[Expression of cytokine IL-1α and S100ß in different types of plaques in Alzheimer's disease].

OBJECTIVE: To study the significance of cytokine IL-1α and S100ß expression in formation and evolution of different types of plaques in Alzheimer's disease. METHODS: Thirty-four autopsy cases of Alzheimer's disease encountered during the period from 1982 to 2008 were retrieved from the archival files of Department of Pathology, Beijing Hospital. Tissue blocks were taken from hippocampus for dual immunostaining for IL-1α/Aß and S100ß/Aß. RESULTS: Immunohistochemical studied for IL-1α/Aß and S100ß/Aß delineated four different types of senile plaques: diffuse non-neuritic plaques, diffuse neuritic plaques, dense-core neuritic plaques and dense-core non-neuritic plaques. The numbers of IL-1α-positive microglias and S100ß-positive astrocytes associated with diffuse neuritic plaques were (7.29 ± 3.04) per mm(2) and (6.49 ± 2.20) per mm(2), respectively. In contrast, the numbers of IL-1α-positive microglias and S100ß-positive astrocytes associated with diffuse non-neuritic plaques, dense-core neuritic plaques and dense-core non-neuritic plaques were (3.24 ± 1.53) per mm(2) and (4.14 ± 1.77) per mm(2), (2.09 ± 1.37) per mm(2) and (2.25 ± 0.83) per mm(2), and (1.38 ± 0.90) per mm(2) and (0.58 ± 0.36) per mm(2), respectively. The numbers of IL-1α-positive microglias and S100ß-positive astrocytes associated with diffuse neuritic plaques were significantly higher than those of the other three types of plaques (P < 0.05). CONCLUSION: The IL-1α-positive microglias and S100ß-positive astrocytes may be of certain significance in transformation of diffuse non-neuritic plaques to diffuse neuritic plaques in Alzheimer's disease.

[Clinicopathologic analysis of vulnerable plaque in autopsy with acute coronary syndrome].

OBJECTIVE: To observe pathohistological features of vulnerable plaques in coronary arteries. METHODS: Autopsy coronary samples from 67 patients died of acute coronary syndrome (ACS) and 60 patients of non-cardiac death from 1992 to 2006 in Beijing Hospital were examined. Morphological features of vulnerable plaques of ACS cases were evaluated in terms of thrombus, ratio of lipid core, the minimal thickness of fibrous cap and the density of inflammatory infiltration. RESULTS: (1) There are 305 plaques in ACS group and the incidence of big lipid core is 153 (50.16%), thin fibrous cap is 187(61.31%), inflammatory infiltration is 263 (86.23%), neovasculature conformation is 217 (71.15%), severe stenosis is 26 (8.52%), calcification is 238 (78.03%), superficial calcified nodule is 26 (8.52%), fissured plaque is 12 (3.93%), endothelial denudation is 3 (0.98%) and intraplaque hemorrhage is 54 (17.70%), which are significantly higher than control samples except endothelial denudation (P < 0.01). (2) The incidence of vulnerable plaques in ACS group is significantly higher than in the control group (89.51% vs. 21.98%, P < 0.01). There are 4.07 sections of vulnerable plaques with high density of inflammatory infiltration out of 4.55 sections reviewed in ACS patients, while there are 0.85 sections of vulnerable plaques with mild inflammatory infiltration out of 3.87 sections reviewed in the control cases. CONCLUSIONS: Formation of vulnerable plaque was an important pathological factor for the development of ACS. The major morphological characteristics of vulnerable plaque are big lipid core, thin fibrous cap, inflammatory infiltration, neovascularization, severe stenosis, plaque rupture, and endothelial denudation suggesting inflammation performed an important role in the formation of vulnerable plaque.

[Pathologic study of diabetic cardiomyopathy].

OBJECTIVE: To study the histopathologic features, differential diagnosis and pathogenesis of diabetic cardiomyopathy. METHODS: The clinicopathologic features of 40 autopsy cases of diabetes mellitus were studied. The hearts from another 40 cases of non-diabetic elderly deceased were used for comparison. RESULTS: In the 40 cases of diabetes studied, 36 cases (90.0%) showed microscopic myocardial cell death. Focal interstitial fibrosis was observed in 37 cases (92.5%). On the other hand, similar myocardial cell death and patchy interstitial fibrosis was seen in 8 cases (20.0%) and 9 cases (22.5%) of non-diabetic hearts, respectively. The difference between the two groups was statistically significant (P < 0.01). The mural thickness of intramyocardial blood vessels was significantly increased in diabetic group (20.6 microm +/- 4.2 microm) than in non-diabetic group (7.2 microm +/- 5.2 microm), P < 0.01.The myocardial changes in diabetic group however were similar to those in non-diabetic group with systemic hypertension. CONCLUSIONS: Pathologic diagnosis of diabetic cardiomyopathy relies on detailed histologic examination of heart tissue and clinical correlation of a long history of diabetes mellitus. Exclusion of other possible etiologies is also essential. The myocardial cell death observed may be due to the ischemic effect induced by diabetic microangiopathy in cardiac muscle.