Purpose To observe the mutation of K-ras gene and expression of Fascin-1 protein in CRC tissues and their relationship with clinical pathological features, and then to analyze the correlation between mutation of K-ras and expression of Fascin-1. Methods In 86 cases of CRC tissues, K-ras mutation was detected by DNA sequencing analysis, and Fascin-1 expression was detected by im-munohistochemical method. Results In CRC tissues the mutation rate of K-ras was 34. 88%, the expression rate of Fascin-1 was 60. 47%. The mutation rate of K-ras in lymph node metastasis group was higher than that of without lymph node metastasis group, and that in distant metastasis group was higher than that of without distant metastasis group(P<0. 05). The expression rate of Fascin-1 in serosa invasion group was higher than that of without serosa invasion group, and that in lymph node metastasis group was higher than that of without lymph node metastasis group, and that in distant metastasis group was higher than that of without distant metastasis group (P<0. 01). There was a correlation between the mutation of K-ras gene and the expression of Fascin-1 in CRC tissues (rp =0. 236, P<0. 05). Conclusions The CRC tissues with mutation of K-ras are more likely to metastasize and the CRC tissues with expression of Fascin-1 are more likely to invade serosa and metastasize. The CRC tissues with mutation of K-ras are more likely to express Fascin-1.

BACKGROUND: Excellent Iow-antigenicity xenogeneic biological valve scaffold is the premise of constructing tissue-engineered valve by using which kind of acellular methods.OBJECTIVE: To explore the optimal preparation method of making tissue engineered heart valves by meesuring efficiency of different acellular methods and ability to preserve the matrix.DESIGN, TIME AND SETTING: The prospective randomly controlled study was performed at the Central Laboratory of Taian Central Hospital from January 2007 to June 2008.MATERIALS: Sixteen specimens of porcine aortic valves were randomly divided into control, NaCI-sodium-dodecyl-sulfate (SDS),trypsin and triton-X100 groups.METHODS: Specimens in the control group were left intact. Three test groups were decelluladzed with NaCI, trypsin andTriton-X100 respectively.MAIN OUTCOME MEASURES: The gross structure, optical and electron microscope ultrastructure of the decelluarated porcineheart valve matrix was compared. The expression of vascular endothelial cell major histocompatibility complex (MHC)- Ⅰ antigenwas detected by immunohistochemical method.RESULTS: Treatment with NaCL-SDS achieved only incomplete decellularization. The main components of extracellular matdxwere reserved completely, but the fibrous components became unclear and swelling. Treatment with trypsin removed cellscompletely, but caused serious structural alterations, with the presence of swollen collagen fiber, crude edge, widen and irregularfiber interspace. Treatment with Triton-X100 achieved both complete decelluarization and preservation of the matrix structure.Valves following treatment of NaCI-SDS, trypsin and Triton-X100 had certain immunogenicity. However, the immunogenicity ofvalves following treatment of trypsin and Triton-X100 was significantly lower compared with the treatment of NaCL-SDS.CONCLUSION: The decellularization method by Triton-X100 is effective and complete. The Triton-X100 method does not changematrix structure and has low immunogenicity.

Objective To observe the effects of A2a adenosine receptor antagonist SCH442416 and ZM241385 on the expression of glutamine synthetase(GS) and L-Glutamate/L-Aspartate Transporter(GLAST) in rat retina under chronic ocular hypertension model.Methods Rat chronic ocular hypertension models were induced in the right eye of 12 male Sprague Dawley rats by blocking three episcleral veins,the left eye as control one.Intraocular pressure (IOP) was measured and compared at postoperative 1 week,2 weeks and 3 weeks.54 male chronic ocular hypertension rats were divided into 3 groups randomly,topically applying A2a adenosine receptor antagonist SCH442416,ZM241385 and carrier,respectively,three times a day for three weeks.At three weeks,mRNA and protein expression of GS and GLAST in rat retina were analyzed by RealTime-PCR and Western-blot.Results The average IOP of the modeling eyes at postoperative 1 week,2 weeks and 3 weeks were higher than that of the control eyes (all P ＜ 0.05).The mRNA and protein expression of GS and GLAST in the retina of SCH442416 and ZM241385 groups increased significantly compared to the carrier group (all P ＜ 0.05).However,the differences of mRNA and protein expression of GS and GLAST between SCH442416 and ZM241385 groups was not significant(all P ＞ 0.05).Conclusion Rat chronic ocular hypertension model can be induced by blocking three episceral veins successfully and effectively.A2a adenosine receptor antagonist SCH442416 and ZM241385 increase the expression of GS and GLAST.There seems no difference between the effects of these two drugs.

