Objective To evaluate the effectiveness of spatio-temporal image correlation with M-mode display ( STIC-M ) in monitoring fetal left ventricular systolic function in fetuses with congenital heart disease(CHD) . Methods Five hundred and thirty-six normal fetuses and 34 fetuses with CHD( 29 without hydrops and 5 with hydrops) were involved in the study . Left ventricular fractional shortening ( LVFS) was measured using STIC-M . The data of normal fetuses was used to construct reference ranges of LVFS for assessment of fetuses with CHD . Results The LVFS of the normal fetuses [ range :26 .8％ - 42 .9％ , mean :( 34 .9 ± 4 .1) ％ ] was negatively correlated with gestational age ( r = - 0 .16 , P < 0 .001) . Compared with the normal controls ,LVFS was significantly decreased in CHD fetuses with hydrops ( P < 0 .001) . However ,there was no significant difference in LVFS between normal controls and CHD fetuses without hydrops ( P > 0 .05) . Conclusions STIC-M is a new method that can be used to measure LVFS to evaluate fetal ventricular systolic function . The fetal ventricular contractile function of CHD fetuses without hydrops may not be damaged or is in compensation stage . The fetuses with cardiac hydrops generally become lower .

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.

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

Objective To investigate the factors of term pregnancy fetal distress at term pregnancy and intervention midwifery cesarean section and vaginal fetal distress. Methods All 104 cases of full-term pregnancy with maternal fetal distress in labor were random divided into observation group and control group from our hospital from October 2012-October 2013, each group had 52 cases. Mothers in the control group were given vaginal midwifery, maternal in the observation group were used cesarean section, fetal distress factors and maternal and neonatal outcomes of two groups were compared and analyzed. Results Fetal distress factor (placenta, umbilical cord factors, maternal factors, fetal factors or amniotic fluid, etc.) of two groups were compared, the difference was not statistically significant (P>0.05). The inci dence of postpartum hemorrhage, neonatal asphyxia, hypoxic ischemic encephalopathy, fetal growth restric-tion,puerperal infection and hypoproteinemia of the observation group were 5.77%,5.77%, 3.85%,1.92%, 11.54%,9.62%,compared with 9.62%, 7.69%, 5.77%, 1.92%, 7.69%, 5.77%in the control group,the difference was not statis-tically significant (P>0.05). Single factor factors Logistic regression analysis results showed that the umbilical cord and placenta, fetal and maternal,amniotic fluid dung are independent risk factors of fetal distress. Multiple factors Logistic regression analysis results showed that fetal and maternal,amniotic fluid dung are independent risk factors of fetal dis-tress. neonatal deaths of two groups did not occur. Conclusion Vaginal delivery applications and cesarean surgery in treatment of fetal distress of full-term pregnancy can get better maternal and neonatal outcomes, should be based on the specific circumstances of women to choose the appropriate mode of delivery.

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.

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 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.

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

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 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.