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)

Changes in shape and the time course of residual coronary artery stenoses following thrombolysis were studied in 36 patients with acute myocardial infarction. The following results were obtained: 1. Residual stenoses after thrombolysis were categorized morphologically in three groups; long segment type (group L, eight patients), segmental type (group S, 18 patients) and filling defect type (group FD, 10 patients). 2. Residual stenoses in group L did not change either as to morphology or severity one month later. Group S did not show morphological change, but 11 of the 18 patients showed slight regression of residual stenoses. In group FD, filling defect images on repeated angiography resolved in all cases within one month. However, characteristic irregularity at the infarct-related coronary arteries were often observed at the same time. 3. Twelve of the 36 patients underwent angiography during three consecutive days to study sequential changes in residual stenoses. Intracoronary thrombi were resolved before the second day, which was compatible with a plasminogen-plasmin system change. 4. Severe coronary artery atherosclerosis may be an important factor in the pathogenesis in group L, while thrombus formation based on ulcerative lesions without significant stenoses may be an important factor in group FD. 5. Mechanical revascularization for the groups L and S patients, and an additional thrombolytic agent for the group FD patients are recommended as further therapy after thrombolysis.
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PMID:[Residual coronary artery stenosis: its shapes immediately after thrombolysis and subsequent time courses]. 263 21

Lipoprotein (a) is an antigenic variant of low density lipoprotein and is present in the plasma of most people. Many epidemiologic studies from Europe and North America have found that when plasma levels of lipoprotein (a) exceed 0.20 g/L, there is a significantly higher risk of coronary and cerebrovascular atherosclerosis. Until recently, there has been little insight into the function of lipoprotein (a) or its potential atherogenic mechanism. Molecular biological studies have shown that the characteristic protein of lipoprotein (a), called apolipoprotein (a), strongly resembles plasminogen, the precursor of the natural anticoagulant plasmin. Furthermore, there is emerging evidence that lipoprotein (a) is the missing link between the lipoprotein and coagulation systems, acting perhaps as a vehicle which delivers cholesterol to the site of intravascular damage, or as an inhibitor of plasminogen activation at the site of an evolving thrombus.
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PMID:Lipoprotein (a): an emerging risk factor for atherosclerosis. 266 28

Human lipoprotein(a) is a low density lipoprotein-like lipoprotein whose concentration in plasma is correlated with atherosclerosis. The characteristic protein component of lipoprotein(a) is apolipoprotein(a) (apo(a)) which is disulfide-linked to apolipoprotein B-100. Sequencing of rhesus monkey apo(a) cDNA suggests that this protein, like human apo(a), is highly similar to plasminogen. Sequence data suggests that a plasminogen-like protease activity and kringle 1-, 2-, 3-, and 5-like domains are unnecessary for apo(a) function, but a highly repeated kringle four-like domain is important. Liver is the major site of apo(a) RNA synthesis; reduced amounts of message were also found in testes and brain. Co-expression with apoB-100 and plasminogen in rhesus tissues is not mandatory.
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PMID:Rhesus monkey apolipoprotein(a). Sequence, evolution, and sites of synthesis. 292 43

Lp(a) represents a genetically transmitted class of plasma LDL having apo B-100 linked by a disulfide bridge to a glycoprotein, apo(a). Lp(a) is heterogeneous in size and density. Apo(a) is also heterogeneous in size (molecular weight between approximately 300,000 and 700,000) due probably to the polymorphism of both polypeptide and carbohydrate chains. Recent studies have shown that apo(a) has a striking amino acid sequence homology with plasminogen, a serine protease zymogen that following activation to plasmin enters the fibrinolytic system. Apo(a) is severalfold larger than plasminogen (molecular weight approximately 90,000) and also differs from it because it fails to be activated to plasmin. This is due to the fact that arginine is replaced by serine at the site of cleavage by streptokinase, urokinase, or tissue plasminogen activator. A single gene locus appears to control the Lp(a) polymorphism as well as the concentration of the Lp(a) phenotypes in the plasma. Patients with high plasma levels of Lp(a) have been shown to have an increased incidence of cardiovascular disease but a causal relationship has not been firmly established. The information that is being rapidly acquired on the structure of Lp(a) should facilitate the understanding of the molecular basis of the polymorphism of this genetic variant and of the role that the various Lp(a) phenotypes play in atherosclerosis and thrombosis. The potential physiologic role of Lp(a) remains open to inquiry.
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PMID:Lipoprotein(a): a genetically determined lipoprotein containing a glycoprotein of the plasminogen family. 297 66

