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

The rat brain-derived neurotrophic factor (BDNF) gene consists of four short 5'-exons linked to separate promoters and one 3'-exon encoding the mature BDNF protein. Using in situ hybridization we demonstrate here that kindling-induced seizures, cerebral ischaemia and insulin-induced hypoglycaemic coma increase BDNF mRNA levels through insult- and region-specific usage of three promoters within the BDNF gene. Both brief (2 min) and longer (10 min) periods of forebrain ischaemia induced significant and major increases only of exon III mRNA in the dentate gyrus. Following hypoglycaemic coma (1 and 30 min), exon III mRNA was markedly elevated in the dentate gyrus and, in addition, exon I mRNA showed a moderate increase. Single and recurrent (n = 40) hippocampal seizures significantly increased expression of exon I, II and III mRNAs in the dentate gyrus granule cells. After recurrent seizures, including generalized convulsions, there were also major increases of both exon I and III mRNAs in the CA3 region, amygdala, piriform cortex and neocortex, whereas in the hippocampal CA1 sector marked elevations were detected only for exon III mRNA. The insults had no effect on the level of exon IV mRNA in the brain. The region- and insult-specific pattern of promoter activation might be of importance for the effectiveness of protective responses as well as for the regulation of plastic changes following brain insults.
 ...
PMID:Brain insults in rats induce increased expression of the BDNF gene through differential use of multiple promoters. 802 13

The safety of autologous blood donation by "high-risk" patients (those with some preexisting medical conditions) has been questioned. The authors reviewed 1393 consecutive blood donation records (207 high-risk autologous [HRA], 665 non-high-risk autologous [NHRA], and 521 directed donors [DD]) to determine the safety and outcome of blood donation by HRA patients as compared with other donors at their center. The HRA group included patients with a history of significant coronary artery on cerebral vascular disease, recent seizures, cardiac arrhythmia, chronic heart failure, valvular or congenital heart disease, symptomatic dyspnea, insulin-dependent diabetes and/or current therapy with two or more antihypertensive medications. Those designated NHRA were all other autologous donors; DD met all criteria for homologous donation. Donor characteristics including predonation hematocrit, pre- and postdonation mean arterial pressure and heart rates were similar in all groups. Eight HRA donors (3.9%) had reactions, compared with 21 NHRA (3.2%) and 23 DD (4.4%), a difference that was without statistical significance. The reaction rate in all autologous donors (HRA and NHRA) was 3.4%. No differences in symptoms reported, hemodynamics or reaction severity were observed among the three groups (P > .05). A multiple logistic regression was performed within and among the groups with the risk factor categories listed above and medication classes including beta blockers, cardiac glycosides, calcium-channel blockers, antihypertensive agents, nitrates, and antiarrhythmic agents (chi 2 = 14.9; P = .0006). Only first-time donation (P = .0001) and cardiac glycoside usage (P = .04) were positively associated with an untoward reaction. The authors conclude that donation by HRA donors is at least as safe as that by donors who meet homologous donation criteria in their population and setting.
 ...
PMID:Comparable safety of blood collection in "high-risk" autologous donors versus non-high-risk autologous and directed donors in a hospital setting. 787 63

When glucose utilisation is impaired due to decreased insulin effect, ketones are produced by the liver from free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe metabolic acidosis and tends to occur in patients with type I (insulin-dependent) diabetes mellitus. In addition, hypovolemia is an almost invariable finding with marked hypoglycemia and is primarily induced by the associated glucosuria. Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of acetone on the patient's breath sometimes suggests that ketoacidosis is present. The classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss. Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including lethargy, seizures or coma. Some patients also have marked vomiting and abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma glucose concentration. Glucosuria and ketonuria can be semiquantitatively detected with reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the metabolic acidosis. Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia and potassium, and phosphate depletion. The mainstays of therapy are the administration of low-dose insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Ketoacidotic diabetic metabolic dysregulation: pathophysiology, clinical aspects, diagnosis and therapy]. 817 67

