Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The intravenous fat-tolerance test and serum lipid and lipoprotein measurements were carried out in ninety-three normal subjects, fifty-one patients with ischaemic heart disease and thirty patients with peripheral vascular disease. 2. The fractional turnover rate of exogenous triglyceride was significantly slower in patients with ischaemic heart disease and in patients with peripheral vascular disease than in normal men. The rate was also slower in normal men than normal women. 3. Serum triglyceride and cholesterol concentrations were higher in both vascular disease groups than in control subjects. 4. The proportion of both groups of patients who had a subnormal fractional turnover rate of exogenous triglyceride was 35%, and 32% of patients had hypertriglyceridaemia in the fasting state; 27% of patients were hypercholesterolaemic. 5. Although the intravenous fat-tolerance test did not provide significantly better discrimination between cardiovascular patients and control subjects than did measurement of serum triglyceride, the results suggest that hypertriglyceridaemia in such patients may be separable into a group in which impaired triglyceride clearance may be partly responsible, and a group in which overproduction of serum triglyceride may be the major mechanism of the hyperlipidaemia.
Clin Sci Mol Med 1976 Oct
PMID:Intravenous fat-tolerance test in ischaemic heart disease and peripheral vascular disease. 18 30

1. Structural changes in the thymus during the evolution experimental renal hypertension were investigated to determine their possible role in the genesis of hypertensive vascular disease. 2. The thymus, adrenal glands and the progression of hypertensive vascular lesions were investigated in rats during the first 30 days after occlusion of the aorta between the two renal arteries. 3. Hypertension was initially accompanied by marked atrophy of the thymus, most pronounced 9 days after operation. During this time, the adrenal glands doubled in size and the heart became enlarged. 4. After 21 days the thymus regenerated and became hypertrophic. Histological features of hyperactivity accompanied by infiltration of plasma cells were evident, while the adrenal glands remained enlarged. 5. The observed structural changes of the regenerated thymus in the presence of sustained adrenal hypertrophy indicate that the thymus may contribute to the production of hypertensive vascular disease.
Clin Sci Mol Med 1978 Aug
PMID:Biphasic changes in thymus structure during evolving renal hypertension. 67 25

1. The syndrome of malignant hypertension in man and animals has three fundamental components: high blood pressure, activation of the renin-angiotensin system and the rapid development of necrotizing arteriolar disease. 2. The high blood pressure can be associated with different conformations of the arteriolar microcirculation. The emergence of an arteriolar reaction pattern characterized by the formation of focal dilatations, with intervening constricted segments, is of fundamental pathophysiological importance. 3. Activation of the renin system is reflected in an increased renin secretion rate from the kidneys and an increased rate of angiotensin II generation in the pulmonary vascular bed. 4. The crucial pathogenetic process, leading eventually to severe arteriolar wall damage, is a penetration of plasmatic macromolecules into the wall of distended arteriolar segments, as observed in states of severe experimental hypertension. 5. Renin can induce vascular disease, but hypersecretion of renin is not a necessary condition for the development of hypertensive arteriolar necrosis.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The renin-angiotensin system and the pathogenesis of vascular disease in malignant hypertension. 107 5

Hereditary cerebral hemorrhage with amyloidosis, Dutch type (HCHWA-D) (or familial cerebral amyloid angiopathy) and familial Alzheimer's disease (FAD) share several properties. Both are autosomal dominant forms of cerebral amyloidosis characterized by beta-amyloid (A beta) deposition. In HCHWA-D the A beta is predominantly found in blood vessels and in early parenchymal plaques, whereas in AD parenchymal A beta deposits in the form of senile plaques and neurofibrillary tangles are a more prominent finding. Point mutations in the amyloid precursor protein (APP) have recently been described, in both conditions. A G to C transversion at codon 618 (extracellular portion of APP695), producing a single amino acid substitution of glutamine instead of glutamine acid, occurs in HCHWA-D; whereas mutations at codon 642 in the intramembrane region of APP695 (phenylalanine, isoleucine, or glycine instead of valine) are associated with early onset FAD. This suggests that the site of particular mutations in the APP gene and the type of amino acid substitution in the APP holoprotein are more important in determining clinicopathological phenotype and age at which A beta is deposited. Thus FAD and HCHWA-D can be regarded as two sides of the same coin.
Mol Neurobiol 1992
PMID:Molecular biology of Alzheimer's amyloid--Dutch variant. 146 89

