Objective: To investigate the effects of FTY720-P on EphA2-EphrinA2 bidirectional signaling in osteoclasts. Methods: Murine RAW264.7 macrophages were induced into osteoclasts by dexamethasone and 1α, 25-dihydroxyvitamin D 3, and identified by tartrate resistant acid phosphatase (TRAP) staining. Then, the osteoclasts were divided into 2 groups. The osteoclasts were treated with 400 ng/mL FTY720-P in experimental group and without FTY720-P in control group, respectively. After 48 hours of culture, the cells in 2 groups were detected by real-time fluorescent quantitative PCR, Western blot, and immunofluorescence staining. The expressions of EphA2, EphrinA2, RhoA, and the bone reconstruction associated proteins［bone morphogenetic protein 2 (BMP-2) and transform growth factor β 1 (TGF-β 1)］were analyzed and compared. Results: RAW264.7 cells were successfully induced into osteoclasts identified by TRAP staining. Compared with control group, the relative expressions of EphA2 and EphrinA2 mRNAs and proteins in experimental group significantly decreased after 48 hours ( P<0.05), and the relative expression of RhoA protein also significantly decreased ( P<0.05). The relative expressions of BMP-2 and TGF-β 1 mRNAs were significantly increased ( P<0.05), and those protein expressions were enhanced. Conclusion: FTY720-P can down-regulate the expression of RhoA and promote the expressions of TGF- β 1 and BMP-2 by affecting the transduction of EphA2-EphrinA2 bidirectional signaling in osteoclasts.

Methods: The MC3T3-E1 cells were divided into the experimental group and the control group. In the experimental group, the cells were induced by the medium containing 400 ng/mL FTY720-P (chloroform as solubilizer) in vitro. In the control group, the cells were cultured with the medium only containing chloroform. The cell morphology of 2 groups were observed by inverted phase contrast microscope; the expression of osteoblast related protein (collagen type Ⅰ and collagen type Ⅲ) was detected by immunofluorescence staining; the alkaline phosphatase (ALP) staining and alizarin red staining were used to observe the formation of osteoblasts and the formation of mineralized nodules in 2 groups; and the TUNEL fluorescence assay was used to detect the cell apoptosis.

Aim To investigate the effect of pioglitazone on the AdipoR1 and AdipoR2 expression of HU-VECs induced by intermittent high glucose.Methods After exposed to intermittent high glucose for 5 d,HUVECs were incubated with pioglitazone(10,1 or 0.1 ?mol?L-1) for 24 hours.The AdipoR1 and AdipoR2 mRNA expression levels in HUVECs were also determined by real-time PCR.Results After exposed to intermittent high glucose for 5 days,HUVECs were treated with pioglitazone(10,1 or 0.1 ?mol?L-1) for 24 h.10,1?mol?L-1 of pioglitazone treatment enhanced AdipoR1 mRNA level(both P

Objective To study the set-up errors by CBCT in IMRT with two different immobilization techniques for thoracic and abdominal tumors.Methods Sixty patients with thoracic and abdominal tumor were included in this study and separated into study group and the control group.The study group were immobilized with carbon fiber holder,vacuum bag and thermoplastic mask.The control group were immobilized with carbon fiber holder and thermoplastic mask.CBCT scan and auto-match online were regularly performed before the treatment.The setup of left-right(x),superior-inferior(y),anterior-posterior (z) were received.The value of the Mptv was calculated,meanwhile.The grouped t-test of was carried out between these two methods.Results The shift errors in x-,y-,z-dimension of the study group were (0.32 ± 2.58) mm,(-0.40 ± 3.89) mm,(-0.75 ± 2.43) mm.The Mrrv were 5.60 mm,6.08 mm,6.32 mm.The translation set-up errors in x-,y-,z-dimension of the control group were(0.62 ±3.60),(2.44 ± 4.93),(0.66 ±2.85) mm,respectively.The MPrv were 8.07,10.63,6.90 mm,respectively.The t-test value were t =-0.78,-5.11,-4.22,P =0.440,0.000,0.000,respectively.Conclusions The immobilization techniques with carbon fiber holder,vacuum bag and thermoplastic mask would be better than the techniques without the vacuum bag in reducing the setup errors.

