AIM:To study the effect of contact system in monocyte adhesion induced by urokinase-type plasminogen activator (U-PA). METHODS:U937 cells were labeled with [3H] thymidine in the culture medium, test reagents were added into the cell suspension in 24-well plates. The counts?min -1 were counted in a liquid scintillation counter. RESULTS:U-PA-induced monocyte adhesion was inhibited by high-molecular-weight kininogen and kallikrein, and promoted by factor Ⅻ and plasminogen. CONCLUSION:these contact system proteins may be important modulators of U-PA-induced monocyte adhesion, a process which is involved in many pathophysiological events.

Adult ; Aged ; Angiography, Digital Subtraction ; Carcinoma, Hepatocellular ; diagnostic imaging ; therapy ; Chemoembolization, Therapeutic ; Female ; Hemangioma ; diagnostic imaging ; therapy ; Humans ; Liver Neoplasms ; diagnostic imaging ; therapy ; Male ; Middle Aged ; Radiography, Interventional ; methods ; Tomography, X-Ray Computed ; methods

AIM: To observe the effects of norepinephrine (NE) on the cardiopulmonary and lung injury in goats with acute respiratory distress syndrome (ARDS) induced by endotoxin. METHODS: A model of septic ARDS was induced by intravenous infusion of low dose endotoxin in six goats. Then 40?10~ -6 NO inhalation was applied to the animals. After 30 min, combined intravenous infusion of NE at concentration of 0.5 mg?kg~ -1 ?min~ -1 was conducted. The dynamic changes in gas exchange and hemodynamics were measured with the aid of Swan-Ganz catheter. Arterial blood gas analysis before and after the onset of ARDS, 30 min after NO inhalation and combined NE was detected. Histology of the lung was also observed. RESULTS: Inhalation of NO rapidly reduced mean pulmonary arterial pressure (MPAP), increased PaO_2, decreased P_ (A-a) O_2 and Qs/Qt in septic ARDS goats. These decrease and increase were more significant than those in NO inhaled alone when animals received NE. The combination of NO inhalation and NE injection resulted in increase in mean arterial pressure. NO inhalation did not ameliorate lung injury and combined NE intravenous injection ameliorated lung injury. CONCLUSION: Injection of low dose norepinephrine improves the beneficial effects of inhaled nitric oxide on lung gas exchange and ameliorates lung injury in goats with acute respiratory distress syndrome induced by endotoxin.

Objective To investigate the expression and clinical significance of RegⅣand EGFR,PI3K proteins in gastric adenocarcinoma .Methods S-P immunohistochemistry was used to detect the expression of RegⅣand EGFR,PI3K proteins in pathological tissues of 73 cases with gastric adenocarcinoma and tumor -adja-cent normal gastric tissues .Results The positive expression rates of RegⅣand EGFR,PI3K proteins in 73 cases with gastric adenocarcinoma tissue were 50.7%(37/73),56.2%(41/73) and 69.9%(51/73) respectively, which were significantly different from the positive expression rates of tumor -adjacent normal gastric tissues ,be-ing 20.5%(15/73),19.2%(14/73),and 21.9%(16/73),respectively(P<0.05).The expression of RegⅣprotein was significantly correlated to differentiation degree ( P<0.05 ) and the expression of EGFR protein was significantly correlated to infiltrative depth,TNM stage,and lymph node metastasis(P<0.05).The expression of PI3K protein was significantly correlated to differentiation degree ,infiltrative depth,TNM stage and lymph node metastasis(P<0.05).There was positive correlation between the expressions of RegⅣ/EGFR,RegⅣ/PI3K and EGFR/PI3K proteins in gastric adenocarcinoma and the values of Spearman coefficient correlation were 0.325, 0.403 and 0.384,respectively(P<0.05).Conclusion RegⅣmay play an important role in gastric adenocarci-noma genesis and progression by activating EGFR /PI3K/Akt signaling pathway .

