OBJECTIVETo investigate the clinical effect of endovascular embolization (EVE) in the treatment of hemoptysis of systemic arterial origin in children.

METHODSA total of 20 children with hemoptysis of systemic arterial origin who underwent EVE from January 2016 to November 2017 were enrolled. The method for embolization was analyzed and the clinical outcome was evaluated.

RESULTSOffending vessels were bronchial artery (BA) in 14 children, non-bronchial systemic artery (NBSA) in 1 child, and BA and NBSA in 5 children. Of all the children, 13 underwent EVE with peripheral embolization agents and 7 underwent EVE with mechanical coils. A total of 41 offending vessels were embolized (34 BAs and 7 NBSAs) and all the children achieved immediate arrest of hemoptysis. Two children experienced recurrence within 6 months after EVE and 2 experienced recurrence with 6-24 months after EVE. The peripheral embolization agent group had a lower overall recurrence rate than the mechanical coil group [8%(1/13) vs 43%(3/7); P=0.10]. One child experienced intracranial ectopic embolism after surgery and had good quality of life during 20 months of follow-up after treatment. No other complications were observed.

CONCLUSIONSEVE is a safe and effective method for the treatment of hemoptysis of systemic arterial origin in children and thus holds promise for clinical application.

Objective : To investigate the role of knockdown of peroxiredoxin-6 ( PRDX6) in injury and adaptive expression of bile acid transporter in human hepatoellular carcinomas ( HepG2 ) cells induced by rifampicin (RFP) . Methods : Cells in logarithmic growth phase were uniformly inoculated in six-well plates , and HepG2 cells were transiently transfected with specific PRDX6-siRNA and control-siRNA to construct the knockdown group and control group . After 24 h of induction with 100 μmol/L RFP , Western blot and qRT-PCR were performed to detect the protein and gene expression levels of PRDX6 , multidrug resistance protein 1 (MDR1) , multidrug resist- ance-associated proteins 2 , 3 and 4 (MRP2 , MRP3 and MRP4) , and Na + /taurine taurocholate cotransporter pro- tein (NTCP) . Annexin V-FITC/PI double staining assay was used to detect the apoptosis rate of cells in each group ; CCK-8 assay was used to detect the changes of cell proliferation in each group; The relative contents of ala- nine aminotransferase ( ALT) , aspartate aminotransferase ( AST) , total bilirubin ( TBIL) , indirect bilirubin (IBIL) and total bile acid (TBA) in the supernatant of cell culture medium of each group were detected by kits . Results : RFP increased the protein and gene expression levels of MRP2 , MRP3 , MRP4 , MDR1 , NTCP and PRDX6 in HepG2 cells (P < 0. 05) , while the protein and gene expression levels of MRP2 , MRP3 , MRP4 , MDR1 and NTCP decreased to different degrees after PRDX6 knockdown (P < 0. 05) . In addition , PRDX6 knockdown re- sulted in increased apoptosis rate of HepG2 cells (P < 0. 05) , decreased cell proliferation ability (P < 0. 05) , and increased levels of cell injury markers (ALT , AST , TBIL , DBIL , TBA) in cell culture supernatants (P < 0. 05) . Conclusion RFP increased the protein and gene expression of bile acid transporter and PRDX6 to increase in HepG2 cells . However , following knockdown of PRDX6 and treatment with RFP , the protein and gene expression levels of the bile acid transporter decreased and cell injury was aggravated , suggesting that PRDX6 played a protec- tive role in RFP-induced adaptive response in HepG2 cells .

Objective : To investigate the effect of mesencephalic astrocyte-derived neurotrophic factor (MANF) on the adaptive expression of bile acid transporter in human hepatoellular carcinomas (HepG2) induced by rifampicin (RFP) ． Methods: The control group cell line (Y07) and the knockdown group cell line (Y25) were constructed by lentiviral stable transfection technology．The Y07 and Y25 cells were treated with RFP of 200 μmol / L for 48 h， and qRT-PCR and Western blot were used to detect the protein and gene expression levels of MANF，bile salt export pump ( BSEP) ，multidrug resistance-related proteins 2 /3 /4 ( MRP2 ，MRP3 ，MRP4) ，multidrug resistance protein 1 (MDR1) ，organic solute transporter a / β ( OSTα/ β) ，organic anion transporter ( OATP2B1) ．The protein and gene expression levels of proliferating cell nuclear antigen ( PCNA) ，proliferating cell marker Ki67 were used to evaluate the proliferation of cells in each group changes in levels．Changes in the protein and gene expression levels of C / EBP homologous protein( CHOP) and cysteinyl aspartate specific proteinase-3 ( Caspase-3) were used to evaluate the apoptosis of cells in each group．The relative contents of alanine aminotransferase(ALT) ，aspartate aminotransferase(AST) ，alkaline phosphatase ( ALP) ，total bilirubin ( TBIL) ，indirect bilirubin ( IBIL) and total bile acid(TBA) in the supernatant of cell culture medium of each group were detected by kits. Results: RFP could induce the protein and gene expression of MANF，BSEP ，MRP2 ，MRP3 ，MRP4 ，MDR1 ，OSTα , OSTβ , OATP2B1 in HepG2 cells (P ＜0. 05 ) ，while the protein and gene expression levels of BSEP ，MRP2 ，MRP3， MRP4，MDR1，OSTα、OSTβ、OATP2B1 decreased after MANF knockdown(P＜0. 05) ．Moreover，under the action of RFP，the protein expression of PCNA and Ki67 in the knockdown group was still higher．The protein and gene levels of CHOP and Caspase-3 significantly increased after MANF knockdown(P＜0. 05) ．The levels of the hepatic cell injury markers in the cell supernatant increased significantly(P＜0. 05) ． Conclusion RFP can induce the expression of bile acid transporter such as BSEP，MRP2，MRP3，MRP4，MDR1，OSTα , OSTβ and OATP2B1 to increase in HepG2 cells(P＜0. 05) ，but the expression of bile acid transporter of HepG2 after MANF knockdown will significantly decrease under the induction of rifampicin(P＜0. 05) ，and cell indury is aggravated，indicating that MANF plays a protective role in RFP-induced adaptive responses by regulating the bile acid transporter.