ABSTRACT
Objective:To observe the effect of emotional stimulation on the formation process of atherosclerosis ( AS) ,and explain the role of hydrogen sulfide ( H2 S) in atherosclerotic lesions. Methods:Twenty-four Sprague-Dawley rats were randomly divided into AS group, qi-stagnation and blood-stasis AS group and the control group. The AS group was fed with special diets, the qi-stagnation and blood-stasis AS group was fed with special diets and emotional stimulation, and the control group was fed with normal diets. During the experiment, the indicators including the characterization score, H2 S content, four items of the natural bleeding and blood coagula-tion, tissue blood flow and blood lipid were respectively detected in the 4 th, 8 th and 12 th week. Results:Compared with those in the AS group, since the 4 th week, the rats in qi-stagnation and blood-stasis AS group were with significantly decreased activity, slow re-sponse, lackluster fur and dark purple tongue (P<0. 01);the level of plasma lipid increased significantly, and increased further with time extension(P<0. 05 or P<0. 01);since the 8 th week, APTT and FIB changed significantly (P<0. 05),the blood flow to skin, liver and kidney decreased significantly (P<0. 05);the content of H2S was significantly higher in the 12 th week (P<0. 01). Con-clusion:Emotional stimulation promotes the formation of AS model,and the gas molecule system of H2 S plays a regulatory role in the qi-stagnation and blood-stasis AS animal model.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the expressions of Sonic hedgehog (Shh) and matrix metalloproteinases 2 (MMP2) in human esophageal squamous cell carcinoma (ESCC) and their association with the clinicopathological features.</p><p><b>METHODS</b>Immunohistochemistry was employed to examine the expressions of Shh and MMP2 in 48 specimens of ESCC and 44 specimens of adjacent tissues.</p><p><b>RESULTS</b>The positivity rate of Shh expression in ESCC (75%) was significantly higher than that in the adjacent tissues (20.45%). Shh expression was located mainly in the cell nuclei and cytoplasm, and was closely correlated with TNM stage. Positive MMP2 expression was detected in 68.75% of the ESCC tissues as compared to 22.72% in the adjacent tissues. MMP2 expression was localized mainly in the cytoplasm, and its expression level was closely correlated with TNM stage and lymph node metastasis. A positive correlation was found between Shh and MMP2 expressions in the 48 ESCC tissues (R=0.037, P=0.019).</p><p><b>CONCLUSION</b>The expression of Shh protein may be involved in tumor invasion and metastasis of ESCC.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Carcinoma, Squamous Cell , Metabolism , Pathology , Esophageal Neoplasms , Metabolism , Pathology , Hedgehog Proteins , Metabolism , Lymphatic Metastasis , Matrix Metalloproteinase 2 , Metabolism , Neoplasm StagingABSTRACT
<p><b>BACKGROUND</b>Tissue microarray provides a convenient shortcut for immunohistochemical staining. The aim of this study is to investigate the clinicopathologic and prognostic values of survivin and cyclooxygenase-2 (COX-2) expression level in patients with non-small cell lung cancer (NSCLC).</p><p><b>METHODS</b>Expression of survivin and COX-2 was detected in 88 cases of NSCLC and 5 cases of normal lung samples by immunohistochemical staining on tissue microarray sections. All cases were followed up for more than 5 years.</p><p><b>RESULTS</b>Cytoplasmic and nuclear expression rate of survivin in NSCLC was 94.3% and 79.5%, respectively, and positive expression rate of COX-2 was 71.6%, however, neither survivin nor COX-2 expression was observed in normal lung tissues (P < 0.005). Nuclear expression of survivin was markedly higher in smokers than that in non-smokers (P=0.002). The positive expression of COX-2 was significantly related to gender, smoking, histologic subtype and lymph node metastasis (P < 0.05). Univariate analysis showed that patients with positive expression of COX-2 had worse overall survival (P=0.014), however, survivin expression was not related to survival. Multivariate analysis showed that neither survivin nor COX-2 was independent prognostic factor for survival.</p><p><b>CONCLUSIONS</b>The results indicate that survivin highly expresses in NSCLC, so the ubiquitous expression makes it a potential novel parameter for diagnosis of NSCLC. Aberrant expression of COX-2 is related to worse overall survival, which may be useful to predict prognosis for NSCLC.</p>
ABSTRACT
<p><b>BACKGROUND</b>The promyelocytic leukaemia (PML) protein has been implicated in control of key tumor-suppressive pathways. However, its role in pathogenesis of lung cancer is still unclear. The objective of this study is to assess expression and clinical significance of PML, P53 and P16INK4A in lung cancer, as well as the relation of these factors.</p><p><b>METHODS</b>The tissue microarrays were created with samples from lung cancers (n=148), pulmonary benign lung tumors (n=5) and normal lung tissues (n=7), and protein expression was analyzed by immunohistochemical staining. The association between protein expression and clinical parameters was evaluated by using Crosstabs method. The Kaplan-Meier method was used to estimate survival. Cox proportional hazards model was used for univariate and multivariate analysis.</p><p><b>RESULTS</b>There was at least triplicate 0.6-mm cores per sample, 4 cases of lung cancer were excluded for lacking of enough tissue. PML was found in the cytoplasm of 14.0% cases of NSCLC and of 39.1% SCLC (P=0.010), and in the nuclei of 31.4% NSCLC and 8.7% SCLC respectively (P=0.026). PML protein was present in 9 patients with SCLC and absent in 14 cases, 5-year cumulative survival rate of the patients was 50% and 23% respectively (Log-rank test, P=0.047). Lacking of PML protein and senior pathologic T-stage were two hazardous factors that influenced prognosis of SCLC. P53 expression was found in 33.3% lung cancer, and absent in benign tumors and normal tissues of the lung (P=0.038). P16INK4A expression was abolished in normal lung tissue, however, increased in lung cancer (28.5%), and especially in lung cancer with non- or poor differentiation (36.5%) and in SCLC (69.6%). There was inverse correlation between PML expression in the nuclei and P16INK4A expression, positive correlation between P53 and P16INK4A expressions in lung cancers. PML was negatively correlated with P53 in squamous cell carcinoma.</p><p><b>CONCLUSIONS</b>As an important suppressor of tumor, PML is related with P53 mutation in squamous cell carcinoma. Increased P16INK4A protein in lung cancer may be the results of gene mutation, and be related with mutant P53 protein.</p>