Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of gene transfer systems to study cell function makes it apparent that overexpression of a transgene can restore or improve the function of a protein and positively influence cell function in a predetermined manner for purposes of counterbalancing cellular pathophysiology. The ability of some gene transfer vehicles to produce transgene product within hours of delivery positions gene transfer as a unique pharmaceutical administration system that can quickly affect production of biologic response modifiers in a highly compartmentalized fashion. This approach can be expected to overcome many of the adverse effects and high costs of systemic delivery of recombinant pharmaceuticals. This review highlights recent advances toward development of gene therapies for acute illnesses with particular emphasis on preclinical models of disease. In this context, a growing body of data suggests that gene therapies for polygenic and non-genetic diseases such as asthma, cardiogenic and non-cardiogenic pulmonary edema, stroke, subarachnoid hemorrhage, seizures, acute myocardial infarction, endovascular thrombosis, and infections may someday be options for the treatment of patients.
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PMID:Gene therapy for acute diseases. 1173 35

Seven related Quarter Horse foals that died by 7 weeks of age were examined for glycogen branching enzyme (GBE) deficiency. Clinical signs varied from stillbirth, transient flexural limb deformities, seizures, and respiratory or cardiac failure to persistent recumbency. Leukopenia (5 of 5 foals) as well as high serum creatine kinase (CK; 5 of 5), aspartate transaminase (AST; 4 of 4), and gamma glutamyl transferase (GGT; 5 of 5) activities were present in most foals, and intermittent hypoglycemia was present in 2 foals. Gross postmortem lesions were minor, except for pulmonary edema in 2 foals. Muscle, heart, or liver samples from the foals contained abnormal periodic acid Schiff's (PAS)-positive globular or crystalline intracellular inclusions in amounts proportional to the foal's age at death. Accumulation of an unbranched polysaccharide in tissues was suggested by a shift in the iodine absorption spectra of polysaccharide isolated from the liver and muscle of affected foals. Skeletal muscle total polysaccharide concentrations were reduced by 30%, but liver and cardiac muscle glycogen concentrations were normal. Several glycolytic enzyme activities were normal, whereas GBE activity was virtually absent in cardiac and skeletal muscle, as well as in liver and peripheral blood cells of affected foals. GBE activities in peripheral blood cells of dams of affected foals and several of their half-siblings or full siblings were approximately 50% of controls. GBE protein in liver determined by Western blot was markedly reduced to absent in affected foals, and in a half-sibling of an affected foal, it was approximately one-half the amount of normal controls. Pedigree analysis also supported an autosomal recessive mode of inheritance. The affected foals have at least 2,600 half-siblings. Consequently, GBE deficiency may be a common cause of neonatal mortality in Quarter Horses that is obscured by the variety of clinical signs that resemble other equine neonatal diseases.
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PMID:Glycogen branching enzyme deficiency in quarter horse foals. 1181 63

A 38-year-old woman presented with massive hemoptysis (>200 mL/ 24 hours) occurring abruptly after generalized tonic clonic seizure. She experienced similar episodes of hemoptysis on three later occasions. Although the coexistence of hemoptysis and seizure has been reported, albeit rarely, as a clinical manifestation of postictal neurogenic pulmonary edema, massive hemoptysis after seizure is an extremely rare event with no recurrent cases of such episodes having ever been reported. The coexistence of hemoptysis and seizure increases the difficulty in diagnosis for the clinician. We describe the differential diagnosis among the diseases capable of causing seizure and hemoptysis.
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PMID:Massive hemoptysis after generalized tonic clonic seizure requiring mechanical ventilation. 1220 46

Cocaine use has increased considerably during the last twenty years and several related complications can be identified. Clinical features of cocaine intoxication are variable, but predominantly involve cardiovascular events. Chest pain is the most main complaint; myocardial ischemia must be ruled out. Other cardiovascular manifestations are left ventricular dysfunction, arrhythmia, endocarditis and aortic dissection. Non-cardiac complications include neurological (seizures, stroke, cerebral hemorrhage), respiratory (asthma, interstitial pneumonitis, pulmonary edema), renal (acute renal failure, rhabdomyolysis) and obstetrical disorders. Detection of cocaine in the urine provides the diagnosis. Symptomatic treatment is generally given, combining conventional treatment of the complication and broad use of benzodiazepines.
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PMID:[Acute complications in cocaine users]. 1221 80

