Expression of fas protein of myocardium in dilated cardiomyopathy / 法医学杂志

OBJECTIVE@#To investigate Fas protein expression of the myocardium in dilated cardiomyopathy (DCM) and its relationship with occurrence of sudden death caused by DCM.@*METHODS@#Nine autopsy cases of sudden death caused by DCM along with the heart samples were chosen from the archives in the Department of Forensic Medicine, Tongji Medical College, HUST from 1997 to 2007. Other 11 cases which died of violence and other diseases were selected as the control group. Expressions of myocardial Fas protein in the samples were quantitatively detected by immunohistochemistry and computerized imaging analysis.@*RESULTS@#Myocardial Fas protein expression increased significantly in the DCM group. Positive color showed brown-yellow granulated or striped distribution in the longitudinal section of myocardial within the cell membrane and cytoplasm, and showed circular brown granules in the cross section of the cell membrane, while these changes were not observed in the control group though there was focal weak staining noted. Statistical significance was observed between the experimental and control groups (P = 0.002), but no statistical significance was found for the average optical density value between these two groups (P = 0.675).@*CONCLUSION@#The expression of Fas protein increased obviously in the DCM group. Such alteration in expression quantity and distribution of myocardial Fas protein may be related to arrhythmia and heart failure in the patients with DCM.

Ischemic stroke in Williams-Beuren syndrome: a case report.

A 15-year-old girl was admitted because of an acute onset of facial palsy and right hemiparesis. The patient had a history of moderate mental retardation and developmental delay. On admission, her vital signs were stable, except for high blood pressure. Magnetic resonance imaging demonstrated an infarct involving the left internal capsule and putamen. Because of the patient's young age, an extensive stroke survey was performed. Williams-Beuren syndrome was finally confirmed by fluorescent in situ hybridization. Compared with the previously reported cases, no evidence of cerebral arterial stenosis or cardiac abnormalities was found by noninvasive imaging techniques. Because Williams-Beuren syndrome is a complex, multiple congenital anomaly syndrome with prominent cardiovascular features, regular assessment and antihypertensive treatment are necessary to minimize the lifelong cardiovascular risk in patients with this syndrome.

Toll-like receptor 4 expression in the coronary atherosclerotic plaques of patients died from sudden cardiac death / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the Toll like receptor 4 (TLR4) expression in the coronary atherosclerotic plaques in patients died from sudden cardiac death (SCD) or non SCD.</p><p><b>METHODS</b>Autopsied coronary artery samples from 75 patients died from SCD (n = 28), non-SCD (n = 28) or non-CHD (n = 19) were examined and the R value (positive cells' areas/scanning areas) and A value (average optical density) of TLR4 expression in the coronary arteries were detected qualitatively by the immunohistochemistry (SABC method) and image analysis technologies.</p><p><b>RESULTS</b>SCD group: 13 (46.4%) cases showed strong positive expression of TLR4; 11 (39.3%), positive expression; 4 (14.3%), weak positive expression. CHD group: 8 (28.6%) cases showed weak positive expression; 17 (60.7%), very weak positive expression; 3 (10.7%), no positive expression. There was no positive expression of TLR4 in non-CHD samples. A (1.140 +/- 0.101) and R value (0.0269 +/- 0.0027) in SCD group were significantly higher than in non-SCD and control groups (all P < 0.01). A value was siginificantly higher in CHD group (0.719 +/- 0.205) than that in control group (0.481 +/- 0.033, P < 0.05) while R value (0.0085 +/- 0.0007, 0.0046 +/- 0.0004) was similar between the groups (P > 0.05).</p><p><b>CONCLUSION</b>The increased positive expressive of TLR4 in the atherosclerotic plaque can be regarded as an important pathological marker of SCD.</p>