Changes in the apoprotein composition of very low density lipoproteins in man following eating.

The concentrations of certain of the very low density human serum lipoprotein apoproteins were found to increase following a meal, while the concentrations of the majority of the apoproteins were found to be unaffected.     

Changes in the apoprotein composition of very low density lipoproteins in man following eating

Summary The concentration of certain of the very low density human serum lipoprotein apoproteins were found to increase following a meal, while the concentrations of the majority of the apoproteins were found to be unaffected. This work was supported by grants from the U.S. Public Health Service.     

Effect of low density lipoprotein and high density lipoprotein on sodium dodecyl sulphate precipitation of very low density lipoprotein from human serum.

In the presence of low density lipoprotein, the sodium sodecyl sulphate(SDS)-very low density lipoprotein(VLDL) complex sedimented, while in the presence of high density lipoprotein the complex floated. This SDS-VLDL aggregate floats at serum triglyceride to cholesterol ratio of 0.7-0.9 and sediments at a ratio of 0.2-0.5.     

High density lipoproteins in ischaemic heart disease.

High density lipoprotein cholesterol concentrations were significantly lower in ischaemic heart disease patients than in healthy subjects when age and sex-matched. This difference was, however, not observed in the older age group (greater than 60 years).     

Effect of low density lipoprotein and high density lipoprotein on sodium dodecyl sulphate precipitation of very low density lipoprotein from human serum

Summary In the presence of low density lipoprotein, the sodium sodecyl sulphate(SDS)-very low density lipoprotein(VLDL) complex sedimented, while in the presence of high density lipoprotein the complex floated. This SDS-VLDL aggregate floats at serum triglyceride to cholesterol ratio of 0.7–0.9 and sediments at a ratio of 0.2–0.5.     

Investigations on the role of low density lipoproteins in the pathogenesis of the essential carbohydrate-induced hypertriglyceridemia

Zusammenfassung Die mit physikochemischen Untersuchungen nachweisbaren LDL-Anomalien bei der essentiellen Hypertriglyceridämie lassen den Schluss zu, dass Störungen der LDL-Kinetik bei der Pathogenese dieser Krankheit eine wichtige Rolle spielen.     

High density lipoproteins in ischaemic heart disease

Summary High density lipoprotein cholesterol concentrations were significantly lower in ischaemic heart disease patients than in healthy subjects when age and sex-matched. This difference was, however, not observed in the older age group (>60 years).Acknowledgment. This investigation was supported by a grant from University of Nigeria, Nsukka.I am grateful to Prof. Barry Lewis, St. Thomas Hospital Medical School, London, for his expert advice.     

Lipoprotein lipase activity in normal human adipose tissue and its absence in human lipomas

Résumé Il a été trouvé que des spécimens de tissus souscutanés humains et des tissus adipeux omentaux hydrolyseraient un substrat triglycéride activé avec du plasma humain quand incubés dans un medium contenant de l'albumine bovine et du sulfate d'ammonium. Les spécimens de lipomes humains n'ont pas montré d'activité lipolytique signifiante. Les homogénates de lipomes n'ont pas diminué l'activité lipolytique des spécimens de tissus adipeux humains.     

An antibody to low density lipoprotein in diabetics

Summary The serum of 21/180 unselected diabetics contains a low titre antibody to human low density lipoprotein. A similar antibody was found in 10/88 persons with tuberculosis.     

Effect of low density lipoprotein on proteoglycan synthesis by aorta cells in culture.

Increasing the content of human serum low density lipoprotein in the growth medium led to greater incorporation of 35S-sulfate into proteoglycan (mostly into dermatan sulfate) by primary aorta cells but did not affect similar incorporation by fibroblast cells. These results suggest a mechanism which can explain the increased deposition of lipid in aorta due to hyperlipidemia.     

Inhibition of Rho-associated kinase relieves C5a-induced proteinuria in murine nephrotic syndrome

Childhood nephrotic syndrome is mainly caused by minimal change disease which is named because only subtle ultrastructural alteration could be observed at electron microscopic level in the pathological kidney. Glomerular podocytes are presumed to be the target cells whose protein sieving capability is compromised by a yet unidentified permeability perturbing factor. In a cohort of children with non-hereditary idiopathic nephrotic syndrome, we found the complement fragment C5a was elevated in their sera during active disease. Administration of recombinant C5a induced profound proteinuria and minimal change nephrotic syndrome in mice. Purified glomerular endothelial cells, instead of podocytes, were demonstrated to be responsible for the proteinuric effect elicited by C5a. Further studies depicted a signaling pathway involving Rho/Rho-associated kinase/myosin activation leading to endothelial cell contraction and cell adhesion complex breakdown. Significantly, application of Rho-associated kinase inhibitor, Y27632, prevented the protein leaking effects observed in both C5a-treated purified endothelial cells and mice. Taken together, our study identifies a previously unknown mechanism underlying nephrotic syndrome and provides a new insight toward identifying Rho-associated kinase inhibition as an alternative therapeutic option for nephrotic syndrome.     

