Female ; Fluoroscopy ; Humans ; Intubation, Intratracheal ; Male ; Middle Aged ; Tracheotomy ; methods

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Objective To investigate the expressions of receptor for advanced glycation endproducts (RAGE) and nuclear factor κB(NF-κB) in brain hippocampus of rat with chronic fluorosis,and to reveal the mechanism of brain damage resulted from chronic fluorosis.Methods Sixty clean grade SD rats were randomly divided to three groups(20 rats in each group,10 female and 10 male) fed with different contents of fluoride,control group with normal tap-water(＜ 0.5 mg/L fluoride),small dosage of fluoride exposure group(10 mg/L fluoride in tap-water) and large dosage of fluoride exposure group(50 mg/L fluoride) for six months.Then the rats were killed by femoral artery bleeding and hippocampus was removed.Protein and mRNA levels of RAGE and NF-κB in the hippocampus were determined by Western blotting and quantitative real time PCR,respectively.Results As compared to the control groups[(100.00 ± 2.60)％,(100.00 ± 7.80)％],the expressions of RAGE and NF-κB at protein level in the hippocampus were significantly increased in the small dosage of fluoride exposure groups [(205.00 ± 15.30)％,(156.00 ± 12.20)％] and the large dosage of fluoride exposure groups[(232.00 ± 10.90)％,(162.00 ± 9.80)％,all P ＜ 0.05]; for the mRNA level of RAGE and NF-κB,the expressions were higher in the small dosage of fluoride exposure groups(1.27 ± 0.09,0.83 ± 0.15) and the large dosage of fluoride exposure groups (2.60 ± 0.19,1.27 ± 0.19) than those of the control groups(0.66 ± 0.18,0.32 ± 0.08,all P＜ 0.05).Conclusions The increased expressions of RAGE and NF-κB in the hippocampus of rat brain are caused by chronic fluorosis,and these changes may be associated with the mechanism of nerve injury.

Objective Aim of the study is to investigate the expression of syndecan-4 and nuclear factor κB(NF-κB) in the kidney of rat with chronic fluorosis,and to reveal the mechanism of kidney damage resulted from the toxicity of excessive amount of fluoride.Methods According to body mass and sex,sixty SD rats were randomly divided to three groups according to body mass and fed with different contents of fluoride:control group with normal tap-water(＜ 0.5 mg/L fluoride),small dosage of fluoride exposure group (adding 10 mg/L fluoride in tap-water) and large dosage of fluoride exposure group (50 mg/L fluoride) for six months.The protein level of syndecan-4 and NF-κB in the kidney was detected by Western blotting and syndecan-4 mRNA level by quantitative real time PCR.Results As compared to the control group[(100.0 + 8.1)％],the expression of syndecan-4 at protein level in the kidney of rat was significantly increased in the small dosage of fluoride exposure group [(198.5 + 5.6)％,P ＜ 0.05] and large dosage of fluoride exposure group [(209.2 + 13.0)％,P ＜ 0.05]; the protein levels of NF-κB in the small dosage of fluoride exposure group[(284.4 + 11.1)％,P ＜ 0.05] and in the large dosage of fluoride exposure group[(343.2 + 2.9)％,P ＜ 0.05] were significantly increased than that of the control group[(100.0 ± 10.7)％].The mRNA levels of syndecan-4 in the kidney in the small dosage of fluoride exposure group and large dosage of fluoride exposure group(0.431 + 0.058 and 0.453 ± 0.065,both P ＜ 0.05,respectively) were significantly increased than that of the control(0.128 + 0.026).Conclusions The increased expression of NF-κB in the kidney is induced by increased expression of syndecan-4,which may be involved in kidney damage of chronic fluorosis.

20 % . In both groups CH was induced with infusion of 0.01 % NTP at a rate 0.5-6.0 ?g?kg-1?min-1 to maintain MAP at 55-65 mm Hg. MAP, HR, CVP and CO were continuously monitored. Arterial lactate concentration was measured by enzyme assay. Arterial and mixed venous blood gases were analyzed, and oxygen delivery (DO2 ) and consumption (VO2) were calculated before AHH (T0) after AHH was performed (T1), 30 min after CH was induced (T2) and 30 min after termination of CH (T3) in group Ⅰ and in group Ⅱ before CH (T1), 30 min after induction of CH (T2) and 30 rain after termination of CH (T3 ) .ResultsIn group Ⅰ(AHH + CH) compared with the baseline values (T0 ) HR significantly decreased while CVP significantly increased after AHH (T1 ) ; cardiac output (CO) significantly increased after AHH (T1 ) and during CH (T2) while DO2 was significantly decreased after AHH (T1) and CH (T3 ) but arterial lactate concentration was significantly decreased during and after CH (T2, T3). In group Ⅱ (CH alone) compared with the baseline values (T1) HR significantly increased while CVP significantly decreased during and after CH (T2, T3 ) ; there was no significant change in CO and DO2 at T2 and T3 but arterial lactate concentration significantly increased during and after CH (T2, T3). There was significantly less blood loss during operation in group I than in group Ⅱ . ConclusionThere was tissue deoxygenation during and after deliberate hypotension as shown by increased arterial lactate concentration while AHH combined with CH can improve tissue perfusion and oxygenation. AHH can also maintain hemodynamic stability during CH.

