Retraction RETRACTION of "Efficacy and safety of nucleoside analogues in preventing vertical transmission of the hepatitis B virus from father to infant", by L.-H. Cao, P.-L. Zhao, Z.-M. Liu, S.-C. Sun, D.-B. Xu, J.-D. Zhang and Z.-H. Shao - Genet. Mol. Res. 14 (4): 15539-15546 (2015).

The retracted article is: Cao L-H, Zhao P-L, Liu Z-M, Sun S-C, et al. (2015). Efficacy and safety of nucleoside analogues in preventing vertical transmission of the hepatitis B virus from father to infant. Genet. Mol. Res. 14: 15539-15546. The article published in Genetics and Molecular Research 14 (4): 15539-15546 (2015) is a very good paper, but it appears that the authors' group submitted this manuscript to multiple journals, which is ethical misconduct. This manuscript (similar language and identical data) was published in the Experimental and Therapeutic Medicine Journal prior to being submitted to GMR. There are parts copied from "Efficacy and safety of nucleoside analogs on blocking father-to-infant vertical transmission of hepatitis B virus", by Li-Hau Cao, Pei-Li Zhao, Zhi-Min Liu, Shao-Chun Sun, et al. Exp. Ther. Med. 9 (6): 2251-2256 (2015) - DOI: 10.3892/etm.2015.2379. The GMR editorial staff was alerted and after a thorough investigation, there is strong reason to believe that the peer review process was failure. Also, after review and contacting the authors, the editors of Genetics and Molecular Research decided to retract this article in accordance with the recommendations of the Committee on Publication Ethics (COPE). The authors and their institutions were advised of this serious breach of ethics.

Efficacy and safety of nucleoside analogues in preventing vertical transmission of the hepatitis B virus from father to infant.

We examined the efficacy and safety of nucleoside analogues in preventing the vertical transmission of hepatitis B virus (HBV) from father to infant. We included 201 patients who visited the liver clinic of our hospital. The patients were positive for HBV surface antigen (HBsAg), HBeAg, anti-HBc, and HBV DNA; 189 patients (94%) had abnormal liver function. In all couples, the fathers were HBV DNA-negative and had normal liver function, and the mothers were anti-HB-positive before pregnancy. The control group comprised 188 couples who visited our hospital during the same time period. The fathers in the control group were positive for HBsAg, HBeAg, anti-HBc, and HBV DNA. The mothers were HBsAg-negative and anti-HBs-positive. No infants in the case group were HBsAg-positive and HBV DNA-positive, and all were anti-HBs-positive, indicating that father to infant HBV vertical transmission was prevented in the case group. In the control group, 147 of 188 newborns (78.2%) were anti-HBs-positive at birth, 28 (14.9%) were HBV DNA-positive, and 19 (10.1%) were HBsAg-positive. A significant difference was observed between the two groups. No statistically significant difference was observed in the gestational age, birth weight, birth length, 1-min and 8-min Apgar score, jaundice, other internal and surgical diseases, delivery mode, and other birth information between the neonates born to couples in the case and control groups; there were no fetal malformations and stillbirths in the two groups. Our results showed that administration of antiretroviral therapy to HBV DNA-positive fathers before pregnancy can cause a decrease in the viral load and prevent father to infant HBV vertical transmission. The use of antiviral nucleoside analogues before pregnancy was safe in fathers, and the fathers who wanted children could continue to use anti-viral therapy. The sample size in our study was small, and further studies with a large sample size and longer follow-up time are required for determining the use of nucleoside analogues from the point view of prenatal and postnatal care.

Fas/FasL in the immune pathogenesis of severe aplastic anemia.

Fas/FasL protein expression of bone marrow hematopoietic cells was investigated in severe aplastic anemia (SAA) patients. Fas expression was evaluated in CD34(+), GlycoA(+), CD33(+), and CD14(+) cells labeled with monoclonal antibodies in newly diagnosed and remission SAA patients along with normal controls. FasL expression was evaluated in CD8(+) cells in the same manner. In CD34(+) cells, Fas expression was significantly higher in the newly diagnosed SAA group (46.59 ± 27.60%) than the remission (6.12 ± 3.35%; P < 0.01) and control (8.89 ± 7.28%; P < 0.01) groups. In CD14(+), CD33(+), and GlycoA(+) cells, Fas levels were significantly lower in the newly diagnosed SAA group (29.29 ± 9.23, 46.88 ± 14.30, and 15.15 ± 9.26%, respectively) than in the remission (47.23 ± 31.56, 67.22 ± 34.68, and 43.56 ± 26.85%, respectively; P < 0.05) and normal control (51.25 ± 38.36, 72.06 ± 39.88, 50.38 ± 39.88%, respectively; P < 0.05) groups. FasL expression of CD8(+) cells was significantly higher in the newly diagnosed SAA group (89.53 ± 45.68%) than the remission (56.39 ± 27.94%; P < 0.01) and control (48.63 ± 27.38%; P <0.01) groups. No significant differences were observed between the remission and control groups. FasL expression in CD8(+) T cells was significantly higher in newly diagnosed patients, and CD34(+), CD33(+), CD14(+), and GlycoA(+) cells all showed Fas antigen expression. The Fas/FasL pathway might play an important role in excessive hematopoietic cell apoptosis in SAA bone marrow. Furthermore, CD34(+) cells are likely the main targets of SAA immune injury.