The cigarette controversy.

This study examines the history of the cigarette controversy using the tobacco documents as a roadmap to explore the following four questions: (a) What did tobacco companies know about the health risks of smoking and when did they know it? (b) What evidence is there that tobacco companies conspired to deliberately mislead the public about the health risks of smoking? (c) How were scientists involved in the cigarette controversy? (d) Have tobacco companies changed the way they do business since signing the 1998 Master Settlement Agreement? The tobacco companies knew and for most part accepted the evidence that cigarette smoking was a cause of cancer by the late 1950s. The documents also reveal that the tobacco companies helped manufacture the smoking controversy by funding scientific research that was intended to obfuscate and prolong the debate about smoking and health. Today, the tobacco companies acknowledge that smoking is a cause of disease, but they have not materially altered the way they do business. In our opinion, it is not sufficient for the tobacco industry to merely concede the obvious point that smoking is a cause of disease when it is evident that decades of misinformation has resulted in a public that is massively ignorant about the risks of smoking low-tar cigarettes, nicotine addiction, and secondhand smoke exposure. Public education efforts are still needed to correct these misperceptions along with government oversight to ensure that the industry is not permitted to mislead the public further. If the past 50 years have taught us anything, it is that the tobacco industry cannot be trusted to put the public's interest above their profits no matter what they say.     

Quality of life and Kaposi sarcoma: using preference techniques to value the health gains from treatment

The goal of this work was to investigate preference techniques to value potential health gains from treatments of Kaposi sarcoma (KS). The study was designed to take the form of face-to-face interviews with a sample of men with a history of HIV/AIDS ( n=15) or HIV/AIDS and KS ( n=17). The main outcome measure was quality of life (QoL) associated with various KS disease states expressed on a scale from 0 (death) to 1 (perfect health), obtained though time trade-off (TTO) and rating scale techniques. For cutaneous lesions only, the mean TTO preference score value was 0.27. In other words, the men were willing to trade a life expectancy of 5 years for a shorter period (1.4 years) in perfect health. More severe KS health states were rated lower (0.07-0.09). The mean rating scale value for cutaneous lesions only was 0.11 and ranged from -0.10 to -0.04 for the more severe conditions; these values were systematically lower than the TTO ( P=0.014). A large overall potential gain in QoL from treatment (partial response minus stable disease) was found for each condition to be reflected in both the TTO (from 0.31 to 0.55) and the rating scale (from 0.38 to 0.44). Respondents associate KS health states with extremely poor QoL and indicate that large gains are possible through modest treatment effects. While TTO returns higher values than the rating scale, potential gains from treatments were similar. The techniques appear to be suitable for application to QoL and economic evaluation of treatments of KS.     

Prevalence of juvenile periodontitis in a circumpubertal population

A cross-sectional radiographic screening was performed on bite-wing pairs (BW) from 1872 10-12 year old schoolchildren in the Greater Worcester, Massachusetts area to assess the prevalence of juvenile periodontitis (JP). The 3-stage screening process entailed: (1) visual identification of possible cases based upon a visual assessment of BW for interproximal crestal bone levels greater than or equal to 2 mm from the cemento-enamel junction (CEJ) on greater than or equal to 1 permanent first molar; (2) identification of probable cases based upon BW from possible cases measured with a transparent ruler calibrated in millimeters; (3) finally, clinical confirmation of JP in consenting probable cases. A total of 1038 subjects were eligible to be included in the study (greater than or equal to 3 mesial sites readable). Of the 1038 eligible subjects, 117 possible and 103 probable cases were identified in stage 1 and stage 2, respectively. A total of 99 probable cases could be contacted and 43 were examined clinically. Two cases of JP were confirmed clinically in stage 3, yielding a prevalence rate of 4.6/1000. Specifically, this report defines a rate of JP in 10-12 year-old schoolchildren for the first time. In addition, these results indicate that BW can be used to identify children with JP from large data sets. However, further studies including complete clinical and radiographic examinations are necessary to determine whether this method is adequate for large epidemiologic studies.     

Plasticity of human motion processing mechanisms following surgery for infantile esotropia

Monocular oscillatory-motion visual evoked potentials (VEPs) were measured in prospective and retrospective groups of infantile esotropia patients who had been aligned surgically at different ages. A nasalward-temporal response bias that is present prior to surgery was reduced below pre-surgery levels in the prospective group. Patients in the retrospective group who had been aligned before 2 yr of age showed lower levels of response asymmetry than those who were aligned after age 2. The data imply that binocular motion processing mechanisms in infantile esotropia patients are capable of some degree of recovery, and that this plasticity is restricted to a critical period of visual development.     

The superoxide anion may mediate short- but not long-term effects of ultraviolet radiation on melanogenesis

Abstract The present study was carried out to examine the role of reactive oxygen species in mediating the melanogenic effects of UVR. B16 mouse melanoma cells responded to a single dose of UVR by showing increases in their melanin content. Although there was a small increase in melanin at 48-72 hours, which was associated with a rise in tyrosinase activity at 48 h, the greatest change occurred at 3 h and this was not associated with an increase in tyrosinase activity. This short-term response, unlike the more delayed melanogenic response, was reduced by superoxide dismut-ase (SOD). Xanthine oxidase (XO), which generates the superoxide anion (O₂). also increased the melanin content of B16 melanoma cells with effects at 3 h and 48 h. As with UVR, the delayed response was accompanied by an increase in tyrosinase activity but no such association was evident at 3 h. In addition, the short-term effect, like that seen with UVR, was reduced with SOD and to a lesser extent with catalase. In contrast to the effects found with XO, glucose oxidase, which generates hydrogen peroxide, had no effect on the melanin content or tyrosinase activity of the B16 cells. These results confirm previous observations that UVR is able to act directly on cells to bring about delayed increases in melanogenesis. They further demonstrate that UVR also stimulates melanogenesis through a more rapid action that is not associated with an activation of tyrosinase. This effect could be mediated by the O₂ which, rather than activating tyrosinase, could act by serving as a substrate for the enzyme.