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)

Our group has been carrying out interdisciplinary studies on the effects of prenatal and postnatal protein malnutrition on the developing rat brain. Anatomical, physiological, biochemical and behavioral approaches using the same animal model have revealed that protein malnutrition affects the brain at various levels, i.e., (1) anatomical, as revealed by Golgi findings of deranged dendritic trees on analysis of cortical and subcortical areas; (2) physiological, as revealed by delayed sleep pattern maturation, disturbances in seizure thresholds, slowing of sensory cortico-cortical and thalamocortical evoked potentials, and changed power in hippocampal theta activity; (3) biochemical, as revealed by marked increases in biogenic amines dating from birth, as well as modifications in tryptophan metabolism; and (4) behavioral, as revealed by various changes in responses to different kinds of aversive stimulation. Reversal studies have revealed that many changes are permanent and not amenable to nutritional rehabilitation even at birth, which is before the brain growth spurt in the rat. Our paradigm closely mimicks the human condition of low level, chronic protein undernutrition and thus reveals the underlying disturbances due to malnutrition. The dietary reversal studies are attempts at pin-pointing critical brain growth periods, beyond which recovery of functions is not possible.
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PMID:Developmental protein malnutrition: influences on the central nervous system of the rat. 4 55

Eighty-eight rats were paired at birth according to sex and weight. One member of each pair received two electroconvulsive seizures a day during the neonatal period (days 2 to 11). Access of its control littermate to the mother was restricted so that the body weights of any two paired rats never diverged by more than 2 gm on any day of life, and were usually within one half gram of each other. This guaranteed that the nutritional status of seizure-treated and control animals was similar throughout development. On day 30 of life, seizure-treated rats had smaller brains (-56 mg, P less than .05) and reduced numbers of brain cells (-13.10(6), P less than .05) compared to their control littermates. It was concluded that the reduction of brain DNA brought about by neonatal seizures was not simply caused by malnutrition of seizure-treated animals.
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PMID:Developmental effects of seizures: role of malnutrition. 125 Jun 55

Despite the generally salutary experience in recent years of managing suppurative pleuropulmonary disease, empyemas and lung abscesses have persisted and increased in incidence in hospitals such as Queens Hospital Center that serve large numbers of the socioeconomically disadvantaged. This study documents the etiology, clinical presentation, treatment, and treatment results of suppurative pleuropulmonary disease at Queens Hospital Center, which serves a large segment of the urban poor, many of whom are black. Results indicate that contributory or antecedent etiologic factors include a history of prior disease (specifically pneumonia, lung abscess, obstructive lung disease, pulmonary neoplasia, and tuberculosis); a predisposition to constitutional or immunologic deficiencies (specifically, alcoholism, anemia/malnutrition, drug abuse, and acquired immunodeficiency syndrome [AIDS]); conditions contributing to tracheobronchial aspiration (specifically, alcoholism and seizure disorders); and a miscellaneous group such as prior surgery, cardiovascular disease, and sepsis syndrome. The patients in this study were young with maximal incidence occurring in the third to fifth decades of life. Patients were predominantly male (75%) and black (66%). There were 18 deaths (23%), with sepsis being the cause in 10 (56%). Most surgical interventions were conservative, ie, bronchoscopies (48), thoracenteses (43), and tube thoracotomies (39). Thirty-one open thoracotomies were performed for drainage, decortication, or pulmonary resection. The surgical mortality was three cases or 5% of the patients who underwent surgery. The designated incidence of proven AIDS in this series (29%) was low, undoubtedly because many patients refused testing, and the multiple gram-positive and gram-negative infections that were seen did not conform to the Centers for Disease Control criteria for diagnosis and case reporting for AIDS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of surgery in treating pleuropulmonary suppurative disease--review of 77 cases managed at Queens Hospital Center between 1986 and 1989. 160 13

