RISING OBESITY: AN UNINTENDED CONSEQUENCE OF THE ANITSMOKING CAMPAIGN?

Obesity is the fastest growing health issue currently in the United States, as its prevalence has risen to over 30%, up from 14% in 1980 (Chou et al. 2004). As a result, the percentage of the population dealing with chronic health conditions has also been on the rise. Although the obesity epidemic is on the rise, smoking rates in the United States have declined from 33% to under 20% over the same time period, and from about 42% in 1965 (Todeschini et al. 2010). Thus, many economists have inferred that the declining smoking prevalence may partially be contributing to the rising obesity epidemic. Existing evidence shows that smoking cessation leads to significant weight gain. This study examines the effects of state expenditures on antismoking programs on BMI and obesity levels overtime. It is hypothesized that the anti-smoking programs, although efficient in increasing the cessation of smoking, are unintentionally increasing obesity prevalence. If this is the case, the anti-smoking campaign may not be as effective in improving the general health of the public as has been assumed. Based on data mainly from the Behavioral Risk Factor Surveillance System for the years 2000 to 2010, and taking into account lagged variables, ordinary least squares regression results show that antismoking expenditures are positively and significantly correlated to BMI and obesity. This paper also tests the theory that the antismoking campaign may be inducing people to adopt healthier lifestyles, as suggested by some previous literature. Results show that rising antismoking expenditures decrease the probability that an individual will be a smoker, but do not affect whether an individual makes other healthier lifestyle choices, measured by exercise and dietary-intake variables. To combat this unintentional consequence of the antismoking campaign, some antismoking expenditures need to be shifted to anti-obesity programs

Anticancer peptide PNC-27 adopts an HDM-2-binding conformation and kills cancer cells by binding to HDM-2 in their membranes

The anticancer peptide PNC-27, which contains an HDM-2-binding domain corresponding to residues 12-26 of p53 and a transmembrane-penetrating domain, has been found to kill cancer cells (but not normal cells) by inducing membranolysis. We find that our previously determined 3D structure of the p53 residues of PNC-27 is directly superimposable on the structure for the same residues bound to HDM-2, suggesting that the peptide may target HDM-2 in the membranes of cancer cells. We now find significant levels of HDM-2 in the membranes of a variety of cancer cells but not in the membranes of several untransformed cell lines. In colocalization experiments, we find that PNC-27 binds to cell membrane-bound HDM-2. We further transfected a plasmid expressing full-length HDM-2 with a membrane-localization signal into untransformed MCF-10-2A cells not susceptible to PNC-27 and found that these cells expressing full-length HDM-2 on their cell surface became susceptible to PNC-27. We conclude that PNC-27 targets HDM-2 in the membranes of cancer cells, allowing it to induce membranolysis of these cells selectively