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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:e155.)
© 2008 American Heart Association, Inc.

In Memoriam

Ross Gerrity, 1945–2008

J.A. Berliner; C.C. Hedrick

From the University of California, Los Angeles (J.A.B.) and the University of Virginia, Charlottesville (C.C.H.).

Correspondence to J.A. Berliner, 13-186 Center for Health Sciences, UCLA, Los Angeles, CA 90024-1723. E-mail jberliner@mednet.ucla.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

We are very sad to report that Dr Ross Gerrity died of a heart attack at his home in Augusta, Ga on Tuesday, July 1, 2008. Ross played a major role in our understanding of the process of atherosclerosis over a period of over 40 years. He was an outstanding pathologist who was also interested in disease mechanisms. His major discoveries included the recognition that in normal animals the areas of aorta susceptible to atherosclerosis had a different cellular composition.¹ He showed that, in animals fed a high-fat diet, lipoproteins first accumulated selectively in these susceptible areas. Today, the idea that inflammation plays an important role in the initiation of atherosclerosis is well accepted. However, in Ross Gerrity’s early career the role of monocytes was considered relatively unimportant. A major contribution of his research was recognition of the predominant role of monocytes in the process of atherogenesis. Ross was the first to document the early entry of monocytes but not neutrophils into the susceptible areas of the vessel wall in cholesterol-fed animals.^2,3 These 2 papers were recognized by Nature Medicine as among the 100 most significant of the 20th century. He demonstrated that these monocytes took up the lipid that had accumulated, and that after some months smooth muscle cells proliferation was also increased in these areas. He documented that monocyte chemotactic factors accumulated in the lesion areas and, in collaborative studies with the UCLA group, that synthesis of one of the chemotactic factors, MCP-1, was induced by incubating endothelial . . . [Full Text of this Article]