The oral and gastrointestinal opportunistic pathogen contamination was compared between tooth mugs placed upward and down-ward(n=9)for 1 4 days.Selective cultivation of the pathogens was uesd to measure the extent of contamination.The colony forming units (CFU)of colibacillus in group up and group down were 4.25 ±0.71 and 2.84 ±1 .40(P=0.046),S.mutans 89 ±0.31 and 2.84 ±1 .40 (P<0.001 ),Candida 2.28 ±1 .36 and 2.53 ±1 .92(P=0.002),fungus 2.44 ±0.99 and 0,respecitvely.Thus,tooth mug placed open-ing down is superior for health.

The objective of this study was to determine the concentrations of calcium,phosphorus and magnesium in blood and compare the differences in seven areas of Heilongjiang province,and then estimate calcuim-phosphorus metabolism of beef cattle in seven beef cattle farms to provi detheoretical foundation for the prevention of calcium phosphorus metabolism diseases of beef cattle.Seven beef cattle farms of Daqing,Shuangyashan,Jiusan and Mudanjiang in Heilongjiang province were selected as the survey sites,which were recorded as group A (both grazing and stall-feeding in Shuangyashan),group B (stall-feeding mode in Shuangyashan),group C (stall-feeding mode in Daqing),group D (grazing mode in Jiusan),group E (both grazing and stall-feeding in Daqing),group F (both grazing and stall-feeding in Daqing) and group G (stall-feeding mode in Mudanjiang).Then the concentrations of Ca,Mg,P,free fatty acid (NEFA),glucose (Glc) and β-hydroxybutyric acid (BHBA) in the blood were compared to estimate the calcuim-phosphorus metabolic states.Results showed that the concentrations of calcium,magnesium and phosphorus in the plasma of 65 beef cattle in seven survey sites were within the normal range,and there was no significant difference in calcium concentration among seven sites.The P contents in group C and G were significantly higher those that in group A and B(P＜0.01),which in group C was significantly higher than those in group D,E and F (P＜0.01),which in group G was significantly higher than those in group D,E and F(P＜0.01).NEFA content in group B was significantly higher than that in group D (P＜0.05),and there was no difference among other groups.The concentration of Glc in group A was significantly higher than that in group E (P＜0.05),which in group B was significantly higher than those in group A and D,and was very significantly higher than those in group E,F and G (P＜0.01),which in group C was very significantly higher than those in group A,D,E,F and G (P＜0.01),which in group C was significantly higher than those in group A,D,E,F and G (P＜0.01),which in group D was significantly higher than that in group E (P＜0.05),and which in group F was significantly higher than that in group E (P＜0.05).The concentration of BHBA in group C,D and E were significantly higher than that in group A (P＜0.01),which in group C was significantly higher than that in group B (P＜0.05),which in group D and E was significantly higher than that in group B (P＜0.01),which in group C was significantly higher than that in group G (P＜0.01),which in group D was significantly higher than those in group F and G (P＜0.01),and in group E was highly significantly higher than that in group F and G (P＜0.01).Overall,there were not calcuim-phosphorus metabolic disorders within the seven beef cattle farms which were selected,but it is also necessary to strengthen feeding management and health care to prevent the occurrence of nutrition and metabolic diseases.

Objective This study aimed to observe the effect of Jiang Tang San Hao Formula(JTSHF)on systemic and intestinal inflammation,as well as on the NLRP3 inflammasome in type 2 diabetic mice(T2DM),and to elucidate its anti-diabetic molecular mechanisms.Methods Four-week-old male C57BL/6 N mice were used to establish the T2DM model using a high-fat diet combined with streptozotocin injection.The diabetic mice were randomly divided into the model,metformin,and JTSHF groups.A control group was also set to provide baseline comparisons.Each group of mice was orally administered with the corresponding medication daily.The metformin group was orally administered with 0.20 g/kg metformin,the JTSHF group was orally administered with 4.26 g/kg JTSHF,and the control group and model group were orally administered with an equal amount of sterile water continuously for 8 weeks.After an 8-week drug intervention via gavage,the lipopolysaccharide(LPS),tumor necrosis factor-alpha(TNF-α),interleukin 1 beta(IL-1β),and interleukin 6(IL-6)serum and colon levels were quantified using an enzyme-linked immunosorbent assay(ELISA).The pathological morphology of the colon was observed using hematoxylin and eosin staining.NOD-like receptor protein 3(NLRP3),apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC),caspase-1,zonula occludens-1(ZO-1),occludin,and G-protein coupled receptor 43(GPR43)protein expression in the colon were assessed using immunohistochemistry.The mRNA expression levels of NLRP3,ASC,caspase-1,ZO-1,Occludin,and GPR43 in the colon were detected using Real-time PCR.Results The ELISA data revealed significant differences in inflammatory markers among the groups.Compared with the model group,the JTSHF group exhibited notably reduced LPS,TNF-α,IL-1β,and IL-6 levels(P<0.05).Moreover,compared with the model group,JTSHF treatment upregulated ZO-1,occludin,and GPR43 protein and mRNA expression in the colon and downregulated NLRP3,ASC,and Caspase-1 protein and mRNA expression(P<0.05).Conclusion The inflammatory reaction of T2DM mice is apparent.JTSHF effectively alleviates the systemic and intestinal inflammatory response of T2DM mice by inhibiting the NLRP3 inflammasome and repairing the intestinal mucosal barrier,highlighting the potential molecular mechanisms of the anti-diabetes effects of JTSHF.

