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 present study evaluated the neurotoxic potential of phospholipase A2 (PLA2) in in vitro (primary neuronal cultures) and in vivo (EEG and behavior) rat models of CNS excitability. In vitro, PLA2 (0.0038-5.8 nM) or melittin (a potent activator of endogenous PLA2; 100-5000 nM), were highly neurotoxic, causing approximately 500 units/ml LDH release. The neurotoxic EC50s for PLA2 and melittin were 1.8 (1.4-2.3) and 848 (501-1280) nM, respectively. Neurotoxic concentrations of PLA2 stimulated neuronal release of [3H]AA. Preliminary in vitro experiments evaluating changes in neuronal calcium flux indicated that PLA2 caused transient, and melittin sustained, increases in [Ca2+]i. In vivo, PLA2 (0.5-5 micrograms i.c.v.) or melittin (2.5-20 micrograms i.c.v.) produced nonconvulsive EEG seizures, which generalized to status epilepticus. While the onset of seizure development was markedly delayed for PLA2 (1.5-4.5 h), the seizure inducing effects of melittin were evident within 3.5 +/- 0.2 min and more severe. Both PLA2 and melittin were lethal, exhibiting LD50s of 0.62 micrograms and 8.4 micrograms, respectively. Pretreatment with (+)-MK801 (5 micrograms, i.c.v.) significantly attenuated melittin, but not PLA2, in vivo neurotoxicity. PLA2 induced neuropathology in surviving rats revealed extensive cortical and subcortical injury to forebrain neurons and fibre pathways. Collectively, these results demonstrate the potent neurotoxic potential of PLA2, the delayed clinical nature of its in vivo neurotoxicity and the applicability of these model systems to future studies on mechanisms of PLA2 neurotoxicity and the development of potential PLA2 antagonists.
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PMID:Phospholipase A2-induced neurotoxicity in vitro and in vivo in rats. 865 97

Plasma aromatic amino acid (AAA) and branched-chain amino acid (BCAA) concentrations were determined in 292 alcoholics. The BCAA/AAA molar ratio in patients with alcohol withdrawal symptoms was compared with the ratio in patients without such symptoms. The BCAA/AAA molar ratio in patients with transient hallucinations or with delirium tremens was significantly lower than that in patients without these symptoms. The BCAA/AAA molar ratio tended to be lower in patients with alcohol withdrawal seizures than in patients without such symptoms. The BCAA/AAA molar ratio had a negative correlation with plasma total bilirubin and LDH, and a positive correlation with plasma cholinesterase and albumin. These results indicate that abnormalities of amino acid metabolism caused by liver damage in alcohol dependence may have an important role in the pathogenesis of the alcohol withdrawal syndrome.
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PMID:Aromatic and branched-chain amino acid levels in alcoholics. 906 12

Rhabdomyolysis is a condition affecting body homeostasis that results from impaired supply of muscles with energy, nutritional factors and blood. Complex pathophysiological mechanism causes that extended myolysis may complicate different clinical conditions, such as: crush syndrome, excessive physical effort (work, seizures), toxic effect of drugs and toxins, water-electrolyte disturbances, congenital enzymatic deficiencies etc. It seems that on the cellular level, essential role is played by excessively high intracytoplasmatic calcium level, which affects metabolic processes. So high calcium level is a consequence of muscular cell injury irrespective to its reason. It manifests clinically as muscular weakness, pal and oedema and laboratory tests reveal elevated CK, GOT, GPT, aldolase and LDH levels as well as dark brown urine colour. Demonstration of elevated serum myoglobin level or its presence in urine directly confirms development of rhabdomyolysis. In unfavorable conditions, rhabdomyolysis may result in acute renal failure. Appropriately early and adequate water supply and alkalization plays an essential role in prevention of impairment in renal function. In advanced phase of renal failure, hemodialysis is a standard treatment.
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PMID:[Rhabdomyolysis: clinical features, causes, complications and treatment]. 974 Nov 96

