Keeping It Political and Powerful: Defining the Structural Determinants of Health.

Policy Points The structural determinants of health are 1) the written and unwritten rules that create, maintain, or eliminate durable and hierarchical patterns of advantage among socially constructed groups in the conditions that affect health, and 2) the manifestation of power relations in that people and groups with more power based on current social structures work-implicitly and explicitly-to maintain their advantage by reinforcing or modifying these rules. This theoretically grounded definition of structural determinants can support a shared analysis of the root causes of health inequities and an embrace of public health's role in shifting power relations and engaging politically, especially in its policy work. Shifting the balance of power relations between socially constructed groups differentiates interventions in the structural determinants of health from those in the social determinants of health.

Theory in Action: Public Health and Community Power Building for Health Equity.

Context: Within the field of public health, there is growing awareness of how complex social conditions shape health outcomes and the role that power plays in driving health inequities. Despite public health frameworks lifting up the need to tackle power imbalances to advance equity, there is little guidance on how to accomplish this as an integral part of health promotion.

Objective: This article addresses the need for public health professionals to better understand power and identifies opportunities for shifting power to achieve more equitable outcomes.

Advancing efforts to achieve health equity: equity metrics for health impact assessment practice.

Equity is a core value of Health Impact Assessment (HIA). Many compelling moral, economic, and health arguments exist for prioritizing and incorporating equity considerations in HIA practice. Decision-makers, stakeholders, and HIA practitioners see the value of HIAs in uncovering the impacts of policy and planning decisions on various population subgroups, developing and prioritizing specific actions that promote or protect health equity, and using the process to empower marginalized communities.

A simulation-approximation approach to sample size planning for high-dimensional classification studies.

Classification studies with high-dimensional measurements and relatively small sample sizes are increasingly common. Prospective analysis of the role of sample sizes in the performance of such studies is important for study design and interpretation of results, but the complexity of typical pattern discovery methods makes this problem challenging. The approach developed here combines Monte Carlo methods and new approximations for linear discriminant analysis, assuming multivariate normal distributions.

The anticancer activity of the transcription inhibitor terameprocol (meso-tetra-O-methyl nordihydroguaiaretic acid) formulated for systemic administration.

Terameprocol (meso-tetra-O-methyl nordihydroguaiaretic acid, formerly known as EM-1421 and M4N) is a semi-synthetic small molecule with antitumor activity occurring via selective targeting of Sp1-regulated proteins, including survivin and cdc2 that control cell cycle and apoptosis. Terameprocol is in clinical development as a site-specific transcription inhibitor in solid refractory tumors. The present studies were designed to investigate the in-vitro and in-vivo anticancer activity of terameprocol in a novel hydroxypropyl beta-cyclodextrin and polyethylene glycol solvent formulation (designated CPE) designed for safe parenteral administration.

Tetra-O-methyl nordihydroguaiaretic acid inhibits growth and induces death of leukemia cells independent of Cdc2 and survivin.

Tetra-O-methyl nordihydroguaiaretic acid (M4N) was shown to induce G2 arrest and suppress human xenograft tumor growth by inhibiting Cdc2 and survivin. We examined the effect of M4N on leukemia and found that M4N inhibited growth and induced cell death in leukemic cell lines and blasts from AML patients. However, no significant changes in Cdc2 and survivin levels and G2 arrest were observed.

An automated, sheathless capillary electrophoresis-mass spectrometry platform for discovery of biomarkers in human serum.

A capillary electrophoresis-mass spectrometry (CE-MS) method has been developed to perform routine, automated analysis of low-molecular-weight peptides in human serum. The method incorporates transient isotachophoresis for in-line preconcentration and a sheathless electrospray interface. To evaluate the performance of the method and demonstrate the utility of the approach, an experiment was designed in which peptides were added to sera from individuals at each of two different concentrations, artificially creating two groups of samples.

Tetra-O-methyl nordihydroguaiaretic acid induces growth arrest and cellular apoptosis by inhibiting Cdc2 and survivin expression.

We previously reported that Sp1-dependent Cdc2 gene expression is inhibited by tetra-O-methyl nordihydroguaiaretic acid (M(4)N) and that M(4)N is likely responsible for causing growth arrest in M(4)N-treated transformed C3 cells. Here, we show that after M(4)N treatment and cell-cycle arrest, expression of the Sp1-dependent survivin gene, a member of the inhibitor of apoptosis family, is also suppressed, and the mitochondrial apoptotic pathway is activated. To confirm that inhibition of Cdc2 and survivin gene expression is necessary for M(4)N-induced growth arrest and apoptosis, we tested the effect of adding Cdc2 and survivin back to M(4)N-treated cells.

Developmental control of blood cell migration by the Drosophila VEGF pathway.

We show that a vascular endothelial growth factor (VEGF) pathway controls embryonic migrations of blood cells (hemocytes) in Drosophila. The VEGF receptor homolog is expressed in hemocytes, and three VEGF homologs are expressed along hemocyte migration routes. A receptor mutation arrests progression of blood cell movement.