The aim of this study is to elucidate the protective and anti-apoptotic effects of insulin-like growth factor 1 ( IGF-1 ) against β-amyloid (Aβ) and investigate the effect of IGF-1 on Aβ-induced tau phosphorylation. Cell viability was measured using the MTT (3-(4,5-dimethylthiazolyl-2 )-2,5-diphenyltetrazolium bromide) assay, early apoptosis and late apoptosis/necrosis were analyzed by flow cytometry using Annexin V-FITC and propidium iodide (PI) double staining, and morphology was examined by Hoechst 33342 staining. Tau phosphorylation was detected using AT8 immunostaining. Preincubation of cultured rat hippocampal neurons with IGF-1 for 24 h prevented cytotoxicity induced by Aβ25-35 for 48 h. The MTT value significantly increased from 54.51% to 61.8% of the control group, and the percentage of Hoechst 33342-positive cells decreased from 30.77% to 22.81%. Incubation with Aβ25-35 for 48 h caused a marked increase in the percentages of Annexin V-FITC single-labeled cells (Annexin V +/PI-) and Annexin V/PI double-stained cells (Annexin V +/PI + ) (3.41% and 19.47% , respectively), which were significantly decreased by pretreatment with 100 ng/ml of IGF-1 for 24 h (to 2.98% and 15.16% , respectively). Aβ25-35 treatment increased tau phosphorylation and AT8 positive cells were 41.84%. This effect could be inhibited by different concentrations of IGF-1. Our findings showed that IGF-1 protected against Aβ-induced cytotoxicity, decreased the percentage of early and late apoptosis/necrosis cells, and inhibited tau phosphorylation, which may be the cellular mechanisms for its neuroprotective action.

Objective To establish the reference ranges of the spatial angles among cardiac chambers and great vessels in second and third trimester fetuses measured by spatiotemporal image correlation (STIC).Methods Volume images of 352 normal fetuses from 20 to 38 weeks of gestation were recruited in the study.An off-line analysis of acquired volume datasets was carried out with multiplanar mode.Parameters measured included angles between:(1) the 4-chamber view and the left ventricular long axis view; (2) the left ventricular long axis view and main pulmonary artery; and (3) the ductal arch and aortic arch.The relationships between above-mentioned angles and gestational age were assessed by correlation and regression analysis.Results The angle between the 4-chamber view and the left ventricular long axis view (range:55.7° - 35.7°,mean:45.7° ± 5.12°) was uncorrelated with gestational age (r = 0.03,P = 0.51).In contrast,the angle between the left ventricular long axis view and main pulmonary artery,and the angle between the ductal arch and aortic arch were correlated with gestational age (P ＜ 0.001),and the correlation coefficient was - 0.53 and 0.57 respectively.The best-fit exponential curve regression equations of the angle between the left ventricular long axis view and main pulmonary artery was:Y = 154- 4.24X +0.05X2 ,and the angle between the ductal arch and aortic arch was:Y = - 20.8 + 2.65X - 0.37X2.Conclusions The angles among cardiac chambers and great arteries of fetuses from 20 to 38 weeks of gestation can be quantitatively measured by STIC.The reference ranges provide a reliable quantitative standard to estimate the spatial relationships of the cardiac large arteries of fetuses,which may be clinically useful in prenatal screening congenital heart disease.

Objective To study the effect of maca extract on sport fatigue and its antioxidant effect.Methods 50 healthy male Wistar rats were randomly divided into control group (normal breeding,without swimming,equal amount of distilled water for gavage),simple swimming group (swimming,equal amount of distilled water for gavage),swimming and medicine group (divided into maca extract 4.0,8.0 and 16.0 g/(kg· bw) groups,respectively),10 rats in each group.All rats were freely swimming in the circulating water flow daily for 15 days.On the 16th day of experiment,liver tissue samples were collected.The liver lipid peroxide (LPO),superoxide dismutase (SOD),glutathione peroxidase (GSH-Px) and liver glycogen level were determined.Results When rats were administered with maca extract at the doses of 4.0,8.0,16.0 g/(kg· bw),respectively,the swimming time before sinking and the total swimming time were increased by 18.99%,64.46% and 90.69%,and 18.99%,56.23% and 94.72%,respectively,while the numbers of times of sinking were decreased by 27.44%,42.86%,64.11% (P<0.01),respectively,compared with the swimming rats without maca extract treatment.The LPO content in the liver of rats treated with maca extract 4.0,8.0,16.0 g/(kg· bw) were reduced by 31.31%,42.00% and 31.31%,respectively,while the levels of SOD,GSH-Px and liver glycogen were enhanced by 25.92%,31.82%,62.09%,12.33%,23.01%,46.36% and 17.83%,44.69%,62.99%,respectively,over those of rats without maca extract treatment.Conclusions Maca extract reduces the liver LPO level,increases liver glycogen level,improves the SOD and GSH-Px activity,therefore,plays a protective role in sport fatigue.

