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Biomedical subjects

H F Hoff

Publications and source records attributed to H F Hoff.

At least 91 records · Page 5Linked to original sources
PubMed1975

Localization patterns of plasma apolipoproteins in human atherosclerotic lesions.

The localization patterns of human plasma lipoproteins and their respective apoproteins and of neutral lipid were determined in normal and atherosclerotic arteries. Specific antisera were prepared against plasma low-density lipoproteins(LDL) and their apoproteins (apoB), high-density lipoproteins(HDL) and one of their major apoproteins (apoA-I1, and apoC-III, which is a major apoprotein of very low-density lipoproteins (VLDL). Using immunofluorescence techniques, the various antigens were localized in arterial samples obtained at surgery or autopsy. The three apoproteins and neutral lipid were localized to the same tissue areas, namely, lipid core regions and certain connective tissue of atherosclerotic lesions, in 61% of the fibrous plaques and 48% of the fatty streaks examined. In marked contrast, none of the uninvolved arterial regions showed the presence of all four factors together. As controls, the localization of other serum proteins was also determined in these arteries using immunofluorescence techniques. Fibrinogen was associated with regions of maximum complementary localization of factors in 37% of the fibrous plaques and 64% of the fatty streaks. However, albumin was found in only 4-5% of these same regions. The present results suggest that not only LDL but also HDL and VLDL or their respective apoproteins as well as fibrinogen are specifically retained by certain tissue components of the atherosclerotic lesion.

Adolescent↗
PubMed1975

Lipoproteins in atherosclerotic lesions. Localization by immunofluorescence of apo-low density lipoproteins in human atherosclerotic arteries from normal and hyperlipoproteinemics.

Using immunofluorescence techniques, apoLDL, the major protein component of human plasma low and very low density lipoproteins was localized in athersclerotic lesions from the aorta, coronary, and carotid arteries in human normolipoproteinemic, type II, and type IV hyperlipoproteinemics. Although no apoLDL was detected in uninvolved arteries, atheromas from advanced lesions as well as certain collagen and elastic fibers from both fatty streaks and advanced lesions were positive for apoLDL. This localization pattern was the same in each lipemic group, except for the presence of apoLDL in some intimal cells from type II cases. However, extensiveness of apoLDL localization was greatest in the type II group, but equal in the normolipemic and type II group. This may be explained by the high concentration gradient between plasma and tissue for apoLDL in the type II group.

Adult↗
PubMed1973

Differential interference contrast microscopy of human atherosclerotic lesions.

Differential interference contrast microscopy was employed to study sections of human cerebral arteries and aorta. When this procedure was used to observe 0.5-mu-thick sections of plastic-embedded arteries, images were obtained with greater definition of detail than corresponding micrographs of the area using conventional bright-field microscopy. Since structures with different refractive indices are shown in geometric relief from one another, an apparent three-dimensional image is seen, which, together with the theoretically higher resolution and contrast achieved by this technic, gives an image with definition between conventional light and low magnification electron microscopy. The morphology of fatty streak lesions with aggregates of round and elongated lipid-filled cells was demonstrated, and clear images of different forms and sizes of intracellular lipid droplets were illustrated at magnifications around 1000. In atheromatous plaques, intra- and extracellular lipid droplets were observed, some with partially extracted cores or surfaces, as were amorphous lipid droplets coalescing with crystals whose centers had been extracted. We conclude that this optical accessory to a research photomicroscope is a valuable supplemental tool in studies on the morphology of atherosclerotic lesions.

Aorta↗
PubMed1972

A histoenzymatic study of human intracranial atherosclerosis.

A light microscopy study on the localization of enzyme activity within atherosclerotic human intracranial arteries was performed on autopsy material obtained within 4 hours of death. The data suggests that the atherosclerotic process first goes through a proliferative phase and then a degenerative phase culminating in the formation of a plaque. In the proliferative phase, smooth muscle cell proliferation has formed a thickened intima. Tetrazolium reductase, adenosine triphosphatase (ATPase) and adenosine monophosphatase (AMPase) activities are present in these cells, while all dehydrogenases and acid phosphatase activities were weak or not present. As the degenerative phase commences, an area of necrosis, lipid and macrophage accumulation is formed on the lumen side of the elastica. This area increases in size until a plaque is formed. Unsaturated polar and nonpolar lipid, cholesterol, alpha-glycerophosphate dehydrogenase, acid phosphatase, and AMPase activities are associated with these areas and in foam cells, which are often found in the thickened intima of the proliferative phase. Tetrazolium reductase and ATPase activities decrease in the thickened intima as the area of necrosis increases in size, while dehydrogenase activity, except that for alpha-glycerophosphate, remains low or not present. Patterns of enzyme alterations for various stages of the disease process in intracranial arteries, the aorta and coronary arteries suggest a similar, if not identical, progression of the atherosclerotic process, irrespective of known differences in the prevalence of atherosclerosis.

Acid Phosphatase↗