Objective To study the effect of application of vascular endoth el ial growth factor (VEGF) and anti-VEGF on the expression of fracture healing rel ated factors and observe the pathological changes at fractured site. Methods Fra cture models were established in 105 rabbits. All rabbits were randomly assigned into controlled group, VEGF treated group and anti-VEGF treated group. The fact ors related to fracture healing were detected, and pathological changes were obs erved at 8, 24, 72 h and 1, 3, 5, 8 weeks after fracture. Results After the appl ication of VGEF, BMP was expressed earlier and the express period was prolonged . On the contrary, anti-VEGF completely inhibited the expression of BMP in the f ractured ends. The fractured sites were filled with fibrous callus, cartilage ca llus and bony callus at the 3rd week and they were converted into woven bone at the 5th week. The fracture reached to normal healing at the 8th week in the VEGF treated group. Cellular necrosis increased in the earlier period in the VEGF po lyclonal antibody treated group, continuous focal necrosis was seen in the fract ured sites between 1st week to 5th week, vascularization reduced obviously at th e 3rd week. Conclusion Fracture healing is the result of mutual modulation and c oordination among many factors. VEGF may be an important factor which plays impo rtant role in the course of fracture healing.

Objective To explore the changed rules and the diagnositic methods of the cardisc functions after chest impact trauma(CIT).Methods The medals of moderate to severity CIT were established using BIM-Ⅱ Bio-impactor in 20 rabbits.The cardiac functions were examined with cardiac catheterization,single photon-emission computed tomography(SPECT)and the Doppler echocardiography at pre end post 1h,4h,8h and 24h after CIT.Results The cardiac functions were changed significantly after CIT.The expressions of the right ventricular dysfunctions mainly were systolic dysfuction while the left ventricular dysfunctions mainly were diastolic dysfunction after CIT.Conclustion All the cardiac catheterization、SPECT and the Doppler echocardiography are beneficial to the diagnosis of cardiac dysfunction afte CIT.The SPEGT is more exactitude and the Doppler echocardiography is more cheaper compared with non-invasive approaches.

Objective To explore the changes and the significance of left ventricular functions after blunt chest trauma(BCT)in rabbits.Methods 36 rabbit models of BCT with BIM-Ⅱ Bio-impactor in were used to observe the changes of left ventricular functions and free calcium,free calmodulin and total calmodulin were detected at pre-injury,the 2nd,4th,8th,12th and 24th hour after injury.Results The cardiac function were impaired.The systolic functions of left ventricle were impaired and recovered during 4-12 hour after BCT.The diastolic functions of left ventricle were impaired but not recovered 24h after BCT.The free calcium and total calmodulin in myocardial cells were increased from the 4th hour,reached,peak at the 8th hour post-BCT(P＜0.01),and then decreased,but were still higher at the 24th hour post-BCT than that of pre-BCT(P＜0.05).The free calmodulin in myocardial cells was low and reached peak at the 8th hour after BCT(P＜0.01).There is remarkable positive correlation between free calcium in myocardial cells and LVEDP and dp/dtmax with cardiac function(P＜0.05,P＜0.01).Conclusion The cardiac function is obviously changed after BCT,especially the diastolic functions of left ventricle.The hish concentration of free calcium in myocardial ceils may be one of the reasons of cardiac dysfunction after BCT.

The effects of tumor necrosis factor (TNF) on the activity of plasmogen acitva-tor inhibitor (PAD and the morphology of the cells were observed in the original passage of cultured human umbilical vein endothelial cells (HUVEC). It was found that the TNF effect on the PAI was determined by the dosage of TNF, that is, 500U/ml of TNF could significantly activate PAT activity while 2500U/ml markedly inhibit it. Morphdogical observation canfirmed that 2500U/ml of TNF could injure HUVEC to form a kind of cells whose morphology was quite similar to that of circulating endothelial cells originating from peripheral blood.These findings suggest that TNF can stimulate HUVEC to increase the PAI acivity but too large a dosage of TNF could injure the metabolic function and structure of HUVEC.

To study the characteristics and preventive methods of road traffic accidents (RTA) in different regions of Chongqing, 2 police teams of traffic management in downtown, 2 teams at the arban suburb junction, 1 team in the county and 1 freeway team were selected randomly, and RTA occurring in the respective listrict, above middle RTA between 1988 to 1997 were investigated and analyzed. In a total of 13121 cases of RTA, there were 6201 RTA with casualties, 14 catastrophic RTA, and 977 serious RTA. In these RTA there were 1086 deaths, 3165 severely wounded and 7327 mildly wounded. Pedestrians and passenger weres constituted 44 0% and 42 5% of total casualties respectively. 57 9% of severely wounded and deaths occurred in pedestrians. As a whole,there was a tendency of rise in RTA every year, having a significant characteristic of time distribution. The majority RTA occurring in Chongqing was related with violation of driving regulations and recklessness in crossing roads. causes of RTA, time distribution and casualties were different in different regions. In order to decreese the rate of RTA,it is deemed essential to enhance propaganda to raise the awareness of traffic accidents and to reinforce traffic management appropriate for respective district of the city.

