Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripartum cardiomyopathy is a classic but uncommon entity in African women about which there is little etiologic understanding. From January 1990 to March 1996 a series of 30 cases of peripartum cardiomyopathy was collected at the Principal Hospital in Dakar, Senegal. Peripartum cardiomyopathy was defined as the occurrence of cardiac insufficiency in a woman with no previous history of heart disease, during the period between the second and twentieth weeks after delivery confirmed by ultrasound evidence of dilated cardiomyopathy. The overall incidence of peripartum cardiomyopathy during the study period was 30 out of 1200 deliveries. The mean age of the women in the study was 34 years and mean parity was 5.2. In 13.3% of cases births involved twins. There were no predisposing socio-economic or climatic factors. The clinical picture was severe cardiac failure in 80.3% of cases and left ventricular insufficiency in 16.6%. In all cases ultrasound findings were typical of dilated cardiomyopathy. Serum selenium and vitamin B1 levels were normal. Measurements of T CD4 and CD8 in eight patients were normal. Conversion enzyme inhibitors were administered to twenty patients. Complete remission was achieved in 14 patients, three patients died, and thirteen patients presented ultrasonic evidence of persistent dilated cardiomyopathy. One patient relapsed after a subsequent delivery. These findings are in agreement with previous reports concerning the clinical and prognostic features of peripartum cardiomyopathy in Africa.
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PMID:[Etiopathogenic, ultrasonographic and prognostic features of postpartum cardiomyopathy]. 913 97

Cancer and heart disease display spatial patterns that suggest the possible involvement of calcium and selenium deficiencies and mercury excess in their aetiologies. As a consequence, longevity tends to be most common in regions where the environment is calcium- and selenium-enriched but contains only low levels of mercury. Examples are cited from West Africa, China, England and the USA.
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PMID:Landscapes of longevity: the calcium-selenium-mercury connection in cancer and heart disease. 916 Feb 92

The purpose of this study was to examine the relationship between arterial hypertension (HTN), chronic heart disease (CHD), and selenium (Se) status. Blood and plasma Se concentrations and Se-dependent GSH-Px activities were determined in 40 patients (HTN = 20; CHD = 20) and 17 healthy volunteers aged 41 to 66 years. Whole blood and plasma Se concentrations were significantly lower in the patients with HTN (19.1% and 26.3%, respectively) and CHD (33.1% and 29.4%, respectively) compared with the values obtained in the controls. The hypertensive patients had lower plasma Se-GSH-Px (26.7%), and those with CHD had both lower whole blood (19.5%) and plasma Se-GSH-Px activities (30.2%). A significant positive correlation between plasma Se-GSH-Px activity and ejection fraction (EF) was found in patients with CHD. There were significant correlations between plasma and whole blood Se concentration, plasma Se concentration and Se-GSH-Px activity, and whole blood Se and Se-GSH-Px activity. Our results showed that hypertensive patients and those with CHD had lower Se levels compared with controls. We conclude that low Se content might be a risk factor for development of HTN and CHD.
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PMID:Blood and plasma selenium levels and GSH-Px activities in patients with arterial hypertension and chronic heart disease. 972 4

Selenium, long recognised as an important 'dietary antioxidant', is now known to be an essential component of the active sites of a number of enzymes, including the glutathione peroxidase selenoenzyme family which scavenge hydroperoxides to prevent cellular damage. Dietary selenium deficiency has been linked to diseases as diverse as cancer, heart disease, arthritis and AIDS, and epidemiological evidence is now emerging for the beneficial effects of selenium supplementation. Thus, the pharmacology, biology and biochemistry of selenium metabolism have become subjects of considerable interest, which are spurring efforts to develop synthetic selenium-containing compounds as potential therapeutic agents. Phenylaminoalkyl selenides were developed in the authors' laboratories as novel, selenium-based pharmacological agents. We demonstrated that these compounds exhibited dose-dependent antihypertensive activity in spontaneously hypertensive rats. Biochemical studies established that as a consequence of the redox properties of their selenium moieties, these phenylaminoalkyl selenides possessed the remarkable property of propagating a cycle of turnover-dependent local depletion of reduced ascorbate when processed by the key enzyme of catecholamine metabolism, dopamine-beta-monooxygenase. On the basis of inductively coupled plasma/mass spectroscopic analyses, corroborated by operant behaviour and locomotor activity investigations, an orally-active phenylaminoalkyl selenide with restricted CNS permeability was successfully developed. To our knowledge, this compound--4-hydroxy-alpha-methyl-phenyl-2-aminoethyl selenide--is the first orally active, selenium-based anti-hypertensive compound ever reported. In the future, we anticipate more widespread efforts to incorporate selenium into rationally designed pharmaceutical agents, with the goal of developing novel compounds which may be of therapeutic benefit toward a variety of human diseases.
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PMID:Selenium-based antihypertensives. Rationale and potential. 987 85

