Fetal Heart ; Heart Failure ; Heart Rate, Fetal ; Humans

Adult ; Antiretroviral Therapy, Highly Active ; Female ; HIV Infections ; drug therapy ; Humans ; Lamivudine ; administration & dosage ; Male ; Middle Aged ; Treatment Outcome ; Zidovudine ; administration & dosage

Amifostine ; pharmacology ; Anemia, Aplastic ; chemically induced ; pathology ; prevention & control ; Animals ; Benzene ; toxicity ; Dose-Response Relationship, Drug ; Male ; Mice

OBJECTIVETo investigate the apoptosis and proliferation effect of matrine on human medulloblastoma cell line D341 in vitro and the effect of the expression of the related caspase 3 and caspase 9 proteins.

METHODSThe D341 cells were cultivated successfully in vitro. Then the cells were divided into 5 groups according to the concentration of matrine (0.5 mg/mI group, 1.0 mg/ml group, 1.5 mg/ml group, 2.0 mg/ml group and the control group was 0 mg/ml). All the experiments were repeated three times. The cell morphologic and structure change was observed with the optical microscope and the transmission electron microscope. The proliferation of D341 cell was analyzed using Cell Counting Kit-8 assay. Apoptosis was detected by Annexin V-FITC/PI double staining. The expression of Caspase3 and Caspase9 was detected by Western blot.

RESULTSWith the effect of matrine, the proliferation inhibition rate gradually increased with drug concentrations increasing, and there was a significant difference (P < 0.01). The inhibitory effect of matrine on cell proliferation was different with the different treatment time, there was a significant difference between the 24 h to 72 h groups (P < 0.01). The apoptotic rate increased with matrine concentrations increasing. There were significant differences between the group of 0.5 mg/mI or 1.0 mg/mI to the group of 1.5 mg/mI or 2.0 mg/mI (P < 0.05). The apoptotic rate increased with the prolonged treatment time. There were significant differences between the group of 24 h or 48 h to the group of 72 h ( P < 0.05). With the increase of matrine concentration, the expression of Caspase 3 and Caspase 9 increased (P < 0.01).

CONCLUSIONMatrine induces the apoptosis, and inhibits the proliferation of human medulloblastoma D341 cells in vitro by up-regulation of the expression level of Caspase3, Caspase9.

Alkaloids ; pharmacology ; Apoptosis ; Caspase 3 ; metabolism ; Caspase 9 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cerebellar Neoplasms ; metabolism ; pathology ; Humans ; Medulloblastoma ; metabolism ; pathology ; Quinolizines ; pharmacology ; Up-Regulation

Arterio-Arterial Fistula ; therapy ; Cardiac Catheterization ; Coronary Vessels ; Female ; Heart Septal Defects, Ventricular ; therapy ; Heart Ventricles ; abnormalities ; Humans

Brain Injuries ; etiology ; Child ; Heart Defects, Congenital ; complications ; Humans

Fetal atrioventricular block (AVB) is a type of fetal bradyarrhythmias. The reported incidence of fetal complete atrioventricular block (CAVB) and mortality of perinatal fetuses and neonates are signiifcantly higher in pregnancies of anti-SSA/Ro-positive mothers than that of anti-SSA/Ro-negative mothers. The auto-antibodies in maternal serum that can be transported into fetal circulation through placenta may damage fetal cardiac conductive system and eventually result in fetal AVB. There are evidences that early diagnosis and proper treatment can improve the prognosis and survival rate of affected fetuses. In this article, the pathogenesis, risk factors, prenatal diagnosis, treatment and prognosis of fetal immune mediated AVB is reviewed.

Objective Through the analysis of cases,to improve the cognition of clinicians on extracranial vas-cular embolism diseases(VED)in children.Methods The clinical information included incidence trend,thrombophi-lia,clinical features,treatment and prognosis of 29 children with VED,who were admitted from January 201 1 to Decem-ber 201 5 in Nanjing Children′s Hospital Affiliated to Nanjing Medical University,and retrospectively analyzed.Results The annual rate of VED increased from 0 to 1 .49 per 1 0 000 hospital admissions from January 201 1 to December 201 5.In 29 cases,there were 20 male and 9 female,with an average age of 6.03 years old (2 h -1 3.83 years old).In-fants accounted for >20%(6 /29 cases).The average age of the female,non infected group,rheumatic disease group and venous thrombosis group was higher than that of the male,the infection group,the non rheumatic disease group and the arterial embolization group,but there was no significant difference(all P >0.05).Thrombophilia were as follows:in-fection disease,heart disease,kidney disease syndrome,rheumatoid disease,tumor,and twins embolization syndrome. Risk factors included central venous line,immobility,dehydration,glucocorticoids use,etc.Heart disease was the leading cause of non thrombotic embolism,while other thrombophilic diseases resulted in thrombotic embolism.Pulmonary em-bolism was mainly seen in patients with severe pneumonia,especially mycoplasma pneumoniae pneumonia (MPP ).The older the age,the more typical clinical manifestations,and significantly elevated D dimer,fibrin/fibrinogen degradation products tips VED.Treatment depends on the degree of risk.Thirty -seven point five percent(3 /8 cases)of children with arterial embolism were less than 1 year old,and the mortality 25.00% (2 /8 cases)was significantly higher than that of venous thrombosis 1 7.65%(3 /1 7 cases)and 1 1 .76% (2 /1 7 cases).Conclusion Heart disease mainly cause arterial embolism and infection,while nephritic syndrome and rheumatic disease mainly cause venous embolism.Pulmona-ry embolism is mainly seen in children with severe pneumonia,especially MPP.The risk of arterial embolization is higher than that of venous embolism.

Objective To find the expression level and the role of ENST00000460164 in luminal A breast cancer.Methods The expression level of ENST00000460164 in breast cancer tissues was detected by RT-qPCR.pll3.7-ENST00000460164-shRNA and empty vector,pll3.7,were transfected into MCF-7 cells.Cell cycle was measured by flow cytometry.Western blot was used to detect the expression of P16INK4A and cyclinD1.Results ENST00000460164 was highly expressed in luminal A breast cancer tissues as compared to the adjacent non-cancer tissues.The knockdown of ENST00000460164 resulted in the G1 cell-cycle arrested,cyclin D1 downregulated and P16INK4A upregulated in MCF-7 cells.Conclusions ENST00000460164 is overexpressed in luminal A breast cancer.ENST00000460164 may control G1/S transition by regulating P16INK4A or cyclin D1 expression.