SDF-1α, a ligand for the chemokine receptor CXCR4, is well known for mediating the migration of breast cancer cells. In a previous study we demonstrated that a synthetic 21-mer peptide antagonist of CXCR4 (NT21MP) derived from the viral macrophage inflammatory protein II could antagonize tumor growth in vivo by inhibiting cellular proliferation and inducing apoptosis in breast cancer cells. However, the role of SDF-1α in the signaling pathways underlying the proliferation of human breast cancer cells and associated signaling pathways and inhibiting signal pathways of NT21MP remained unclear. The present study investigated the mechanism of NT21MP on anti-tumor in breast cancer in vitro. The effect of NT21MP on the viability of cells was determined by the MTT assay. Annexin V-FITC and PI staining was performed to detect early stage apoptosis in SKBR3 cells treated with SDF-1α and AMD3100 or NT21MP. Western blotting techniques were used to assay the composition of phosphoproteomics and total proteins present in the SKBR3 breast cancer cells. RT-PCR and Western blotting technique were used to detect the effect of NT21MP and AMD3100 on Bcl-2 and Bax expression. The results indicated that SDF-1α prevented apoptosis and promoted the proliferation of SKBR3 human breast cancer cells. As compared with untreated SKBR3 cells, Treatment with SDF-1α significantly increased cell viability, and NT21MP abolished the protective effects of SDF-1α dose-dependently (P<0.05). There was a significant decrease in the percentage of apoptotic cells after SDF-1α treatment as compared with control group (2.7%±0.2% vs. 5.7%±0.4%, P<0.05). But pretreatment of SKBR3 cells with NT21MP significantly attenuated the antiapoptotic effects of SDF-1α as compared with SKBR3 cells without NT21MP pretreatment. The proliferative and anti-apoptotic effects of SDF-1α in SKBR3 cells were associated with an increase in AKT and ERK1/2 phosphorylation as well as a decrease in Bax expression and an increase in Bcl-2 expression. These changes in intracellular processes were blocked by NT21MP in a dose-dependent manner(P<0.05). In conclusion, NT21MP efficiently inhibits SDF-1α-induced proliferation and antiapoptosis in SKBR3 cells by reducing the levels of phosphorylated AKT and ERK1/2, as well as decreasing the ratio of expression of Bcl-2 relative to Bax.

3.0 cm in diameters.Contrast-enhancement CT showed tumors with abundant blood vessel,1 case appeared as uniform enhancement and was difficult to distinguish between tumor body and internal carotid and external carotid because of the iso-density of them.On MRI,the flow void blood vessels inside the tumors could be identified and internal carotid and external carotid separated.MRA displayed all the relation between the tumors and carotid and its branches.DSA could demonstrate the supply arteries of the tumors.Conclusion Ultrasonics,CT,MRI and DSA have own definitely characteristic value in diagnosing carotid body tumor.

Objective To evaluate the MRI diagnostic value for truncus arteriosus, and to improve the non invasive diagnostic level. Methods Twelve cases of truncus arteriosus were examined by X ray, Ultracardiography, and MRI, and all were confirmed by cardioangiography (CAG). Among them, 6 cases were confirmed by operation. Results Truncus arteriosus was classified and diagnosed accurately by MRI in 10 cases, and MR could show the intracardic structure and the site at which the pulmonary artery originated from truncus arteriosus. Conclusion MRI had the definite applied value, and could remedy the shortcoming of echocardiography on the classification and diagnosis of truncus arteriosus. The combined usage of MRI and echocardiography could improve the clinical non invasive diagnostic level of truncus arteriosus.