Sudden infant death syndrome (SIDS) occurs silently usually during sleep and, though remaining unexplained after autopsy, leaves footprints creating a pattern analogous to that which follows a flood of nitric acid (NO). These footprints in SIDS are associated with serious pathological changes, viz. elevated hepatic iron, bone marrow hyperplasia, hypomyelinated respiratory control centres, elevated lung immunoglobulins, cerebral hypoperfusion resembling lesions induced by chronic hypoxemia, ischemia, congenital heart disease and congenital myopathy. Hypoxia stimulates the immune response and the over-arousal of the immune response triggers a flood of NO. Adenosine triggers sleep. NO and adenosine are additive as dilators of coronary blood vessels. Blood pressure collapses. Selenium increases the activity of the enzyme ferrochelatase during incorporation of heme into cytochrome oxidase. NO binds to cytochrome oxidase, inhibiting respiration. When NO reaches dangerous levels, the cell turns on production of heme oxygenase. Heme is broken down to iron (Fe) carbon monoxide (CO) and bile pigments. NO has a huge affinity for hemoglobin which catalyses NO degradation to nitrate. Furthermore, NO is a product of smoke and SIDS incidence is higher in smoking mothers.
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PMID:Association of sudden infant death syndrome with grossly deranged iron metabolism and nitric oxide overload. 1079 Jul 39

Overall use of nutrient and botanical dietary supplements (DS) has increased for years across all major categories. Many DS are simply taken as part of a healthy lifestyle, but some are used to reduce risk of or modulate risk factors for specific chronic diseases, such as heart disease (vitamin E, folic acid, garlic), cancer (selenium, vitamin E, garlic) and certain birth defects (folic acid). Other DS are used for short-term benefits such as sleep management (valerian, melatonin) and enhanced physical performance (pyruvate, creatine). DS are regulated under food law, but with certain provisions that apply only to DS. Thus, DS are eligible for Food and Drug Administration (FDA)-authorized health claims under the Nutrition and Labeling Education Act (NLEA). Health claims have already been authorized for folic acid and calcium, but not for several others. In 1994, when the Dietary Supplement Health and Education Act (DSHEA) was passed, it expanded and clarified the definition of DS, specified additional requirements for safety and provided for four types of claims of nutritional support. These include prevention of classic nutritional deficiencies, structure or function (S/F) effects, mechanisms for S/F effects and general well-being. Although S/F effects result from both foods and drugs, representation that a product will treat, cure, mitigate or diagnose a disease is reserved for drugs. Therefore, the wording of S/F claims for DS has become a difficult issue in the proposed DS labeling regulations.
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PMID:Dietary supplements: how they are used and regulated. 1123 28

During a 2-year period from January 1, 1999, to December 31, 2000, 77 diagnoses of mulberry heart disease (MHD) were documented at the Iowa State University Veterinary Diagnostic Laboratory. Mean (+/- SD) liver vitamin E concentrations were lower (P < 0.05) in pigs with MHD (3.12 +/- 1.12 ppm, wet weight) than in pigs that died of causes other than MHD (4.80 +/- 3.2 ppm, wet weight). The majority of the pigs affected with MHD ranged in age from 3 to 7 weeks. Statistical influence of age was found on the concentration of vitamin E (P < 0.01) but not on concentration of selenium in liver in pigs with MHD. Concentrations of vitamin E below 2 ppm were considered deficient. Hepatic vitamin E concentrations below 2 ppm were measured in 25% of the pigs with gross and microscopic lesions of MHD. In contrast, liver selenium concentrations were adequate in all pigs.
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PMID:Vitamin E and selenium concentrations in livers of pigs diagnosed with mulberry heart disease. 1229 94

