Objective To observe the effect of heroin on EGF and IL-2 positive cells in the submandibular gland of rats. Methods Normal SD rats were divided into normal control group (NGC),saline control group (SCG)and heroin dependence group (HDG). The heroin dependent model of rats was established by subcutaneous injection of heroin, and submandibular glands were excised on the following days respectively: the 10th, 17th, 24th, 31th and 38th. Immunohistochemical SABC method, image analysis and cells calculation were used in the study. Results 1. As compared with those of the NCG, the number of EGF and IL-2 positive cells and the intensity of staining in SCG didn't change obviously. 2. During heroin dependence, the immunohistochemical staining showed that the number of EGF and IL-2 positive cells increased obviously(P

Characters of one Candida intermedia yeast strain which isolated from nature can produce ethanol from xylose-fermenting been systemic studied. In conditions 28?C, 120 r/min, 72 h, it can produce 6.480 g/L ethanol from 7% xylose and 43.70% theoretical production of ethanol from 3% xylose. It can produce up to 21.225 g/L ethanol when incubation time prolong to 156 h from 8% xylose. It also can ferment 13% glucose produce 47.647 g/L ethanol and reach 76.90% of theoretical ethanol production, respectively. Compared to CK, ethanol productivity can be improved 9.91% when add 8% xylose in three times as 3%, 2% and 3%, respectively. Glucose can be first utilized in the mixture sugar medium. When the ratio of xylose vs. glucose is 3:1in mixture sugar, the productivity of ethanol can be improving 25%.

Objective To evaluate the characteristics of abdominal aorta wall motion in different stages of rats atherosclerosis with velocity vector imaging (VVI) technique. Methods Twenty-four healthy SD rats were on high-fat feeding after one week ordinary diet. Abdominal aortic intima-media thickness (IMT), end-systolic blood vessel diameter (Ds), peak systolic velocity (Vs), resistance index (RI), pulsatility index (PI) were measured before and at the end of 8th and 12nd week. Artery wall peak velocity (V_(max)), maximum tangential strain (S_(max)) and the maximum tangential strain rate (SR_(max)) were caculated with VVI. Results Abdominal aortic intima was rough and a small amount of foam cells were found under the light microscope at the end of 8 weeks of high-fat feeding. The values of Smax and SRmax measured at the end of 8th week of high-fat feeding decreased significantly than those of before high-fat feeding (P<0.05). At the end of 12nd week, abdominal aortic intimal was thicker and atherosclerotic plaque appeared somewhere. There were significant differences in artery IMT, Ds, Vs, RI, PI between before and the end of 2nd week of high-fat feeding (P<0.05);the values of V_(max), S_(max), SR_(max) decreased significantly than those of before and at the end of 8th week of high-fat feeding (P<0.05). Conclusion VVI can quantitatively evaluate the vessel wall elasticity in different stage of arteriosclerosis rats.

This study was aimed to observe changes of key molecular in insulin signaling pathway in the hypothala-mus of rats to explore the mechanism of spleen yin deficiency diabetes-associated cognitive decline (DACD) and Zibu Piyin Recipe (ZBPYR) in order to provide new ideas and new clues for treatment of DACD. Rats were randomly divided into five groups, which were the control (Cont) group, diabetes (DM) group, spleen yin deficiency (pi) group, spleen yin deficiency diabetes (piDM) group and the ZBPYR group. Insulin receptor substrate 1 (IRS-1) serine phos-phorylation levels and protein kinase B (PKB/Akt) serine phosphorylation levels which were involved in the insulin signaling were observed by western blotting in the hypothalamus to determine whether there were insulin signaling obstacles in the hypothalamus of rats. The results showed that the expression of p-IRS-1ser in the DM group, pi group and piDM group was increased compared with the Cont group (P< 0.05); while the p-Akt expression of the DM group and piDM group was decreased (P< 0.05). The expression of p-IRS-1ser in the ZBPYR group decreased compared with the DM group and piDM group (P< 0.05); while the level of p-Akt increased compared with the DM group and piDM group (P < 0.05). It was concluded that insulin signaling was not transduced normally in the hy-pothalamus of the DM group, pi group and piDM group. Insulin resistance may occur in the hypothalamus. And ZBPYR can correct insulin signaling transduction disorder.

