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

Serum lipoproteins were determined 8-12 weeks after the onset of ischemic cerebro-vascular disease (ICD) in 61 patients, 38 males and 23 females, before the age of 55. The results were compared with those of a matched control material. The diagnosis was based on clinical findings, CSF spectrophotometry, computer tomography, and angiography. Hyperlipoproteinemia was no common finding in these young and middle-aged patients with ICD. The normal mean total serum cholesterol concentration was the result of a slight increase in VLDL cholesterol and a concomitant HDL cholesterol reduction. In men, the HDL cholesterol concentration was lower than expected for any VLDL-TG concentration. The mean value of the HDL cholesterol concentration in the patients was 18% lower than in the control group. On agarose electrophoresis the lipoprotein variants "late prebeta", "sinking prebeta" and "rapid beta" lipoproteins could be demonstrated in the same frequency as in controls. There was no significant correlation between the degree of atherosclerosis, estimated by angiography, and any serum lipoprotein fraction. Several recent studies have stressed the importance of a low HDL concentration as an independent risk factor for atherosclerosis. The decreased HDL cholesterol levels found in the present material require further attention to the possible beneficial role of HDL in ICD.
Atherosclerosis 1978 Jul
PMID:Dyslipoproteinemia in patients with ischemic cerebro-vascular disease: a study of stroke before the age of 55. 20 3

One hundred seventeen patients, 31 with TIA and 86 with cerebral infarction, had angiographically verified atherosclerosis within the relevant carotid artery territory and normal CSF. They were treated with anticoagulants for a mean of 11.1 months. No TIA but 1 cerebral infarction, appearing during inadequate anticoagulant therapy, was registered. Seventy-six of the patients, 20 with TIA and 56 with infarction, were followed for a mean of 4.4 months after cessation of anticoagulants or during inadequate antinecessitating re-institution of anticoagulant therapy. Long-term, anticoagulant treatment can be recommended in carefully selected patients with TIA, and also with infarction in the carotid territory.
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PMID:Prognosis in patients with infarction and TIA in carotid territory during and after anticoagulant therapy. 50 92

An operative case of 12-year-old boy with a saccular aneurysm at the anterior communicating artery was reported. He had episodes of occasional headache during one year before admission. He was attacked by a severe headache associated with nausea and vomiting, and was admitted to Ooita Pref. Hospital under the diagnosis of subarachnoid hemorrhage four days later. On admission physical examinations revealed almost normal findings except for moderate dehydration and a blood pressure of 130/70 mmHg. Routine examinations (blood, serum including total cholesterol, urine, ECG and plain chest X-film) were normal. Neurologically there were lethalgic state, moderate nuchal rigidity and bilateral abducens paresis. Slightly hemorrhagic and xanthochromic CSF was demonstrated by a spinal puncture. An aneurysm was found at the anterior communicating artery on the right carotid arteriogram. The left carotid and the left vertebral arteriograms showed no pathologic findings. Operation via right fronto-temporal approach disclosed a berry aneurysm about 4 mm in diameter arising from the bifurcation of the right anterior cerebral and the anterior communicating artery. There was a plaque presumably an atherosclerotic change at the neck of the aneurysm. Clipping of the aneurysmal neck was done. The aneurysm was not visualized on the postoperative arteriogram, and the patient was discharged in good condition two weeks after the operation. It is true that this patient had a lesion which seemed to be an atherosclerotic plaque at the neck of the aneurysm macroscopically, but he did not have any evidence of generalized atherosclerosis or other metabolic disturbance. This plaque may be of special significance in etiological respect. In general, however, degenerative lesions like atherosclerosis occur predominantly in larger arteries than smaller arteries of the brain. Also the location of this aneurysm was at the anterior communicating artery which is reported to be implicated in anomalous vascularity on occasion. From these facts the authors considered combined congenital and acquired factors in the development of this aneurysm.
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PMID:[Intracranial aneurysm in a child--a case report and some considerations on etiology (author's transl)]. 94 72