We report a seizure-related death in a patient with juvenile myoclonic epilepsy 3 months following a previous generalised tonic-clonic seizure complicated by pulmonary oedema. Seizure-related pulmonary oedema is rare but may indicate an increased susceptibility to epilepsy related death. We consider possible preventative measures for patients presenting with seizure-related pulmonary oedema.
Seizure 2002 Oct
PMID:Sudden unexplained death in epilepsy (SUDEP) following previous seizure-related pulmonary oedema: case report and review of possible preventative treatment. 1223 72

In this work we submitted adult male Wistar rats to intracerebroventricular (icv) and iv microinjections of the fraction tityostoxin (TsTX) from the Tityus serrulatus scorpion venom, to address whether the CNS could account for the systemic alterations previously reported: cardiac arrhythmias, lung edema, and seizures. Animals were injected icv, total volume of 1.0 microl, with either sterile saline (n = 4) or differing doses of TsTX (1.74, n = 5; 0.174, n = 4; 0.087, n = 5; and 0.058 microg, n = 4). The peripheral effect of the highest dose of TsTX used (1.74 microg) was tested through iv injections in the femoral vein (n = 4). All animals were recorded by a Video EEG/ECG system for a maximum period of 90 mins or until death. After recording, the lungs were harvested and weighed to evaluate edema (lung/body wt x100). Our results show that icv injections of TsTX, but not iv injections, were able to provoke heart arrhythmias, lung edema, and seizures. Furthermore, the toxin was capable of producing epileptiform discharges in all animals injected with 1.74 microg of the toxin. In conclusion, the action of TsTX in the CNS may solely account for the peripheral alterations observed in severe cases of Tityus serrulatus scorpion poisoning.
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PMID:Centrally injected tityustoxin produces the systemic manifestations observed in severe scorpion poisoning. 1262 85

Sodium azide, used mainly as a preservative in aqueous laboratory reagents and biologic fluids and as a fuel in automobile airbag gas generants, has caused deaths for decades. Its exposure potential for the general population increases as the use of airbags increase. In order to characterize the known health effects of sodium azide in humans and the circumstances of their exposure, the authors conducted a systematic review of the literature from 1927 to 2002 on human exposure to sodium azide and its health effects. The most commonly reported health effect from azide exposure is hypotension, almost independent of route of exposure. Most industrial exposures are by inhalation. Most laboratory exposures or suicide attempts are by ingestion. Most of the reported cases involved persons working in laboratories. The time between exposure and detection of hypotension can predict outcome. Fatal doses occur with exposures of >or=700 mg (10 mg/kg). Nonlethal doses ranged from 0.3 to 150 mg (0.004 to 2 mg/kg). Onset of hypotension within minutes or in less than an hour is indicative of a pharmacological response and a benign course. Hypotension with late onset (>1 hour) constitutes an ominous sign for death. All individuals with hypotension for more than an hour died. Additional health effects included mild complaints of nausea, vomiting, diarrhea, headache, dizziness, temporary loss of vision, palpitation, dyspnea, or temporary loss of consciousness or mental status decrease. More severe symptoms and signs included marked decreased mental status, seizure, coma, arrhythmia, tachypnea, pulmonary edema, metabolic acidosis, and cardiorespiratory arrest. The signs and symptoms from lower exposures (<700 mg) are physiological responses at the vascular level and those at or above are toxicological responses at the metabolic level. There is no specific antidote for sodium azide intoxication. Recommended preventive measures for sodium azide exposure consist of education of people at high risk, such as laboratory workers, regarding its chemical properties and toxicity, better labeling of products containing sodium azide, and strict enforcement of laboratory regulations and access control.
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PMID:Human health effects of sodium azide exposure: a literature review and analysis. 1285 Nov 50

