Elevated carcinoembryonic antigen levels correlating with disease recurrence in a patient with adenoid cystic carcinoma.

Background: Carcinoembryonic antigen (CEA) is an oncofetal glycoprotein involved in cell recognition and adhesion. Serum CEA has been extensively studied as a potential chemical marker for malignancy, most notably in patients with colon carcinoma. Serum CEA measurements have not been reported for patients with salivary gland carcinomas.

erbB-2 and myc oncoproteins in sera and tumors of breast cancer patients.

This study compares the prevalence of elevated serological levels of erbB-2 and myc proteins in 36 breast cancer patients and 25 healthy, ambulatory female controls. The controls were frequency matched to the cases by age and ethnicity. Oncoprotein levels were determined blind to the "case-control status" of the individual from whom the specimen was derived.

Fine-needle aspiration of breast biopsy specimens: correlation of histologic and cytologic findings.

The accuracy of fine-needle aspiration (FNA) cytologic diagnosis of nonpalpable breast lesions and the prevalence of neoplasm occurring in areas unrelated to the radiologic abnormality were studied. Template-guided FNA cytologic examination was performed in 101 surgically excised breast specimens. The exact area of the mammographic abnormality was aspirated with radiographic control.

Virus-induced atherosclerosis. Herpesvirus infection alters aortic cholesterol metabolism and accumulation.

Infection of normocholesterolemic, specific-pathogen-free chickens with Marek's disease herpesvirus (MDV) has been shown histologically to lead to chronic atherosclerosis like that in humans. The development of herpesvirus-induced atherosclerosis in vivo and the presence of specific Marek's antigen within aortic cells suggested that MDV infection may modify lipid metabolism and lead to significant lipid accumulation. Experiments reported herein were designed to determine the types and quantity of lipid present in aortas from MDV-infected and uninfected chickens between 2 and 8 months of age following infection and assess one possible mechanism of lipid accumulation by evaluating the effect of MDV infection on aortic cholesterol and cholesteryl ester (CE) metabolism.

Insoluble low-density lipoprotein-proteoglycan complexes enhance cholesteryl ester accumulation in macrophages.

The interaction of arterial proteoglycans (PGs) and low-density lipoproteins (LDLs) has been postulated to be an important factor in extracellular cholesterol accumulation in the arterial wall. In the present study, insoluble complexes of LDL and PG (LDL-PG) were prepared and their effects on cholesteryl ester accumulation in mouse peritoneal macrophages was tested. The cholesteryl ester content of macrophages incubated with LDL-PG for 3 days was greater than 20 times that observed in cells incubated with LDL alone.

Altered glycosaminoglycan metabolism in injured arterial wall.

Glycosaminoglycans (GAG) are believed to be important in the pathogenesis of atherosclerosis. We have previously demonstrated that areas of injured aorta that have been re-endothelialized accumulate increased amounts of lipid and GAG when compared to areas remaining de-endothelialized. We have now examined the net incorporation of labeled precursors into the individual GAG present in both re-endothelialized and de-endothelialized areas of rabbit aorta.

Lipoprotein-heparin-fibronectin-denatured collagen complexes enhance cholesteryl ester accumulation in macrophages.

The sequestration of low-density lipoprotein (LDL) by components of the vascular extracellular matrix has long been recognized as a contributing factor to lipid accumulation during atherogenesis. The effects, however, that components of the extracellular matrix might have on LDL catabolism by scavenger cells have been little investigated. For these purposes we have prepared insoluble complexes of LDL, heparin, fibronectin, and denatured collagen (gelatin) and examined their effects on lipid accumulation, LDL uptake and degradation, and cholesteryl ester synthesis in mouse peritoneal macrophages.

Lipoprotein and albumin accumulation in reendothelialized and deendothelialized aorta.

Although arterial injury is believed to be an important factor in the pathogenesis of atherosclerosis, little is known about lipoprotein accumulation in the injured arterial wall. In experiments reported here, the authors quantitated the accumulation of iodinated lipoprotein and albumin in reendothelialized and deendothelialized rabbit aorta. Results indicate that over the experimental period, insudated lipoprotein but not albumin is retained in the reendothelialized aorta.

Effect of endothelium on glycosaminoglycan accumulation in injured rabbit aorta.

Previous studies have indicated that reendothelialized regions of injured rabbit aortas are more susceptible to diet-induced atherosclerosis than persistently deendothelialized regions or uninjured aortas. However, the mechanism responsible for this selective lipid deposition is not understood. One possibility is that these regions differ with respect to the quantity and type of glycosaminoglycan-containing proteoglycans which are known to interact with lipoproteins.

Herpesvirus-induced atherosclerosis in chickens.

Repeated experiments have established that infection with Marek's disease herpesvirus (MDV) leads to atherosclerosis in specific pathogen free (SPF) normocholesterolemic chickens. Neither normocholesterolemic nor hypercholesterolemic uninfected SPF chickens develop this disease. The MDV-induced arterial disease is remarkably similar to chronic human atherosclerosis.

Arterial neutral cholesteryl esterase. A hormone-sensitive enzyme distinct from lysosomal cholesteryl esterase.

We describe here an activable neutral cholesteryl esterase (EC 3.1.1.

Prostacyclin modulates cholesteryl ester hydrolytic activity by its effect on cyclic adenosine monophosphate in rabbit aortic smooth muscle cells.

