Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was conducted to compare the effects of experimental immune complex disease on the development of glomerulonephritis and aortic and coronary artery atherosclerosis. Fourteen adult male macaques (Macaca fascicularis) were fed a mildly atherogenic diet. Ten of these animals were given repeated intravenous injections of bovine serum albumin (BSA), and the remaining 4 were given similar injections of saline. Three of the monkeys given BSA responded with a high antibody titer, 4 with a moderate titer, and 3 with a low level titer to BSA. In all 4 monkeys with the moderate antibody response glomerulonephritis developed, characterized by increased glomerular cellularity, electron-dense deposits in the glomerular capillary basal lamina, and deposits of IgG, IgM, C3, C4, and BSA. Glomerulonephritis was not seen in the other 6 monkeys given BSA or the 4 control monkeys. Aortic lesions seen at necropsy consisted of a few fatty intimal streaks with no differences between test monkeys (given BSA) and control monkeys (given saline). There was no correlation between total serum cholesterol concentration, high-density lipoprotein cholesterol concentration, or BSA antibody levels and the degree of aortic atherosclerosis. Immunochemical stains for immunoglobulins and complement components revealed increased intimal staining when intimal thickness increased. Medial staining for immunoglobulin and complement components appeared to be slightly increased in monkeys with moderately high-level titers of BSA. The extent of atherosclerosis in the coronary arteries of monkeys given BSA was greater than in the control animals. Differences in the extent and severity of the atherosclerotic lesions were most pronounced in the proximal portions of the main coronary arteries, suggesting an increased susceptibility of this site to immune-complex-exacerbated atherosclerosis. In addition to the increased lesion severity in monkeys given BSA, there were numerous granulocytes seen within, attached to, and penetrating into the intima of the coronary lesions. No correlation was seen between the development of glomerulonephritis and either aortic or coronary artery atherosclerosis.
 ...
PMID:Increased atherosclerosis and glomerulonephritis in cynomolgus monkeys (Macaca fascicularis) given injections of BSA over an extended period of time. 622 52

The results of integrated estimations of a complex of lipid indices are presented. Their abnormalities are considered to be atherosclerosis risk factors in the evolution of glomerulonephritis and its different variants, types and stages. The quantitative and qualitative peculiarities of the indicated abnormalities are revealed, in particular, their major expressiveness in chronic form, nephrotic variant and in the stage of renal failure. Two aspects of correction of actual abnormalities are singled out: 1. indirect, i.e. treatment of the renal pathologic process with preparation of pathogenetic therapy (glucocorticoids, indomethacin), and 2. direct, i.e. with medications exerting a corrective influence on lipid metabolism (clofibrate, nicotinic acid, curantil). The selection of corrective methods is determined by the stage of disease and by the character of the changes in lipid metabolism.
 ...
PMID:Abnormalities of lipid metabolism and methods of their correction in patients with glomerulonephritis. 653 84

Serum and lipoprotein lipids were determined in 42 female transplant recipients and compared with age-matched and serum lipid-matched normal subjects. Eight patients had glomerulonephritis as the pre-transplant etiology of renal disease, 22 had analgesic nephropathy, 6 polycystic kidneys and 6 ureteric reflux. A number of abnormalities were observed: (i) Serum triglycerides and phospholipids were elevated in all patients. Serum cholesterol levels were increased in analgesic nephropathy, polycystic kidney and ureteric reflux, but not in glomerulonephritis patients. The serum esterified/free cholesterol ratio was reduced in all patients except those with polycystic kidneys as the pre-transplant diagnosis; (ii) All VLDL lipids were raised in transplant patients regardless of etiology of renal disease prior to transplantation; (iii) LDL lipids, cholesterol, triglyceride and phospholipid were elevated in analgesic nephropathy, polycystic kidney and ureteric reflux patients, but were normal in glomerulonephritis patients: (iv) HDL cholesterol and triglycerides were elevated in all patients regardless of etiology. HDL phospholipid levels also tended to be raised, but this was significant only in glomerulonephritis patients. Lipoprotein--lipid ratio data indicated that lipoprotein--lipid composition deviated less from normal in glomerulonephritis patients than in the other patient groups.
Atherosclerosis 1980 Sep
PMID:The influence of pre-transplant etiology of renal disease on lipoprotein lipids in female renal allograft receipients. 700 88

