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TSRI Scientific Report 2004



Cover Artwork


On the front cover: In 1918, the great flu pandemic swept the world, killing an estimated 20 million to 40 million people, making it the largest and most destructive outbreak of any infectious disease in recorded history. The cover illustrates the devastation and the scale of the epidemic that the world experienced in 1918 (photograph of influenza ward at Camp Funston, Kansas). From another army ward in Fort Jackson, South Carolina, lung biopsy material was removed from a dead soldier and fixed in formalin. A section stained with hematoxylin and eosin (overlay) shows acute bronchiolitis and alveolitis. This lung sample was recently examined by Jeffery Taubenberger, M.D., Ph.D. Using reverse transcriptase–polymerase chain reaction, he found that the sample contained influenza virus RNA, enabling deduction of the coding sequence for the viral hemagglutinin (partial sequence of the 1918 gene at top in background). From this reassembled gene, the crystal structure of the 1918 hemagglutinin was determined by James Stevens, Ph.D., in the laboratory of Ian A. Wilson, D.Phil., Department of Molecular Biology, Scripps Research. Both are members of 1918 flu consortium funded by the National Institutes of Health. Members of the consortium are using a multidisciplinary approach to understand the virulence of this extinct virus. Photos courtesy of the National Museum of Health and Medicine and Dr. Taubenberger, Armed Forces Institute of Pathology, Washington, D.C.
 

Inside front cover: Detail (circular inset) of an atherosclerotic lesion in the intima of an artery and initial stages of removal of cholesterol from the intima via the reverse cholesterol transport pathway. In atherosclerosis, circulating monocytes infiltrate the vessel intima in response to inflammatory mediators. Once there, the monocytes differentiate into macrophages, take up cholesterol, and become foam cells. The only way these foam cells can remove their intracellular stores of cholesterol is by actively transporting the cholesterol out of the cell through the actions of the ABC-A1 cassette transporter. Only preβ-high-density lipoprotein (preβ-HDL), composed of a single apolipoprotein A-I (apoA-I) molecule, can accept cholesterol from macrophages. This preβ-HDL is derived from native HDL spheres within the intima and is a crucial rate-limiting step. Concentrations of apoA-I in the plasma are a major determinant of the size of atherosclerotic lesions. The recent discovery that phospholipid transfer protein (PLTP), a key molecule responsible for the generation of preβ-HDL from HDL, is secreted in large amounts by foam cells loaded with cholesterol suggests that PLTP may be a therapeutic target. Work done by Linda K. Curtiss, Ph.D., David T. Valenta, Ph.D., and Catherine Desrumaux, Ph.D., Department of Immunology. Image by Dr. Valenta.

Inside back cover: Electron cryomicroscopy and image reconstruction of 4 types of flock house virus particles that differed in RNA and protein content revealed almost identical capsid shells (gray scale). Despite differences in the encapsidated RNA (electrophoretic profiles in center of figure), a substantial fraction of the packaged nucleic acid, either viral or heterologous, was organized as a dodecahedral cage of duplex RNA. Molecular graphics by Kelly A. Dryden, Ph.D., and Mark Yeager, M.D., Ph.D., Department of Cell Biology. For details, see reports from the laboratories of Anette Schneemann, Ph.D., Department of Molecular Biology, and Dr. Yeager.