A large body of documented evidence shows that smoking during pregnancy is harmful to both the mother and fetus. Prenatal exposure to nicotine in various forms alters neurologic development in experimental animals and may increase the risk for neurologic conditions in humans. There is a direct association between maternal smoking and SIDS; however the connection with depression, attention disorders, learning and behavior problems, and nicotine addiction in humans is not straightforward. Nicotine’s action on the production and function of neurotransmitters makes it a prime suspect in the pathology of these diseases. Nicotine accentuates neurotransmitter function in adults but desensitizes these functions in prenatally exposed infants and children. This desensitization causes an abnormal response throughout the lifespan. Furthermore, nicotine use in the adolescent and adult can alleviate some of the symptoms caused by these neurotransmitter problems, but it also increases the risk for nicotine addiction. Although nicotine replacement drugs are allowed for pregnant women, there is no clear indication that they improve outcomes during pregnancy, and they may add to the damage to the developing neurologic system. Understanding the effects of nicotine exposure is important in providing safe care for pregnant women, children and families and for developing appropriate smoking cessation programs during pregnancy.
Customizing EMR with clinical practice guidelines improved adherence to recommendations for screening and identification of childhood overweight and obesity. Increased recognition and diagnosis will lead to improved interventions and improve outcomes for childhood obesity.
Data increasingly implicate a possible role of immune and inflammatory responses to infection in sudden infant death syndrome (SIDS). We have previously described a dual challenge model that results in pathology, organ damage, vascular collapse and unexplained death similar to that seen in SIDS. In this study, we examined changes in inflammatory cytokine mRNA in the lung and liver and regulation of pathways associated with nitric oxide production. Our data suggest that priming of the immune system by mild viral infection disturbs normal inflammatory response to endotoxin. This results in an increased nitric oxide synthase production, most likely the cause of liver pathology and clotting abnormalities.
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