Serum and lipoprotein lipids have been compared in male and female transplant recipients with glomerulonephritis or analgesic nephropathy as etiology of pre-transplant renal disease, and a number of differences were observed. (1) Serum cholesterol and phospholipid levels were elevated in glomerulonephritis and female analgesic nephropathy, but not in male analgesic nephropathy patients. (2) Glomerulonephritis patients had normal low density lipoprotein (LDL) cholesterol levels whereas these were elevated in female and depressed in male analgesic nephropathy patients. (3) LDL phospholipid, on the other hand, was normal in male and elevated in female transplant recipients irrespective of etiology of pre-transplant renal disease, while high density lipoprotein (HDL) phospholipid levels were elevated in female glomerulonephritis patients only. Mild hypertriglyceridemia and a tendency to increased HDL cholesterol were observed in all patients. These results provide further evidence for the complexity of lipoprotein lipid abnormalities in renal disease.
Atherosclerosis 1981 May
PMID:Lipoprotein lipids in renal transplant recipients of different pre-transplant etiology of renal disease. A comparison of male and female patients. 701 3

Cultured mouse peritoneal macrophages secrete a growth-promoting activity that stimulates 3 types of nonlymphoid mesenchymal cells in vitro: fibroblasts, vascular smooth muscle, and vascular endothelium. Production of this macrophage-derived growth factor (MDGF) is directly related to the number of viable macrophages and their time in culture, and is independent of platelet- or plasma-derived serum growth factors. Treatment of cultured macrophages with latex, bacterial lipopolysaccharide, or phorbol myristate acetate results in increased growth factor activity. Preliminary biochemical characterization of MDGF indicates that it is a heat labile (100 degrees C, 2 min), non-dialyzable protein, which contains at least 1 essential disulfide bond. Growth-promoting activity is not adsorbed by CM-Sephadex chromatography, under conditions that effectively remove platelet-derived growth factor(s). Serine protease activity is not required for the action of MDGF. Secretion of macrophage-derived growth factor may be relevant to the function of mononuclear phagocytes in several pathologic processes, including the neovascularization and fibroplasia of wound healing, smooth muscle hyperplasia in atherosclerosis, and proliferative glomerulonephritis.
 ...
PMID:Stimulation of nonlymphoid mesenchymal cell proliferation by a macrophage-derived growth factor. 720 74

Clusterin is a heterodimeric glycoprotein produced by a wide array of tissues and found in most biologic fluids. A number of physiologic functions have been proposed for clusterin based on its distribution and in vitro properties. These include complement regulation, lipid transport, sperm maturation, initiation of apoptosis, endocrine secretion, membrane protection, and promotion of cell interactions. A prominent and defining feature of clusterin is its induction in such disease states as glomerulonephritis, polycystic kidney disease, renal tubular injury, neurodegenerative conditions including Alzheimer's disease, atherosclerosis, and myocardial infarction. The expression of clusterin in these states is puzzling, from the specific molecular species and cellular pathways eliciting such expression, to the roles subserved by clusterin once induced. This review will discuss these physiologic and pathophysiologic aspects of clusterin and speculate on its role in disease.
 ...
PMID:Clusterin: physiologic and pathophysiologic considerations. 764 19