Vascular smooth muscle cell is a major cell component involved in the process of atherosclerosis. In the present study, we investigated the effects of platelet-derived growth factor (PDGF)-BB dimer on the expression of macrophage-colony stimulating factor (M-CSF) in vascular smooth muscle cells isolated from human umbilical artery. On Northern blot analysis of total RNAs isolated from smooth muscle cells, with human cDNA for M-CSF, a marked dose-dependent reduction of mRNA level was found in PDGF-BB-treated smooth muscle cells. Cellular production of M-CSF was estimated by immunoblot analysis of cell lysate with specific polyclonal antibody against recombinant human M-CSF. A concentration of 10 ng/ml PDGF-BB significantly reduced M-CSF mass in smooth muscle cells compared with that in the absence of PDGF-BB. These results suggest that PDGF-BB plays an important role in the cellular metabolism of vascular wall by regulating the rate of M-CSF production in vascular smooth muscle cells.
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PMID:Platelet-derived growth factor BB-dimer suppresses the expression of macrophage colony-stimulating factor in human vascular smooth muscle cells. 137 30

Biosynthesis of apolipoprotein (apo) E has been previously demonstrated to be regulated in macrophages by intracellular free cholesterol levels as well as by macrophage activating factors. In this report, the regulation of apo E secretion by cytokines detected within atherosclerotic lesions has been investigated. Granulocyte macrophage-colony stimulating factor (GM-CSF) stimulated macrophages had a 3-5-fold reduction in apo E secretion, comparable to that observed for gamma interferon (IFN gamma), while tumor necrosis factor alpha (TNF alpha) and interleukin 1 beta (IL-1 beta) resulted in a 2-fold decrease. In contrast to the reduction in apo E secretion by these cytokines, transforming growth factor beta (TGF-beta) stimulated macrophages secreted 3-fold greater amounts of apo E than controls. The reduced secretion of apo E by GM-CSF was reversible, heat labile, dose dependent, maximal 48 h after cytokine exposure and was coincident with an increase in fibronectin secretion. The opposing effects of GM-CSF and TGF-beta on apo E secretion were consistent with similar changes detected in apo E mRNA levels. Cytokine effects on apo E secretion in cholesterol loaded macrophages were also investigated and found to be similar to the non-loaded cells with GM-CSF decreasing and TGF-beta increasing apo E secretion. The observed differences in apo E secretion did not correlate with any significant changes in either cellular cholesterol distribution in the non-cholesterol loaded macrophages or in basal ACAT activity. In addition to changes in apo E secretion, cytokine treated macrophages pulsed with [14C]oleate and acetylated LDL for 2-6 h had a 2-fold increase (GM-CSF) or decrease (TGF-beta) in cholesterol esterification. Therefore, GM-CSF and TGF-beta mediated changes in apo E secretion may occur through a mechanism independent of changes in cellular free cholesterol levels. These results suggest that cytokines expressed within an atheroma may play an important role in the modulation of macrophage mediated reverse cholesterol transport.
Atherosclerosis 1992 Oct
PMID:Cytokine regulation of macrophage apo E secretion: opposing effects of GM-CSF and TGF-beta. 146 52

The early atherosclerotic lesion is characterized by the presence of macrophage-derived foam cells. Macrophage colony stimulating factor (M-CSF) specifically stimulates the functions of the monocyte-macrophages. To elucidate the effects of M-CSF in the atherogenic process in vivo, we administered human recombinant M-CSF into Watanabe heritable hyperlipidemic (WHHL) rabbits, an animal model for familial hypercholesterolemia. Three hundred micrograms of M-CSF were intravenously injected into WHHL rabbits aged 2.5 months, three times a week for 8.5 months. After the M-CSF treatment, we found very retarded progression of atherosclerosis. The accumulation of cholesterol ester was remarkably decreased in the aortae of M-CSF-treated animals (0.60 +/- 0.32 mg/g tissue), as compared to those of controls (4.32 +/- 0.61 mg/g tissue). Furthermore, the percentage of the surface area of the aorta with macroscopic plaque in animals treated with M-CSF was 14.3 +/- 6.2%, much less than that in controls receiving saline injection (38.8 +/- 8.0%). Thus, M-CSF definitely prevented the progression of atherosclerosis in WHHL rabbits by influencing macrophage functions.
Atherosclerosis 1992 Apr
PMID:Macrophage colony stimulating factor prevents the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbits. 159 Aug 29