The effects of prenatal protein malnutrition upon the efficacy of excitatory synaptic transmission at the level of the perforant path/dentate granule cell synapse were examined during development of perforant path kindling in chronically implanted adults rats. Rats born to dams fed a low protein (6% casein) or control protein (25% casein) diet were fostered to lactating dams fed the 25% casein diet 24 h after birth and were maintained on this diet throughout life following weaning. Beginning at 90-120 days of age, animals received daily kindling stimulations applied to the perforant path. Extracellular field potentials recorded from the granule cell layer of the dentate gyrus in response to single-pulse stimulation of the perforant path were analyzed to determine the effects of prenatal protein malnutrition on the efficacy of synaptic transmission during the kindling process. Measures used for these analyses included the EPSP slope, an indicator of the level of synaptic drive, the population spike amplitude which is a measure of postsynaptic activation and cellular firing, and the ratio of the population spike amplitude relative to the corresponding EPSP slope value, which was used to evaluate the overall efficacy of synaptic transmission. animals of the 6%/25% diet group were found to have significantly lower afterdischarge thresholds, yet required significantly more daily kindling stimulations to develop generalized motor convulsions (stage 5 seizure) than control animals. Examination of dentate field potentials obtained prior to kindling revealed no significant between group differences in measures of EPSP slope or population spike amplitude. Statistically significant increases in measures of both the population EPSP slope and population spike amplitude were observed in both diet groups 24 h after the first kindled afterdischarge. The degree of increase in both of these measures was significantly greater in animals of the 6%/25% group. Evaluation of input/output measures obtained during kindling revealed a steady increase in the population EPSP slope for both diet groups with animals of the 6%/25% group showing significantly greater levels of enhancement in this measure than controls. Enhancement of population spike amplitudes reached maximal values in animals of the 25%/25% group within the first few kindling stimulations and these levels remained unchanged until the first stage 5 seizure. In contrast, animals of the 6%/25% group showed a continuous increase in the population spike amplitude measure during the entire kindling process. Appearance of the first generalized motor convulsion (stage 5 seizure) resulted in a decrease in population spike amplitudes in both diet groups, with animals of the 6%/25% group showing a significantly greater decrease in this measure than controls.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of prenatal protein malnutrition on kindling-induced alterations in dentate granule cell excitability. I. Synaptic transmission measures. 164 74

Deficiency of 3-hydroxy-3-methylglutaryl-CoA lyase has been studied in 11 Saudi infants. The diagnosis was established by the measurement of enzyme activity in lymphocytes, in fibroblasts and, in seven patients, by the gas chromatography/mass spectrometer pattern of excreted organic acids in the urine. In seven infants the disease caused a devastating acidotic attack within the first day of life, while in two the crisis occurred by the third day of life. In two infants from one family the disease appeared later in infancy. The clinical presentation of an acidotic attack is lethargy, hyperpnoea, tachypnoea and seizures, either at birth (two infants), following first feeding (in five infants), or following vomiting or refusal of food in later infancy. The acidotic attacks recurred later in life following minor illness or refusal to eat. The acidosis of this enzyme deficiency progresses rapidly, leading to cardiopulmonary arrest and death within hours of onset unless treated promptly. In four surviving infants diagnosed and treated early, development is normal. Magnetic resonance and computerized tomography brain scans in these infants, however, show white matter lesions and mild atrophy.
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PMID:3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) lyase deficiency in Saudi Arabia. 188 3

Complications that can lead to death during shigellosis include intestinal as well as systemic manifestations. The former include intestinal perforation, toxic megacolon, and dehydration, and the latter include sepsis, hyponatremia, hypoglycemia, seizures and encephalopathy, hemolyticuremic syndrome, pneumonia, and malnutrition. Data on the frequency of these complications come primarily from hospital-based studies, in which sepsis-either with Shigella or with other Enterobacteriaceae-and hypoglycemia are the most common causes of death. Management of these two complications requires broad-spectrum empiric antibiotic treatment of all severely ill, malnourished patients with shigellosis as well as frequent feedings to prevent hypoglycemia. Unfortunately, in developing countries, access to parenteral broad-spectrum antimicrobial agents is often limited, and frequent feedings are often precluded by the severe anorexia that is characteristic of shigellosis. Realistic approaches to the reduction of mortality from shigellosis must continue to focus on prevention and early antimicrobial therapy rather than on treatment of established complications.
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PMID:Potentially lethal complications of shigellosis. 204 57

Experimental epilepsy was induced in developing normal, undernourished and subsequently rehabilitated rats by locally injecting graded doses of Kainic acid (KA) in the right frontal cortex. Frequency and power spectral analysis of EEG was carried out to assess the progressive changes in EEG during KA-epileptogenesis. Undernourished animals were highly susceptible to seizure discharge. They exhibited generalized tonic-clonic discharge and had episodes of clinical seizures even after temporary neuronal recovery. Increase in power of delta, theta and decrease in alpha power was observed in the compressed spectral array (CSA) of undernourished animals. Delayed neuronal recovery with reduced background EEG and marked electrosilence in response to intra-rectal sodium valproate was observed in undernourished animals. Rehabilitated animals exhibited partial recovery which was related to the body weight gain. Spike frequency, spike amplitude and neuronal recovery time were not significantly differet between normal and undernourished animals at lower doses of KA (7.5-60 ng) whereas at higher doses (120-500 ng) marked differences were observed in these parameters. In KA treated undernourished rats 3H-glycine incorporation was significantly higher than normal in the hippocampus and spinal cord and lower in the cerebellum.
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PMID:Kainic acid induced epileptogenesis in developing normal & undernourished rats--a computerised EEG analysis. 207 64

