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)

This review concerns the acute phase of stroke. It describes incidence, prevalence, etiology, diagnosis and treatment together with the possibilities for prevention. The incidence of stroke in the Danish population is about 2/1000 person years and has been largely unchanged during the last 20 years. About 85 per cent of strokes are caused by cerebral infarcts, ten percent by intracerebral haemorrhages and about five per cent by subarachnoid bleeding. The incidence increases with age. Up till age 65 years the ratio between men and women is two to one, while the ratio in the oldest age group approaches one to one. The most important risk factors for stroke are smoking, arterial hypertension, previous cerebrovascular disease, heart disease and diabetes mellitus. Till now, no treatment has been documented as effective in reducing the cerebral damage caused by acute stroke. Ongoing controlled clinical trials in the acute state of ischaemic stroke are testing the effect of thrombolytic therapy, treatment with calcium antagonists, glutamate receptor antagonists, aspirin and heparin. The general medical treatment including nursing and physiotherapy in the acute phase is described. Within recent years benefit of various strategies of stroke prevention has been documented.
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PMID:[Apoplexy--the acute stage]. 841 52

For the first time, the GluR-1 subtype of AMPA receptor was identified in the sympathetic nervous system of neonatal swine, an animal model of human development and heart disease. The rationale was to seek evidence of a role ascribed to glutamate in cardiorespiratory regulation in the laboratory rat. The receptor was demonstrated with the avidin-biotin immunoperoxidase technique by using an affinity-purified polyclonal antibody judged to be specific to Glu-R1 in several species. Glu-R1 immunoreactivity was regionally distributed in the thoracic spinal gray, and present intracellularly in neurons and within the surrounding neuropil. Sympathetic preganglionic neurons in the intermediolateral cell column of upper and lower thoracic spinal segments were intensely labeled and surrounded by labeled neuropil. High concentrations of Glu-R1 distinguished laminae II: substantia gelatinosa and the outer region of lamina III. Laminae I and V of the dorsal horn but not IV contained immunolabeled neurons. Arrays of moderately immunoreactive perikarya extended from an intermediate zone of laminae VII to the central gray. Glia and perivascular processes were not labeled, confirming previous observations [Tachibana, M., Wenthold, R.J., Morioka, H., Petralia, R.S., 1994. Light and electron microscopic immunocytochemical localization of AMPA-selective glutamate receptors in the rat spinal cord. J. Comp. Neurol. 344, 431-454]. Neuronal staining patterns corroborated evidence in rats indicating a postsynaptic localization of Glu-R1 associated with plasma membranes and cytoplasmic organelles [Martin, L.J., Blackstone, C.D., Levey, A.I., Huganir, R.L., Price, D.L., 1993. AMPA glutamate receptor subunits are differentially distributed in rat brain. Neuroscience 53, 327-358.; Rubio, M.E., Wenthold, R.J., 1997. Glutamate receptors are selectively targeted to postsynaptic sites in neurons. Neuron 18, 939-950]. Our data predict a role for L-glutamate in postnatal development of cardiorespiratory reflexes in swine.
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PMID:Presence of a non-NMDA glutamate receptor subtype in the sympathetic nervous system of neonatal swine. 986 84

Nearly a dozen antiepileptic drugs have been shown to prevent attacks in patients with partial epilepsy, whether used alone, or in combination when successive single-agent well-conducted treatments have failed. Perampanel (Fycompa, Eisai) an AMPA glutamate receptor antagonist, has been granted marketing authorisation in the European Union and United States, for use in combination with other antiepileptic drugs in patients aged 12 years or older with partial epilepsy. Perampanel has not been compared with other antiepileptic drugs in clinical trials. Its evaluation is based on three comparative, double-blind, placebo-controlled trials, in which perampanel was added to other antiepileptic drugs considered to be inadequately effective. In these trials, after 19 weeks of treatment, its efficacy was only modest: the response rate was at best only about 20% higher than with placebo. Indirect comparison, albeit inherently unreliable, suggests that perampanel is no better than other antiepileptic drugs. Perampanel has frequent and often dose-dependent adverse effects; they mainly include irritability, aggression, impaired alertness and coordination, and weight gain. Cardiac disorders were observed during a long-term trial of perampanel. This possible adverse effect requires further study. Perampanel led to stunted growth in experimental animals. It is not known whether adolescents are also at risk. Perampanel does not appear to be a potent inducer or inhibitor of the cytochrome P450 enzyme system, but its drug interaction profile requires further evaluation. In animal studies, perampanel exposure resulted in increased perinatal mortality. In practice, there is no evidence that perampanel represents a therapeutic advance for patients with partial epilepsy. In addition to its known adverse effects, there are concerns over possible long-term cardiac toxicity and a deleterious effect on growth. Other acceptable solutions, based on better-known drugs, should be discussed with epileptic patients.
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PMID:Perampanel. Just another anticonvulsant for partial epilepsy: no progress. 2516 90