In order to explore the effect of anti vegf on fracture healing process,rabbits with left radius fracture were used as an animal model and divided randomly into control and experiment groups.VEGF polyclonal antibody was given to the animals of the experiment group films were thken at the fracture sites after 1,3,5 and 8 weeks of the fracture.the results showed that the cellular necrosis increased in the experiment group shortly after the fracture.Although there was fibroblast proliferation at 72 hours after the fracture,continuous focal necrosis was seen from 1 to 5 weeks in the fracture sites,and the vascularization reduced obviously 3 weeks after the injury.The organelle degeneration was observed in the fibroblasts and osteoblasts under microscope.The fracture sites were filled with fibrous tissue at the 8 th week and nonunion was ween in the fracture sites on X ray films.These results suggest that the lack of VEGF in the fracture sites might be one of the important reasons of fracture healing.

The uncontrolled inflammatory response is commonly seen and plays an important role in the pathogenesis of post traumatic complications. Bacterial endotoxin or lipopolysaccharide (LPS) is one of the most potent mediators in inducing uncontrolled inflammatory response.Several LPS associated receptors have been identified on the surface of monocytes/macrophages, which are shown to be initial factors to recognize LPS and trigger inflammatory response. Scanvenger receptor (SR), CD14and toll like receptor4 (TLR4)act as high affinity or sensitive LPS receptorS. SRhas been shown to be responsibe for clearance and neutralization of LPS by macrophages,whereas CD14 and TLR4have been foand to be important receptors mediating cell activation induced by LPS. TLR2, ? 2 integrin and L selectin have been considered to be low affinity LPSreceptors, and they may play an important catalytic role in LPS induced pro inflammatory and anti inflammatory responses as "secondary LPS receptors". In addition, TLR4 might be the receptor pathway through which LPS could activate blood endothelial cells. Down regulation of defense receptors such as SR and up regulation of excitatory receptors such as CD14, TLR4, and TLR2might be an important mechanism to turn monocytes/macrophages into effector cells (release of pro and anti inflammatory mediators) during the course of infection. Further investigation of transmembrane LPS signaltransduction mechanisms. might help discover some novel strategies for effective control or modulation of uncontrolled inflammatory response.

AIM: To explore the pathophysiological bases in the pathogenesis of the lasting emotional behavioral disorders following posttraumatic stress disorder (PTSD). METHODS: 240 male Wistar rats were divided randomly into 3 groups. Group SE ( n =96) for rats with PTSD-like behavior by constant pulsating current of 100 ?A with intratrain frequencies of 16 Hz, pulsating duration of 1 ms, train duration of 10 s and interstimulus interval of 7 min for 5 days with 8 times per day. Group CE ( n =96) for control with electrode implanted in hippocampus without stimulation, and Group NC ( n =48) for normal control. The activities of Na +-K +-ATPase and Ca 2+ -ATPase, levels of intracellular calcium and free calmodulin (CaM), and the total CaM expression were detected in hippocampi of experimental rats. RESULTS: The activities of Na +-K +-ATPase and Ca 2+ -ATPase in mitochondria of hippocampal cells in Group SE rats were significantly decreased at 48 h and 72 h after the last stimulation, respectively. The intracellular free calcium levels were increased, and the mean channel fluorescence of intracellular free CaM decreased remarkably at 72 h poststimulation, while the expression of total CaM was significantly elevated at 48 h after the last stimulation in hippocampi of Group SE rats. CONCLUSION: The lasting increased levels of intracellular free calcium and expression of Ca 2+ -CaM in hippocampus, as well as the dysfunction of Na +-K + pump and Ca 2+ -ATPase in mitochondria may play important roles in the long-term neuropsychological sequelae in PTSD.

Objective To evaluate the expressive varieties of Nogo-A mRNA in injured optic nerves of rats. Methods Reverse transcription polymerase chain reaction (RT-PCR) method was used to hemi-quantitatively analyze the levels of Nogo-A mRNA in the optic nerves 3, 7, 9, 15, 21, and 25 days respectively after injury. Results The level of the expression of Nogo-A mRNA was low in the normal optic nerves, while it was significantly high in the optic nerves 3 days after injury, and kept the high level still after 25 days. Conclusion The expression of Nogo-A mRNA in injured optic nerves is increased.

Objective To observe the alterations of nitric oxide (NO) level and the neuronal NOS (nNOS) expression in rats with posttraumatic stress disorder (PTSD) like behavior following subconvulsive electrical stimuli. Methods After the establishment of the PTSD animal model following subconvulsive stimuli to hippocampus, the nitric oxide (NO) and NO synthase (NOS) levels and the neuronal NOS (nNOS) expression in hippocampus and frontal cortex of experimental rats were investigated by neurochemistry and Western blotting, respectively. Results The NO level in hippocampus of experimental rats with PTSD like behavior following subconvulsive stimulation increased significantly at 12 h after the last stimulation (4.65?1.22 ?mol/g protein, P