Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The basis for life is the ability of the cell to maintain ion gradients across biological membranes. Such gradients are created by specific membrane-bound ion pumps [adenosine triphosphatases (ATPases)]. According to physicochemical rules passive forces equilibrate (dissipate) ion gradients. The cholesterol/phospholipid ratio of the membrane and the degree of saturation of phospholipid fatty acids are important factors for membrane molecular order and herewith a determinant of the degree of non-specific membrane leakiness. Other operative principles, i.e. specific ion channels can be opened and closed according to mechanisms that are specific to the cell. Certain compounds called ionophores can be integrated in the plasma membrane and permit specific inorganic ions to pass. Irrespective of which mechanism ions leak across the plasma membrane the homeostasis may be kept by increasing ion pumping (ATPase activity) in an attempt to restore the physiological ion gradient. The energy source for this work seems to be glycolytically derived ATP formation. Thus an increase in ion pumping is reflected by increased ATP hydrolysis and rate of glycolysis. This can be measured as an accumulation of breakdown products of ATP and end-products of anaerobic glycolysis (lactate). In certain disease entities, the balance between ATP formation and ion pumping may be disordered resulting in a decrease in inter alia (i.a.) cellular energy charge, and an increase in lactate formation and catabolites of adenylates. Cardiac syndrome X is proposed to be due to an excessive leakage of potassium ions, leading to electrocardiographic (ECG) changes, abnormal Tl-scintigraphy of the heart and anginal pain (induced by adenosine). Cocksackie B3 infections, a common agent in myocarditis might also induce an ionophore-like effect. Moreover, Alzheimer's disease is characterized by the formation of extracellular amyloid deposits in the brain of patients. Perturbation of cellular membranes by the amyloid peptide during the development of Alzheimer's disease is one of several mechanisms proposed to account for the toxicity of this peptide on neuronal membranes. We have studied the effects of the peptide and fragments thereof on 45Ca2+-uptake in human erythrocytes and the energetic consequences. Treatment of erythrocytes with the beta 1-40 peptide, results in qualitatively similar nucleotide pattern and decrease of energy charge as the treatment with Ca2+-ionophore A23187. Finally, in recent studies we have revealed and published in this journal that a rare condition, Tarui's disease or glycogenosis type VII, primarily associated with a defect M-subunit of phosphofructokinase, demonstrates as a cophenomenon an increased leak of Ca2+ into erythrocytes.
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PMID:Imbalance of plasma membrane ion leak and pump relationship as a new aetiological basis of certain disease states. 1464 92

These analyses examined the relationship between dementia and comorbid conditions with respect to degree of functional impairment and emotional impact. Analyses were conducted using National Health Interview Survey (2001 through 2005) data from a subset of individuals aged > or =60 years with activity limitations attributed to dementia, senility, or Alzheimer disease compared with those whose limitations were attributed to other conditions. The mean number of limited activities was 6.84 (95% confidence interval: 6.48-7.20) for persons with dementia-related limitations and 4.87 (95% confidence interval: 4.81-4.93) for those with limitations not dementia related. Both groups reported similar prevalence of diabetes, acute myocardial infarction, heart disease, prostate cancer, breast cancer, angina, and emphysema; respondents with dementia-related functional limitations were more likely to report diabetes, depression or anxiety, and vision problems as being related to functional limitations. Persons with dementia-related functional limitations were also more likely than persons with non-dementia-related functional limitations to report feeling sad, hopeless, worthless, nervous, and that "everything is an effort." Improving or maintaining functional independence in patients with dementia will likely require a multifaceted approach across disease states. Additional research will help define the impact of dementia on the development and progression of functional limitations related to comorbidities.
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PMID:Prevalence and impact of dementia-related functional limitations in the United States, 2001 to 2005. 1956 54