Objective To investigate the correlation between miR-221 and epithelial-mesenchymal transition (EMT) in drug-resistant glioma cells. Methods The expression levels of miR-221, PTEN, p-Akt, E-cadherin, vimentin, and MRP1 were quantitatively analyzed in Z1 cells (primary drug-resistant cells), Z2 cells (drug-sensitive cells) and Z2-BCNU cells (drug-resistant cells) using fluorescent real-time PCR and Western blotting. Results The expression levels of PTEN were significantly increased in Z2 cells compared with Z1 and Z2-BCNU cells which overexpressed miR-221 and vimentin. The expression levels of vimentin, p-Akt and MRP1 were significantly decreased in Z2 cells overexpressing E-cadherin. Conclusion MiR-221 regulates the expression of EMT-related genes through down-regulation of PTEN and activation of PI3-K/Akt signaling.

Objective To explore the molecular mechanisms by which mitochondrial estrogen receptorβ(ERβ) suppresses non-small cell lung cancer cell apoptosis induced by apoptotic stimulations. Methods The mitochondrial localization of ERβin non-small cell lung cancer cell lines A549 and 201T was determined using immunofluorescence and Western blotting. The changes of apoptosis of the cells with mitochondrial ERβ overexpression or knockdown in response to cisplatin and STS treatments were assessed, and mitochondrial ERβ interaction with the pro- apoptotic protein Bad was detected using co-immunoprecipitation and Western blotting. Results ERβ was localized in the mitochondria in A549 and 201T cells. ERβoverexpression significantly reduced while ERβknockdown increased Bax activation and cell apoptosis induced by cisplatin and STS. Mitochondrial ERβinteraction with pro-apoptotic protein Bad may suppress Bax activation and its translocation to the mitochondria. Conclusion Mitochondrial ERβ can suppress apoptosis of non-small cell lung cancer cells induced by cisplatin or STS through interaction with Bad, suggesting the value of mitochondrial ERβ as a new therapeutic target for treatment of non-small cell lung cancer.

Objective To investigate the correlation between miR-221 and epithelial-mesenchymal transition (EMT) in drug-resistant glioma cells. Methods The expression levels of miR-221, PTEN, p-Akt, E-cadherin, vimentin, and MRP1 were quantitatively analyzed in Z1 cells (primary drug-resistant cells), Z2 cells (drug-sensitive cells) and Z2-BCNU cells (drug-resistant cells) using fluorescent real-time PCR and Western blotting. Results The expression levels of PTEN were significantly increased in Z2 cells compared with Z1 and Z2-BCNU cells which overexpressed miR-221 and vimentin. The expression levels of vimentin, p-Akt and MRP1 were significantly decreased in Z2 cells overexpressing E-cadherin. Conclusion MiR-221 regulates the expression of EMT-related genes through down-regulation of PTEN and activation of PI3-K/Akt signaling.

Objective To explore the molecular mechanisms by which mitochondrial estrogen receptorβ(ERβ) suppresses non-small cell lung cancer cell apoptosis induced by apoptotic stimulations. Methods The mitochondrial localization of ERβin non-small cell lung cancer cell lines A549 and 201T was determined using immunofluorescence and Western blotting. The changes of apoptosis of the cells with mitochondrial ERβ overexpression or knockdown in response to cisplatin and STS treatments were assessed, and mitochondrial ERβ interaction with the pro- apoptotic protein Bad was detected using co-immunoprecipitation and Western blotting. Results ERβ was localized in the mitochondria in A549 and 201T cells. ERβoverexpression significantly reduced while ERβknockdown increased Bax activation and cell apoptosis induced by cisplatin and STS. Mitochondrial ERβinteraction with pro-apoptotic protein Bad may suppress Bax activation and its translocation to the mitochondria. Conclusion Mitochondrial ERβ can suppress apoptosis of non-small cell lung cancer cells induced by cisplatin or STS through interaction with Bad, suggesting the value of mitochondrial ERβ as a new therapeutic target for treatment of non-small cell lung cancer.