We studied the clinical and CT findings of 3 children with acute encephalopathy associated with adenovirus type 7 (AD-7) infection. Seizures in all the patients developed from 8 to 10 days after the onset of pyrexia. The values of serum AST, LDH and CRP elevated and those of WBC and serum protein decreased at the onset of encephalopathy. None of the patients had CSF leukocytosis. CT showed mild brain atrophy in all patients. A steroid pulse therapy was effective in one patient. The pathogenesis of encephalopathy is unknown. However, its onset and the success of the steroid pulse therapy suggested that it is a post infectious encephalitis. These findings, as well as the data of blood examination and of previous reports, implicated adverse effects of cytokines in the pathogenesis of this encephalopathy.
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PMID:[Three cases with acute encephalopathy related with adenovirus type 7 infection]. 1065 55

As seizures in infants and children often originate from the neocortex, neocortical epilepsy models may be appropriate for studying epileptiform activity and seizure-induced injury in the developing nervous system. However, the characterization of epileptiform activity or seizure-induced injury in cultured developing cortical neurons has seldom been reported. Therefore, We attempted to establish a cultured developing cortical neuronal epilepsy model, and to study the subsequent effect on neurons. Cultures were exposed to Mg(2+)-free media for 3 h, and then returned to regular media. Using whole-cell patch-clamp intracellular recording techniques, we found that spontaneously recurrent epileptiform discharges for at least 72 h could be induced after transient Mg(2+)-free treatment. Neuron morphology following Mg(2+)-free treatment demonstrated no prominent alterations. At different time points (6, 24 and 72 h) after Mg(2+)-free treatment, neuronal viability, identified by trypan blue staining and LDH activity, and apoptosis, measured by flow cytometry, showed modest but non-significant (P>0.05) changes compared with the age-matched control group after various culture periods (6 and 17 days) in vitro. Mitochondrial metabolic activity, measured by MTT assay, significantly decreased by 15% at 6 h after Mg(2+)-free treatment (P<0.05) in neurons cultured for 6 days, and at 24 h showed a 29% decrease in neurons cultured for 17 days (P<0.05). In conclusion, brief Mg(2+)-free treatment constitutes a cultured developing cortical neuron 'seizure' model, and can induce transient mitochondrial dysfunction without cell loss.
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PMID:Effect of recurrent epileptiform discharges induced by magnesium-free treatment on developing cortical neurons in vitro. 1269 39

The aim of this study was to assess the validity of serum and CSF oxidative status of patients with IE in their initial stage through the d-ROM (Diacron-Reactive Oxygen Metabolites, Italy) test, compared to those with other neurological diseases. The study was conducted on the following four groups: (1) influenza virus-associated encephalopathy (IE, n = 8), including four patients showing neurological sequelae or mortal; (2) influenza virus-associated febrile seizures (IFS, n = 11); (3) febrile convulsion (FC, n = 10): (4) enterovirus-associated encephalopathy (EE, n = 4), including one patient with neurological sequelae. The CSF d-ROM levels in the IE group were significantly higher than those in the IFS and the FC groups but not in the EE group. In addition, general laboratory findings such as leukocytes, platelets, C-reactive protein, aspartate aminotransferase, creatinine, creatinine kinase and LDH, including interleukin-6 (IL-6), were analyzed in each group. The CSF d-ROM levels in the IE group were significantly higher than those in the IFS and FC groups but not in the EE group. As for the serum d-ROM levels and general laboratory findings, with the exception of CSF IL-6 levels in IE, no significant differences were detected compared with the other groups. In patients with IE, the CSF d-ROM levels could be a valid predictive biomarker of the severity, and oxidative stress may be related to the pathogenesis of IE.
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PMID:Diagnostic and predictive value of CSF d-ROM level in influenza virus-associated encephalopathy. 1641 81

We describe a 16 year old female who developed thrombotic thrombocytopenic purpura (TTP) following infection due to Streptococcus. Initially presenting a fever and systemic upset she progressed to develop dialysis dependent acute renal failure, seizures, thrombocytopenia and a haemolytic anaemia--the pentad of features seen in TTP. Prior to the diagnosis she was found to have unexplained and previously undescribed MRI findings of diffuse increased signal intensity in the white matter of the left cerebellar hemisphere posteriorly and also increased signal intensity in the overlying cortex. She was commenced on plasmapheresis, and her anaemia, thrombocytopenia, creatinine and LDH all fully responded. In addition, she had no further seizures following plasmapheresis and has not relapsed to date. We review both the rare association of TTP and streptococcal infection, and the neuroradiological findings described in the literature. This is only the third case report describing TTP following streptococcal infection, and only the second in the era of plasmapheresis.
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PMID:Thrombotic thrombocytopenic purpura secondary to Streptococcus. 1661 15