Oxidized lipoproteins have been identified in atherosclerotic plaques and in early lesions in humans as well as in animals. There is accumulating evidence that such oxidized lipoproteins have an important role in atherosclerosis. Treatment of endothelial cells with altered lipoproteins stimulates monocyte binding as well as the production of chemotactic factors for monocytes. Both these findings could be relevant to the accumulation of monocytes-macrophages in the arterial wall during the early stages of lesion development. We now report that treatment of endothelial cells (EC) with modified low-density lipoproteins obtained by mild iron oxidation or by prolonged storage, results in a rapid and large induction of the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage CSF (M-CSF) and granulocyte CSF (G-CSF). These growth factors affect the differentiation, survival, proliferation, migration and metabolism of macrophages/granulocytes, and G-CSF and GM-CSF also affect the migration and proliferation of EC. Because EC and macrophages are important in the development of atherosclerosis, the expression of the CSFs by these cells could contribute to the disease.
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PMID:Induction of endothelial cell expression of granulocyte and macrophage colony-stimulating factors by modified low-density lipoproteins. 169 Mar 54

The elongation and ectatic course of the basilar artery (BA), called megadolichobasilar artery anomaly (MDBAA) is a macroscopic description of a neuroradiologic finding. Clinically ischemic brain stem syndromes and peripheral cranial nerve disturbances especially of the trigeminal and facial nerves, cerebellar dysfunction and CSF circulation disturbances are observed. Seldom a subarachnoid hemorrhage is proven. In CT and MRI often a tumorlike mass with a ringlike contrast enhancement combined with a nonhomogeneous lesion due to partial thrombosis, is detected. Angiography in most cases shows fusiform dilatation of the BA, elongation of the top of the basilar trunk, asymmetric tortuosity or dislocation of the irregular shaped wall of the BA. Fifteen patients within the last 12 years are demonstrated. The role of reticular fiber deficiency in the media and defects of the elastic lamina as the basis of these malformations is reported. We discuss coincidental findings of MDBAA with atherosclerosis, congenital factors causing generalized vasculopathy, metabolic disturbances in form of so called inborn errors of metabolism and endocrine deficiencies. In cases with clinical signs the morbidity is remarkably high.
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PMID:Clinical signs associated with megadolichobasilar artery anomaly. 179 46

We present the clinical and laboratory findings of 8 patients with cerebrotendinous xanthomatosis. The clinical features consisted of a combination of bilateral Achilles tendon xanthomas, cataracts, low intelligence, pyramidal signs, cerebellar signs, convulsions, peripheral neuropathy, foot deformity, cardiovascular disease or atherosclerosis, EEG abnormality, and increased CSF protein. Increased cholesterol was present in the serum, CSF and red cell membrane of all 8 patients. The bile of one patient with late age onset of the disease showed an attenuated production of bile acids and bile alcohols. Three of the 7 had obstruction and/or marked narrowing of the coronary arteries. Data on 136 patients reported throughout the world are reviewed.
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PMID:Cerebrotendinous xanthomatosis: clinical and biochemical evaluation of eight patients and review of the literature. 207 21

We investigated the action of monocyte colony-stimulating factor (M-CSF) on plasma cholesterol metabolism. Recombinant human monocyte colony-stimulating factor (rhM-CSF) was intravenously injected into Watanabe heritable hyperlipidemic (WHHL) rabbits that were deficient in LDL receptor. The treated rabbits showed decreases in plasma total cholesterol levels from 493 +/- 39 to 416 +/- 45 mg/dl (about 15%) during the treatment. The decrease in total plasma cholesterol level was due to decreased levels of lipoproteins containing apo B 100 such as VLDL, IDL, and LDL. The effect of M-CSF on the LDL-receptor-deficient animal in vivo and evidence from Northern blot analysis of liver suggested that M-CSF lowers plasma cholesterol level through activated uptake of lipoproteins containing apo B 100 via pathways other than the hepatic LDL receptor. We have started a clinical study to evaluate the plasma cholesterol-lowering effect of M-CSF in patients with familial hypercholesterolemia, and have observed a decreased in total plasma cholesterol level in one of three patients treated with M-CSF. M-CSF may provide new insight into plasma cholesterol metabolism and a possible new tool to treat patients with hypercholesterolemia and atherosclerosis.
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PMID:Plasma cholesterol-lowering activity of monocyte colony-stimulating factor (M-CSF). 219 82


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