Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149958 (complex partial seizures)
 2,563 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Deletions which removed rfa genes involved in lipopolysaccharide (LPS) core synthesis were constructed in vitro and inserted into the chromosome by linear transformation. The deletion delta rfa1, which removed rfaGPBI, resulted in a truncated LPS core containing two heptose residues but no hexose and a deep rought phenotype including decreased expression of major outer membrane proteins, hypersensitivity to novobiocin, and resistance to phage U3. In addition, delta rfa1 resulted in the loss of flagella and pili and a mucoid colony morphology. Measurement of the synthesis of beta-galactosidase from a cps-lacZ fusion showed that the mucoid phenotype was due to rcsC-dependent induction of colanic acid capsular polysaccharide synthesis. Complementation of delta rfa1 with rfaG+ DNA fragments resulted in a larger core and restored the synthesis of flagella and pili but did not reverse the deep rough phenotype or the induction of cps-lacZ, while complementation with a fragment carrying only rfaP+ reversed the deep rough phenotype but not the loss of flagella and pili. A longer deletion which removed rfaQGPBIJ was also constructed, and complementation studies with this deletion showed that the product of rfaQ was not required for the functions of rfaG and rfaP. Thus, the function of rfaQ remains unknown. Tandem mass spectrometric analysis of LPS core oligosaccharides from complemented delta rfa1 strains indicated that rfaP+ was necessary for the addition of either phosphoryl (P) or pyrophosphorylethanolamine (PPEA) substituents to the heptose I residue, as well as for the partial branch substitution of heptose II by heptose III. The substitution of heptose II is independent of the type of P substituent present on heptose I, and this results in four different core structures. A model is presented which relates the deep rough phenotype to the loss of heptose-linked P and PPEA.
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PMID:Role of the rfaG and rfaP genes in determining the lipopolysaccharide core structure and cell surface properties of Escherichia coli K-12. 134 43

The Salmonella enterica group C1 O antigen structure has a Man-Man-Man-Man-GlcNAc backbone with a glucose branch, which differs from the S. enterica group B O antigen structure which has a Man-Rha-Gal backbone with abequose as side-chain. We have cloned the group C1 rfb (O antigen) gene cluster from serovar montevideo strain M40, using a low-copy-number cosmid vector. The restriction map of the group C1 (M40) rfb gene cluster was compared with that of group B strain LT2 by Southern hybridization and restriction enzyme analysis. The results indicate that the flanking genes are very similar in the two strains, but there is no detectable similarity in the rfb regions. We localized the mannose pathway genes rfbM and rfbK and one of the genes, rfbK, shows considerably similarity to cpsG of strain LT2, suggesting that part of the mannose pathway in the group C1 rfb cluster is derived from a gene of the M antigen (cps) cluster. The M antigen, which forms a capsule, is comprised of four sugars, including fucose. The biosynthetic pathway of GDP-fucose has steps in common with the GDP-mannose pathway, and the cps cluster has isogenes of rfbK and rfbM, presumably as part of a fucose pathway. We discuss the structure and possible evolution of the group C1 rfb gene cluster.
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PMID:Cloning and structure of group C1 O antigen (rfb gene cluster) from Salmonella enterica serovar montevideo. 137 35

We compared the relative sensitivity of two interictal PET techniques, bolus injection of [15O] labeled water for estimation of cerebral blood flow (H2(15)O CBF-PET), and 18F 2-deoxyglucose (18FDG-PET) for cerebral glucose metabolism (CMRglc), and T2-weighted magnetic resonance imaging, in 28 patients with medically intractable complex partial seizures undergoing evaluation for surgery. There were statistically significant associations between lateralization by 18FDG-PET, and MRI, but not H2(15)O CBF-PET, and lateralization of the epileptic focus as defined by scalp-sphenoidal ictal EEG. Fifteen patients had surgery or subdural electrodes. 18FDG-PET was more closely associated with a good outcome than H2(15)O CBF-PET, which, in addition, showed hypoperfusion contralateral to the epileptic temporal lobe in several cases. H2(15)O sensitivity may have been reduced by technical factors, but 18FDG-PET appears to be more specific for localization of epileptic zones.
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PMID:Comparison of PET measurements of cerebral blood flow and glucose metabolism for the localization of human epileptic foci. 146

