Over 100 papers describing and utilizing the Stanford Health Assessment Questionnaire (HAQ) have been published since 1980. A brief overview of the HAQ is presented along with a guide to the accumulated literature. The topics covered include: studies using the disability, pain, economic, and drug side effect dimensions of the HAQ; reliability and validity studies; applications to various rheumatic diseases; language adaptations; modifications and derivative scales; studies correlating the HAQ with sociodemographic, health status, laboratory, and physical measures; and randomized controlled trials and observational studies using the HAQ. A few comments regarding future directions for research are also presented.

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Background-Atherosclerosis is a complex disease requiring improvements in diagnostic techniques and therapeutic treatments. Both improvements will be facilitated by greater exploration of the biology of atherosclerotic plaque. To this end, we carried out large-scale gene expression analysis of human atherosclerotic lesions. Methods and Results-Whole genome expression analysis of 101 plaques from patients with peripheral artery disease identified a robust gene signature (1514 genes) that is dominated by processes related to Toll-like receptor signaling, T-cell activation, cholesterol efflux, oxidative stress response, inflammatory cytokine production, vasoconstriction, and lysosomal activity. Further analysis of gene expression in microdissected carotid plaque samples revealed that this signature is differentially expressed in macrophage-rich and smooth muscle cell-containing regions. A quantitative PCR gene expression panel and inflammatory composite score were developed on the basis of the atherosclerotic plaque gene signature. When applied to serial sections of carotid plaque, the inflammatory composite score was observed to correlate with histological and morphological features related to plaque vulnerability. Conclusions-The robust mRNA expression signature identified in the present report is associated with pathological features of vulnerable atherosclerotic plaque and may be useful as a source of biomarkers and targets of novel antiatherosclerotic therapies. (Circ Cardiovasc Genet. 2011;4:595-604.)Key Words: plaque Ⅲ macrophage Ⅲ smooth muscle cell Ⅲ correlation Ⅲ coexpression A therosclerosis and its clinical sequelae, coronary heart disease, stroke, and peripheral vascular disease, represent significant medical problems. In the United States, approximately 13 million patients have diagnosed coronary heart disease, and almost 800 000 deaths in 2007 were due to cardiovascular disease or its complications. 1 Despite recent advances in pharmacological intervention, identification and prevention of processes leading to atherosclerotic plaque rupture remain incomplete. Understanding the molecular mechanisms that drive this process is a critical step toward development of therapies to slow or reverse progression of atherosclerosis. Clinical Perspective on p 604Currently, few validated targets are available for pharmacological treatment of atherosclerosis, and a limited number of diagnostic techniques can accurately predict either plaque progression or response to treatment. Gene expression microarray technology and systems biology allow comprehensive characterization of the pathological processes associated with atherosclerosis, making possible the identification of new targets to treat this disease and new diagnostic measures of disease progression. 2 To understand the underlying disease pathophysiology and gain insights into plaque biology that could facilitate the discovery of new therapies, we have undertaken gene expression profiling of human plaque. Because of its availability and documented similarity ...

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