Objective To discuss the method of interventional intravascular treatment in traumatic carotid cavernous fistula(TCCF)and the significance of clinical application in emergency.Methods In 297 cases of TCCF,36 cases were treated by interventional intravaseular embolization by detachable balloon, embolization orificium or occlusion in one side of carotid artery.In the 36 cases,serious epistaxis occurred in 22 cases,cortical vein inflow in 9 cases,intracranial hemorrhage in 3 cases,aggravation of eyesight in 3 cases,and limb dysfunction in 2 cases.Results Fistula was successfully embolized and internal carotid artery remained patent in 19 cases.Complete embolization of orificium or internal carotid artery was achieved in 17 cases.The serious epistaxias in 22 cases and intracranial hemorrhage in 3 cases stopped.Eyesight recovered in 2 cases and improved in 1 case.Limb dysfunction improved evidently in 2 cases. Conclusion Intravascular embolization treatment is the first therapeutic choice for TCCF,especially in emergency.It is necessary,safe and effective.

Objective To evaluate the role of JNK signal pathway in brain injury after resuscitation in a rat model of asphyxia cardiac arrest.Methods Forty healthy male SD rats 'weighing 300-350 g were randomly divided into 4 groups ( n =10 each):sham operation group (group SH) ; cardiac arrest group (group CA) ; group SP600125-JNK inhibitor (group SP) and dimethyl sulfexide (DMSO) group.The rats were anesthetized with intraperitoneal pentobarbital 45 mg/kg,tracheostomized and mechanically ventilated.PETCO2 was maintained at 35-45 mm Hg.Femoral artery and vein were cannulated for BP monitoring and fluid infusion.Cardiac arrest was induced by clamping tracheal tube until ECG activity disappeared and MAP ＜ 10 mm Hg.Resuscitation was started at 3 min after cardiac arrest.MAP ＞ 60 mm Hg and HR ＞ 250 bpm were considered to be signs of successful resuscitation.SP600125 20 mg/kg and DMSO 0.2 ml were injected iv as soon as chest compression was started in groups SP and DMSO respectively.The animals were sacrificed at 5 h after successful resuscitation and their brains were removed for determination of wet/dry (W/D) weight ratio and microscopic examination of hippocampus.Neuronal apoptosis was detected by TUNEL.Results Cardiac arrest significantly increased W/D ratio and the number of apoptotic cells in group CA.SP600125 iv significantly attenuated the cardiac arrest-induced increase in W/D ratio and the number of apoptotic cells but DMSO did not.Conclusion JNK signal pathway is involved in the brain injury after resuscitation in a rat model of asphyxia cardiac arrest.

Objective To investigate the effects of sevoflurane anesthesia on the expression of c-Jun N-terminal kinase (JNK) and neuronal apoptosis in hippocampus in juvenile rats.Methods Forty healthy male SD rats, aged 30-35 days, weighing 100-110 g, were randomly divided into 2 groups (n = 20 each): control group (group C) and sevoflurane group (group S) . Group C inhaled a gas mixture of oxygen and air for 5 h and group S 3% sevoflurane for 5 h. The concentration of oxygen in both groups was maintained at 30% . Ten rats in each group were scarified at 1 h after regaining consciousness and the hippocampi removed for determination of phospho-JNK expression (by immuno-histochemistry and Western blot) and neuronal apoptosis (by TUNEL) . Another 10 rats were selected at 24 h after regaining consciousness to assess the cognitive function using Morris water maze. Results Compared with group C, phospho-JNK expression was significantly up-regulated, the number of apoptotic neurons increased, the latency prolonged and the duration of staying at the original platform quadrant shortened in group C ( P ＜ 0.05 or 0.01) . Conclusion Inhalation of 3.0% sevoflurane can induce neuronal apoptosis in hippocampus by activating JNK signaling pathway, thus leading to cognitive decline in juvenile rats.