Objective To prepare mouse model with heat stress and determine its pathological changes of the lung and brain during heat stress. Methods BALB/c mouse were randomly (random number) divided into two groups, control group and heat stress group. The animals in the control group were sham- heated at a temperature of ( 25 ± 0.5) ℃ and humidity of (35 ± 5 ) %. The animals of heat stress group were placed in a prewarmed incubator maintained at (35.5 ± 0.5) ℃ and relative humidity of (60 ± 5) %. Rectal temperature (Tc) was monitored, and when Tc respectively reached 39 ℃, 40 ℃ , 41 ℃ and 42 ℃, those study animals were killed. The other animals were removed from the incubator and allowed to cool at an ambient temperature of (25 ±0. 5)℃ and humidity of (35 ±5)% , respectirvely for 12 and 24 hrs when Tc reached 41 ℃ , and for 6 hrs when Tc reached 42 ℃. The lung and brain of all the animals were isolated. Hematoxylin and eosin stain and light microscope were used to detect their pathological changes. Results All the animals displayed uniform response to the heat stress. Low degree of heat stress could induced obviously pathological changes of the lung, progressively greater damage to lung with further congestion of lung matrix, asystematic hemorrhage of alveolar space, abscission of alveolar epithelial cell and disappear of pulmonary alveolus tissue structure were detected with the rise of Tc to 42 ℃. However, absorption of congestion and hemorrhage and recovery of pulmonary alveolus tissue structure could also be seen with cooling at ambient temperature. With low degree of heat stress, the brain only showed moderate edema. Neuronal denaturation and necrosis were detected when Tc reached to 42 ℃. Interestingly, the lesions of brain further aggravated even through cooling treatment after Tc reached to 42 ℃ , but recovery could been observed after cooling treatment followed with Tc of 41 ℃. Conclusions The pathological changes of the lung and brain showed distinctive lesions to heat stress and cooling treatment, and these changes were correlated with the timing and time of cooling treatment, which provide the experimental basis to further study the mechanisms between the heatstroke and multiple organ dysfunction syndrome (MODS).

OBJECTIVE To investigate the correlation between vascular endothelial function and aortic compliance in patients with obstructive sleep apnea hypopnea syndrome(OSAHS) and hypertension. METHODS A total of 103 OSAHS cases were divided into simple OSAHS group(n=55) and OSAHS complicated with hypertension group(n=48, OSAHS+HT group). 20 patients with simple hypertension were included into the hypertension group, and 20 healthy people served as controls. Vascular endothelial function was evaluated by detecting flow mediated dilation of the brachial artery(FMD) with color Doppler; the changes of aortic compliance in patients were detected by echocardiography. RESULTS The FMD, aortic tension and aortic distensibility index levels of OSAHS with hypertension group were significantly lower than the normal control group, hypertension group and OSAHS group(P<0.05); The aortic stiffness index level of OSAHS hypertension group was significantly higher than the normal group, the high blood pressure group and OSAHS group(P<0.05); Analysis of Spearman correlation coefficient of patients in OSAHS with hypertension group found aortic FMD were positively correlated with aortic stiffness index, negatively correlated with aortic tension index and aortic expansion; The aortic FMD, aortic tension, swelling index and aortic stiffness index in OSAHS hypertension group had positive correlation with AHI (P<0.05), and negative correlation with LSaO2(P<0.05). CONCLUSION OSAHS is associated with vascular endothelial dysfunction and decreased aortic compliance. When combined with hypertension, vascular endothelial function and aortic compliance will be significantly affected. The severity of OSAHS was closely related to the decrease of vascular endothelial function and the changes of aortic compliance.

STGC3, a novel tumor related gene, was cloned recently. The previous studies indicated that STGC3 can inhibit the proliferation of CNE2 cell line in vitro. To examine the effect of STGC3 on the tumorigenicity of CNE2 cell line and explore its mechanism in nude mice. The Tet/pTRE/CNE2-STGC3 cell line was planted under the front leg skin of nude mice and induced by doxycycline (Dox). The mRNA and protein level of STGC3 in transplanted tumor tissues were detected with RT-PCR and Western Blotting. The apoptosis ratio of the tumor cell was analyzed with flow cytometry. STGC3, Bcl-2 and Bax proteins were examined by immunohistochemistry method. The results indicated that high level of STGC3 expression can inhibit tumorigenicity of CNE2 cell line in nude mice. Tumor grew slowly, later and smaller. Cell apoptotic percentage increased. Bcl-2 protein expression was down-regulated and Bax protein expression was up-regulated in Tet/pTRE/CNE2-STGC3 cell line (P

Objective To study the effect of caveolin-1 gene expression on the proliferation of human gastric adenocarcinoma cells,and to explore the possibility for its future usage in gene therapy.Methods The full-length caveolin-1 gene was stably transfected into the MGC803 cell line by lipofectin.The Pcl neo vector was transfected at the same time as mock control.The expression of caveolin-1 was detected by Western blot in both the caveolin-1 gene transfected MGC803 cells and the controls.The cell cycle was analyzed by flow cytometry.Results After transfected with caveolin-1,MGC803 cells significantly up-regulated the expression of caveolin 1 and extended their doubling time.The cell proliferation was inhibited and the cell cycle was arrested in the G_0/G_1 phase.Conclusion Caveolin-1 can inhibit the proliferation of MGC803 cells and induce cell cycle arrest in G_0/G_1 phase.

