Budd-Chiari syndrome(BCS).</p><p><b>METHODS</b>MRV examination was performed on 44 cases of BCS, and the images of obstructive interface morphology of the inferior vena cava were reviewed by two radiologists.</p><p><b>RESULTS</b>In all 44 cases, there were 37 cases with complete obstruction and 7 with incomplete obstruction. MRV showed 4 cases with membrane with hole of incomplete obstruction. The morphologies MRV demonstrated that the proximal part of the 37 cases with complete obstruction were mainly divided into the cone type (36 cases) and the planum type (1 case). Besides, the type of distal end of obstruction were the cone type (30 cases), the planum type (4 cases) and the irregular type (3 cases). The overall sensitivity, specificity, positive and negative predictive values for the diagnosis of MRV were respectively 100%%, 57.1%, 92.5% and 100% as compared to the DSA.</p><p><b>CONCLUSION</b>The examination of MRV is capable of revealing the obstructive interface morphology of the inferior vena cava, especially for the distal end of obstruction. MRV can provide guidelines in interventional treatment of Budd-Chiari syndrome.</p>

Signal transducer and activator of transcription-3 activation after focal cerebral ischemia and reperfusion in rats / 中华神经医学杂志

Objective To investigate the activation of signal transducer and activator of transcription-3 (STAT3) in rats following focal cerebral ischemia/repeffusion (IR) and explore the correlation between STAT3 activation and the cerebral infract volume. Methods Ninety-nine SD rats were randomized into sham-operated group (n=9) and two IR groups with right middle cerebral artery occlusion with thread for 2 h (n=45) and 6 h (n=45) followed by reperfusion. At different time points after the end of the ischemia, the rats were sacrificed to obtain the brain tissue for triphenyltetrazolium chloride (TTC) staining to determine the infract volume. Immunohistochemistry and Western blot were used to detect the expressions of STAT3 and phosphorylated STAT3 (P-STAT3) in the brain tissue, and their correlations to the infarct volume were analyzed. Results Cerebral ischemia induced obvious infraction in the right hemisphere of the rats, where TTC staining was absent. Ischemia for 6 h resulted in more extensive areas without TTC staining than ischemia for 2 h (P<0.05). Reperfusion for 24 h after a 2-hour ischemia was associated with obviously reduced area free of TTC staining (P<0.05), whereas reperfusion for 24 h following a 6-hour ischemia only caused mild reduction of the TTC staining-free area. Immunohistochemistry of the brain tissue demonstrated the presence of STAT3 protein expression in the cytoplasm and P-STAT3 in the cell nuclei. IR was found to cause changes in the expression of P-STAT3 but not STAT3 protein, and the expression of P-STAT3 increased with the reperfusion time, reaching the peak level at 24 h of reperfusion. The activation level of STAT3 protein was inversely correlated to the dimension of the TTC staining-free area in the brain. Conclusion STAT3 is expressed in the cytoplasm and P-STAT3 in the cell nucleus of the brain tissue. Without causing obvious changes in STAT3 expression level, cerebral ischemia and reperfusion increases the phosphorylation level of STAT3 in inverse correlation to the size of the infarct area.