Tangier disease is a very rare autosomal recessive inherited disorder characterized by markedly reduced high-density lipoprotein (HDL) levels, characteristic large, yellow-orange tonsils, and enlarged liver, spleen and lymph nodes. It is caused by mutations in the ABCA1 gene. There is no specific treatment, and medications traditionally used to increase HDL are ineffective. A number of patients with non-classical Tangier disease have been described in the literature, who presented with low HDL levels, corneal lesions, hepatosplenomegaly, and thrombocytopenia. We report here about a 45-year-old female with a past medical history of early coronary artery disease, myocardial infarction, multiple episodes of angina, immeasurable HDL, and a history of idiopathic thrombocytopenia purpura. She had a tonsillectomy performed previously, but did not remember if the tonsils were of any unusual color. There was no history of peripheral neuropathy. Her family history is significant for her father and mother having Alzheimer disease and hypertension, respectively. On physical examination she did not have any hepatosplenomegaly or corneal opacities. She was found to have three mutations in the ABCA1 gene. These were designated A1046D (c.3137C>A) in exon 22; Y1532C (c.4595A>G) in exon 34, and W1699C (c.5097G>T) in exon 37. All three have been reported to be deleterious in functional studies. The patient has immeasurable HDL, which leads us to assume that two mutations are on one allele and one mutation on the other. We suspect that this condition is under-diagnosed, and as more patients are reported in the literature, the phenotype of Tangier disease will be elucidated further.
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PMID:A Non-classical Presentation of Tangier Disease with Three ABCA1 Mutations. 2343 Sep 4

Between 1961 and 1971, military herbicides were used by the United States and allied forces for military purposes. Agent Orange, the most-used herbicide, was a mixture of 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid, and contained an impurity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Many Korean Vietnam veterans were exposed to Agent Orange during the Vietnam War. The aim of this study was to evaluate the association between Agent Orange exposure and the prevalence of diseases of the endocrine, nervous, circulatory, respiratory, and digestive systems. The Agent Orange exposure was assessed by a geographic information system-based model. A total of 111,726 Korean Vietnam veterans were analyzed for prevalence using the Korea National Health Insurance claims data from January 2000 to September 2005. After adjusting for covariates, the high exposure group had modestly elevated odds ratios (ORs) for endocrine diseases combined and neurologic diseases combined. The adjusted ORs were significantly higher in the high exposure group than in the low exposure group for hypothyroidism (OR=1.13), autoimmune thyroiditis (OR=1.93), diabetes mellitus (OR=1.04), other endocrine gland disorders including pituitary gland disorders (OR=1.43), amyloidosis (OR=3.02), systemic atrophies affecting the nervous system including spinal muscular atrophy (OR=1.27), Alzheimer disease (OR=1.64), peripheral polyneuropathies (OR=1.09), angina pectoris (OR=1.04), stroke (OR=1.09), chronic obstructive pulmonary diseases (COPD) including chronic bronchitis (OR=1.05) and bronchiectasis (OR=1.16), asthma (OR=1.04), peptic ulcer (OR=1.03), and liver cirrhosis (OR=1.08). In conclusion, Agent Orange exposure increased the prevalence of endocrine disorders, especially in the thyroid and pituitary gland; various neurologic diseases; COPD; and liver cirrhosis. Overall, this study suggests that Agent Orange/2,4-D/TCDD exposure several decades earlier may increase morbidity from various diseases, some of which have rarely been explored in previous epidemiologic studies.
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PMID:Agent Orange exposure and disease prevalence in Korean Vietnam veterans: the Korean veterans health study. 2490 69

Exfoliation syndrome is an age-related disease characterized by the production and progressive accumulation of a fibrillar extracellular material in many ocular tissues. It leads to the most common identifiable cause of open-angle glaucoma worldwide, comprising the majority of glaucoma in some countries. The material in the eye appears as white deposits on the anterior lens surface and/or pupillary border. During pupillary movement, the iris scrapes exfoliation material from the lens surface, while the material on the lens causes rupture of iris pigment epithelial cells, with concomitant pigment dispersion into the anterior chamber and its deposition on anterior chamber structures. Exfoliation material can be found in many different organs. It is an ischemic disease and is associated with elevated serum homocysteine. Systemic associations include transient ischemic attacks, hypertension, angina, myocardial infarction, cerebrovascular and cardiovascular disease, aortic aneurysm, Alzheimer disease, and hearing loss. The discovery in 2007 of nonsynonymous single nucleotide polymorphisms in the LOXL1 (lysyl oxidase-like 1) gene are expected to make a major impact not only in understanding exfoliation syndrome, but in leading to new avenues of therapy.
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PMID:Ocular and systemic manifestations of exfoliation syndrome. 2527 96