Clusterin is a widely distributed glycoprotein with a wide range of biologic properties. A prominent and defining feature of clusterin is its marked induction in such disease states as glomerulonephritis, cystic renal disease, renal tubular injury, neurodegenerative conditions, atherosclerosis, and myocardial infarction. The expression of clusterin in these states is intriguing given the apparent incongruity of the conditions listed, the variety of stimuli eliciting such expression, and the multiple proposed roles once induced. This review will outline the conditions associated with clusterin induction and speculate on its role in disease.
 ...
PMID:The role of clusterin in tissue injury. 765 21

Human leucocyte elastase is a serine proteinase involved in phagocytosis, defence against invading micro-organisms, degradation of elastin, collagen, proteoglycans, fibrinogen and fibrin, being also responsible for the digestion of damaged tissues and of the bacterial degradation products. Lack of the enzyme regulation is at the basis of pathological states, such as pulmonary emphysema, cystic fibrosis, rheumatoid arthritis, atherosclerosis and glomerulonephritis. A detailed characterisation of the enzyme:inhibitor recognition process, based on extensive thermodynamic, kinetic and structural information, as well as on the comparative analysis with the homologous proteinase from porcine pancreas, is reported in the present review.
 ...
PMID:Molecular bases for human leucocyte elastase inhibition. 804 99

The small leucine-rich proteoglycan biglycan is involved in several physiological and pathophysiological processes through the ability of its core protein to interact with other extracellular matrix molecules and transforming growth factor-beta (TGF-beta). To learn more about the regulation of biglycan core protein expression, we have cloned and sequenced 1218 base pairs from the 5'-flanking region of the human biglycan gene, demonstrated functional promoter activity, and investigated the molecular mechanisms through which various agents modulate its transcriptional activity. Sequencing revealed the presence of several cis-acting elements including multiple AP-2 sites and interleukin-6 response elements, a NF-kappaB site, a TGF-beta negative element, and an E-box. The TATA and CAAT box-lacking promoter possesses many features of a growth-related gene, e.g. a GC-rich immediate 5' region, many Sp1 sites, and the use of multiple transcriptional start sites. Transient transfections of the tumor cell lines MG-63, SK-UT-1, and T47D with various biglycan 5'-flanking region-luciferase reporter gene constructs showed that the proximal 78 base pairs are sufficient for full promoter activity. Several agents among them interleukin-6, and tumor necrosis factor-alpha. were capable of altering biglycan promoter activity. However, in MG-63 cells, TGF-beta1 failed to increase either activity of the biglycan promoter constructs or specific transcription from the endogenous biglycan gene. Since TGF-beta1 also did not alter the stability of cytoplasmic biglycan mRNA as determined from Northern analysis after inhibition of transcription with 5,6-dichloro-1beta-D-ribofuranosylbenzimidazole, an as yet unidentified nuclear post-transcriptional mechanism was considered responsible for the TGF-beta effect in this cell type. These results might help to elucidate the molecular pathways leading to pathological alterations of biglycan expression observed in atherosclerosis, glomerulonephritis, and fibrosis.
 ...
PMID:Transcriptional regulation of the human biglycan gene. 866 74

Some fibrinolytic parameters, whole blood and plasma serotonin were studied in normotensive and hypertensive patients with glomerulonephritis. Diminished activity of tissue plasminogen activator (tPA) and a significant prolongation of the euglobulin clot lysis time was observed in hypertensive and normotensive patients with glomerulonephritis when compared to healthy volunteers. Antigen and activity of inhibitor of tissue plasminogen activator (PAI) was found to be higher in hypertensive patients relative to control group. Whole blood serotonin was significantly lower, whereas plasma serotonin was higher in normotensive and hypertensive patients with glomerulonephritis when compared to healthy subjects. Impairment in fibrinolysis and elevated plasma serotonin levels may contribute to the increased risk of thromboembolic complications and accelerated atherosclerosis in these patients.
 ...
PMID:[Fibrinolytic and peripheral serotonergic system in patients with glomerulonephritis]. 883 42


<< Previous 1 2 3 4 5 6 7 8 Next >>