Objective To analyze and compare the HBV DNA contents in serum and breast milk after injection of hepatitis B im‐munoglobulin (HBIG) in different periods of pregnant and lying‐in women to provide the experimental basis for blocking the mater‐nal‐neonatal transmission(PMTCT) and breast feeding scheme .Methods 140 pregnant women carrying hepatitis B virus with HB‐sAg(+ ) by antenatal examination in the obstetric outpatient department of our hospital from June 2012 to June 2014 were selected and divided into the research group and the control group according to the voluntary and secretive principle .Among them ,75 cases in the research group were intramuscularly injected by high titer HBIG 200 U at 28 ,32 ,36 weeks of pregnancy ,while 65 cases in the control group were injected by HBIG at the end of pregnancy due to different causes .Serum HBV‐DNA content before injection and before delivery was detected in the two groups ,and which in neonatal serum and breast milk within 3-5 d also detected .The differences and correlation between the two groups were analyzed .Results The HBV‐DNA content <500 copies/mL ,500-1 × 106 copies/mL ,>1 × 106 copies/mL before HBIG injection in the research group were 28 cases ,17 cases ,30 cases respectively ,which before delivery were 35 cases ,20 cases ,20 cases respectively ;which in antenatal twice detection in the control group were 19 cases , 21 cases ,25 cases and 20 cases ,17 cases ,28 cases respectively ;neonatal serum HBV‐DNA positive in the research group and control group had 1 case(5 .3% ) and 5 cases (7 .7% ) respectively ;the breast milk HBV‐DNA positive in the two groups had 3 cases(4% )/and 8 cases(12 .3% ) respectively .Conclusion HBIG injection at late pregnancy in the pregnant women carrying HBV could influ‐ence the HBV replication ,thus reduces the probability of neonatal intrauterine infection ,at the same time reduces the HBV‐DNA positive rate of postpartum breast milk .

Objective To develop a simple microfluidic chip technology for analyzing the electrotaxis of cancer cells . Methods The basic structure of the proposed microfluidic electrotaxis chip included a straight microchannel and liquid storage pools located on both sides of the microchannel .Two platinum electrodes were inserted into the liquid pools to create a controllable direct current ( DC ) field in the microchannel .The distribution and strength of the DC field in the microchannel was analyzed by the finite element analysis software COMSOL multiphysics and experiment tests .Finally, the electrotactic behavior of the rhabdomyosarcoma RD cells in the DC field of different strength was characterized using the accumulated distance, average velocity, x forward migration index ( xFMI) and y forward migration index ( yFMI) as quantitative parameters.Results The results of element analysis and experiments showed that the structure of the designed microfluidic electrotaxis chip was able to guarantee a uniform and strength-controllable DC field in the microchannel .The experiment of cell electrotaxis showed that the RD cells migrated toward the anode of the DC field .Meanwhile , the values of xFMI and accumulated distance for RD cells increased with the enlargement of the DC field , with the strength ranging from 188 to 1320 V/m.Conclusion The microfluidic chip technology developed in this paper for assaying the electrotaxis of cancer cells is simple and easily implementable , and it can be used for studies of the electrotactic behavior and underlying mechanisms of various cancer cells and normal cells in the future .

Background and objective It has been proven that miR-133b could inhibit cancer cell growth, the expression level of miR-133b was significant reduction in lung cancer tissue and serum of patients, and increase the radiation sensitivity of squamous cell carcinoma by targeting PKM2, but the exist mechanisms is not clear. The aim of this study is to explore the effect of miR-133b on proliferation in A549 lung cancer stem cells and drug sensitivity in DDP, and to explore the relationship between miR-133b and PKM2 gene, as well as the effect of cancer stem cells. Methods Using miRBase and miRNAMap database to sequence comparison miR-133b and PKM2 gene. Using im-mune magnetic separation method to select the CD133+/CD34+lung cancer stem cells from A549 cells, and using flow cytometry to detect the purity. The expression of miR-133b mRNA was detected by real-time fluorescence quantita-tive PCR (qRT-PCR). Cell proliferation was detected by CCK8 assay. 15 μg/mL DDP was treated to cells which was transfected with miR-133b, and apoptosis was detected by flow Cytometry at 0 h, 12 h, 24 h, 72 h. The expression of PKM2 protein was detected by Western blot. Results Gene binding site report that PKM2 gene may be the target gene of miR-133b; the results of flow cytometry showed that the purity of CD133+/CD34+ stem cells was (92.15±4.27)%. qRT-PCR results showed that compared with the control group, after overexpression of miR-133b, miR-133b was up-regulated and miR-133b was down regulated after miR-133b inhibition (P<0.05). Compared with the control group, cell proliferation of miR-133b mimics group was significantly decreased (P<0.05), PKM2 protein levels were signifi-cantly lower (P<0.05); and cell proliferation of the miR-133b inhibitor group and PKM2 level was increased (P<0.05). The apoptosis of miR-133b mimics group was significantly higher than that of control group (P<0.05) after DDP treat-ment with 12 h. The expression of PKM2 protein in miR-133b mimics+DDP group was significantly lower than that in control group (P<0.05). Conclusion Overexpression of miR-133b can inhibit the growth and proliferation of lung cancer stem cells by down regulating PKM2, and can enhance the sensitivity of lung cancer stem cells to DDP.