AIM:To study whether the pulmonary infection of Escherichia coli (E.coli) interferes the glu-colipid metabolism in high-fat diet-induced obese mice.METHODS:High-fat diet-induced obese mice (n=48) and nor-mal chow-fed control mice ( n=48) were intranasally infused with 40 μL fluid containing 4 ×109 CFUs E.coli.The ser-um, periepididymal adipose tissue and liver were obtained at 0 d, 1 d, 2 d, 3 d and 4 d after infection.The body mass, periepididymal adipose tissue and liver were weighed , and the levels of fasting blood glucose (FBG), fasting blood insulin ( FINS) , free fatty acid ( FFA) and very-low-density lipoprotein ( VLDL) were measured by ELISA .The serum total cho-lesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol ( LDL-C) , and hepatic TG contents were detected , and the hepatic steatosis was observed under microscope with oil red O staining.RESULTS:Compared with day 0, the body mass, fat mass and fat index were decreased significantly from day 1 to day 4 after infection (P<0.05).The levels of FBG, FINS and HOMA-IR were apparently raised from day 2 to day 4 af-ter infection (P<0.05).The contents of serum FFA, TG and VLDL were increased markedly from day 1 to day 4 after in-fection (P<0.05).However, the concentrations of serum TC, LDL-C and HDL-C were decreased obviously from day 1 to day 3 ( P<0.05 ) .The liver mass , liver index and TG content were significantly increased from day 1 to day 4 ( P<0.05 ) .Consistently , the lipid droplet accumulation in the liver cells was increased obviously at day 2 and day 4 after infec-tion.Compared with control group , except the levels of serum TC , LDL-C and HDL-C in obese group substantially de-creased, the other indexes were increased by different degrees during the whole experiment period (P<0.05).CONCLU-SION:Pulmonary infection of Escherichia coli exacerbates the disorder of glucose and lipid metabolism in high-fat diet-in-duced obese mice , which contributes the development of insulin resistance and hepatic steatosis .

OBJECTIVETo explore the expression of integrin alpha 6 in hepatic sinusoidal capillaration.

METHODSThe rat hepatic fibrosis model was established by injection of carbon tetrachloride subcutaneously. Then the expression of laminin and integrin alpha 6 subunit was observed by immunohistochemistry and dot immuno-blotting.

RESULTSWe observed sinusoidal capillaration formed by deposition of laminin along sinusoids in Disse interspace by immunohistochemistry staining. In normal rat the expression of integrin alpha 6 was restricted to portal vascular endothelial cells and bile duct epithelial cell membranes. No expression was observed in sinusoidal endothelial cell membranes. When capillaration integrin alpha 6 was detected in a continuous pattern along the sinusoids, the content of integrin alpha 6 was significantly higher in fibrotic liver tissues than in normal liver tissues as measured by dot immuno-blotting (P<0.05).

CONCLUSIONSDuring fibrogenesis, laminin continuously accumulate in liver tissues and form basement membrane resulting in sinusoidal capillaration, and then induce the expression of integrin alpha 6 on SEC membranes.

Animals ; Antigens, CD ; biosynthesis ; Carbon Tetrachloride ; Immunoblotting ; Immunohistochemistry ; Integrin alpha6 ; Laminin ; metabolism ; Liver ; metabolism ; pathology ; Liver Cirrhosis, Experimental ; chemically induced ; metabolism ; pathology ; Male ; Rats ; Rats, Wistar ; Time Factors

ObjectiveTo evaluate the application of multi-slice CT (MSCT) perfusion scan technique in predicting renal function recovery after unilateral hydronephrosis treatment.MethodsThirtyeight patients with unilateral obstructive hydronephrosis not shown on intravenous urography (IVU) and a normal contralateral kidney were recruited for this study.Patients were divided into detected (D) and undetected (UD) groups depending on whether the IVU detected urinary tract obstruction.All patients underwent plain abdominal X-ray,gray-scale ultrasonography,excretory urography and MSCT perfusion scan before and after the treatment.Patients were followed-up at six months or more after the treatment for a mean duration of 12.5 months (range from 6 to 22 ).ResultsOf the 38 cases,22 cases were in group D,16 cases were in group UD.On MSCT,renal cortex blood flow (BF) and blood volume ( BV ) value after treatment in group D were 561.1 ± 165.4 ml/( 100 g · min) and 35.9 ± 11.3 ml/100 g compared with before treatment rates of 361.6 ±109.7 ml/(100g· min) and24.1 ±10.2 ml/100g,t=-3.38,-2.34,P＜0.01,0.05.In the UD group,the differences of these parameters were after treatment 38.7 ± 15.4 ml/(100 g · min),10.306 ± 4.925 ml/100 g and before treatment 39.1 ± 22.5 ml/( 100 g · min) and 8.7 ± 4.4 ml/100 g,P ＞ 0.05.In the aspects of BF and BV,there were statistically significant differences between group D and group U D both before and after the treatment,t=9.09,4.15,P ＜ 0.01.ConclusionsM SCT perfusion can provide a valuable prediction technique of the renal function recovery in patients with unilateral obstructive hydronephrosis.Improvement of renal function can be expected after relief of obstructive hydronephrosis if the patients have a BF 361.6 ml/( 100 g · min) and BV 24.1 ml/100 g or greater measured by MSCT perfusion.

