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Qiu T.-L.,Shaoxing Municipal Peoples Hospital | Jin G.-L.,Shaoxing Municipal Peoples Hospital | Wang X.-M.,Shaoxing Municipal Peoples Hospital
National Medical Journal of China | Year: 2010

Objective: To analyze the correlative factors of traumatic embolism in superficial cerebral vein and explore their corresponding treatments. Methods: A total of 74 cases were divided into 3 groups according to their injury mechanisms. Group A: traumatic brain injury in superficial cerebral vein with cerebral contusion, acute intracerebral hematoma and subdural hematoma in the same place; Group B: traumatic brain injury in superficial cerebral vein with acute intracerebral hematoma, subdural hematoma and skull fracture in the same place; Group C: traumatic brain injury in superficial cerebral vein with acute subdural hematoma and skull fracture in the same place, without cerebral contusion or acute intracerebral hematoma. They were divided into different groups according to gender, age, pre-operative GCS and cerebral hernia. Results: Among 74 cases, 28, 39 and 7 cases belonged to groups A, B and C respectively. There was significant difference among injured veins in three groups (P < 0.01). Cerebral infarction was found in 37 cases in groups A and B while only 2 cases in group C. Cerebral infarction had no correlation with sex, age, pre-operative GCS and cerebral hernia. Conclusion: Injuries in superficial cerebral vein are mainly caused by skull fracture, contre-coup injury and shearing force. Cerebral infarction often exists if there is cerebral contusion. It is necessary to protect injured primary superficial cerebral veins and ambient venous network, remove intracranial hematoma and large bone flap to reduce intracranial hypertension and dilute blood post-operatively to prevent venous embolism. Copyright © 2012 by the Chinese Medical Association. Source


Xu W.-Y.,Zhejiang University | Zheng L.-R.,Zhejiang University | Guo H.-Y.,Shaoxing Municipal Peoples Hospital | Peng F.,Shaoxing Municipal Peoples Hospital | Lv H.-T.,Wenzhou Medical College
Journal of Shanghai Jiaotong University (Medical Science) | Year: 2012

Objective: To investigate the influence of insulin resistance on the ventricular remodeling, and to observe the intervention effect of rosuvastatin and explore its possible mechanism. Methods: Forty male LDLR-/- mice aged 6 weeks were randomized into control group (NC group, fed with normal diet), high fat and high fructose diet group (HFF group, fed with normal diet+21.1% fat+20% fructose), rosuvastatin intervention group(HFFR group, intervention with rosuvastatin on the basis of that in HFF group) and rosuvastatin and mevalonic acid intervention group (HFFRMA group, fed with mevalonic acid on the basis of that in HFFR group), with 10 mice in each group. Mice were sacrificed 12 weeks after treatment, the fasting blood sugar (FBS) was determined by oxygen electrode method, fasting plasma insulin (FINS) was detected by ELISA, homeostasis model insulin resistance index (HOMA-IR) and left ventricular weight index (LVWI) were calculated, collagen volume fraction (CVF) of myocardial tissues was calculated with Picric-Sirius Red staining, and the expression of PPARα and MMP-9 protein in myocardial tissues was detected by Western blotting. Results: FBS, FINS, HOMA-IR, LVWI, CVF and the expression of PPARα and MMP-9 protein in HFF group, HFFR group and HFFRMA group were significantly higher than those in NC group(P<0.05). After treatment with rosuvastatin, FBS, FINS and HOMA-IR in HFFR group and HFFRMA group were significantly improved, and LVWI, CVF and the expression of PPARα and MMP-9 protein in HFFR group and HFFRMA group were significantly lower than those in HFF group (P<0.05). However, there was no significant difference in these parameters between HFFR group and HFFRMA group (P>0.05). Conclusion: Insulin resistance can be induced in LDLR-/- mice 12 weeks after high fat and high fructose diet. Insulin resistance may contribute to myocardial fibrosis and ventricular remodeling. Rosuvastatin can inhibit ventricular remodeling and improve insulin resistance, and the mechanism may be associated with the down-regulation of expression of MMP-9 and PPARα protein, which is independent of lipid-lowering effect. Source


Sun G.-Y.,Wenzhou Medical College | Wu J.-X.,Shaoxing Municipal Peoples Hospital | Wu J.-S.,Wenzhou Medical College | Pan Y.-T.,Wenzhou Medical College | Jin R.,Wenzhou Medical College
Chinese Journal of Cancer Research | Year: 2012

Objective: To investigate the expressions of caveolin-1, E-cadherin and β-catenin in gastric carcinoma, precancerous gastric and chronic non-atrophic gastritis tissues, and evaluate the correlation of these expressions with the development of gastric cancer. Methods: The expressions of caveolin-1, E-cadherin and β-catenin were detected by biotin- streptavidinperoxidase (SP) immunohistochemistry on 58 gastric cancer tissues, 40 precancerous gastric tissues and 42 chronic non-atrophic gastritis tissues. The correlation between the expressions of caveolin-1, E-cadherin and β-catenin, and the clinicopathologic parameters of gastric cancer was analyzed retrospectively. Results: The positive rates of caveolin-1 and E-cadherin expressions in gastric carcinoma were significantly lower than precancerous gastric and chronic non-atrophic gastritis tissues (P<0.01). An abnormal rate of β-catenin expression in gastric carcinoma was higher than precancerous gastric and chronic non-atrophic gastritis tissues (P<0.01). Moreover, low expressions of caveolin-1, E-cadherin and β-catenin correlated with tumor size, depth of invasion, lymph node metastasis and TNM stage (P<0.05). The positive rates of caveolin-1 and E-cadherin expressions decreased (P<0.01), while an abnormal rate of β-catenin expression increased inversely, with the degree of atypical hyperplasia (P<0.01). Caveolin-1 expression correlated positively with E-cadherin (r=0.41, P<0.05). Caveolin-1 (r=-0.36, P<0.05) and E-cadherin (r=-0.45, P<0.05) expressions negatively correlated with abnormal β-catenin expression. Conclusion: These results suggested that dysregulated expressions of caveolin-1, E-cadherin and β-catenin correlated with the development of gastric cancer and its biological behavior. © 2012 Chinese Anti-Cancer Association and Springer-Verlag Berlin Heidelberg. Source

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