Appeal No. 94-4009 Paper No. 32 Application No. 07/953,716 Page 11 increase in thickness. At this stage, the lipid composition of the intima consists mainly of phospholipids (lecithins, cephalins and sphingomyelins; [cited pages not of record]). Some cholesterol is present, but cholesterol esters are generally absent. We find nothing in Bowman that shows that atherosclerotic intimal thickening necessarily precedes other contributors to atherosclerosis like hyperlipidemia or hypercholesterolemia. We do, however, find a reasonable suggestion that it was conventional to delay both the development and the progression of atherosclerosis by treating hypercholesterolemia and hyperlipidemia (Bowman at 23.62, col. 2 ("Treatment of atherosclerosis")). Even if we accepted Appellants' narrower construction that treatment must occur before any atherosclerotic intimal thickening had occurred, Appellants identify hyperlipidemia as a promoter of smooth muscle cell activation (Paper No. 1 (Spec.) at 2). Consequently, Fujikawa's hyperlipidemia patients would inherently be treated for atherosclerotic intimal thickening. Note that, since the claimed treatment begins prior to atherosclerotic intimal thickening, the patients are still healthy in terms of intimal thickening. Consequently, the clinician would have to have had some reason to suspect that the patient would benefit from prophylactic treatment for intimal thickening. At the hearing, we askedPage: Previous 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 NextLast modified: November 3, 2007