Platelet-activation factor (PAF), one of the potent proinflammatory mediators, is produced from a large range of cells, including polymorphonuclear neutrophils, monocytes, and natural killer cells. To study the role of PAF in the pathogenesis of silicosis, we determined the PAF in silicotic patients and in healthy persons. The results showed that the concentration of PAF in the plasma of silicotic patients was significantly higher than that of healthy persons. Our in vitro experimental results showed that the total numbers of fibroblasts were markedly raised with added PAF from 0 to 1 μ g/ml. Adding 1 μ g/ml PAF significantly increased the total numbers of fibroblasts after culture for 48, 72, 96 hrs. Therefore, we suggest that PAF be possibly involved in the pathogenesis of silicosis. However, the mechanism remains to be further elucidated.
Platelet Activating Factor ; g <3> ; Pathogenesis ; /mL ; Effective

Objective To investigate the activity of recombinant Vibrio vulnificus hemolysin (rVvhA) on the apoptosis of J774A.1 cells and the related mechanism. Methods The cytotoxic effect of rVvhA on the growth of J774A.1 cells was identified by MTT, celluar and mitochondrial morphology were observed by transmission electron microscopy, apoptosis or necrosis and mitochondrial membrane potential in J774A.1 cells were measured by flow cytometry, activities of caspase-3 ,-8,-9 were detected by spectrophotometry. Results The viability of J774A.1 cells exposed to rVvhA was inhibited, and it is dependent on dose. Celluar and mitochondrial uhrastructure both occurred to change obviously observed by transmission electron microscopy in J774A.1 treated by 2.0 HU/ml and 3.0 HU/ml rVvhA after 8 hours; and 3.0 HU/ml rVvhA group had a better cytotoxic effect on J774A.1 than that of 3.0 HU/ml rVvhA group. The percentage of apoptosis is (7.80±0.62)%, (12.33±0.12)%, respectively. Besides, the mitochondriai membrane potential also reduced, because the rate of fluorescence which is green increase 1.0% (normal) to 9.8% (2.0 HU/ml rVvhA) and 39.2% (3.0 HU/ml rVvhA). At the same time, the caspase-3, -9 activity increased gradually, but caspase-8 remained unchanging. In J774A.1 cells treated by 3.0 HU/ml rV-vhA + caspase-3 inhibitor(Ac-DEVD-FMK) or caspase-9 inhibitor(Ac-LEHD-FMK), The apoptosis of was reduced to(6.23±3.95)% ,(9.60±3.14)%, and the activity of caspase-3, -9 reduced, too. Conclusion The rVvhA has cytotoxic effect on J774A.1. Mitochondria-mediated apoptosis pathway which is dependent on caspase may be related to apoptosis induced by rVvhA in J774A.1.

Aim To investigate the effects of harpagide on cerebral ischemia and the mitochondria mediated Caspase dependent apoptotic signaling pathway in mice.Methods The MCAO was employed to establish MCAO model.When the models were established, the mice were given harpagide (4, 8, 12 mg·kg-1) and edaravone (3.2 mg·kg-1) [0.1 ml·(10 g)-1] by tail vein injection after MCAO immediately.And the model and control mice were given equivalent normal saline by the same way.After MCAO for 6 h, the behavior, volume of cerebral ischemia and pathological changes in the brain were observed.Westernblot was employed to determine the contents of Cyt C in mitochondrion and pro-caspase-3 in endochylema.Results Compared with the model group, harpagide (4, 8, 12 mg·kg-1) could significantly decrease the increased nerve functional score, brain index, brain water content and volume of cerebral ischemia induced by cerebral ischemia.Harpagide (4, 8, 12 mg·kg-1) could reduce the contents of Cyt C in mitochondrion and pro-caspase-3 in endochylema.Conclusion Harpagide may have protective effect on the cerebral ischemia injury in mice, which might be related to the inhibition of the cerebral mitochondria mediated Caspase dependent apoptotic signaling pathway.

Objective To evaluate image quality of 640-slice coronary CT angiography by combined anesthesia in Tibet minipigs. Methods Tibet minipigs underwent 640-slice coronary CT angiography after anesthesia with xylazine hydrochloride and pentobarbital sodium. The effect of anesthesia was observed and the image quality was evaluated.Results The anesthesia maintained in 40 minutes.The heart rate was (66.66±6.62)beat per minutes.The respiratory frequency was (15.62±1.53)beat per minutes.The revived time was 30 -60 minutes. All of images were good enough to be diagnosed.Conclusion Combined anesthesia with xylazine hydrochloride and pentobarbital sodium has excellent anesthetic effect.It is also simple,convenient and safe.Therefore,it is one of ideal anesthetic methods on such study for 640-slice coronary CT angiography in Tibet minipigs.