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

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 .

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 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 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.

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.

OBJECTIVEThis study aimed to induce carcinogenesis of lingual mucosa in C57BL/6 mice by feeding them 4-nitroquinoline 1-oxide (4NQO) solution.

METHODSA total of 85 C57BL/6 mice were randomly divided into distilled water control group (DD group, n=5), 1,2-propylene glycol control group (PG group, n=5), and experimental group (EP group, n= 75). The mice in the experimental group were medially fed in 15 cages. By contrast, the mice in DD, EP, and PG groups were watered with distilled water, 50 mg.L-1 4NQO solution, and 1,2-propylene glycol solution. The mice in EP group were executed every two weeks from week 0, and the mice in the control groups were sacrificed at the 28th week. The mice were weighed. Mucosal lesions were measured by macroscopic observation and histopathologic detection.

RESULTSOne mouse in EP group died of unknown reason. The weight of the mice in EP group presented weight loss compared with the mice in DD and PG groups after the 24th week. Seventy-nine macroscopic lesions were observed in the lingual mucosa, oral floor, and upper palatal and buccal mucosa. A total of 70 macroscopic lesions (88.6%) were located in the lingual mucosa. Mucosal lesions changed from simple hyperplasia to squamous cell carcinomas. Well-differentiated squamous cell carcinomas were observed in all mice of EP group by pathological section at the 28th week. No lesion was found in the mice of DD and PG groups.

CONCLUSIONThe animal model of lingual squamous cell carcinomas was successfully established. The periods from 12th to 16th week and 20th to 28th week were the ideal times for the research on pathogenesis of early and medial-advanced stage during carcinogenesis of squamous cell carcinomas.

Objective To improve the gene targeting efficiency with C57BL/6 embryonic stem ( ES) cells.Meth-ods Three different genetically modified C57BL/6 ES cell lines, named TLX3, Ai3K and SL, were microinjected into ICR, B6( Cg)-Tyrc-2J and BALB/c mouse blastocysts, respectively.The efficiency was statistically evaluated according to three aspects:blastocyst collection, chimera production and germline transmission.Results None of the three ES cell lines was germline transmitted with B6(Cg)-Tyrc-2J mice as blastocyst donors, while it was achieved with both BALB/c and ICR mouse blastocysts.Compared in the aspect of blastocysts collection, ICR mouse was much better than BALB/c mouse (P<0.05), and the chimera production efficiency of ICR mouse was comparable to that of BALB/c mouse (P =0.115). As to the germline transmission efficiency, that of BALB/c mice is significantly higher than that of the ICR mice ( P<0.01).Conclusions The germline transmission efficiency of BALB/c mouse is highest among these three mouse strains. However, it has the disadvantages of blastocyst collection, developmental delay and zona pellucida fragility, compared with ICR mouse.Therefore, ICR mouse is also a good candidate as blastocyst donor for embryonic stem cell microinjection.

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.