Cardiovascular disease represents the major cause of morbidity and mortality in noninsulin-dependent diabetic patients. While it was once thought that atherosclerotic vascular disease was responsible for all of these adverse effects, recent studies support the notion that one of the major adverse complications of diabetes is the development of a diabetic cardiomyopathy characterized by defects in both diastolic and systolic function. Contributing to the development of the cardiomyopathy is a shift in myosin isozyme content in favor of the least active V3 form. Also defective in the noninsulin-dependent diabetic heart is regulation of calcium homeostasis. While transport of calcium by the sarcolemmal and sarcoplasmic reticular calcium pumps are minimally affected by noninsulin-dependent diabetes, significant impairment occurs in sarcolemmal Na(+)-Ca2+ exchanger activity. This defect limits the ability of of the diabetic heart to extrude calcium, contributing to an elevation in [Ca2+]i. Also promoting the accumulation of calcium by the diabetic cell is a decrease in Na+, K+ ATPase activity, which is known to increase [Ca2+]i secondary to a rise in [Na+]i. In addition, calcium influx via the calcium channel is stimulated. Although the molecular mechanisms underlying these defects are presently unknown, the possibility that they may be related to aberrations in glucose or lipid metabolism are considered. The evidence suggests that classical theories of glucose toxicity, such as excessive polyol production or glycosylation, appear to be insignificant factors in heart. Also insignificant are defects in lipid metabolism leading to accumulation of toxic lipid amphiphiles or triacylglycerol. Rather, the major defects involve membrane changes, such as phosphatidylethanolamine N-methylation and protein phosphorylation, which can be attributed to the state of insulin resistance.
Mol Cell Biochem 1991 Sep 18
PMID:Cardiomyopathy associated with noninsulin-dependent diabetes. 166 89

Continuous or repeated injury of rabbit aortae by indwelling vascular catheters caused the deposition of platelets on the injured vessels and the formation of thrombi rich in platelets and fibrin at sites where flow was most disturbed and injury was most extensive. Incorporation of 51Cr platelets into the thrombi reached a maximum between 3 and 24 hr. The platelet-fibrin-rich thrombi remained reactive to circulating platelets for at least 14 days. Continuing reactivity of thrombi and the turnover of platelets in the thrombi were accompanied by an increase in the proportion of platelets that separated in the least dense fraction on Stractan density gradients. Platelet survival was also shortened (43.5 +/- 5.9 hr in animals with catheters, compared with 62.6 +/- 4.5 hr in animals with a sham operation), indicating that some platelets that had taken part in thrombus formation or had interacted with the injured vessel wall were rapidly cleared from the circulation. Platelets from rabbits that had had indwelling aortic catheters in place for 3 or 6 days survived significantly longer than those from animals with a sham operation upon injection of the platelets into normal animals; thus, continuous turnover of platelets on injured vessels and thrombi, and the clearance of altered platelets, leads to a population of younger platelets that survive longer. The continuing reactivity of thrombi may in part account for repeated occlusive episodes in vascular disease. The contribution of thrombin generation and fibrin formation to the platelet-rich thrombi is substantial and warrants the ongoing evaluation of treatment with a combination of anticoagulant and antiplatelet agents in arterial thrombosis and in thrombus formation on vascular catheters.
Exp Mol Pathol 1990 Dec
PMID:The relation among vessel injury, thrombus formation, and platelet survival in rabbits. 225 31

