The "turning off" of excessive cell replicative activity in advanced XXXX of @entity1707 by a regression diet.

@entity1707 @entity39 @entity665 @entity731 @entity165
We studied progression of @entity731 in the coronaries and abdominal aortas of @entity1707 fed hyperlipidemic (HL) diets producing serum @entity165 levels of about 700 mg/dl for up to 18 months with killings at 9, 13.5 and 18 months on diet. We studied changes in lesions in subsets given after 9 months on the HL diet a low fat, low @entity165 mash diet with killings at 4.5 and 9 months on the regression diet. Lesion cell numbers were evaluated using mean nuclear profiles per cross-section (Np/Cx) in an anatomically defined portion of artery as an index. Lesion sizes were evaluated using mean cross-sectional area (area/Cx) as an index. Tritiated thymidine labeling indices (LI) were used as an index of cell proliferative activity in the coronaries. We also determined the percentage of lesions occupied by lipid rich calcific @entity39 . For further comparisons all of the same values were determined for normal intimal cell masses (ICM) in control groups fed a low fat, low @entity165 mash diet throughout. The @entity731 in the HL @entity1707 appeared to arise mainly in the ICM. These became lesions and increased tremendously in size and cell numbers. The greatest increase was in the abdominal aorta even when lesion values were normalized by being expressed as percentages of the wall (intima + media). Lipid-rich calcific @entity39 occupied about 25% of the lesion by 9 months and the percentage was similar at 18 months although size of lesions and their @entity39 regions had increased 3-fold over the 9-month interval. Lesion @entity665 LIs were 3-4-fold greater than in the control ICM. In the period 9-18 months on an HL diet lesions increased about 3-fold in size and cell numbers. In the @entity1707 put on a regression diet for the 9-18 month period growth of the lesions stopped completely. In fact, there was a numerical decrease in lesion sizes and cell numbers and this was statistically significant for the left anterior descending coronary. The lesion growth stoppage was partly accounted for by the "turning off" of excessive DNA synthesis activity of the lesion cells as indicated by the return of @entity665 LIs to the normal values in the mash controls. Another factor was the lack of increase and in fact marked reduction in the size of the regions of lipid rich @entity39 .(ABSTRACT TRUNCATED AT 400 WORDS)