Sudden unexpected death in epilepsy (SUDEP) accounts for approximately 2% of deaths in population-based cohorts of epilepsy, and up to 25% of deaths in cohorts of more severe epilepsy. When it occurs, SUDEP usually follows a generalised tonic-clonic seizure. Unresponsiveness, apnoea, and cardiac arrest occur in SUDEP, rather than the typical gradual recovery. The great majority of tonic-clonic seizures occur without difficulty and how the rare seizure associated with SUDEP differs from others is unknown.Three mechanisms have been proposed for SUDEP: cardiac arrhythmia, neurogenic pulmonary oedema, and postictal suppression of brainstem respiratory centres leading to central apnoea. Recent studies have found that the incidence of SUDEP increases with the severity of epilepsy in the population studied. The duration of epilepsy, number of tonic-clonic seizures, mental retardation, and simultaneous treatment with more than two antiepileptic drugs are independent risk factors for SUDEP. Some studies have reported that carbamazepine use, carbamazepine toxicity, and frequent, rapid changes in carbamazepine levels, may be associated with SUDEP. Other evidence indicates that carbamazepine could potentially increase the risk for SUDEP by causing arrhythmia or by altering cardiac autonomic function. However, this evidence is tenuous and most studies have not found an association between the use of carbamazepine or any other individual antiepileptic drug and SUDEP. There is little information regarding antiepileptic drugs other than phenytoin and carbamazepine. The incidence of SUDEP with gabapentin, tiagabine, and lamotrigine clinical development programmes is in the range found in other populations with refractory epilepsy. This suggests that these individual antiepileptic drugs are no more likely to cause SUDEP than antiepileptic drugs in general. Best current evidence indicates that the risk of SUDEP can be decreased by aggressive treatment of tonic-clonic seizures with as few antiepileptic drugs as necessary to achieve complete control. At present there is no strong reason to avoid any particular antiepileptic drug. Further studies are needed to elucidate the potential role of individual antiepileptic drugs in SUDEP and establish clinical relevance, if any. These studies may be challenging to conduct and interpret because SUDEP is relatively uncommon and large numbers will be necessary to narrow confidence intervals to determine the clinical relevance. Also adjustments will be needed to account for the potent risks associated with other independent factors.
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PMID:Do antiepileptic drugs play a role in sudden unexpected death in epilepsy? 1286 2

A method has been described for the study of the central effects produced by the intracerebral injection of drugs in the unanaesthetized mouse. The effects observed were in good agreement with those obtained after similar injections in cats, dogs and human beings. After intracerebral injection, drugs of diverse structure produced certain generalized effects: changes in positioning of the tail, stupor, hyperexcitability and tachypnoea. Both acetylcholine and methacholine produced an akinetic seizure and depression, but the latter compound also caused lacrimation and salivation. Atropine produced piloerection, increased sensitivity to sound and touch, clonic convulsions and scratching, whereas hexamethonium caused Parkinsonian-like muscle tremors and peripheral vasodilatation. After adrenaline, hyperexcitability, exophthalmos, stupor and death from pulmonary oedema were observed, but (+)-methylamphetamine produced only piloerection and exaggerated activity in response to sound and touch. Ergotamine caused a decreased sensitivity to sound and touch, micturition, and stupor, while ergometrine caused clonic convulsions, piloerection, defaecation and stupor.
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PMID:Pharmacological effects produced by intracerebral injection of drugs in the conscious mouse. 1341 44

Scorpion human envenoming is a public health hazard in the southwest of Venezuela. Tityus zulianus is one of the scorpion species whose venom causes lung edema and cardiac failure in children. These occasionally deadly manifestations have been attributed to a massive sympathetic discharge. The intraperitoneal administration of T. zulianus venom (20 micrograms/g mouse) to anesthetized mice during subcutaneous microdialysis caused increased secretions, dyspnea, seizures and death between 30 min to 2 h. Seven amino acids were analyzed by capillary electrophoresis with laser induced fluorescence detection (CE-LIFD) in the collected samples before and after the venom administration. We found an increase of arginine (39%), phenylalanine (40%) and glutamate (94%), with no changes in valine, serine and aspartate, changes were significant when the injection of venom and vehicle were compared and before vs after venom injection. Further investigation is needed to know if the observed changes could be related to the molecular mechanisms of the venom or some of its components and therefore with the envenoming symptoms. To our knowledge, this is the first report with subcutaneous microdialysis and CE-LIFD coupling in scorpion envenomation studies in vivo, in mice.
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PMID:[Amino acid changes following intraperitoneal administration of Tityus zulianus scorpion venom in mice. Study with subcutaneous microdialysis and capillary electrophoresis]. 1472 83


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