Objective To examine the expression of inhibitory chondroitin sulfate proteoglycans (CSPGs) and in-vestigate their potential effects on neural plasticity in the peri-infarct cortex and ipsilateral thalamus after focal cerebral infarction in hypertensive rats. Methods Twenty-four adult renovascular hypertensive Sprague-Dawley rats per group were subjected to permanent right middle cerebral artery occlusion(MCAO) or sham operation. Twelve rats which were se-lected randomly from per group at each time point were decapitated and their brains were removed and cut into coronal sections at 7 and 14 days post MCAO. The expression of CSPGs, NG2 and Neurocan was examined using immunostaining and western blot. Results All rats displayed neurological deficits to varying degrees and the expression of CSPGs, NG2 and full length Neurocan was increased in the peri-infarct cortex and ipsilateral thalamus at 7 and 14 days (P<0.05). However, there were no significant difference in either expression of CSPGs, NG2 and full-length Neurocan between 7 and 14 days or the expression of C-terminal fragment Neurocan at 7 and 14 days (all P>0.05). Conclusions CSPGs may play a negative role in neural plasticity through induction of inhibitory environment in the peri-infarct cortex and ipsilat-eral thalamus following focal cerebral infarction in hypertensive rats.

Objective To investigate the dynamic levels of autophagy after intimal injury of carotid artery. Meth-ods In this study ,40 male SD rats were randomly assigned to operated(n=20)and control groups(n=20). Balloon inju-ry was induced in the left carotid artery in operated groups .Rats in control groups just received carotid artery exposure without injury. Western blot was used to detect the levels of Beclin-1, LC3 and p62 at the third and seventh days. Immu-nofluorescence was used to examine the expression of Beclin-1 and LC3 at the third and seventh days. Results The ex-pression levels of Beclin-1 and LC3 were increased while the levels of P62 were decreased at the third and seventh days after carotid balloon injury. Beclin-1 and LC3 were present in neointima and medintima. The numbers of both Beclin-1 positive cells and LC3 positive cells were increased at the third and seventh days after carotid injury. The numbers of Be-clin-1 positive cells were 18.60 ± 1.34 in neointima and 6.40 ± 0.55 in medintima at third day, (27.6 ± 2.19 in neointima and 6.40±0.55 in medinitima at the seventh day,(all P=0.000,n=5). The numbers of LC3 positive cells were 10.60±1.52 in neointima and 3.00 ± 0.71 in medintima at third day, (P=0.000,n=5;at the seventh day 21.20 ± 2.49;3.00 ± 0.71,P=0.000,n=5). Conclusions This study domenstrates that autophagy was activated after carotid injury and the chang is dy-namic, which may contribute to neointima formation.

Objective:To investigate the expression of Rho GTPases signaling pathway in non-small cell lung carcinoma (NSCLC)and its clinical significance.Methods:Molecules of Rho GTPases signaling pathway including RhoC, E-cadherin, MMP-2, and MMP-9 were detected by RT-PCR and immunohistochemistry in 36 specimens of non-small cell lung carcinoma (NSCLC). The relationship between RhoC mRNA and prognosis of patients was evaluated by using Kaplan-Meier survival curve analysis.Results:There was a significant difference in the expression of RhoC mRNA between NSCLC tissues and para-cancerous tissues (P<0.01). The expression of RhoC mRNA in NSCLC was not correlated with gender, age, invasion degree, lymph node metastasis, tumor size, histological classification, and differentiation degree but correlated with different TNM stage (P<0.05). There was a significant positive correlation between the expression of RhoC protein and MMP-2 protein (r=0.474, P=0.003). The survival time of patients with weak expression of RhoC mRNA was longer than those with over-expression of RhoC mRNA, but there was no significant difference between the two groups (P>0.05). Conclusion:Over-expression of RhoC mRNA is closely correlated with the tumorigenesis and progression of NSCLC, and may be related with invasion and metastasis of NSCLC early to middle stage.

Objective To investigate the expression,clinicopathological significance and correlation of S100A4,EGFR and PI3K in lung adenocarcinoma.Methods Immunohistochemical method (EnVision two steps) was used to detect the expression of S100A4,EGFR and PI3K proteins in 84 lung adenocarcinoma tissue samples and 30 normal lung tissue samples.The relationship of S100A4,EGFR and PI3K expression with clinicopathologic factors,post-operative five-year survival and the correlations among the three proteins were analyzed.Results The positive expression rates of S100A4,EGFR and PI3Kin lung adenocarcinoma tissues were higher than those in normal tissues,respectively [(69.0 ％,58/84) vs (6.7 ％,2/30),(64.3 ％,54/84) vs (16.7 ％,5/30),(52.4 ％,44/84) vs (13.3 ％,4/30),P ＜ 0.01].The expression of S100A4,EGFR and PI3K proteins were positively correlated with the differentiated degree,lymph node metastasis,clinical stages,and five-year survival (P ＜ 0.05),but not correlated with other clinicopathologic factors (P ＞ 0.05).The expression of S100A4 was positively correlated with EGFR and PI3K in lung adenocarcinoma (P ＜ 0.01),and the expression of EGFR was positively correlated with PI3K (P＜ 0.01).Conclusions S100A4,EGFR and PI3K were closely related with the occurrence,development,metastasis and prognosis of lung adenocarcinoma.S100A4 might be an important marker in estimating biological behavior and metastasis tendence of lung adenocarcinoma.S100A4 may be correlated with EGFR and PI3K.