The first disease due to disturbances in a cell organelle was discovered in 1959-62, and its basis was loose-coupling of oxidative phosphorylation in the skeletal muscle mitochondria accompanied by severe alterations of their structure (Luft's disease). During the 1980s, functional disturbances and structural alterations in the mitochondria were observed in more than 100 disease entities, mainly in parts of the central nervous system and skeletal muscles. A second breakthrough in this area was the discovery in 1963-64 that mitochondria had their own DNA, mtDNA. Following the observation in 1988 of mutations of mtDNA in mitochondrial diseases, such mutations--mainly deletions and point mutations--were observed in almost all mitochondrial diseases. A remarkable extension of the area is the notion that "normal" ageing is accompanied by decreased oxidative phosphorylation and the appearance of mtDNA mutations. During the last two years, such changes have been demonstrated in diseased states in tissues and organs, which are especially reliant on oxygen supply: in the central nervous system (Parkinson's disease, some types of epilepsy and seizures, Huntington's disease, possibly also in Alzheimer's disease); in heart muscle (cardiomyopathies) and in skeletal muscle. Type 2 diabetes or NIDDM engages two tissues most reliant on oxygen consumption, the pancreatic islets (insulin secretion) and skeletal muscle (insulin sensitivity). Both these functions are genetically determined, the latter to a high degree also controlled by "environmental" factors. The evident age factor in the development of NIDDM could be on a par with the "normal" ageing process.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Physiopathology of mitochondria. From Luft's disease to aging and diabetes]. 836 14

Hypoglycemia, a commonly encountered metabolic emergency, is most often easily diagnosed and rapidly treated with satisfactory patient outcome. If not recognized and treated promptly, hypoglycemia may cause irreversible central nervous system injury; it rarely results in death. The classic presentation of hypoglycemia, a patient with diabetes mellitus on medical therapy (Insulin or oral hypoglycemic agents) who presents with an altered sensorium, is frequently seen in the emergency department (ED). Less often, patients with this metabolic emergency present to the ED in a manner suggestive of a situation other than hypoglycemia. Patients may present with seizure activity or focal neurological deficits, leading the physician to treat a primary neurological syndrome and not immediately recognize the primary cause of the problem. Alternatively, patients with hypoglycemia will present to the ED with an altered mental status after a traumatic event. The physician may again assume that the alteration in consciousness has resulted from a head injury and not a metabolic disorder. Four cases are presented in which the medical history of the event (i.e., trauma) suggested head injury as an explanation of the presentation when, in fact, hypoglycemia was responsible for the altered sensorium. The diagnosis of hypoglycemia is easily made with the performance of a bedside screening test which can be subsequently confirmed by laboratory blood analysis. It is imperative that emergency physicians consider hypoglycemia in all patients with any mental status abnormality, focal neurological deficit, or seizure activity, even when the findings seem to be explained initially by other etiologies.
 ...
PMID:Acute hypoglycemia masquerading as head trauma: a report of four cases. 885

To determine risk factors for ankle and foot fractures, data collected from 9704 women 65 years of age or older from four areas of the United States were analyzed. Self-reported baseline questionnaires covered areas such as lifestyle factors (physical activity, diet, and smoking habits) and functional impairment (history of fracture, falling, and other diseases). Bone mineral density (BMD) and performance on neuromuscular tests were also measured. During 5.9 years of follow-up, 191 women fractured an ankle and 204 women fractured a foot. Proportional hazard models were used to estimate relative risks. In multivariable models, factors associated with ankle fracture included one or more falls in the year prior to baseline (relative risk [RR] 1.5; 95% confidence interval [CI] 1.1-2.1), greater vigorous physical activity (RR per 2 times/week, 1.2; CI 1.1-1.3), weight gain since age 25 (RR per 20% gain, 1.4; CI 1.2-1.5), self-reported osteoarthritis (RR 0.5; CI 0.3-0.8), a sister's history of hip fracture after age 50 (RR 1.7; CI 1.0-3.0), out of house < or = 1 per week (RR 3.0; CI 1.4-6.6), and low distal radius BMD (RR per -0.1 g/cm2, 1.2; CI 1.0-1.4). Factors associated with foot fracture included insulin-dependent diabetes (RR 2.9; CI 1.2-7.2), use of seizure medications (RR 2.3; CI 1.0-5.7) or of benzodiazepines (RR 1.5; CI 1.1-2.2), history of hyperthyroidism (RR 0.5; CI 0.3-1.0), poor far depth perception (RR 0.7; CI 0.5-1.0), and low distal radius BMD (RR per -0.1 g/cm2, 1.3; CI 1.1-1.5). Ankle and foot fractures have different profiles of risk factors that are largely independent of low bone mass.
 ...
PMID:Predictors of ankle and foot fractures in older women. The Study of Osteoporotic Fractures Research Group. 886 10

