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To provide a basis for further optimization of the polio sequential immunization schedule, this study evaluated the effectiveness of booster immunization with one dose of bivalent oral poliovirus vaccine (bOPV) at 48 months of age after different primary polio immunization schedules. At 48 months of age, one dose of bOPV was administered, and their poliovirus types 1-3 (PV1, PV2, and PV3, respectively)-specific neutralizing antibody levels were determined. Participants found to be negative for any type of PV-specific neutralizing antibody at 24, 36, or 48 months of age were re-vaccinated with inactivated polio vaccine (IPV). The 439 subjects who received a bOPV booster immunization at the age of 48 months had lower PV2-specific antibody levels compared with those who received IPV. One dose of IPV during basic polio immunization induced the lowest PV2-specific antibody levels. On the basis of our findings, to ensure that no less than 70% of the vaccinated have protection efficiency, we recommend the following: if basic immunization was conducted with 1IPV + 2bOPV (especially Sabin strain-based IPV), a booster immunization with IPV is recommended at 36 months of age, whereas if basic immunization was conducted with 2IPV + 1bOPV, a booster immunization with IPV is recommended at 48 months of age. A sequential immunization schedule of 2IPV + 1bOPV + 1IPV can not only maintain high levels of antibody against PV1 and PV3 but also increases immunity to PV2 and induces early intestinal mucosal immunity, with relatively good safety. Thus, this may be the best sequential immunization schedule for polio in countries or regions at high risk for polio.
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Objective To evaluate the antibody titer distributions after primary vaccination by different sequential schedules of Sabin strain-based inactivated poliovirus vaccine(sIPV) and bivalent oral attenuated live poliomyelitis vaccine against types 1 and 3 (bOPV) in Drug Candy(DC) form or liquid dosage form. Methods Eligible infants of 2 months old selected in Liuzhou were assigned randomly in a ratio of 1:1:1:1 to 4 groups as following: sIPV+2bOPV(DC), sIPV+2bOPV(liquid), 2sIPV+bOPV(DC), 2sIPV+bOPV(liquid), and were vaccinated at 0, 28, 56 days. Polio neutralizing antibody titers against poliovirus types 1, 2 and 3 were tested prior to Dose 1 and at 28 days after Dose 3. Results The antibody titer distribution for type 1 was statistically different between sIPV+2bOPV(DC) and sIPV+2bOPV(liquid) (Z=-2.589, P=0.010) while no significant differences were detected between the two groups for type 2(Z=-0.331, P=0.741) and type 3(Z=-1.556, P=0.120). There were no significant differences between 2sIPV +bOPV(DC) and 2sIPV+bOPV(liquid) for the distributions(All P>0.05) (type 1: Z=-1.249, P=0.212; type 2: Z=-1.658, P=0.097; type 3: Z=-1.436, P=0.151). In the same dosage forms with different sequential schedules, the antibody titer distributions were significantly different between 2 doses sIPV and 1 dose sIPV groups(All P<0.05)(sIPV+2bOPV(liquid) vs 2sIPV+bOPV(liquid): type 1: Z=-2.766, P=0.006; type 2: Z=-9.137, P<0.001; type 3: Z=-5.529, P<0.001. sIPV+2bOPV(DC) vs 2sIPV+bOPV(DC): type 1: Z=-3.748, P<0.001; type 2: Z=-7.660, P<0.001; type 3: Z=-6.030, P<0.001). Conclusions Different dosage forms have similar immune effects, so appropriate dosage forms should be selected for vaccination according to the effectiveness, characteristics of subjects and the population density. In the case of sufficient supply of sIPV, 2 doses sIPV sequential program should be the first choice to complete the primary immunization.
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<p><b>OBJECTIVE</b>To investigate the effect and mechanism of Factor Xa on the differentiation of Meg-01 cells into platelet-like particles.</p><p><b>METHODS</b>The Meg-01 cells were used as experimental object, Factor Xa was used as agonist. Cell proliferation was detected by CCK-8 assay. The viability of platelet-like particles was analyzed by AlamaBlue kit. MAPK/ERK pathway and PI3K/AKT pathway were assayed by Western blot. The expression of CD41b was analyzed by Western blot and flow cytometry. Cell cycle and apoptosis were detected by flow cytometry.</p><p><b>RESULTS</b>The Factor Xa (1 µg/ml) inhibited cell viability, induced apoptosis. Factor Xa triggered cell arrest at the G(2)/M stage and down-regulated the expression of SKP2. After Meg-01 cells were stimulated by Factor Xa, the expression of CD41b was up-regulated and the MAPK/ERK pathway and PI3K/AKT pathway were activated. The platelets-like particles stimulated by FXa activation were viable.</p><p><b>CONCLUSION</b>The Factor Xa maybe display some effect on the differentiation of megakaryocytes into platelets.</p>
Assuntos
Humanos , Apoptose , Plaquetas , Biologia Celular , Pontos de Checagem do Ciclo Celular , Diferenciação Celular , Linhagem Celular , Proliferação de Células , Sobrevivência Celular , Fator Xa , Farmacologia , Sistema de Sinalização das MAP Quinases , Megacariócitos , Biologia Celular , Fosfatidilinositol 3-Quinases , Metabolismo , Proteínas Proto-Oncogênicas c-akt , MetabolismoRESUMO
This study was aimed to investigate the expression of cdx2 gene in pediatric patients with acute leukemia and its clinical implication. The bone marrow and peripheral blood were collected from 33 newly diagnosed pediatric patients with acute leukemia, the cdx2 gene expression in each AL subtypes and normal controls was detected by RT-PCR, the relationship between cdx2 expression and response to treatment was observed. The results showed that the expression of cdx2 was positive in 25 out of 30 AL cases (83.3%), to be exact, in 20 of 21 ALL cases (95.2%) and in 5 of 9 AML cases (55.6%), which showed statistical difference (p < 0.05). The cdx2 mRNA could be detected also in 1 of 3 CML cases. However, no expression of cdx2 was observed in all normal control which revealed significant difference between patient group and normal control group. 21 AL patients with cdx2 positive expression (17 ALL and 4 AML patients) and 4 AL patients with cxd2 negative expression (1 ALL and 3 AML patients) all reached complete remission (CR) after treatment, which showed no correlation with CR rate. 8 patients with positive cdx2 expression were followed up. As a result, the cdx2 positive expression at initial diagnosis of patients remained positive at reaching CR, but it gradually turned to negative along with prolonging of CR, while the cdx2 negative expression at initial diagnosis of patients remained negative at CR in bone marrow level. It is concluded that cdx2 positive expression is observed in the majority of pediatric AL patients, even positive rate in ALL patients is higher than that in AML patients, while the cdx2 expression also can be observed in CML patients. The cdx2 positive expression is not related to the CR rate in AL patients.