OBJECTIVETo investigate the effects of polyunsaturated fatty acids (PUFA) ω-3 and ω-6, and their middle metabolites PGE2 and PGE3 on angiogenesis formation of gastric cancer, and to explore associated mechanism.

METHODSThe effects of ω-3, ω-6, PGE2, PGE3 on the proliferation and migration of human umbilical vein endothelial cell (HUVEC) were measured by proliferation and migration assay respectively. The angiogenesis assay in vivo was used to measure the effects of ω-3, ω-6, PGE2 and PGE3 on neovascularization. In all the assays, groups without ω-3, ω-6, PGE2 and PGE3 were designed as the control.

RESULTSWith the increased concentration of ω-6 from 1 μmol/L to 10 μmol/L, the proliferation ability of HUVECs enhanced, and the number of migration cells also increased from 28.2±3.0 to 32.8±2.1, which was higher than control group (21.2±3.2) respectively (both P<0.05). With the increased concentration of ω-3 from 1 μmol/L to 10 μmol/L, the proliferation ability of HUVECs was inhibited, and the number of migration cells decreased from 15.8±2.0 to 11.0±2.1, which was lower than control group (22.1±3.0) respectively (both P<0.05). In the angiogenesis assay, compared with control group (standard number: 43 721±4 654), the angiogenesis ability of HUVECs was significantly enhanced by ω-6 in concentration-dependent manner (1 μmol/L group: 63 238±4 795, 10 μmol/L group: 78 166±6 123, all P<0.01). Meanwhile, with the increased concentration of ω-3 from 1 μmol/L to 10 μmol/L, the angiogenesis ability was significantly decreased from 30 129±3 102 to 20 012±1 541(all P<0.01). The proliferation and migration ability of HUVECs were significantly promoted by ω-6 metabolites PGE2 (P<0.05) in a concentration-dependent manner. In contrast, ω-3 metabolites PGE3 significantly inhibited the proliferation and migration ability of HUVECs in a concentration-dependent manner (all P<0.05). After rofecoxib (a COX-2 specific inhibitor) inhibited the expression of COX-2, the expression level of PGE2 was significantly decreased in a dose-dependent manner. In co-culture system, whose gastric cancer cells expressed positive COX-2, ω-6 could increase angiogenesis of gastric cancer cells(P<0.01), but ω-3 could inhibit such angiogenesis(P<0.01). In co-culture system, whose gastric cancer cells did not express COX-2, ω-3 could inhibit the angiogenesis of gastric cancer cells (P<0.05), but ω-6 had no effect on angiogenesis.

CONCLUSIONSThe PUFA ω-6 can enhance the angiogenesis via the promotion of proliferation and migration of HUVECs, and COX-2 and PGE2 may play an important role in this process, whereas, the ω-3 can inhibit the angiogenesis through its middle metabolites PGE3 to inhibit the proliferation and migration of HUVECs. Results of this experiment may provide a new approach to inhibit and prevent the spread of gastric cancer.

Alprostadil ; analogs & derivatives ; pharmacology ; Angiogenesis Inducing Agents ; metabolism ; pharmacology ; Angiogenesis Inhibitors ; pharmacology ; Cell Count ; methods ; Cell Line, Tumor ; drug effects ; physiology ; Cell Migration Assays ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Coculture Techniques ; Cyclooxygenase 2 ; pharmacology ; Dinoprostone ; metabolism ; pharmacology ; Fatty Acids, Omega-3 ; pharmacology ; Fatty Acids, Omega-6 ; metabolism ; pharmacology ; Fatty Acids, Unsaturated ; pharmacology ; Human Umbilical Vein Endothelial Cells ; drug effects ; physiology ; Humans ; Lactones ; pharmacology ; Neovascularization, Pathologic ; physiopathology ; Stomach Neoplasms ; physiopathology ; Sulfones ; pharmacology