Numerical Simulation of Fire in Underground Commercial Street.

In this study, while aiming at the prevention of fire accidents in underground commercial streets, an underground commercial street is selected as a research object, and the building fire is numerically simulated using the PyroSim software. Fire simulation scenarios are divided according to different fire zones by analyzing the temperature, carbon monoxide (CO) concentration, and visibility in the smoke layer inside a building. The available safe evacuation time is calculated according to the critical fire hazard judgment conditions. We found that the time when the flue gas temperature and CO concentration reached the critical value in the fire site was longer than the time when the visibility reached the critical value reducing or even avoiding the spread of smoke from the fire area to the evacuation stairs can provide effective help for crowd evacuation. Finally, the safety of the building is evaluated, and fire prevention countermeasures are defined based on the actual situation and fire numerical simulation results to reduce fire incidence, casualties, and economic losses.

Effect of Repaglinide on Blood Glucose, Endothelial Function, Lipid Metabolism, and Inflammatory Reaction in a Rat Model of Atherosclerosis.

OBJECTIVE: To investigate the protective effect of repaglinide on rat with atherosclerosis. METHODS: Sprague Dawley (SD) rats were divided into control, model, repaglinide, and metformin groups. In addition to the normal group, rats were given intraperitoneal injection of streptozotocin and high-fat diet (HFD). Meanwhile, repaglinide or metformin was administrated to the treatment rats, respectively, for 4 weeks. Serum, plasma, liver, epididymal fat, and aorta thoracica were obtained to observe the protective effect of repaglinide on rat with atherosclerosis. RESULTS: Compared to the control group, blood glucose was increased in the model group (P < .05), while it was decreased in the drug-administered groups. In addition, the levels of endothelin 1, TG, TC, low-density lipoprotein cholesterol, atherogenic index, liver index, and epididymal fat index were significantly increased, but the levels of high-density lipoprotein cholesterol, plasminogen activator inhibitor 1, and antiatherogenic index were decreased significantly in the model group compared to the control group (P < .05, respectively). And these effects were reversed by treatment with repaglinide (P < .05, respectively). CONCLUSION: Our results suggested that repaglinide may regulate the formation of early atherosclerosis through the abovementioned mechanisms.

Excessive copper induces the production of reactive oxygen species, which is mediated by phospholipase D, nicotinamide adenine dinucleotide phosphate oxidase and antioxidant systems.

Tobacco BY-2 suspension cells were used to study the chemical damage and its associated mechanisms caused by Cu2+. Treatment with 100 micromol/L Cu2+ generated a large amount of H2O2 and thiobarbituric acid-reactive substances (TBARS) in cells. Using phospholipase D (PLD) specific inhibitor (1-butanol) or phosphatidic acid (PA), we demonstrated that PLD plays an important role in the generation of H2O2 and TBARS. Semi-quantitative reverse-transcriptase polymerase chain reaction and enzyme activity assays with wild type and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-overexpressing BY-2 cells revealed that PLD and PA are the key factors leading to NADPH oxidase activation, which is responsible for H2O2 and TBARS production induced by Cu2+. Moreover, the content of ascorbic acid (AsA), an effective antioxidant, was sharply reduced in BY-2 cells exposed to excessive Cu2+. Furthermore, a significant downregulation of the enzymes of AsA biosynthesis and the antioxidant system was found. This evidence suggests that excessive Cu2+-elevated reactive oxygen species (ROS) production is caused by upregulated PLD that elevates the activity of NADPH oxidase and its collapsed antioxidant systems that scavenges ROS.

[Effects of two different dosages of octreotide on portal pressure and hepatic hemodynamics in cirrhotic portal hypertensive patients after portal-azygous devascularization and splenectomy].

OBJECTIVE: Increased portal inflow and intrahepatic resistance may play a part of the role in pathogenesis of portal hypertension in cirrhotic patients. Some vasoactive substances may play an important role in the regulation of hepatic hemodynamics. The aim of this study is to investigate the effects of two different dosages of octreotide on portal pressure and hepatic hemodynamics. METHODS: 26 cirrhotic patients who underwent portal-azygous devascularization and splenectomy were investigated in a randomized and double-blind study. Patients were assigned to receive treatment either with a bolus of octreotide 100 microg, followed by infusion of 50 microg/h for 72 h (Group A, n = 12) or with a bolus of octreotide 100 microg, followed by infusion of 25 microg/h for 72 h (Group B, n = 14). The portal pressure was dynamically measured via a catheter placed in portal vein. The indexes of hepatic hemodynamics, including maximal and mean velocity of portal vein flow (PFV(max), PFV(mean)), maximal and minimal velocity of hepatic artery flow (HAV(max), HAV(min)) were measured using colour sonography at baseline, 72 h after infusion octreotide and 7 days after cessation of the infusion. RESULTS: The portal pressure declined 15.4% on average either in group A or group B after surgery. Portal pressure was significantly decreased after infusion of octreotide in both group A and B as compared with that at baseline. The mean decrease of portal pressure was 20.6%. The portal pressure showed a sustained decrease in group A, but it returned to baseline in group B after stopping of octreotide infusion. The portal pressure in group A and B was statistically different 24 h after stopping octreotide infusion (24.8 +/- 6.5 vs 29.4 +/- 5.8), 48 h (25.3 +/- 6.7 vs 29.9 +/- 7.0), P < 0.05. However, no differences of portal pressure between group A and B before surgery (41.0 +/- 6.6 vs 38.5 +/- 4.7), baseline (32.8 +/- 4.9 vs 33.6 +/- 6.5) and during octreotide infusion were observed. PFV(max) and PFV(mean) were significantly decreased as compared with baseline either before surgery or octreotide infusion. However, HAV(max) and HAV(min) were significantly increased as compared with baseline and before surgery. No relationship between portal pressure and sonography indexes was observed. CONCLUSIONS: Both dosages of octreotide infusion 50 microg/h and 25 microg/h can significantly reduce portal pressure, although with 25 microg/h of octreotide is reflects it seen returned to baseline. The dosage 50 microg/h of octreotide infusion may be more rational for prevention rebleeding of varices in cirrhotic portal hypertensive patients.