Objective To investigate the effect and its mechanism of cyclin dependent protein kinase inhibitor Olomoucine treatment on experimental herpes simplex encephalitis(HSE). Methods 45 mice were randomly assigned to HSV-1 sham-infected group (n=15), HSV-1 infected control group (n=15) and Olomoucine treated group (n=15). Flow cytometry was used to detect the expression of brain cells surface antigen CD11b. The reverse transcription polymerase chain reaction (RT-PCR) to detect the expression of tumor necrosis factor-? (TNF-?) and Interleukin-6 (IL-6). TUNEL method was adopted to detect neural cells apoptosis. Pathologic slices of brain tissues were used to identify tissue morphology differences. The survival rates were compared between the treatment groups Acyclovir (n=20) and Olomoucine (n=20) by the method of Kaplan-Meier 2 weeks after HSV-1 infection. Results After HSV-1 infection, the expression of brain tissue CD11b, TNF-?, IL-6 were significantly increased compared with sham-infected group (allP

A total of 79 tibial fracture patients (47 males and 32 females; 16 to 73 years old) were selected from Department of Orthopedics, Huangbu Hospital of Huidong City, including 19 cases of open fractures and 60 of closed fractures. Forty-eight fractures in 79 patients were fixed with interlocking nails, 19 by revolving self-locking nail, and 12 by auto compressive locking nail. Operations were all successful. The average operation time was (102 ?10) minutes in the interlocking group, (65?10) minutes in the revolving self-locking nail group and (100?10) minutes in the auto compressive locking nail group. The patients were followed up for 6-10 months. In the interlocking group, one breakage of the screws was found, with one superficial infection and the other 3 achieved delayed bone fracture. The healing time of interlocking group was (21.0?3.2) weeks and the excellent rate of function recovery was (85.42?5.20)% by Johner-Wruh. In the revolving self-locking nail group, one developed delayed bone facture and the other one achieved dislocation; the healing time was (20.0?3.6) weeks and the excellent rate of function recovery was (84.21?4.10)%. In the auto compressive locking nail group, one had loosening screw and the other one achieved superficial infection. The healing time was (17.0?2.8) weeks and the excellent rate of function recovery was (91.67?3.70)%. The excellent and good rate in auto compressive locking nail group was significantly greater than the other groups (P

bThis study explored whether the transplantation of modified marrow stromal cells (MSCs) has angiogenic effects in a left middle cerebral artery occlusion infarction/reperfusion (MCAO I/R) rat model and preliminarily examined the mechanism of angiogenesis following cerebral infarction. MSCs were isolated by using a direct adherent method and cultured. Vascular endothelial growth factor (VEGF) was transfected into MSCs by employing the liposome transfection. The transfection efficiency was measured by the optical density method. The protein expression of VEGF gene before and after transfection was measured by Western blotting. SD rat model of transient occlusion of the left middle cerebral artery was established by using an approach of intra-luminal occlusion. Tetrazolium (TTC) and HE staining were performed to observe the cerebral infarction. ELISAs were used to measure the levels of VEGF in the rat cerebral tissues. The expression patterns of angiopoietin-2 (Ang-2) and CD34 in cells surrounding the area of infarction were immunohistochemistrically observed. Ang-2 protein expression in the tissue surrounding the area of infarction was measured by Western blotting. VEGF expression in the MSCs increased after transfection at a rate of approximately 28%±3.4%. ELISA showed that the expression of VEGF in the cerebral tissue was significantly increased after induction of infarction, peaking on the 4th day and decreasing to the levels of the sham surgery group (normal) within 7 to 10 days. The VEGF level was significantly higher at each time point in the VEGF-MSC and MSC groups compared to the model group. Moreover, the VEGF level was higher in the VEGF-MSC group than in the MSC group and stayed relatively high until the 10th day. The immunohistochemical results showed that 10 days after the infarction, the number of Ang-2 and CD34-expressing cells in the area surrounding the infarction was significantly higher in the VEGF-MSC group and the MSC group compared to the model group. Moreover, the VEGF level was higher in the VEGF-MSC group than the MSC group. A similar trend in Ang-2 protein expression was revealed by Western blotting. In the MCAO rat model transfected with modified MSCs over-expressing VEGF, compared to the MSC transplantation group, the concentration of VEGF was significantly increased in the brain tissue after cerebral infarction. In addition, the level of Ang-2 was up-regulated, with angiogenesis promoted, the blood supply to the areas surrounding the cerebral infarction increased, and neurological function improved. We are led to speculate that the synergistic effects of VEGF and Ang-2 may be responsible for the angiogenesis following cerebral infarction.

bThis study explored whether the transplantation of modified marrow stromal cells (MSCs) has angiogenic effects in a left middle cerebral artery occlusion infarction/reperfusion (MCAO I/R) rat model and preliminarily examined the mechanism of angiogenesis following cerebral infarction. MSCs were isolated by using a direct adherent method and cultured. Vascular endothelial growth factor (VEGF) was transfected into MSCs by employing the liposome transfection. The transfection efficiency was measured by the optical density method. The protein expression of VEGF gene before and after transfection was measured by Western blotting. SD rat model of transient occlusion of the left middle cerebral artery was established by using an approach of intra-luminal occlusion. Tetrazolium (TTC) and HE staining were performed to observe the cerebral infarction. ELISAs were used to measure the levels of VEGF in the rat cerebral tissues. The expression patterns of angiopoietin-2 (Ang-2) and CD34 in cells surrounding the area of infarction were immunohistochemistrically observed. Ang-2 protein expression in the tissue surrounding the area of infarction was measured by Western blotting. VEGF expression in the MSCs increased after transfection at a rate of approximately 28%±3.4%. ELISA showed that the expression of VEGF in the cerebral tissue was significantly increased after induction of infarction, peaking on the 4th day and decreasing to the levels of the sham surgery group (normal) within 7 to 10 days. The VEGF level was significantly higher at each time point in the VEGF-MSC and MSC groups compared to the model group. Moreover, the VEGF level was higher in the VEGF-MSC group than in the MSC group and stayed relatively high until the 10th day. The immunohistochemical results showed that 10 days after the infarction, the number of Ang-2 and CD34-expressing cells in the area surrounding the infarction was significantly higher in the VEGF-MSC group and the MSC group compared to the model group. Moreover, the VEGF level was higher in the VEGF-MSC group than the MSC group. A similar trend in Ang-2 protein expression was revealed by Western blotting. In the MCAO rat model transfected with modified MSCs over-expressing VEGF, compared to the MSC transplantation group, the concentration of VEGF was significantly increased in the brain tissue after cerebral infarction. In addition, the level of Ang-2 was up-regulated, with angiogenesis promoted, the blood supply to the areas surrounding the cerebral infarction increased, and neurological function improved. We are led to speculate that the synergistic effects of VEGF and Ang-2 may be responsible for the angiogenesis following cerebral infarction.
Angiopoietin-2 ; genetics ; metabolism ; Animals ; Bone Marrow ; metabolism ; pathology ; Cerebral Infarction ; genetics ; metabolism ; pathology ; Male ; Neovascularization, Pathologic ; genetics ; pathology ; Rats ; Rats, Sprague-Dawley ; Stromal Cells ; metabolism ; pathology ; Vascular Endothelial Growth Factor A ; genetics ; metabolism