Objective To establish a simple , fast and economic total DNA extraction method to serve the rapid identification of model mouse genotype in large number of mice .Methods Three methods, i.e.phenol extraction, isopropyl alcohol precipitation and mouse ear boiling methods were used to extract the total DNA from ten C 57-rasmodel mice.The purity and yield of DNA obtained by the three methods were compared , and polymerase chain reaction ( PCR) assay was used to compare the efficacy of the three extraction methods .Results Among the three methods , phenol extraction was the best and isopropyl alcohol precipitation was the poorest in DNA yield .In terms of DNA purity , the phenol extraction was the best and the mouse ear boiling method was the poorest .All the three methods could be used to extract the total DNA from mice serving as template of PCR reaction for the mouse genotype identification .The time consumption of three methods are 12.5 hr ,13 hr and 0.18 hr.Mouse ear boiling method was significantly lower than that of the other two methods ( P <0.01 ) ,.The obtained total DNA can be stored at conventional -20℃for 7 days and 30 days later still can be used as a template for PCR reaction .Conclusions Among the three methods studied , the mouse ear boiling method is simple and with the lowest cost , so it is feasible for total DNA extraction in scaled genotyping experiments .

Objective To investigate the effect of propofol on the activation of c-Jun N-terminal kinase (JNK) in hippocampus following asphyxial cardiac arrest-resuscitation in rats.Methods Forty male Sprague-Dawley rats,aged 6 months,weighing 350-380 g,were randomly divided into 4 groups (n =l0 each):sham operation group (group S),asphyxial cardiac arrest-cardiopulmonary resuscitation group (group CA-CPR),propofol group (group P) and normal saline group (group NS).All the rats were tracheostomized and mechanically ventilated after anesthetization.Cardiac arrest was induced by clamping the tracheal tube at the end of exhalation until ECG activity disappeared and MAP ＜ 10 mm Hg.Resuscitation was started 3 min later.MAP ＞ 60 mm Hg and HR ＞ 250 bpm were considered to be signs of successful resuscitation.Propofol 2 mg/kg was injected intravenously at 30 min before asphyxia,followed by propofol infusion at a rate of 4 mg· kg-1 · h-1 until the start of resuscitation in group P,while the equal volume of normal saline was given in group NS.At 12 h after successful resuscitation,the animals were sacrificed and brains were harvested for determination of wet/dry brain weight (W/D) ratio in brain tissues and expression of phosphor-JNK (p-JNK) in hippocampus (by immuno-histochemistry and Western blot),and for examination of the pathological changes of hippocampus.Results Compared with group S,W/D ratio was significantly increased and the expression of p-JNK in hippocampus was up-regulated in CA-CPR,P and NS groups (P ＜ 0.05 or 0.01).Compared with group CA-CPR,W/D ratio was significantly decreased and the expression of p-JNK in hippocampus was down-regnlated in group P (P ＜ 0.05 or 0.01),and no significant change was found in the indexes mentioned above in group NS (P ＞ 0.05).The pathological changes of hippocampus were significantly attenuated in group P compared with group CA-CPR.Conclusion Propofol can inhibit the activation of JNK in hippocampus following asphyxial cardiac arrest-resuscitation in rats and thus reducing brain injury.

Objective To evaluate the role of c-Jun N-terminal kinase (JNK) in lipopolysaccharide (LPS)-induced acute lung injury ( ALI) in rats.Methods Eighty male SD rats weighing 250-300 g were randomly divided into 4 groups ( n = 20 each) : control group (group C) ; ALI group; LPS + SP600125 (JNK inhibitor)group (group S) and LPS+ DMSO (the solvent) group (group DMSO) . ALI was induced by intravenous LPS 5mg/kg. In S and DMSO groups, SP600125 30 mg/kg and DMSO 0.2 ml were injected intravenously after LPS administration respectively. Ten animals were sacrificed by exsanguinafions at 4 h after LPS administration in each group. The broncho-alveolar lavage fluid (BALF) was colleted. The TNF-α and IL-1β concentrations in BALF were measured. The lungs were removed for microscopic examination and determination of W/D lung weight ratio. The other 10 animals in each group were observed for 48 h survival rate. Results Intravenous LPS significantly increased TNF-α and IL-1β concentrations in BALF and W/D lung weight ratio, decreased 48 h survival rate and induced histologic damage. Intravenous SP600125 30 mg/kg significantly attenuated the above-mentioned LPS-induced changes. Conclusion Activation of JNK is involved in the development of endotoxin-induced ALI in rats.