Maternal immunoglobulin G (IgG) was derived from Wistar rats that just delivered the new offsprings. We examined the effect of this maternal IgG on infantile spasms induced by N-methyl-d-aspartate (NMDA) in immature rats. Pup animals were treated subcutaneously with 10 mg/kg/day maternal IgG from day 11 to day 15 after birth followed by a single intraperitoneal dose of NMDA (15 mg/kg). Administration of maternal IgG decreased the severity and increased the number of ACTH immunoreactive cells in the cortex of rats with NMDA-induced spasms. Furthermore, maternal IgG inhibited NMDA-induced intracellular LDH activity in cultured hippocampal neurons in a dose-dependent manner. The results indicate that maternal IgG can attenuate NMDA-induced seizures. In infantile spasms, some factors may during pregnancy negatively affect the transfer of maternal IgG from mother to fetus thereby causing a decrease in the amount of protective maternal IgG.
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PMID:Maternal IgG suppresses NMDA-induced spasms in infant rats and inhibits NMDA-mediated neurotoxicity in hippocampal neurons. 1702 92

Screening for pulmonary hypertension (pHTN) has not yet become routine in sickle cell disease (SCD), despite clinical evidence of its high prevalence and associated mortality. Our objectives are to identify clinical conditions and laboratory findings predictive of/or associated with pHTN. One hundred twenty-five adult outpatients with Hb SS, SC, SOArab, Sbeta(0), or Sbeta(+) thalassemia, who underwent echocardiography and/or right heart catheterization due to cardiorespiratory symptoms, were studied. pHTN was identified in 36% (28/77) of SS/Sbeta(0) and in 25% (12/48) of SC/SOArab/Sbeta(+) patients studied. In SS/Sbeta(0) patients, pHTN was associated with low hemoglobin, low GFR, increasing age, no history of treatment with hydroxyurea and a history of leg ulcers, with trends for associations with higher total bilirubin, LDH levels, systolic systemic blood pressure, history of avascular necrosis, seizures, and cerebrovascular events. Twelve (40%) of the SS/Sbeta(0) patients with pHTN had >or= 1+ proteinuria. (P<0.039). The presence of proteinuria correlated with lower GFR and had a high positive predictive value (0.60) for pHTN in subjects with SS/Sbeta(0). The data also provided evidence that pHTN in this population is associated with right heart failure, with echocardiographic evidence of right ventricle enlargement and pericardial effusion. This study confirmed that even relatively mild elevations in pulmonary pressure are associated with high prospective mortality (hazard ratio: 15.9). We concluded that pHTN has a high prevalence in all Hb S related syndromes and is associated with increased mortality in SS/Sbeta(0). Kidney dysfunction, as indicated by proteinuria or decreased GFR, also represents sufficient reason to screen for pHTN.
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PMID:Pulmonary hypertension associated with sickle cell disease: clinical and laboratory endpoints and disease outcomes. 1772 99

This paper describes very rare chemical poisoning and characteristics of patients with acute endosulfan mass poisoning in a rural area of Turkey and our experiences of these patients. We included 41 patients who were treated in our hospital with the diagnosis of endosulfan poisoning. After the first vital intervention they were examined in terms of age, sex, symptoms and physical examination findings, laboratory results, treatment and outcome. Forty-one patients were admitted to the emergency department (ED) after triage. Nineteen (46.3%) of the patients were female, 22 (53.7%) were male. The mean age was 27.9+/-16.0 years (1-67 years). The mean time to the ED was 4.1+/-0.9 h (3-6.5 h). The most common symptoms were anxiety (97.6%), nausea (56.1%) and vomiting (48.8%). Tests of the blood samples obtained at the ED revealed leucocytosis (11 070.6+/-4302.5/microl), increased blood glucose, LDH, CK and CK-MB levels. Toxicological analysis of blood and urine samples revealed endosulfan as the causative agent. Especially in the rural areas, cases with acute repetitive seizures should suggest endosulfan intoxication when the aetiology is uncertain even in the absence of any signs of intoxication. Health care professionals should understand the hazards associated with the pesticide use as well as diagnosis and treatment of these types of poisonings.
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PMID:Experiences with endosulfan mass poisoning in rural areas. 1893 18


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