The present study was undertaken to evaluate the antiseizure activity spectrum of insulin against various behavioral seizure models in rats. Insulin was injected intraperitoneally (i.p.) at a test dose of 1 U/kg. Dextrose (3 g/kg) was administered simultaneously with insulin to counteract its hypoglycemic effect and induce a normoglycemic state. Insulin was found to significantly decrease the incidence, intensity and mortality rate and prolong the latency of generalized tonic-clonic convulsions induced by pentylenetetrazole (60 mg/kg i.p.) and significantly decrease the intensity and mortality rate and prolong the latency of generalized tonic-clonic convulsions induced by penicillin (2000 U/intracerebrocortical). Insulin was not only found to prolong the latency of all the seizure components but was found to reduce the incidence of focal myoclonic twitches and generalized tonic-clonic convulsions induced by kainic acid (12 mg/kg i.p.) as well. Insulin was shown to be ineffective to suppress ouabain (5 micrograms/intracerebroventricular) induced seizures. These findings indicate that insulin possesses a broad spectrum of antiseizure activity in rats. Interaction with brain Na(+)-K(+)-ATPase has been discussed as a possible mechanism of action.
 ...
PMID:Antiseizure activity of insulin: insulin inhibits pentylenetetrazole, penicillin and kainic acid-induced seizures in rats. 895 15

The amounts of cortisol and testosterone in the plasma or urine of Mongolian gerbils exposed to stress factors or treated subcutaneously with insulin (2 IU), vasopressin (1 IU), ACTH (6 IU) or dexamethasone (50 micrograms) were determined. Increased plasma cortisol was observed in animals stressed by ether anesthesia or immobilisation (1-4 hours), or treated with insulin, vasopressin or ACTH. Cortisol levels were reduced after dexamethasone administration. Plasma testosterone was elevated in animals stressed by ether anesthesia or handling plus seizure; no other treatment altered testosterone levels. An augmented cortisol excretion, which lasted one day, occurred in gerbils immobilised for one as well as for four hours. A much more prolonged stimulation of cortisol excretion, lasting three days, was seen in animals receiving ACTH or dexamethasone plus ACTH. Testosterone excretion was stimulated by ACTH and dexamethasone plus ACTH; it was not influenced by any other treatment. The present study shows that analysis of circulating steroid levels is the only reliable approach to assess the secretory activity of Mongolian gerbil adrenals or testes. In some experimental conditions (e.g. after stressor application or ACTH treatment) cortisol excretion may be used as an index of adrenal secretory function. In contrast, the striking differences between cortisol values present in plasma and urine of peptide-or dexamethasone-treated gerbils indicate that urinary cortisol does not reflect short-term changes of adrenal function. Similarly, the striking differences of testosterone values in plasma and urine indicate that urinary testosterone monitoring cannot be used to determine the secretory activity of gerbil testes.
 ...
PMID:Dissociation of plasma and urinary steroid values after application of stressors, insulin, vasopressin, ACTH, or dexamethasone in the Mongolian gerbil. 902 44

We report on a male infant with congenital hypoparathyroidism who developed primary hypothyroidism at 3 months and insulin-dependent diabetes mellitus at 25 months. He had evidence of widespread and progressive neurologic dysfunction characterized by severe developmental delay, blindness, deafness, seizures, atrophy of the cerebellar and frontal lobes, and elevated spinal fluid protein. Also noted were renal hypoplasia, hyporeninemic hypoaldosteronism, chronic anemia, persistent elevation of liver transaminase levels, abnormal intraventricular cardiac conduction, reduction in numbers of helper T-cells, and distinctive facial anomalies. The child died of multiorgan failure at 29 months. A mitochondrial basis for the syndrome was considered but a molecular mechanism has, as yet, not been identified.
 ...
PMID:Multiple endocrinopathies in an infant with fatal neurodegenerative disease. 909 56

Severe partial seizures may be the presenting feature of nonketotic hyperglycemia in older adults, but cases in children are rare. We report three teenagers with well-controlled epilepsy who suddenly developed intractable partial seizures poorly responsive to anticonvulsants. Blood glucose levels were measured only after several days of hospitalization for frequent seizures when mild polyuria and polydipsia were first noted. Glucose levels were high with mild ketosis and acidosis in one patient and no ketosis in two. With institution of insulin, there was prompt cessation of seizures. The patients were diagnosed as having type I insulin-dependent diabetes mellitus and require ongoing insulin treatment. Hyperglycemia should be considered in children with epilepsy who develop intractable seizures.
 ...
PMID:Insulin-dependent diabetes mellitus presenting in children as frequent, medically unresponsive, partial seizures. 913 91


<< Previous 1 2 3 4 5 6 7 8 9 10