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A number of authors have attempted to defend ecologic (aggregate) studies by claiming that the goal of those studies is estimation of ecologic (contextual or group-level) effects rather than individual-level effects. Critics of these attempts point out that ecologic effect estimates are inevitably used as estimates of individual effects, despite disclaimers. A more subtle problem is that ecologic variation in the distribution of individual effects can bias ecologic estimates of contextual effects. The conditions leading to this bias are plausible and perhaps even common in studies of ecosocial factors and health outcomes because social context is not randomized across typical analysis units (administrative regions). By definition, ecologic data contain only marginal observations on the joint distribution of individually defined confounders and outcomes, and so identify neither contextual nor individual-level effects. While ecologic studies can still be useful given appropriate caveats, their problems are better addressed by multilevel study designs, which obtain and use individual as well as group-level data. Nonetheless, such studies often share certain special problems with ecologic studies, including problems due to inappropriate aggregation and problems due to temporal changes in covariate distributions.
Ecologic versus individual-level sources of bias in ecologic estimates of contextual health effects.

CONTEXT The long-term risk for developing hypertension is best described by the lifetime risk statistic. The lifetime risk for hypertension and trends in this risk over time are unknown.
OBJECTIVES To estimate the residual lifetime risk for hypertension in older US adults and to evaluate temporal trends in this risk.
DESIGN, SETTING, AND PARTICIPANTS Community-based prospective cohort study of 1298 participants from the Framingham Heart Study who were aged 55 to 65 years and free of hypertension at baseline (1976-1998).
MAIN OUTCOME MEASURES Residual lifetime risk (lifetime cumulative incidence not adjusted for competing causes of mortality) for hypertension, defined as blood pressure of 140/90 mm Hg or greater or use of antihypertensive medications.
RESULTS The residual lifetime risks for developing hypertension and stage 1 high blood pressure or higher (greater-than-or-equal to 140/90 mm Hg regardless of treatment) were 90% in both 55- and 65-year-old participants. The lifetime probability of receiving antihypertensive medication was 60%. The risk for hypertension remained unchanged for women, but it was approximately 60% higher for men in the contemporary 1976-1998 period compared with an earlier 1952-1975 period. In contrast, the residual lifetime risk for stage 2 high blood pressure or higher (greater-than-or-equal to 160/100 mm Hg regardless of treatment) was considerably lower in both sexes in the recent period (35%-57% in 1952-1975 vs 35%-44% in 1976-1998), likely due to a marked increase in treatment of individuals with substantially elevated blood pressure.
CONCLUSION The residual lifetime risk for hypertension for middle-aged and elderly individuals is 90%, indicating a huge public health burden. Although the decline in lifetime risk for stage 2 high blood pressure or higher represents a major achievement, efforts should be directed at the primary prevention of hypertension.
Residual lifetime risk for developing hypertension in middle-aged women and men: The Framingham Heart Study.

The alpha-pyrone antibiotic myxopyronin (Myx) inhibits bacterial RNA polymerase (RNAP). Here, through a combination of genetic, biochemical, and structural approaches, we show that Myx interacts with the RNAP "switch region"--the hinge that mediates opening and closing of the RNAP active center cleft--to prevent interaction of RNAP with promoter DNA. We define the contacts between Myx and RNAP and the effects of Myx on RNAP conformation and propose that Myx functions by interfering with opening of the RNAP active-center cleft during transcription initiation. We further show that the structurally related alpha-pyrone antibiotic corallopyronin (Cor) and the structurally unrelated macrocyclic-lactone antibiotic ripostatin (Rip) function analogously to Myx. The RNAP switch region is distant from targets of previously characterized RNAP inhibitors, and, correspondingly, Myx, Cor, and Rip do not exhibit crossresistance with previously characterized RNAP inhibitors. The RNAP switch region is an attractive target for identification of new broad-spectrum antibacterial therapeutic agents.
The RNA Polymerase "Switch Region" Is a Target for Inhibitors