Toxic injury is one of the many ways by which the functional integrity of the heart may become compromised. Any of the subcellular elements may be the target of toxic injury, including all of the various membranes and organelles. Understanding the mechanisms underlying cardiotoxicity may lead to treatment of the toxicity or to its prevention. Doxorubicin and its analogs are very important cancer chemotherapeutic agents that can cause cardiotoxicity. Other agents which are cardiotoxic and which have profound public health implications include the alkaloid emetine in ipecac syrup, cocaine, and ethyl alcohol. The most important cardiotoxic mechanisms proposed for doxorubicin include oxidative stress with its resultant damage to myocardial elements, changes in calcium homeostasis, decreased ability to produce ATP, and systemic release of cardiotoxic humoral mediators from tissue mast cells. Each of the first 3 mechanisms can lead to each of the other 2, and the causal relationships between all of these mechanisms are not clear. New evidence suggests that doxorubicinol, one of the metabolites of doxorubicin may be the moiety responsible for cardiotoxicity. Several other potential mechanisms also have been proposed for doxorubicin. Emetine in ipecac syrup is the first aid treatment of choice for many acute toxic oral ingestions and the alkaloid, itself, is used to treat amebiasis. Cardiotoxicity occurs following chronic exposure, such as occurs therapeutically in amebiasis and with ipecac abuse by bulemics. A number of mechanisms are proposed for emetine cardiotoxicity, but the current mechanistic literature is quite scarce. Cocaine abuse recently has caught the public interest, in particular because of the drug-related sudden deaths of certain athletes. Cocaine can cause hypertension, arrhythmias, and reduced coronary blood flow, each of which can contribute to its lethality. However, it may be possible that cocaine sudden death episodes are more related to hyperthermia and convulsive seizures, rather than to cardiovascular toxicity. Chronic alcohol use leads to dilated cardiomyopathy and failure as part of the general physical degeneration that occurs with alcoholism. Several mechanisms are proposed for the cardiomyopathy, but only 2 things seem clear. The cardiotoxicity is due to an intrinsic effect of alcohol, rather than to malnutrition or co-toxicity, and abstinence is the only effective treatment for the cardiomyopathy. Recent articles indicate that very moderate use of alcohol may be beneficial and protect against cardiovascular-related morbidity. One explanation for these findings seems to be that the non-drinking groups, against whom the moderate drinking comparisons were made, were enriched in former drinkers with significant alcohol-related cardiovascular pathology.
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PMID:Toxic mechanisms of the heart: a review. 209 Dec 37

The seizure threshold and therapeutic potential of intrarectal sodium valproate were studied in young developing normal and undernourished rats, using the penicillin model. Undernourished rats were highly susceptible to seizure discharge. They exhibited generalised electrocortical inhibition and repeated episodes of epileptic discharges even after temporary neuronal recovery. Delayed spontaneous and drug induced neuronal recovery, low spike frequency and amplitude (P less than 0.001) reduced background EEG and marked electrocortical silence in response to intrarectal (25 mg/kg) sodium valproate treatment, was observed in the undernourished animals. Rehabilitated animals exhibited partial neuronal recovery which was related to the improvement in body weight. Analysis of spike frequency, spike amplitude and neuronal recovery time showed that both normal and undernourished animals behaved in a similar fashion at lower doses of penicillin (2.5 to 15 IU). Significant differences in the electrophysiological parameters were observed between the two groups at higher doses of penicillin (20 to 30 IU).
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PMID:Seizure susceptibility & intra rectal sodium valproate induced recovery in developing undernourished rats. 211 23

Mutations in the enhancer of seizure (e(sei] locus have been isolated on the basis of their ability to cause temperature-induced paralysis of alleles at the seizure (sei) locus at temperatures at which these mutations ordinarily do not paralyze. This enhancer is specific to the seizure locus and is without effect on other temperature-sensitive paralytic mutants including para, nap, tip-E and shi. This suggests that the enhancer responds specifically to the mechanism of paralysis mediated by the seizure mutations. The e(sei) is a recessive mutation which maps to 39.0 on the left arm of chromosome 3. Deficiency mapping has placed it at 69A4-B5 on the salivary gland polytene chromosome map. When a new enhancer allele was isolated following P-M hybrid dysgenesis, there was a concomitant P-element insertion at 69B. In the absence of seizure mutations, the enhancer mutation causes non-temperature dependent hyperactivity when agitated and interferes with the climbing response. Electrophysiological studies examined the effects of increasing temperature on electrical activity in the adult giant fiber/flight muscle system. Neuronal hyperactivity was seen in both e(sei) and sei single mutant homozygotes, but not in wild type. The hyperactivity was more severe in the sei;e(sei) double mutants. The correlation between the physiological effects and the mutant behavior suggests that both sei and e(sei) cause membrane excitability defects. Since previous work has shown that seizure mutants affect [3H]saxitoxin binding to the voltage-sensitive sodium channel, e(sei) may code for a gene product which interacts with this channel.
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PMID:Enhancer of seizure: a new genetic locus in Drosophila melanogaster defined by interactions with temperature-sensitive paralytic mutations. 244 Jul 63


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