Objective To explore the characteristic and effect of psychoeducational family intervention for schizophrenic patients.Methods 200 patients with schizophrenia were divided into two groups:drug treatment plus psychoeducational family intervention(n=100),drub treatment(n=100),to carry cut a nine-month follow-up comparative study.Results Compared with drug treatment,intervention group had more essential knowledge about the disease and improved their caring attitudes to the patients,and the patients were more compliant in treatment(P

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.

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.