[Methodology of DNA staining by Azure A].
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Biomedical subjects
Publications and source records attributed to Song He.
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This paper introduces a pathological information network and image analysis system designed by ourselves. The system offers an efficient means for modern medical diagnosis and treatment, teaching, research and management in the department of pathology.
OBJECTIVE: To investigate the expression, localization and interrelationship of P27(kip1) and cyclin D3 in non-Hodgkin's lymphoma (NHL). METHODS: The expressions of P27(kip1), cyclin D3 and index Ki-67 was detected in 100 NHL and 20 reactive lymph nodes by immunohistochemical technique. The expression and localization of P27(kip1) and cyclin D3 in 3 NHL cell lines were detected by Western blot, double immunolabelling and laser scanning confocal microscopy, respectively. RESULTS: In general the expression of P27(kip1) in NHL was lower than in control group, and was negatively related to the tumor aggressiveness and proliferating activity; the expression of cyclin D3 in NHL was higher than in control group, and was positively related to the tumor aggressiveness and proliferating activity. There was a negative correlation between P27(kip1) and cyclin D3. Nevertheless, anomalous high P27(kip1) expression was found in a few NHL tissues with high expression of cyclin D3 and Ki-67. Overexpression and colocalization of P27(kip1) and cyclin D3 was found in Raji cell line. CONCLUSIONS: Under expression of P27(kip1) and overexpression of cyclin D3 may play a role in the occurrence and development of NHL. Anomalous high P27(kip1) expression and its interaction with cyclin D3 may be another mechanism for tumor genesis of NHL.
BACKGROUND & OBJECTIVE: Previous studies showed that expression of phosphatase and tensin homology deleted on chromosome ten (PTEN), gap junction protein connexin 43 (Cx43) and vascular endothelial growth factor (VEGF) may play an important role in tumor occurrence and progression. This study was designed to investigate the relationship among the protein expression of PTEN, Cx43, and VEGF in carcinogenesis and progression of hepatocellular carcinoma. METHODS: The expression of PTEN, Cx43 and VEGF were determined in 47 cases of HCC by streptavidin peroxidase immunohistochemistry. RESULTS: In the hepatocellular carcinoma, the total positive rates of PTEN, Cx43 and VEGF were 76.4%, 42.6%, and 70.2%, respectively. With progression of tumor course, PTEN and Cx43 positive rates decreased (P< 0.05), but the VEGF positive rate significantly increased (P=0.001). In comparison with the group of intrahepatic vascular embolism, PTEN positive rate increased apparently in the group without intrahepatic vascular embolism (P=0.006). Cx43 positive rate was lower in the group with cirrhosis background than that in the group without cirrhosis background (Chi(2)=4.713 5, P=0.03). No significant difference of PTEN positive rate was observed in tumor size, differentiation degree in cancerous tissue and cirrhosis background, Cx43 positive rate in tumor size, differentiation degree in cancerous tissue and intrahepatic vascular embolism, VEGF positive rate in tumor size, differentiation degree in cancerous tissue, cirrhosis background and intrahepatic vascular embolism. Correlation analysis revealed that PTEN positive rate was positively correlated with Cx43 positive rate (Cramer's V=0.394 9, P=0.023), negatively correlated with VEGF positive rate (Cramer's V=0.393 7,P=0.024), but no significant association was observed between Cx43 positive rate and VEGF positive rate (Cramer's V=0.307 2, P=0.064). CONCLUSION: The aberrant expression of PTEN, Cx43, and VEGF may play a role in occurrence, progression, and intrahepatic metastasis of the hepatocellular carcinoma. Determining the expression of PTEN, Cx43, and VEGF may contribute to synthetically evaluating the biological behavior of hepatocellular carcinoma.