Presence in and effects of pineal indoleamines at very low level of phylogeny

The unicellular organism Tetrahymena contains serotonin and is able to take up the hormone from its mileiu. The serotonin content of the cell changes as a function of the presence of foreign exogenous hormones. This indicates a possible role of serotonin as a chemical mediator. Exogenous serotonin stimulates the RNA synthesis of Tetrahymena, and it was the only one among the hormones studied which kept the RNA level durably high. Serotonin stimulates phagocytosis and growth of Tetrahymena, and its precursors also stimulate growth. Serotonin can imprint Tetrahymena, and as a consequence of this the effect of the hormone increases in the case of further encounters. Treatment with serotonin-related molecules soon after imprinting can reduce the effect of imprinting. Melatonin can contract the pigment cells of Planaria; however, its precursors serotonin and tryptamine can do this more intensely. Both melatonin and serotonin can influenc the regeneration of Planaria, with effects which differ when different phenomena are studied. Evolutionary theories are discussed.     

Reduced bactericidal capacity of polymorphonuclear leucocytes in nephrotic syndrome and effect of steroid therapy

Zusammenfassung Es wird der Nachweis erbracht, dass die bakterizide Wirkung der polymorph-kernigen Leukozyten bei Patienten mit nephrotischem Syndrom vermindert ist und dass Prednisolon einen günstigen Einfluss auf die Bakterizidie polymorph-kerniger Leukozyten beim nephrotischen Syndrom hat.     

Net transport of cholesterol from cells of the human EA.hy 926 endothelial cell line to high density lipoproteins

EA.hy 926 cells, a human endothelial cell line, show characteristics of differentiated endothelial cells. The cells express saturable binding of apo E-free¹²⁵I-high density lipoprotein₃ (HDL₃). B_max increased from 71 to 226 ng HDL₃ bound/mg cell protein after cholesterol loading of the confluent endothelial cells with cationized low density lipoprotein (LDL). The affinity did not change after cholesterol enrichment (K_d was 37 g HDL₃ protein/ml for control cells and 31 g/ml, for loaded cells). Incubation of cholesterol-loaded EA.hy 926 cells with native HDL and LDL had different effects on cellular cholesterol levels. Incubation with HDL decreased both esterified and unesterified cellular cholesteryl, but LDL did not change total cellular cholesterol However, LDL tended to increase cellular cholesteryl esters, with a concomitant decrease of unesterified, cellular cholesterol. Incubation of endothelial cells with both HDL and LDL also resulted in decreased total cellular cholesterol levels. These data show that cationized LDL-loaded human endothelial EA.hy 926 cells can be used to study the net transport of cellular cholesterol to HDL, the first step in reverse cholesterol transport.     

Effect of vitamin A deficiency on rat hepatic and colon epoxide hydrase.

Rat liver microsomes and homogenized mucosal linings prepared from vitamin A-supplemented and deficient male rats were used in metabolic studies of 7-3H-styrene oxide. The colon tissue in deficient animals exhibits a significantly higher value of Vmax than the same tissue from vitamin-supplemented animals. The implications of this finding in addition to our earlier observation 10 is discussed in relation to colon carcinoma.     

Mosaicism for sulfoiduronate sulfatase deficiency in carriers of Hunter's syndrome

Summary Using an assay for sulfoiduronate sulfatase based on the degradation of³⁵S mucopolysaccharides in a cellfree system, two clonal populations have been demonstrated in fibroblasts of heterozygotes for Hunter's syndrome. The locus responsible for sulfoiduronate sulfatase deficiency in thisX-linked mucopolysaccharidosis is therefore subjected to dosage compensation in females.Acknowledgments. The technical assistance of Mr.Antonio De Falco and Mrs.Carmela Salzano is gratefully acknowledged. The authors are indebted to Dr.H. Kresse (Münster, BRD) for helpful suggestions.