Objective To evaluate the short-term efficiency and risk factors for effects after percutaneous radiofrequency ablation (RFA) for hepatic malignant tumors under the guidance of sonography.Methods The clinical data and the follow-up radiographic images of the patients with hepatic malignant tumors treated by percutaneous RFA were reviewed between June 2011 and May 2012,and the short-term incomplete ablation rate,recurrance rate and tumor progression rate were calculated,and the factors affecting the incomplete ablation rate,recurrence rate and progression rate were analyzed.Results 610 lesions were ablated in the total of 462 RFA procedures for 405 patients under the guidance of sonography with percutaneous method.The average size of the tumor was (2.5 ± 1.1)cm.During at least 3-month follow-up,complete and incomplete ablation rate was 89.2％ (544/610) and 10.8％ (66/610)separately,and recurrance rate and progression rate of tumor was 17.5％ (81/462) and 23.8％ (110/462).The numbers (≥3) and the size (≥3 cm) and the location (close to vessels) of the lesions reduced the complete ablation rate.The numbers (≥3) of lesions affected the recurrence rate and progression rate of lesions as only risk factor.Recurrent hepatocellular carcinoma (HCC) and metstasis from gastrointestine or non-gastrointestine had higher recurrence rate and progression rate comparing with primary HCC.Conclusions RFA can effectively control local progression of hepatic maglinant tumors,and the tumor's size,number and location close to velssels could effect complete ablation rate,the number of tumors could effect the recurrence and porgression rate.Recurrent HCC and metstasis from gastrointestine or nongastrointestine had higher recurrence and progression rate comparing with primary HCC.

After the reform from "4+1" to "3+2",an undergraduate teaching model of clinical medicine,has been implemented in our university,higher demands are set on the training of students' abilities and creativity.This paper explored the basic medicine teaching from the perspectives of creative concepts,teaching staff,curriculum design and practice.

This study was aimed to observe the protection ofZi-Bu Pi-Yin recipe (ZBPYR) on the cortex mitochondrial dysfunction of diabetes-associated cognitive dysfunction rats. SD rats were randomly divided into four groups, which were the control (Con) group, the diabetes (DM) group, the ZBPYR treatment (ZBPYR1) group and the ZBPYR protection (ZBPYR2) group. Morris water maze test was taken to evaluate the learning and memory ability of rats. The transmission electron microscope (TEM) was used to detect the ultrastructure and quantity changes of cortex mitochondria. Western blot was used to detect the expression of Cyto C. The results showed that compared to Con group, the learning and memory ability were decreased in the DM group (P < 0.05); the learning and memory ability of the ZBPYR1 group was improved compared to the DM group (P < 0.05); compared to the DM group, the ZBPYR2 group was significantly improved (P < 0.01). Compared with the Con group, the number of cortex mitochondria in DM group was decreased (P< 0.05), and the structure was disordered, blurred, or even completely destroyed. After ZBPYR intervention, these pathological changes were reduced obviously. And the number of mitochondria in the ZBPYR2 group was increased than that of the DM group (P < 0.05). The expression of Cyto C in cytoplasm of the DM group was significantly higher than that of the Con group (P < 0.01). After ZBPYR intervention, the expression of Cyto C was decreased. It was concluded that ZBPYR regulated the mitochondrial morphology and changes of volume in the cortex, prevented the releasing of Cyto C from mitochondria to cytoplasm, and improved the cognitive function of diabetes 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.

Objective To explore the mechanism of Zibu Piyin Recipe (ZBPYR) on spleen yin deficiency diabetes-associated cognitive disorder (DACD). Methods The rats were randomly divided into control group, diabetes mellitus (DM) group, spleen yin deficiency group, spleen yin deficiency DM group and spleen yin deficiency DM+ZBPYR group (treatment group). Type 2 DM models were established by high-fat food feeding and low dose STZ intraperitoneal injection for 4 weeks. Then the classical compound method was used to construct spleen yin deficiency rat models by improper diet, over exertion and yin fluids exhaustion. The treatment group was given ZBPYR by gavage for 15 days, and the other groups were given the same amount of normal saline. Then cerebral cortex, hippocampus, stomach and liver were obtained and the changes of protein expression of PDHE1α in them were observed by Western Blot. Results The protein expression of PDHE1αin cortex of DM group and spleen yin deficiency DM group were lower than control group (P<0.05). PDHE1α expression of treatment group in cortex and stomach increased more significantly than spleen yin deficiency DM group (P<0.05). The expression of PDHE1α protein showed no significant difference among all groups in hippocampus and liver. Conclusion ZBPYR improved spleen yin deficiency DACD by regulating PDHE1αin cortex and stomach.