The role of the heart in hypertension has finally emerged as a major issue of cardiovascular concern by the clinician, physiologist, pharmacologist, biochemist, and molecular biologist. This discussion provides an overview of the present state of knowledge and current areas of investigation in this active area of broad interest. Generally, these relate to: the active participation of the heart (e.g. hemodynamic, humoral, autocrine/paracrine); the adaptive response of the heart (i.e. hemodynamic); non-hemodynamic relationships (vis-a-vis, age, race, gender, humoral, coexistent disease); and current thoughts on mechanisms of so-called regression of left ventricular hypertrophy. Several antihypertensive classes of compounds are characterized by decreasing cardiac mass and left ventricular wall thicknesses. The angiotensin converting enzyme inhibitors are included among these agents; their physiological effects in producing "regression" are under active study as are the mechanisms responsible for these changes. These concerns are no longer of incidental or theoretical interest but have major impact on selection of antihypertensive therapy and the management of the patient with hypertension. Thus, the heart may participate actively in the pathogenesis and maintenance of the disease; it adapts to the vascular disease hemodynamically; but in this regard the response has both positive beneficial concerns as well as negative implications as an independent risk factor. These latter concerns should be explored in great depth before conclusions are made with respect to the long-term implications of antihypertensive therapy on the heart.
J Mol Cell Cardiol 1989 Dec
PMID:Overview of hemodynamic and non-hemodynamic factors associated with left ventricular hypertrophy. 253 39

The relationship between inhibition of aortic histamine synthesis induced by varied dosages of alpha-hydrazinohistidine (alpha HH) and aortic uptake of fluorescein-labeled bovine serum albumin (FITCBSA) was examined in 40 male Wistar rats made diabetic by streptozotocin. Compared to nondiabetic animals, aortic uptake of FITCBSA in untreated diabetic animals was increased 43%. alpha HH administration produced essentially a complete inhibition of this accelerated histamine synthesis in diabetic animals at all dosages examined and likewise prevented an increase in aortic FITCBSA uptake among these animals. In diabetic animals, aortic histamine synthesis and aortic FITCBSA uptake showed a significant, strong positive correlation (r = 0.822, P less than 0.001) when examined in relation to the degree of inhibition of accelerated aortic histamine synthesis achieved among the individual animals. These data support the hypothesis that elevations in de novo aortic histamine formation, and thus elevations in the inducible histamine pool, are responsible, at least in part, for increased aortic uptake of macromolecules in diabetes. Since increases in various permeability characteristics occur early in atherogenesis, these data also indicate that expansion of the nascent histamine pool occurring in diabetes may be an important factor in the predisposition of diabetics to atherosclerotic vascular disease.
Exp Mol Pathol 1985 Jun
PMID:Aortic histamine synthesis and aortic albumin accumulation in diabetes: activity-uptake relationships. 399 55

Senile cerebral amyloidosis has been investigated using immunoperoxidase and enzyme histochemical techniques in six unfixed brains. Our findings do not support the opinion that vascular and senile plaque amyloid are immunoglobulin-derived. In contrast with recent reports we did not detect prealbumin in senile plaques and congophilic angiopathy lesions. All senile plaques contain complement factors C1q, C3 and C4. The highest peroxidase activity was found in the amyloid nucleus but the corona also showed evident peroxidase activity.
Virchows Arch B Cell Pathol Incl Mol Pathol 1984
PMID:An immunohistochemical study on cerebral vascular and senile plaque amyloid in Alzheimer's dementia. 615 Dec 85

The microdistribution of type V collagen, fibronectin, and laminin on the luminal surface of perfusion-fixed normal rat aortic endothelium has been studied by an immunoelectron microscopic method using monospecific antibodies and a protein A-gold complex. Gold particles indicating the presence of these biologically active connective tissue proteins were localized in groups on and in the vicinity of the interendothelial border. They were also found on the small flaps of cell junctions as well as on certain cell projections and scattered on the cell surface. Correlative transmission electron-microscopic examinations proved the specificity of these localizations. The endothelial cells of the aorta differed markedly in the amount of scattered connective tissue proteins on their surface, suggesting that there are several types of aortic endothelial cells with distinct functional differences. The findings provide evidence that connective tissue proteins may contribute to the surface pattern of the normal endothelium, especially on cell borders. It is likely that these proteins influence functions such as the permeability and chemotactic activity of the endothelium pertinent to the development of vascular disease.
Exp Mol Pathol 1984 Jun
PMID:Presence of connective tissue proteins on the endothelium of the rat aorta. 637 59


1 2 3 4 5 6 7 8 9 10 Next >>