The effects of intake of dried garlic on blood coagulation, fibrinolysis, platelet aggregation, serum cholesterol levels, and blood pressure were studied in 20 patients with hyperlipoproteinemia over a period of four weeks. Fibrinogen and fibrinopeptide A significantly decreased by 10%. Streptokinase activated plasminogen and fibrinopeptide B beta 15-42 significantly increased by about 10%. Serum cholesterol levels significantly decreased by 10%. Systolic and diastolic blood pressure decreased. ADP and collagen induced platelet aggregation were not influenced.
Atherosclerosis 1988 Dec
PMID:Effect of dried garlic on blood coagulation, fibrinolysis, platelet aggregation and serum cholesterol levels in patients with hyperlipoproteinemia. 324 Mar 34

Blood samples were taken for haemostatic analysis from 225 patients with angina pectoris who were admitted to hospital for coronary angiography. beta thromboglobulin, platelet factor 3, platelet factor 4, factor VII:C, factor VIII:C, von Willebrand factor antigen, activated partial thromboplastin time, fibrinogen, antithrombin III, protein C:Ag, plasminogen, and antiplasmin were measured before angiography. Patients who had had a myocardial infarction in the two months before the investigation were excluded from the study. Multiple linear regression analysis showed that none of the haemostatic variables contributed independently to the prediction of an angiographic score that indicated the extent of coronary atherosclerosis. History of myocardial infarction, male sex, worsening of angina pectoris, serum triglycerides, and ejection fraction were independently associated with the angiographic score. There were some significant correlations between haemostatic variables and conventional risk factors for coronary heart disease. Thus data obtained from haemostatic analyses of peripheral venous blood do not permit the presence or the extent of atherosclerosis in coronary arteries to be predicted.
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PMID:Lack of association between haemostatic variables and the presence or the extent of coronary atherosclerosis. 325 21

Epidemiological studies of oral contraceptives pertaining to premenopausal women are briefly reviewed. Therapeutic considerations are noted. The clinical effects of aging and hormone replacement therapy are indicated in terms of metabolism, the endometrium, and bone mass. The pharmacological advantages and consequences of nonhormonal and hormonal contraception are explored. For aging women over 40, there is a need for relief of menopausal symptoms, contraception, and reduction of risks for atherosclerosis, hypertension, coronary heart disease, endometrial carcinoma, breast cancer, and osteoporosis. With the availability and use of low estrogen products, women over 40 can insure tissue support and prevent bone loss as long as the therapy is instituted within 3 years of the last menses. Over-40 women who drink and smoke should not use oral contraceptives. Sterilization does not satisfy longterm hormonal needs, and has other reported menstrual side effects. The dose and duration regimen of hormonal therapy must be carefully considered due to the effects on the endometrium., the coagulation system, the liver, lipids, and bone. Combination estrogen and progestogen is necessary, but consideration must be given to existing levels of endogenous hormones. Lipid patterns may change due to hormone replacement or as a result of aging and contribute to coronary heart disease. Hormone replacement can reverse the atherogenic pattern of increased low density lipoprotein levels and decreased high density lipoprotein levels; a chart gives the effects on lipids and coagulation from various estrogen or estrogen plus progestogen products. For the estrogen-deficient menopausal woman, high estrogen can decrease antithrombin III plasminogen and alpha-antitrypsin antigen levels. Lower dose progestogens are recommended. Studies of dose and effects on bone mass are reviewed and vaginal rings and transdermal steroid patches, triphasic formulations, and new progestational agents such as 19-nortestosterone derivatives are described. Newer low dose formulations are needed for the aging woman, as well as further research on what product best suits the variability of women aged 40-50
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PMID:Contraception for the perimenopausal patient. 330 20