This study was aimed to observe different forms of β-amyloid peptide (Aβ) and insulin degrading enzyme (IDE) in the hippocampus and cortex in order to further explore the role of Aβ and IDE on spleen yin deficiency di-abetes-associated cognitive decline (DACD), and the effect of Zi-Bu Pi-Y in method. The rats were randomly divided into five groups, which were the blank control (Cont) group, diabetes (DM) group, spleen yin deficiency (pi) group, spleen yin deficiency diabetes (piDM) group and Zi-Bu Pi-Y in recipe (ZBPYR) group. Soluble and insoluble Aβ in the hippocampus and cortex of rats were extracted by gradient centrifugation, and then measured by ELISA. The ex-pression of IDE was observed by western blot. The results showed that the content of soluble and insoluble Aβ1-42 in the hippocampus and cortex of the DM group and piDM group were higher than the Cont group. The soluble and in-soluble Aβ1-42 content in the hippocampus and cortex of the ZBPYR group were reduced compared with the DM group and the piDM group. The soluble Aβ1-40 in the cortex of the DM group, pi group and piDM group were in-creased compared with the Cont group (P < 0.05). The soluble Aβ1-40 content of the ZBPYR group was decreased compared with the DM group and the piDM group (P < 0.05). The expression of IDE protein was decreased in the hippocampus of the DM group and the piDM group compared with the Cont group (P< 0.05), and the IDE protein level in the hippocampus of the ZBPYR group was increased compared with the DM group and the piDM group (P<0.05). The expression of IDE protein in the cortex of the DM group, pi group and piDM group was lower than the Cont group (P< 0.05). The IDE protein level in the cortex of the ZBPYR group was reduced compared to the DM group (P< 0.05). It was concluded that the increased Aβ1-42 in brain may be a major pathological change of DACD and spleen yin deficiency DACD. The decreased IDE expression may be one of the reasons to induce increasing of Aβ1-42 level. The Zi-Bu Pi-Y in method may decrease the Aβ1-42 content by upregulating IDE protein expression.

BACKGROUND: Following bone marrow mesenchymal stem cells (BMMSCs) infusion therapy, which factor promotes BMMSCs migrated to correct position is a key point, currently, adhesion molecule is thought to be playing an important role in mediating BMMSCs migration. OBJECTIVE: To investigate the expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) in rat BMMSCs. METHODS: BMMSCs were in vitro separated from rat bone marrow by directly adherence method. The expression of VCAM-1 and ICAM-1 were identified by using immunocytochemical staining, and the expression rates of antigen were tested by flow cytometry, in addition, their mRNA expressions were measured by RT-PCR. RESULTS AND CONCLUSION: Immunocytochemistry demonstrated that BMMSCs weakly expressed VCAM-1, but strong expressed ICAM-1. Flow cytometry showed that the expression rate of VCAM-1 was 6%, and the expression rate of ICAM-1 was 100%. RT-PCR showed that BMMSCs expressed a low level of VCAM-1 mRNA but a high level of ICAM-1 mRNA. It revealed under physiological condition, BMMSCs expressed a low level of VCAM-1, whereas they expressed a high level of ICAM-1.

