Fetal gene can cause preeclampsia

Preeclampsia is a pregnancy complication characterized by high blood pressure and signs of damage to kidneys and liver. Preeclampsia usually starts after 20 weeks of pregnancy in women whose blood pressure had been normal. Slight rise in blood pressure may be a sign of preeclampsia.

Pregnant women risk of preeclampsia can be linked in some cases to genes from fetus. Preeclampsia usually starts with a problem in the placenta, which is mainly composed of fetal cells.
Researchers analysed a large number of women, and discovered several genetic variables that identified  the same gene associated with the risk.

The genetic variants identified by the researchers are associated with the FLT-1 gene, which encodes a protein that, in soluble form, is known as a biomarker for preeclampsia.

The protein contributes to damaging the mother's vascular system causing high blood pressure and an increased amount of protein in the urine. This happens as a result of problems with the placenta, essentially because fetal cells in the placenta produce the protein.

The risk of the disease may be because changes in the gene affect how the protein works and how it affects the mother. This is a fetal gene that gives the mother an increased risk of developing preeclampsia.
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Air pollution can damage children's DNA

Children exposed to high levels of traffic-related air pollution have evidence of a specific type of DNA damage called telomere shortening.

Young people with asthma also have evidence of telomere shortening, according to the preliminary research by John R. Balmes, MD, of University of California, Berkeley, and colleagues.

The results suggest that telomere length may have potential for use as a biomarker of DNA damage due to environmental exposures and chronic inflammation.

The study included 14 children and adolescents living in Fresno, California -- the second-most polluted city in the United States. The researchers assessed the relationship between polycyclic aromatic hydrocarbons (PAHs), a "ubiquitous" air pollutant caused by motor vehicle exhaust; and shortening of telomeres, a type of DNA damage typically associated with aging.

As the exposure to PAHs increased, telomere length decreased, children with asthma were exposed to higher PAH levels than those without asthma.
The relationship between PAH level and telomere shortening remained significant after adjustment for asthma and other factors.

 Research suggested that children may have different telomere shortening regulation than adults, which might make them more vulnerable to the damaging effects of air pollution.

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