We tested the hypothesis that prostacyclin (PGI2), 6-keto-prostaglandinF1 alpha(6-keto-PGF1 alpha), and several E series prostaglandins (PG) may affect the activity of cholesteryl ester (CE) hydrolase since our previous experiments indicated that smooth muscle cells (SMC) in neointima of injured rabbit aorta (a) acquire the capacity to produce PGI2 and (b) have increased lysosomal CE hydrolytic (acid cholesteryl ester hydrolase [ACEH])activity. Using cultured SMC from rabbit thoracic aorta, we demonstrated that PGI2, 6-keto-PGF1 alpha, and 6-keto-PGE1 enhanced ACEH activity fourfold. No significant effects on ACEH activity were observed with PGE1 or PGE2.

Studies on the exocytosis of cultured mast cells derived from mouse bone marrow.

Mast cells were obtained from mouse bone marrow cells cultured for 14 days in medium derived from Concanavalin A (Con A) stimulated mouse spleen cells. Upon passive sensitization of the cultured cells with immunoglobulin E (IgE), histamine release from mast cells was approximately 200% above control within 1 min of incubation with anti-IgE. The calcium inonophore A 23187 also evoked a concentration-dependent (10(-8) M to 6 x 10(-7) M) histamine release following a 6 min incubation.

Diet-induced hypercholesterolemia inhibits the recovery of prostacyclin production by injured rabbit aorta.

The effect of diet-induced hypercholesterolemia on the recovery of prostacyclin (PGI2) synthetic capacity was assessed at the luminal surface of previously injured rabbit aorta. Prostacyclin synthesis and release were measured by radioimmunoassay following arachidonic acid stimulation of deendothelialized and reendothelialized aortas of hypercholesterolemic rabbits. Assay of PGI2 production by aorta was performed at 15, 35, and 70 days following removal of endothelium with a balloon catheter.

Herpesvirus infection enhances cholesterol and cholesteryl ester accumulation in cultured arterial smooth muscle cells.

In our previous experiments, atherosclerosis similar to that in humans was reproducibly induced in both normocholesterolemic and hypercholesterolemic specific-pathogen-free (SPF) chickens by infection with Marek's disease herpesvirus (MDV). In contrast, uninfected chickens fed either relatively cholesterol-poor or cholesterol-supplemented diets did not develop this arterial disease. In experiments reported here, the hypothesis that infection of arterial smooth muscle cells (SMCs) with MDV would enhance lipid accumulation in these cells was tested.

Recovery of prostacyclin production by de-endothelialized rabbit aorta. Critical role of neointimal smooth muscle cells.

Prostacyclin (PGI2) synthetic capacity was assayed at the surface of aortas at various intervals after removal of endothelium with a balloon catheter. Results were correlated with morphologic changes in the vessel wall seen by light microscopy, scanning and transmission electron microscopy. To assay PGI2 synthetic capacity, we applied an incubation chamber to the luminal surface of the aortas; after arachidonic acid stimulation we assayed the PGI2 synthesized with a bioassay and radioimmunoassay.

Endothelium modifies the altered metabolism of the injured aortic wall.

Results of previous experiments in this laboratory indicate that lipids, especially cholesterol and cholesteryl ester, preferentially accumulate in re-endothelialized, as compared with de-endothelialized, areas of aorta (Am J Pathol 1980, 99:81-104). In the experiments reported here, the hypothesis that this lipid accumulation results from alterations in arterial wall metabolism induced by injury and modified by endothelium was tested. Activities of the two cholesterol-ester-metabolizing enzymes acyl CoA: cholesterol acyltransferase and acid cholesteryl esterase were assayed in uninjured aortas and in de-endothelialized and re-endothelialized areas of balloon-catheter-injured aortas from normocholesterolemic and hypercholesterolemic rabbits.

Enhancement of cholesterol and cholesteryl ester accumulation in re-endothelialized aorta.

The purpose of the experiments reported here was to determine chemically the character and quantity of lipid in re-endothelialized and de-endothelialized areas of rabbit aortas. The aortas of 22 rabbits, Groups I and II, were de-endothelialized with a balloon catheter, and the rabbits were maintained on a lipid-poor diet for 4 weeks. Thirteen rabbits, Group II, were then fed an egg-supplemented diet for 6 weeks.

Atheroarteriosclerosis induced by infection with a herpesvirus.

Atheroarteriosclerosis closely resembling that in humans was induced in normocholesterolemic and hypercholesterolemic chickens by infection with Marek's disease herpesvirus (MDV). Four comparably sized groups of chickens were used. Each group was initially fed a diet relatively poor in cholesterol.

Role of endothelium and hypercholesterolemia in intimal thickening and lipid accumulation.

In experiments reported here we tested the hypothesis that persistent absence of endothelium favors intimal thickening, lipid accumulation, and atherosclerosis. Rabbit aortas were de-endothelialized with a balloon catheter at Day 0. Initially, all rabbits were fed a diet low in lipid.

Virus-induced atherosclerosis.

Of four groups of chickens, two (groups I and II) were infected with MDV and two were not (groups III and IV). Groups I and III were fed diets low in lipid, and groups II and IV were fed cholesterol-supplemented diets. Striking grossly visible atherosclerotic lesions were seen in large coronary arteries, aortas, and major aortic branches of infected normocholesterolemic and hypercholesterolemic chickens (groups I and II).