The association of ToRCH infection and congenital malformations: A prospective study in China.

OBJECTIVE: ToRCH infections (toxoplasmosis, rubella, cytomegalovirus and Herpes simplex virus) have long been known to be associated with bad obstetric outcomes. Little information is available about the impact of ToRCH infection on reproduction in china nearly for ten years. We designed a prospective study among 1863 pregnant women to investigate the association of ToRCH infection and congenital malformations. STUDY DESIGN: All participants had set up a maternal health Handbook and were managed through the maternal and child health care system. They underwent regular pregnancy check-up, including physical measurements (weight, abdominal circumference and blood pressure), laboratory examinations (blood, urine) and ultrasound scan. ToRCH IgM antibodies were tested by chemiluminescence immunoassay. RESULTS: 102 participants were infected with ToRCH and the total infection rate was 6.06% (102/1683). CMV infection rate (3.15%, 53/1683) was the highest. The positive rate of ToRCH IgM antibodies increased significantly in participant with upper respiratory tract infection (14.6%, 32/219) or with adverse pregnancy history (4.8%, 70/1464). Among 85 ToRCH infected participants, adverse pregnancy outcome were observed in 57 cases which included abortions (31.8%, 27/85), premature births (8.2%, 7/85), congenital malformations (12.9%, 11/85), and stillbirths (9.4%, 8/85). Furthermore, congenital malformations was much higher than that in those without ToRCH infection (1.1%, 17/1598) (P＜0.001). CONCLUSION: ToRCH infection was a significant risk factor of severe damage to the fetus, especially congenital malformations. ToRCH screening for pregnant women can reduce the incidence of adverse pregnancy and prevent birth defects in china.

Interference of the long noncoding RNA CDKN2B-AS1 upregulates miR-181a-5p/TGFßI axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells.

Long noncoding RNA (lncRNA) CDKN2B-AS1 has been shown to play a crucial role in the development as well as in the prognosis of various human cancers, including cervical cancer. However, the underlying mechanisms need to be further explored between CDKN2B-AS1 and cervical cancer. In the present study, RT-PCR showed that the mRNA level of CDKN2B-AS1 was significantly upregulated while the miR-181a-5p was downregulated in cervical cancer cell lines. In addition, the interference of CDKN2B-AS1 by shRNA resulted in the suppression of cell proliferation, invasion, migration and promotion of apoptosis and senescence, and either CDKN2B-AS1 overexpression or miR-181a-5p showed reversed results. Further studies demonstrated that CDKN2B-AS1 could directly interact with miR-181a-5p, and that there was an inverse correlation between miR-181a-5p and CDKN2B-AS1. In addition, we found that TGFßI was a target of miR-181a-5p and could be downregulated by CDKN2B-AS1 knockdown. Moreover, the in vivo experiments further demonstrated the contribution of CDKN2B-AS1 in cervical cancer including tumor growth, apoptosis inhibition and senescence inhibition, and CDKN2B-AS1 knockdown could inhibit the aforementioned activities. In summary, our study demonstrated that the CDKN2B-AS1/miR-181a-5p/TGFßI axis might play a vital role in cervical cancer development.

Long non-coding RNA GAS5 inhibits ovarian cancer cell proliferation via the control of microRNA-21 and SPRY2 expression.

In recent decades, numerous long non-coding (lnc)RNAs, including growth arrest-specific transcript 5 (GAS5), have been demonstrated to exert promoting or suppressive effects in human cancers. Decreased expression of the lncRNA GAS5 was reported to promote cell proliferation, migration and invasion and indicate poor prognosis in ovarian cancer. However, the exact underlying molecular mechanism through which GAS5 is involved in ovarian cancer growth remains unknown. The present study aimed to investigate the regulatory mechanism of GAS5 in ovarian cancer cell proliferation. Quantitative polymerase chain reaction and western blot analysis were used to examine RNA and protein expression, respectively. An MTT assay was used to examine cell proliferation. A luciferase reporter gene assay was conducted to verify the targeting relationship. It was identified that the expression levels of GAS5 and Sprouty homolog 2 (SPRY2) were significantly downregulated, while the expression level of microRNA (miR)-21 was significantly upregulated in ovarian cancer tissues and cell lines compared with adjacent non-tumor tissues and normal ovarian epithelial cells, respectively. Downregulation of GAS5 was significantly associated with advanced clinical stage. Luciferase assay data indicated that miR-21 was a direct target of GAS5 and that SPRY2 was a target gene of miR-21 in ovarian cancer-derived A2780 cells. GAS5 overexpression significantly inhibited the proliferation of ovarian cancer cells, which was accompanied by the downregulation of miR-21 and the upregulation of SPRY2. The overexpression of miR-21 caused a significant decrease in A2780 cell proliferation, which was accompanied by reduced SPRY2 expression. Furthermore, miR-21 overexpression attenuated the suppressive effects of GAS5 on A2780 cell proliferation and rescued the promoting effects of GAS5 on SPRY2 expression. In addition, the knockdown of SPRY2 also rescued the suppressive effects of GAS5 on the proliferation of A2780 cells. In summary, our study demonstrates that GAS5 exerts a suppressive effect on the proliferation of ovarian cancer cells, at least in part via the inhibition of miR-21 expression and subsequent increased SPRY2 expression. These findings suggest that the GAS5/miR-21/SPRY2 signaling pathway may be a potential therapeutic target in ovarian cancer.

[Application of Epstein-Barr virus-transformed B lymphoblastic cells in identification of CTL epitopes specific for Hantaan virus].

AIM: To establish Epstein-Barr virus (EBV)-transformed B lymphoblastic cell lines (B-LCL) to present peptides as antigen-presenting cells (APC) and stimulate short-cultured T cells secreting IFN-gamma, by which the T cell epitopes are identified. METHODS: PBMCs from patients with hemorrhagic fever with renal syndrome (HFRS) were transformed using EBV from supernatant of B95-8 cells. ELISPOT assay was then employed to evaluate the IFN-gamma production of short-cultured G9L-specific CD8(+) T cells stimulated with peptide-pulsed autologous B-LCL cells. RESULTS: B-LCL pulsed with G9L or G9L-nested V15R can stimulate G9L-specific CD8(+) T cells producing IFN-gamma, but not B-LCL pulsed with non-homologous I15P. CONCLUSION: B-LCL can efficiently and specifically present peptides to peptide-specific T cells as non-professional APC.