Objective This study aimed to observe the effect of Jiang Tang San Hao Formula(JTSHF)on systemic and intestinal inflammation,as well as on the NLRP3 inflammasome in type 2 diabetic mice(T2DM),and to elucidate its anti-diabetic molecular mechanisms.Methods Four-week-old male C57BL/6 N mice were used to establish the T2DM model using a high-fat diet combined with streptozotocin injection.The diabetic mice were randomly divided into the model,metformin,and JTSHF groups.A control group was also set to provide baseline comparisons.Each group of mice was orally administered with the corresponding medication daily.The metformin group was orally administered with 0.20 g/kg metformin,the JTSHF group was orally administered with 4.26 g/kg JTSHF,and the control group and model group were orally administered with an equal amount of sterile water continuously for 8 weeks.After an 8-week drug intervention via gavage,the lipopolysaccharide(LPS),tumor necrosis factor-alpha(TNF-α),interleukin 1 beta(IL-1β),and interleukin 6(IL-6)serum and colon levels were quantified using an enzyme-linked immunosorbent assay(ELISA).The pathological morphology of the colon was observed using hematoxylin and eosin staining.NOD-like receptor protein 3(NLRP3),apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC),caspase-1,zonula occludens-1(ZO-1),occludin,and G-protein coupled receptor 43(GPR43)protein expression in the colon were assessed using immunohistochemistry.The mRNA expression levels of NLRP3,ASC,caspase-1,ZO-1,Occludin,and GPR43 in the colon were detected using Real-time PCR.Results The ELISA data revealed significant differences in inflammatory markers among the groups.Compared with the model group,the JTSHF group exhibited notably reduced LPS,TNF-α,IL-1β,and IL-6 levels(P<0.05).Moreover,compared with the model group,JTSHF treatment upregulated ZO-1,occludin,and GPR43 protein and mRNA expression in the colon and downregulated NLRP3,ASC,and Caspase-1 protein and mRNA expression(P<0.05).Conclusion The inflammatory reaction of T2DM mice is apparent.JTSHF effectively alleviates the systemic and intestinal inflammatory response of T2DM mice by inhibiting the NLRP3 inflammasome and repairing the intestinal mucosal barrier,highlighting the potential molecular mechanisms of the anti-diabetes effects of JTSHF.

Objective This study aimed to observe the effect of Jiang Tang San Hao Formula(JTSHF)on systemic and intestinal inflammation,as well as on the NLRP3 inflammasome in type 2 diabetic mice(T2DM),and to elucidate its anti-diabetic molecular mechanisms.Methods Four-week-old male C57BL/6 N mice were used to establish the T2DM model using a high-fat diet combined with streptozotocin injection.The diabetic mice were randomly divided into the model,metformin,and JTSHF groups.A control group was also set to provide baseline comparisons.Each group of mice was orally administered with the corresponding medication daily.The metformin group was orally administered with 0.20 g/kg metformin,the JTSHF group was orally administered with 4.26 g/kg JTSHF,and the control group and model group were orally administered with an equal amount of sterile water continuously for 8 weeks.After an 8-week drug intervention via gavage,the lipopolysaccharide(LPS),tumor necrosis factor-alpha(TNF-α),interleukin 1 beta(IL-1β),and interleukin 6(IL-6)serum and colon levels were quantified using an enzyme-linked immunosorbent assay(ELISA).The pathological morphology of the colon was observed using hematoxylin and eosin staining.NOD-like receptor protein 3(NLRP3),apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC),caspase-1,zonula occludens-1(ZO-1),occludin,and G-protein coupled receptor 43(GPR43)protein expression in the colon were assessed using immunohistochemistry.The mRNA expression levels of NLRP3,ASC,caspase-1,ZO-1,Occludin,and GPR43 in the colon were detected using Real-time PCR.Results The ELISA data revealed significant differences in inflammatory markers among the groups.Compared with the model group,the JTSHF group exhibited notably reduced LPS,TNF-α,IL-1β,and IL-6 levels(P<0.05).Moreover,compared with the model group,JTSHF treatment upregulated ZO-1,occludin,and GPR43 protein and mRNA expression in the colon and downregulated NLRP3,ASC,and Caspase-1 protein and mRNA expression(P<0.05).Conclusion The inflammatory reaction of T2DM mice is apparent.JTSHF effectively alleviates the systemic and intestinal inflammatory response of T2DM mice by inhibiting the NLRP3 inflammasome and repairing the intestinal mucosal barrier,highlighting the potential molecular mechanisms of the anti-diabetes effects of JTSHF.