Objective To explore the pulse oxygen saturation instrument in the application of vaginal delivery newborn, and analyze the pulse oxygen saturation in the clinical application value of vaginal delivery newborn. Methods From May 2012 to May 2013 in our hospital, 100 cases was born of the gestational age between 37 weeks to 42 weeks of vaginal delivery term newborns were randomly selected, and randomly divided into two groups in digital method: ob-servation group and control group, 50 cases in each group, after birth, the observation group with pulse oxygen satu-ration meter records the pulse of the fetus within 1 h each time values,and blood oxygen saturation, the control group was using Apgar score record the pulse of the fetus within 1 h each time values, and blood oxygen saturation, then put the two methods respectively recorded data entry into SPSS19.0 statistical software for analysis processing, analysis and comparison of pulse oxygen saturation and Apgar score in vaginal delivery was how to apply in the newborn and appli-cation value. Results Neonatal pulse oxygen saturation in observation group 1 min-monitoring value, 5 min-the moni-toring value of 10 min-monitoring value, 30 min-monitoring values were significantly higher than that of control group, significant difference was found in two groups, with statistical significance(P<0.05); Newborns in observation group 60 min-pulse oxygen saturation monitoring values similar to the control group, no significant differences between the two groups, no statistically significant (P>0.05);Neonatal pulse monitoring value in observation group, 1 min value, pulse pulse value when the 5 min,when 10 min pulse value, pulse value when 30 min, when 60 min pulse value were significantly higher than that of control group, significant difference, the two groups have statistical significance (P<0.05). Conclusion Pulse oxygen saturation meter compared with traditional Apgar score detection method, pulse oxy-gen saturation meter advantage in the application of vaginal delivery neonate, and reliability is extremely strong, ap-plication prospect, is worthy of popularization and application in clinical work.

OBJECTIVETo explore the molecular mechanisms by which mitochondrial estrogen receptor β (ERβ) suppresses non-small cell lung cancer cell apoptosis induced by apoptotic stimulations.

METHODSThe mitochondrial localization of ERβ in non-small cell lung cancer cell lines A549 and 201T was determined using immunofluorescence and Western blotting. The changes of apoptosis of the cells with mitochondrial ERβ overexpression or knockdown in response to cisplatin and STS treatments were assessed, and mitochondrial ERβ interaction with the pro-apoptotic protein Bad was detected using co-immunoprecipitation and Western blotting.

RESULTSERβ was localized in the mitochondria in A549 and 201T cells. ERβ overexpression significantly reduced while ERβ knockdown increased Bax activation and cell apoptosis induced by cisplatin and STS. Mitochondrial ERβ interaction with pro-apoptotic protein Bad may suppress Bax activation and its translocation to the mitochondria.

CONCLUSIONMitochondrial ERβ can suppress apoptosis of non-small cell lung cancer cells induced by cisplatin or STS through interaction with Bad, suggesting the value of mitochondrial ERβ as a new therapeutic target for treatment of non-small cell lung cancer.

Apoptosis ; Carcinoma, Non-Small-Cell Lung ; pathology ; Cell Line, Tumor ; Cisplatin ; Estrogen Receptor beta ; metabolism ; Humans ; Mitochondrial Proteins ; metabolism ; bcl-Associated Death Protein ; metabolism

OBJECTIVETo investigate the correlation between miR-221 and epithelial-mesenchymal transition (EMT) in drug-resistant glioma cells.

METHODSThe expression levels of miR-221, PTEN, p-Akt, E-cadherin, vimentin, and MRP1 were quantitatively analyzed in Z1 cells (primary drug-resistant cells), Z2 cells (drug-sensitive cells) and Z2-BCNU cells (drug-resistant cells) using fluorescent real-time PCR and Western blotting.

RESULTSThe expression levels of PTEN were significantly increased in Z2 cells compared with Z1 and Z2-BCNU cells which overexpressed miR-221 and vimentin. The expression levels of vimentin, p-Akt and MRP1 were significantly decreased in Z2 cells overexpressing E-cadherin.

CONCLUSIONMiR-221 regulates the expression of EMT-related genes through down-regulation of PTEN and activation of PI3-K/Akt signaling.

Cadherins ; metabolism ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; metabolism ; Multidrug Resistance-Associated Proteins ; metabolism ; PTEN Phosphohydrolase ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; Signal Transduction ; Vimentin ; metabolism