The effect of ambient air pollution on birth outcomes in Norway.

BACKGROUND: Ambient air pollution can be harmful to the fetus even in countries with relatively low levels of pollution. Most of the established literature estimates the association between air pollution and health rather than causality. In this paper, I examine the causal effects of ambient air pollution on birth outcomes in Norway. METHODS: With the large sample size and geographic division of sub-postal codes in Norway, I can control for a rich set of spatio-temporal fixed effects to overcome most of the endogeneity problems caused by the choice of residential area and date of delivery. After controlling for a rich set of spatio-temporal fixed effects, my paper uses the variance in ambient air pollutant concentrations over narrow time intervals and in a small geographic area of Norway to determine how prenatal air pollution exposure affects birth outcomes. My data contain extensive information about parents as well as meteorological conditions that can be used to control for potential confounding factors. RESULTS: I find that prenatal exposure to ambient nitric oxide in the last trimester causes significant birth weight and birth length loss under the same sub-postcode fixed effects and calendar month fixed effects, whereas other ambient air pollutants such as nitrogen dioxide and sulfur dioxide appear to be at safe levels for the fetus in Norway. In addition, the marginal adverse effect of ambient nitric oxide is larger for newborns with disadvantaged parents. Both average concentrations of nitric oxide and occasional high concentration events can adversely affect birth outcomes. CONCLUSIONS: Prenatal exposure to NO pollution has an adverse effect on birth outcomes. This suggests that government and researchers should pay more attention to examining NO pollution and that health care providers need to advise pregnant women about the risks of air pollution during pregnancy.

Anti-HER-2 engineering antibody ChA21 inhibits growth and induces apoptosis of SK-OV-3 cells.

BACKGROUND AND AIMS: Anti-HER-2 antibodies targeting distinct epitopes have different biological functions on cancer cells. In a previous study, we demonstrated that anti-HER-2 engineering antibody ChA21 was able to bind to subdomain I of HER-2 extracellular domain. In this study, The effects of ChA21 on growth and apoptosis against ovarian carcinoma cell SK-OV-3 over-expressing HER-2 in vitro and in vivo were investigated. METHODS: Cell growth inhibition was evaluated by MTT assay. Apoptosis was detected by TUNEL stain, transmission electron microscopy and flow cytometry on cultured cells and tissue sections from nude mice xenografts. The apoptosis-related proteins Bax and Bcl-2 were assessed by immunohistochemistry. RESULTS: We found that treatment of ChA21 caused a dose-dependent decrease of cell proliferation in vitro and a significant inhibition of tumor growth in vivo. ChA21 therapy led to a significant increase in the induction of apoptosis, and up-regulated the expression of Bax, while the expression of Bcl-2 was down-regulated. CONCLUSION: These data suggest that ChA21 inhibits the growth and induces apoptosis of SK-OV-3 via regulating the balance between Bax and Bcl-2.

[Effects of anti-HER-2 chimeric antibody chA21 on proliferative inhibition of SKOV3 cells and inducing their apoptosis].

AIM: To explore the effects of anti-HER-2 chimeric antibody chA21 on proliferation and apoptosis of ovarian cancer cell lines SKOV3. METHODS: MTT colorometric assay, HE staining, transmission electron microscopy, flow cytometry and TUNEL staining were used to study the proliferative inhibition and apoptotic induction of SKOV3 cells by chA21 in vitro. RESULTS: Proliferative inhibition rate and apoptotic rate of SKOV3 cells were increased with dose and action time by chA21 (0.2 mg/L-5.4 mg/L). CONCLUSION: chA21 can remarkably inhibit proliferation of SKOV3 cells in vitro and induction of apoptosis may be a principal way.