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BackgroundTo evaluate the efficacy and safety of treating HBV-positive mothers with telbivudine in early and middle pregnancy to prevent mother-to-infant HBV transmission.MethodsThe subject population comprised pregnant women with chronic hepatitis B (CHB; n = 188) from January 2013 to June 2015, with HBV DNA ≥1.0 × 107copies/mL and increased alanine aminotransferase levels. Groups A (n = 62) and B (n = 61) were treated with telbivudine starting at 12 weeks or 20–28 weeks after gestation, respectively. Telbivudine was discontinued at postpartum 12 weeks. Group C (n = 65) received no antiviral. All infants were vaccinated with hepatitis B immunoglobulin (200 IU) and HBV vaccine (20 with hepatitis B The maternal HBV DNA levels of the groups were compared. Mother-to-infant transmission of HBV was indicated by the presence of HBsAg in infants 7 months after birth.ResultsBefore treatment, the HBV DNA levels of the 3 groups were similar. Before delivery and 12 weeks after delivery, the HBV DNA levels of groups A and B were similar, but both were significantly lower than that of group C (P < 0.01, all). No infants in groups A and B were HBsAg-positive, but the infection rate of group C was 18.4% (P < 0.01). The HBV infection rate of infants was positively associated with the HBV DNA levels of the pregnant mothers.ConclusionAdministration of telbivudine to HBV-infected mothers, started during early and middle pregnancy, completely blocked mother-to-infant HBV transmission.Trial registrationThe study was registered retrospectively on Janurary 25 in 2016 at Chinese Clinical Trial Registry (ChiCTR-OPC-16007899).

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PurposeDefine the effectiveness of teriparatide (TPTD) treatment on reducing the incidence of new vertebral compression fractures (NVCFs) and back pain and improving quality of life after percutaneous kyphoplasty (PKP).MethodsTwo years of clinical follow-up data from primary osteoporotic women who had experienced initial osteoporotic vertebral compression fractures (OVCFs) and received PKP plus 12-month TPTD (n=113) or basic treatment (BT) of calcium and vitamin D supplements (n=208) were retrospectively collected. The risk of NVCFs over each 6-month period in the TPTD group was evaluated and compared with the BT group using a logistic regression. Health-related quality of life (HRQoL, EQ-5D questionnaire), back pain [100 mm visual analog scale (VAS)] and bone mineral density (BMD) of the spine were analyzed using linear mixed models for repeated measures (LMMRM).ResultsLogistic regression analysis adjusting for baseline characteristics showed that patients in the TPTD group had a lower risk of NVCFs compared with those receiving BT during the final three observation intervals (6–12 months, OR=0.189, 95% CI=0.030–0.681, p=0.046; 12–18 months, OR=0.009, 95% CI=0.0001–0.111, p=0.001; 18–24 months, OR=0.024, 95% CI=0.0009–0.264, p=0.009, respectively). Significant improvements in adjusted EQ-5D and back pain VAS scores were identified in the TPTD group compared with the BT group, and this improvement was sustained for at least 12 months after teriparatide treatment was discontinued (both p<0.001). The BMD of the spine also showed a higher T-value in the TPTD group compared with the BT group (p<0.001).ConclusionIn routine clinical practice, for patients with OVCFs who receive the PKP procedure, TPTD treatment may be a preferable subsequent therapy because of its ability to reduce the incidence of NVCFs and sustain a high quality of life and back pain alleviation.

Colorectal cancer (CRC) is the fourth leading cause of cancer-induced mortality. Histone deacetylase 2 (HDAC2) is involved in prognosis and therapy of CRC. This study aimed to explore novel therapeutic targets for CRC. The alteration of HDAC2 expression in CRC tissues was estimated by qRT-PCR. After lentivirus transfection, HDAC2 knockdown was confirmed by western blot analysis. The effect of HDAC2 knockdown on cell proliferation was then assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Screened by TargetScan, microRNA (miR)-455 was predicted to bind to 3 0 UTR of HDAC2 and the prediction was verified by luciferase assay. Finally, cells were transfected, respectively, with miR-455 mimics or miR-455 negative control (miR-NC) and the expression of HDAC2, cell proliferation and apoptosis of transfected cells were respectively evaluated by western blot analysis, MTT assay and flow cytometry. Results showed that the HDAC2 expression was up-regulated in CRC tissues (Po0.05). HDAC2 knockdown significantly decreased cell viability at day 3 (Po0.05), day 4 (Po0.01), and day 5 (Po0.001) after infection. Then, miR-455 was verified to directly target HDAC2, resulting in a significant difference in luciferase activity (Po0.01). Moreover, miR-455 decreased the expression of HDAC2 (Po0.01). miR-455 remarkably decreased cell viability at day 3 (Po0.05), day 4 (Po0.01), and day 5 (Po0.001) after transfection while inducing cell apoptosis (Po0.001). In conclusion, miR-455 inhibited cell proliferation while inducing cell apoptosis by targeting HDAC2 in CRC cells.