Objective To observe the effects of different concentrations of SB203580, the inhibitor of P38MAPK, in process of high glucose (GS)-induced renal tubular epithelial-myofibroblast transdifferentiation (TEMT). Methods The cultured human renal tubular epithelial cells (HK-2) were divided into control group (5.5 mmol/L GS), GS (30 mmol/L GS) group and different concentrations of SB203580 (30 mmol/L GS +5, 10, 20 and 30 μmol/L SB203580) groups. The treat?ments were for 48 hours. MTT assay was used to observe cell proliferation. The median inhibiting concentration (IC50) was cal?culated. Western blot assay was used to detect the expressions of P38MAPK, P-P38MAPK andα-smooth muscle actin (α-SMA) in control group, high-glucose group and S30 group. The expression ofα-SMA was also detected by the method of im?munofluorescence. Results 1.Compared with control group, there was no significant inhitory effect on proliferation rate in DMSO group (P>0.05). There were increased HK-2 cells in high glucose group and S5group (P<0.05). Proliferation rates were significantly decreased in S20 and S30 groups (P<0.05). Compared with high glucose group, the proliferation rates of HK-2 cells were inhibited in S5, S10, S20 and S30 groups (P<0.05). 2. The expression of P-P38MAPK was significantly higher in high glucose group and S30 group than that of control group (P<0.05). Compared with high glucose group, the ex?pression of P-P38MAPK was significantly decreased in S30 group (P<0.05), whereas no significant difference in the expres?sion of P38MAPK between the two groups (P>0.05). 3. Compared with control group, the expression ofα-SMA was signifi?cantly increased in high glucose group and S30 group (P<0.05). Compared with high glucose group, the expression of α-SMA was significantly decreased in S30 group (P < 0.05). Conclusion The 30 mmol/L GS can lead to TEMT in HK-2 cells. The more suitable inhibitory concentration of SB203580 in the process of TEMT is 30μmol/L. SB203580 can slow down the process of TEMT by inhibiting P38MAPK activation and inhibiting proliferation and the expression ofα-SAM s of HK-2 cells.

Objective To explore the effect and the possible pathway of different concentrations of QLT0267,which was the inhibitor of the integrin-linked kinase (ILK),on the process of high glucose-induced tubularepithelial-myofibroblast transdifferentiation (TEMT) in human renal tubular epithelial cells (HK-2).Methods HK-2 cells were exposed to 30 mmol/L GS,and TEMT model was established.After excluding the effect of high osmotic in TEMT,HK-2 cells were divided into 6 groups by different concentrations of GS and QLT0267 for 48 hours.The rate of the cell proliferation was calculated by MTT.The expression of ILK and α-smooth muscle actin (α-SMA) were determined by immunofluorescence and Western blot,and the expression of protein kinase B (AKT),phosphorylated protein kinase B (p-AKT),and E-cadherin were determined by Western blot.Results (1) The expression of ILK,p-AKT,and α-SMA in HK-2 cells were unregulated and the expression of E-cadherin was downregulated for 48 hours with glucose treating vs control (P ＜ 0.05);(2) The proliferation rate in high glucose group was higher than the group which concentration of QLT0267 was greater than 5 μmol/L (P ＜ 0.05);(3) With the concentrations of QLT0267 increased,the expression of p-AKT,α-SMA was gradually decreased (all P ＜ 0.05),and the expression of E-cadherin was gradually increased (all P ＜ 0.05).Conclusions 30 μmol/L of GS can lead to TEMT in HK-2 cell.The QLT0267 with concentration greater than 5 μmol/L may prevent the activation of ILK downstream proteins,then partially inhibits cell proliferation and TEMT in HK-2 cell.

Biliary atresia is a serious congenital malformation that threatens the life of newborns.At present, the treatment of biliary atresia mainly relies on Kasai portoenterostomy which is also named hepatoportoenterostomy to correct the dysplastic biliary system.Cholangitis is the most common and intractable complication after Kasai portoenterostomy.The pathogenesis is still unidentified.Many factors including ascending infection of intestinal bacteria, abnormal development of intrahepatic bile duct, surgical injury, reflux of intestinal contentscan and so on can affect the occurrence and development of the disease.The initial time and frequency of cholangitis can affect the postoperative primary liver function, so it is especially important to diagnose and treat it timely.The diagnosis of post-Kasai cholangitis is lack of specificity, mainly based on clinical manifestations, biochemical abnormalities and surgical history.For intractable cholangitis should consider completing radioisotope hepatobiliary imaging, percutaneous cholangiography and single or double-balloon enteroscopy.The main focus of prevention and treatment lies in preoperative care, surgical improvement and postoperative care, as well as drug prevention during disease follow-up.