Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study describes the demographic and biophysical characteristics of rural menopausal women in Western Kenya. Menopause occurs as the gradual unresponsiveness of the human ovary to gonadotropins, premature ovarian failure at under 40 years, and menopause following surgical procedures of the uterus and ovaries. A 3-phase process starts with low serum estradiol and progesterone, followed by a rise in follicle stimulating hormone, and a rise in luteinizing hormone. Clinical symptoms include vasomotor ones, genitourinary ones, osteoporosis and increased incidence of bone fractures, increased incidence of thromboembolic and ischemic heart disease, and psychological symptoms of anxiety, depression, and memory loss. The age of menopause varies with socioeconomic conditions, race, parity, height, weight, skinfold thickness, lifestyle, and education. Data were obtained for this study from a sample of 1078 women from 7 sublocations in Vihiga division, Kenya. Women were aged 40-60 years. The most populous ethnic group was the Luhya. 81.6% were married, 15.6% were widowed, and 0.7% were divorced. 4 women had never been married. 75.1% had a primary school education; 18.6% had not received any formal education. 30.1% had husbands who were unskilled workers, 28.8% had husbands who were farmers, and 20.6% had husbands who were skilled workers. 1.3% had no children, and 1 woman had 17 children. The average number of children was 7.74. 9 of the nulliparous women were menopausal. The mean height was 161.1 cm. The median age at menopause was 48.28 years. Almost all women were menopausal by 55 years. The total fertility period averaged 35 years. Female life expectancy was 59 years.
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PMID:Median age at menopause in a rural population of western Kenya. 952 44

Electroconvulsive therapy (ECT) is used widely in the treatment of psychiatric conditions; however, its use is not without controversy with some recommending a moratorium on its clinical use. Complications and side effects of ECT include memory loss, injury, problems originating from sympathetic stimulation such as arrhythmias and myocardial ischemia and the risk of general anesthesia. Nitrous oxide (laughing gas) could potentially substitute for ECT as it shares some similar effects, has potential beneficial properties for these psychiatric patients and is relatively safe and easy to administer. Nitrous oxide induces laughter which has been described as nature's epileptoid catharsis which one might surmise would be beneficial for depression. It also produces a central sympathetic stimulation similar to ECT and causes release of endogenous opioid peptides, which are potential candidates for the development of antidepressant drugs. Nitrous oxide is also associated with seizure like activity itself. Administration of nitrous oxide as a substitute for ECT is eminently feasible and could be given in a series of treatments similar to ECT therapy.
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PMID:Nitrous oxide (laughing gas) inhalation as an alternative to electroconvulsive therapy. 2000 16

Carbon monoxide (CO) is a colorless, odorless, nonirritant gas that accounts for numerous cases of CO poisoning every year from a variety of sources of incomplete combustion of hydrocarbons. These include poorly functioning heating systems, indoor propane-powered forklifts, indoor burning of charcoal burning briquettes, riding in the back of pick-up trucks, ice skating rinks using propane-powered resurfacing machines, and gasoline-powered generators that are not in correct locations. Once CO is inhaled it binds with hemoglobin to form carboxyhemoglobin (COHb) with an affinity 200 times greater than oxygen that leads to decreased oxygen-carrying capacity and decreased release of oxygen to tissues leading to tissue hypoxia. Ischemia occurs with CO poisoning when there is loss of consciousness that is accompanied by hypotension and ischemia in the arterial border zones of the brain. Besides binding to many heme-containing proteins, CO disrupts oxidative metabolism leading to the formation of free radicals. Once hypotension and unconsciousness occur with CO poisoning, lipid peroxidation and apoptosis follow. Because COHb has a short half-life, examination of other biomarkers of CO neurotoxicity that reflect inflammation or neuronal damage has not demonstrated consistent results. The initial symptoms with CO exposure when COHb is 15-30% are nonspecific, namely, headache, dizziness, nausea, fatigue, and impaired manual dexterity. However individuals with ischemic heart disease may experience chest pain and decreased exercise duration at COHb levels between 1% and 9%. COHb levels between 30% and 70% lead to loss of consciousness and eventually death. Following resolution of acute symptoms there may be a lucid interval of 2-40 days before the development of delayed neurologic sequelae (DNS), with diffuse demyelination in the brain accompanied by lethargy, behavior changes, forgetfulness, memory loss, and parkinsonian features. Seventy-five percent of patients with DNS recover within 1 year. Neuropsychologic abnormalities with chronic CO exposure are found even when magnetic resonance imaging (MRI) and magnetic resonance spectroscopy are normal. White-matter damage in the centrum semiovale and periventricular area and abnormalities in the globus pallidus are most commonly seen on MRI following CO exposure. Though not as common, toxic or ischemic peripheral neuropathies are associated with CO exposure in humans and animals. The cornerstone for treatment for CO poisoning is 100% oxygen using a tight-fitting mask for greater than 6 hours. The indications for treatment with hyperbaric oxygen to decrease the half-life of COHb remain controversial.
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PMID:Carbon monoxide intoxication. 2656 90