Objective This study aimed to observe the effect of Jiang Tang San Hao Formula(JTSHF)on systemic and intestinal inflammation,as well as on the NLRP3 inflammasome in type 2 diabetic mice(T2DM),and to elucidate its anti-diabetic molecular mechanisms.Methods Four-week-old male C57BL/6 N mice were used to establish the T2DM model using a high-fat diet combined with streptozotocin injection.The diabetic mice were randomly divided into the model,metformin,and JTSHF groups.A control group was also set to provide baseline comparisons.Each group of mice was orally administered with the corresponding medication daily.The metformin group was orally administered with 0.20 g/kg metformin,the JTSHF group was orally administered with 4.26 g/kg JTSHF,and the control group and model group were orally administered with an equal amount of sterile water continuously for 8 weeks.After an 8-week drug intervention via gavage,the lipopolysaccharide(LPS),tumor necrosis factor-alpha(TNF-α),interleukin 1 beta(IL-1β),and interleukin 6(IL-6)serum and colon levels were quantified using an enzyme-linked immunosorbent assay(ELISA).The pathological morphology of the colon was observed using hematoxylin and eosin staining.NOD-like receptor protein 3(NLRP3),apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC),caspase-1,zonula occludens-1(ZO-1),occludin,and G-protein coupled receptor 43(GPR43)protein expression in the colon were assessed using immunohistochemistry.The mRNA expression levels of NLRP3,ASC,caspase-1,ZO-1,Occludin,and GPR43 in the colon were detected using Real-time PCR.Results The ELISA data revealed significant differences in inflammatory markers among the groups.Compared with the model group,the JTSHF group exhibited notably reduced LPS,TNF-α,IL-1β,and IL-6 levels(P<0.05).Moreover,compared with the model group,JTSHF treatment upregulated ZO-1,occludin,and GPR43 protein and mRNA expression in the colon and downregulated NLRP3,ASC,and Caspase-1 protein and mRNA expression(P<0.05).Conclusion The inflammatory reaction of T2DM mice is apparent.JTSHF effectively alleviates the systemic and intestinal inflammatory response of T2DM mice by inhibiting the NLRP3 inflammasome and repairing the intestinal mucosal barrier,highlighting the potential molecular mechanisms of the anti-diabetes effects of JTSHF.

Objective This study aimed to observe the effect of Jiang Tang San Hao Formula(JTSHF)on systemic and intestinal inflammation,as well as on the NLRP3 inflammasome in type 2 diabetic mice(T2DM),and to elucidate its anti-diabetic molecular mechanisms.Methods Four-week-old male C57BL/6 N mice were used to establish the T2DM model using a high-fat diet combined with streptozotocin injection.The diabetic mice were randomly divided into the model,metformin,and JTSHF groups.A control group was also set to provide baseline comparisons.Each group of mice was orally administered with the corresponding medication daily.The metformin group was orally administered with 0.20 g/kg metformin,the JTSHF group was orally administered with 4.26 g/kg JTSHF,and the control group and model group were orally administered with an equal amount of sterile water continuously for 8 weeks.After an 8-week drug intervention via gavage,the lipopolysaccharide(LPS),tumor necrosis factor-alpha(TNF-α),interleukin 1 beta(IL-1β),and interleukin 6(IL-6)serum and colon levels were quantified using an enzyme-linked immunosorbent assay(ELISA).The pathological morphology of the colon was observed using hematoxylin and eosin staining.NOD-like receptor protein 3(NLRP3),apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC),caspase-1,zonula occludens-1(ZO-1),occludin,and G-protein coupled receptor 43(GPR43)protein expression in the colon were assessed using immunohistochemistry.The mRNA expression levels of NLRP3,ASC,caspase-1,ZO-1,Occludin,and GPR43 in the colon were detected using Real-time PCR.Results The ELISA data revealed significant differences in inflammatory markers among the groups.Compared with the model group,the JTSHF group exhibited notably reduced LPS,TNF-α,IL-1β,and IL-6 levels(P<0.05).Moreover,compared with the model group,JTSHF treatment upregulated ZO-1,occludin,and GPR43 protein and mRNA expression in the colon and downregulated NLRP3,ASC,and Caspase-1 protein and mRNA expression(P<0.05).Conclusion The inflammatory reaction of T2DM mice is apparent.JTSHF effectively alleviates the systemic and intestinal inflammatory response of T2DM mice by inhibiting the NLRP3 inflammasome and repairing the intestinal mucosal barrier,highlighting the potential molecular mechanisms of the anti-diabetes effects of JTSHF.