Impaired fibrinolysis is believed to promote atherosclerosis and contribute to myocardial infarction. The major triggering factor for fibrinolysis is vascular tissue plasminogen activator (t-PA), and the aim of this study was to evaluate the capacity of human arterial smooth muscle cells (SMC) for induction of fibrinolysis. SMC were plated on labeled fibrin gels, and lysis was measured as release of label. Fibrinolytic capacity was dependent on the phenotypic state of SMC. The "multilayered phenotype" to which SMC modulate after cellular injury had a much lower fibrinolysis-inducing capacity than the more ordinary "monolayered" SMC type. Fibrinolysis was mediated by activation of plasminogen. In long-term experiments under conditions imitating thrombolysis, platelet-derived growth factor promoted fibrinolysis indirectly by increase of SMC number, and a direct effect on cellular production of t-PA was not detected. SMC from atherosclerotic intima had a much lower capacity for induction of fibrinolysis than cells from adjacent nonatherosclerotic intima. SMC also displayed several structurally detectable interactions with the fibrin substratum, such as organization of the gel by means of extension of numerous filamentous processes and contraction and wrinkling of the gel. In conclusion, human arterial SMC in vitro induce fibrinolysis by activation of plasminogen. This capacity is dependent on phenotype and lowered for SMC from atherosclerotic intima, suggesting impairment after arterial injury and in atherosclerosis.
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PMID:Impaired fibrinolysis-inducing capacity for postinjury phenotype of cultivated human arterial and human atherosclerotic intimal smooth muscle cells. 335 71

Abnormalities of the fibrinolytic system can result in unusual or unexplained clotting that occurs spontaneously or after minor trauma. We identified five patients with limb-threatening arterial thrombosis of the upper extremity associated with either a low level of plasminogen or an abnormal immunoreactive plasminogen. All patients had extensive thrombosis of the brachial, radial, and ulnar arteries. Two patients had concomitant thrombus of the subclavian artery, which in one patient was associated with distal embolization to the hand. There was no evidence of atherosclerosis in any patient. Detection of an abnormal plasminogen level was done by immunoelectrophoresis of the patient's serum with antiplasminogen sera. In these patients a separate immunoreactive band located near the anode and distinct from the normal single plasminogen band was detected. Because of extensive thrombosis of the arterial system, exploration of the brachial artery, as well as the origin of all the forearm vessels, was necessary for complete balloon catheter thrombectomy. Prompt diagnosis and treatment are necessary to prevent the catastrophic complication of arm or hand amputation. Patients with an abnormal plasminogen level should receive perioperative heparin therapy and long-term warfarin to prevent recurrent thrombotic episodes.
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PMID:Abnormalities of the fibrinolytic system as a cause of upper extremity ischemia: a preliminary report. 336 30

Apolipoprotein(a) [apo(a)], the glycoprotein associated with the lipoprotein(a) [Lp(a)] subfraction of plasma lipoproteins, has been shown to exhibit heritable molecular weight isoforms ranging from 400-700 kDa. Increased serum concentrations of Lp(a) correlate positively with the risk of atherosclerosis. Variations in Lp(a) plasma levels among individuals are inherited as a codominant quantitative trait. As part of an effect to define the basis of these variations and further clarify the expression of the protein, we have determined the chromosomal location of the human apo(a) gene. Blot hybridization analysis of DNA from a panel of mouse-human somatic cell hybrids with an apo(a) cDNA probe revealed a complex pattern of bands, all of which segregated with chromosome 6. In situ hybridization yielded a single peak of grain density located on chromosome 6q26-27. Apo(a) cDNA sequences exhibit striking homology to those of the plasma protease plasminogen, and, therefore, we have reexamined the chromosome assignment of the plasminogen gene. We conclude that both the apo(a) and plasminogen genes reside on human chromosome 6q22-27, consistent with a gene duplication mechanism for their evolutionary origin. The results are of significance for the genetic control of apo(a) expression and genetic influences predisposing to atherosclerosis.
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PMID:The apolipoprotein(a) gene resides on human chromosome 6q26-27, in close proximity to the homologous gene for plasminogen. 341 Apr 59


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