Objective To investigate the effects of vascular endothelial growth factor receptor?2 ( VEGFR?2) on proliferation, migration, invasion, and apoptosis after radiotherapy in lung cancer cell line Calu?1, and to explore the probable mechanisms. Methods Small interference RNA ( siRNA )?mediated silencing of VEGFR?2 gene was performed on Calu?1 cells, and the mRNA and protein expression of VEGFR?2 was determined by quantitative real?time PCR and Western blot, respectively. The cells were divided into control group, vascular endothelial growth factor ( VEGF ) group, VEGFR?2 specific siRNA (siKDR) group, and siKDR+VEGF group. The changes in proliferation, migration, and invasion were evaluated by the CCK8 assay, cell scratch wound?healing assay, and transwell migration assay, respectively. The protein expression of VEGFR?2 and proteins in the related downstream signaling pathway was measured by Western blot. Apoptosis in each group was determined after radiotherapy. Results After RNA interference?mediated silencing of VEGFR?2, the mRNA and protein expression of VEGFR?2 was significantly reduced ( P=0. 001,P=0. 000);the proliferation, migration, and invasion of Calu?1 cells were also significantly reduced ( P=0. 000,P=0. 000,P=0. 000);the phosphorylation levels of AKT, ERK 1/2, and p38 were significantly reduced in Calu?1 cells ( P=0. 336,P=0. 986,P=0. 553);the apoptosis in Calu?1 cells was significantly elevated ( P=0. 0012);the protein expression of HIF?1α was significantly inhibited ( P= 0. 016 ) . Conclusions The VEGFR?2 gene silencing significantly inhibits several physiological functions of Calu?1 cells and elevates the apoptosis rate after radiotherapy.

Objective To determine the effects of endostatin on the expression of vascular endothelial growth factor receptor?2 ( VEGFR?2 ) in non?small cell lung cancer cells ( human A549 lung adenocarcinoma cells and human Calu?1 lung carcinoma cells) , and to investigate the possible mechanisms underlying its radiosensitizing effect. Methods The CCK8 method was used to determine the inhibitory effect of endostatin on cell proliferation and calculate the drug concentration that caused a 20% reduction in cell proliferation within 24 h ( IC20 ) . RT?PCR and Western blot assays were used to assess the mRNA and protein expression of VEGFR?2, proteins within its related signaling pathways, and HIF?1α, respectively. The radiosensitivity of cells in each group was determined by colony formation assay;cell apoptosis and cell cycle distribution were determined by flow cytometry. Comparison of mean values between multiple samples was made by one?way analysis of variance, and comparison of mean values between two samples was made by t test. Results Endostatin significantly inhibited the proliferation of Calu?1 cells ( F=50?36,P<0?01) with an IC20 of 296?5 μg/ml;the mRNA and protein expression of VEGFR?2 and HIF?1α was also significantly inhibited in endostatin?treated Calu?1 cells ( F=25?43,10?44, all P<0?05) . Moreover, the phosphorylation of Akt, ERK 1/2, and p38 was significantly reduced in endostatin?treated Calu?1 cells ( F=2?89,0?24, 1?09, all P<0?05) . The radiosensitivity enhancement ratios for Calu?1 cells and A549 cells were 1?38 and 1?09, respectively. Endostatin significantly induced apoptosis ( F=44?15, P<0?01) and G2/M blockage ( F= 104?24, P< 0?01 ) in Calu?1 cells. Conclusions Endostatin induces apoptosis and enhances radiosensitivity in Calu?1 cells with high expression of VEGFR?2, but it has a limited impact on A549 cells with low expression of VEGFR?2.

Objective To study the effects of toys for laboratory animals on reproductive performance and growing development of experimental mice.Methods ICR mice were fed with toys, the informations of reproductive performance and growing development were recorded.Results All the data of reproductive performance of the test group were higher than the control group except the number of newborn mice, and showed significant difference ( P <0.05 ) .The data of growing development of the test group were higher than the control group too, but showed no significant difference ( P >0.05).Conclusion Toys for laboratory animals have good effects on reproductive performance and growing development of mice, and suggested to be used into the process of experimental mice raising.

Objective To study absorption of shegan heji marker components in blood and their excretion in urine and feces of rats, after intragastric administration of shegan heji. Methods LC-MS/MS was used for determination of marker compounds. Rat metabolic cage technology was employed. Results Excretion of marker components were completed 24 hours after administration. Conclusion Ephedrine can be excreted from rats within 24 hours. The possibility of mutual transformation of flavonoids exists in the body. Taking shegan heji will not cause accumulation of ephedrine and flavonoids in the body.