OBJECTIVE: To investigate the relationship between expression of c-erbB-2, CD44v6 and nm23 gene proteins and the clinicopathological features of colorectal carcinomas. METHODS: Immunohistochemical technique was adopted to detect the protein expression of c-erbB-2, CD44v6 and nm23 genes in 92 cases of colorectal carcinomas. Of the 92 cases, 28 cases were followed up for more than 10 years, in which the prognosis was analyzed. RESULTS: Expression of c-erbB-2 and CD44v6 was correlating with UICC staging (P < 0.05), and c-erbB-2 was associated with prominent peritumoral lymphocytic infiltration (P < 0.05). In the 28 cases with followed-up data, univariant analysis revealed that the survival rate was correlated with histological grading, UICC staging, tumor growth pattern, peritumoral lymphocytic infiltration, and expression of c-erbB-2, CD44v6 and nm23. However, Cox stepwise proportional hazards analysis showed that only UICC staging, c-erbB-2 and nm23 status retained significant independently in prospecting prognosis. CONCLUSIONS: Besides UICC III and IV stage, overexpression of c-erbB-2 and decreased expression of nm23 are considered acceptable as the parameters in predicting of poor prognosis in colorectal carcinoma.
OBJECTIVE: To reclassify retrospectively 370 cases of malignant lymphomas. METHODS: According to the WHO new classification, the clinical features and pathology as well as immunophenotype of 370 lymphomas were analysed. RESULTS: In the 370 lymphomas, there were 359 non-Hodgkin's lymphomas (NHL) (97.03%) and 11 Hodgkin's lymphomas (HL) (2.97%). Of the 359 NHL, 246 were B-cell lymphomas (68.52%), 108 T-cell lymphomas (30.08%), 1 each histiocytic lymphoma and follicular dendritic cell sarcoma, and 3 NK cell lymphomas. The extranodal lymphomas were 196 cases (54.6%) and the nodal lymphomas 163 cases (45.4%). The incidence of NHL categories were in proper order as follows: diffuse large B cell lymphoma (173 cases, 48.2%) > peripheral T cell lymphoma (54 cases, 15.0%) > mucosa associated lymphoid tissue (MALT) lymphoma (31 cases, 8.6%) > NK/T cell lymphoma (25 cases, 7.0%) > follicular lymphoma (21 cases, 5.8%) > anaplastic large cell lymphoma (12 cases, 3.3%). CONCLUSION: The results suggested that the study of malignant lymphomas with WHO new classification have important clinical significance.
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OBJECTIVE: To observe the expression of lipopolysaccharide binding protein (LBP) and CD14 mRNA in alcohol-induced liver disease (ALD) and evaluate the relationship between the expression of LBP and CD14 mRNA and the severity of liver injury in alcoholic-fed rats. METHODS: Twenty Wistar rats were divided into two groups: ethanol-fed group and control group. Ethanol-fed group were fed ethanol (by intragastric infusion of 500 ml/L ethanol orally, dose of 5~12 g/kg/d) and control group received dextrose instead of ethanol. Rats of both groups were sacrificed at 4 weeks and 8 weeks, respectively. Levels of endotoxin and alanine transaminase (ALT) in blood were measured, and liver pathology was observed by light and electronic microscopy. Expression of LBP and CD14 mRNA in liver tissues were determined with the reverse transcription polymerase chain reaction (RT-PCR) analysis. RESULTS: Plasma endotoxin levels were increased significantly in ethanol-fed rats [(129 21) pg/ml and (187 35) pg/ml at 4 weeks and 8 weeks] than in control rats [(48 9) pg/ml and (53 11) pg/ml, respectively, t=11.2, 11.6, P<0.05]. Mean values for plasma ALT levels were increased dramatically in ethanol-fed rats after 4 weeks and 8 weeks [(112 15) U/L and (147 22) U/L, respectively] than in the control animals [(31 12)U/L and (33 9)U/L, respectively, t=5.9, 20.6, P<0.05]. In liver sections from ethanol-fed rats, there was marked pathological changes (steatosis, cell infiltration and necrosis). In the control rats, there was no significant difference in the levels of LBP and CD14 mRNA at the two time points. In ethanol-fed rats, ethanol administration led to a significant increase in LBP and CD14 mRNA levels as compared with the control group (P<0.05). CONCLUSIONS: Ethanol administration lead to a significant increase in endotoxin levels of the serum and LBP and CD14 mRNA expression in liver tissues in ethanol- fed rats when compared with the control rats. Increase of LBP and CD14 mRNA expression may result in greater sensitivity to endotoxin and thus lead to liver injury.