Selenium is an essential trace element that is an integral part of many proteins, with catalytic and structural functions. The antioxidant properties of some selenoproteins, such as glutathione peroxidase, may be particularly important in carcinogenesis and heart disease. The content of selenium in food depends on the selenium content of the soil where the plants are grown or the animals are raised. Moreover, the metabolism of selenium is determined by its dietary form: some forms are better utilized than others. Therefore, wide variations have been found in selenium status in different parts of the world. In animal studies, selenium deficiency is associated with cardiomyopathy and sudden death, as well as reduced T-cell counts and impaired lymphocyte proliferation and responsiveness. Abnormalities in liver function, brain, heart, striated muscle, pancreas and genital tract have also been reported. In humans, selenium deficiency has been implicated in the etiology of cardiovascular disease and other conditions in which oxidative stress and inflammation are prominent features, but there is still only limited evidence from epidemiological and ecological studies for this, and the therapeutic benefit of selenium administration in the prevention and treatment of cardiovascular diseases remains insufficiently documented. Interventions studies are currently in progress to assess the benefits of selenium supplements in primary and secondary prevention of atherosclerosis. The results to date are inconclusive and further controlled trials are needed.
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PMID:The controversy surrounding selenium and cardiovascular disease: a review of the evidence. 1255 53

The severity of the heart damage caused by a coxsackievirus infection in mice is determined by several factors, including the genotype of the infecting virus as well as the genetic background of the infected host. Earlier work by us showed that the cardiovirulence of a given coxsackievirus genotype could be increased substantially by feeding the host a diet nutritionally deficient in either selenium or vitamin E. Here we report that host genetic background as a determinant of viral infection outcome is superseded by feeding the host a diet nutritionally deficient in both selenium and vitamin E. Mice of the C57Bl/6 strain, normally resistant to coxsackievirus B3-induced myocarditis, become susceptible when fed such a doubly deficient diet. Our results demonstrate the powerful influence of host nutritional status on the course of viral infection compared to other variables traditionally considered to play major roles in determining the extent of virally induced inflammatory heart disease.
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PMID:Coxsackievirus B3-resistant mice become susceptible in Se/vitamin E deficiency. 1272 14

Dietary intake of selenium has been implicated in a wide range of health issues, including aging, heart disease and cancer. Selenium deficiency, which can reduce selenoprotein levels, has been associated with several striated muscle pathologies. To investigate the role of selenoproteins in skeletal muscle biology, we used a transgenic mouse (referred to as i6A-) that has reduced levels of selenoproteins due to the introduction and expression of a dominantly acting mutant form of selenocysteine transfer RNA (tRNA[Ser]Sec). As a consequence, each organ contains reduced levels of most selenoproteins, yet these mice are normal with regard to fertility, overall health, behavior and blood chemistries. In the present study, although skeletal muscles from i6A- mice were phenotypically indistinguishable from those of wild-type mice, plantaris muscles were approximately 50% heavier after synergist ablation, a model of exercise overload. Like muscle in wild-type mice, the enhanced growth in the i6A- mice was completely blocked by inhibition of the mammalian target of rapamycin (mTOR) pathway. Muscles of transgenic mice exhibited increased site-specific phosphorylation on both Akt and p70 ribosomal S6 kinase (p70S6k) (P < 0.05) before ablation, perhaps accounting for the enhanced response to synergist ablation. Thus, a single genetic alteration resulted in enhanced skeletal muscle adaptation after exercise, and this is likely through subtle changes in the resting phosphorylation state of growth-related kinases.
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PMID:Selenoprotein-deficient transgenic mice exhibit enhanced exercise-induced muscle growth. 1451 90


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