Twenty-three patients with complex partial seizures were evaluated with 18F-2-deoxyglucose positron emission tomography and with the Beck Depression Inventory. Five of 10 patients with left and zero of eight with right temporal electroencephalographic foci had depressive symptoms; one of five patients with poorly localized electroencephalographic foci also scored in the depressed range. Temporal, frontal, caudate, and thalamic normalized glucose metabolic rates among five patients with depressive symptoms and well-localized left temporal epileptogenic regions were compared with five patients without depressive symptoms but with similar electroencephalographic characteristics. Multifactorial analysis of variance yielded a significant nonlateralized mood by region interaction. Of nine individual regions compared, only inferior frontal cortex showed a significant difference in normalized regional metabolic rate between depressed and nondepressed patients. Metabolism in this region also distinguished patients with depressive symptoms from normal control subjects. Depressive symptoms in patients with complex partial seizures are associated with a bilateral reduction in inferior frontal glucose metabolism, compared with patients without depressive symptoms and normal control subjects. The frontal lobe hypometabolism observed in patients with depressions associated with epilepsy, Parkinson's disease, and primary affective disorder suggests that similar frontal lobe metabolic disturbances could underlie these conditions.
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PMID:Cerebral metabolism and depression in patients with complex partial seizures. 159 97

Many biologically active tracers are available for positron emission tomography (PET) investigations, but most studies of epilepsy have utilized 18F-fluorodeoxyglucose (FDG) to measure local cerebral metabolic rate for glucose. Over 70% of patients with medically refractory partial seizures demonstrate an interictal zone of hypometabolism corresponding to the epileptogenic region. This metabolic defect commonly involves the temporal lobe in patients with complex partial seizures of mesial temporal origin, and is encountered less consistently with seizures of extratemporal neocortical origin. Although false localization is less likely with FDG-PET than with EEG, the hypometabolic zone merely reflects a focal functional deficit and its epileptogenicity must still be demonstrated electrophysiologically. When hemispherectomy or large multilobar resections are planned in small children, FDG-PET also provides useful supporting evidence that the contralateral hemisphere is functioning normally. It is difficult to obtain FDG-PET scans and to interpret results during spontaneous partial seizures. Ictal scans can be more easily obtained with single photon emission computed tomography (SPECT), which may provide information for planning surgical resections.
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PMID:PET scanning in partial epilepsy. 177 75

123I-Iomazenil SPECT was performed in 17 patients who were considered candidates for surgery of epilepsy because of medically intractable complex partial seizures. In addition to this examination their presurgical evaluation consisted of long term ictal EEG-CCTV monitoring, CT, MRI and 18FDG PET. In eight patients intracranial ictal EEG recordings were performed. SPECT was assessed visually while PET data were analyzed quantitatively. Both SPECT and PET were compared to ictal EEG data and showed asymmetries in over 80% of patients in agreement with EEG findings. These three methods were in agreement in 65% of patients. SPECT showed abnormality contralateral to the EEG focus in one patient (6%) while PET always demonstrated ipsilateral dysfunction. It is concluded that 123I-Iomazenil SPECT may be considered a more economical and more widely available alternative to 18FDG PET in the presurgical evaluation of patients with medically intractable complex partial seizures. In this respect 123I-Iomazenil specifically reflects functional changes in the membranes of neurons while 18FDG is related to glucose metabolism not only of neurons but also of glial cells.
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PMID:Identification of the side of epileptic focus with 123I-Iomazenil SPECT. A comparison with 18FDG-PET and ictal EEG findings in patients with medically intractable complex partial seizures. 196 75

Clinical applications of experimental models of complex partial seizure were studied using kainic acid-induced limbic seizures and amygdaloid kindling models. The following experiments were done aiming to study the basic approach for the treatment of the intractable complex partial seizures. 1) Degenerative focal lesions were made in bilateral substantia nigra and substantia innominata by a local microinjection of the ibotenic acid and influences upon limbic seizures were studied. Substantia innominata has a facilitatory effect upon secondary generalization of the limbic seizure while substantia nigra has an inhibitory influence. Degenerative lesions of the bilateral hippocampus inhibited development process as well as establishment of the kindling. 2) Resection of the primary epileptic focus in a limbic seizure status resulted in seizure control in cats with a single focus but not in another with multiple foci. 3) An autoradiography was done during limbic seizure status induced by kainic acid microinjection, and local cerebral glucose utilization (LCGU) and local cerebral blood flow were studied in order to study the relationship between cerebral metabolism and cerebral blood flow during limbic seizures. In the pyramidal cell of the hippocampus, an increased ratio of LCGU (x 4.1) is larger than that of LCBF (x 1.6). This uncoupling may be one reason of the neuronal cell damage during the limbic seizure status. 4) Autoradiography of the calcium suggested that one of the causes of hippocampal degeneration in intractable complex partial seizures should be a consequence of calcium influx into pyramidal cells during repeated limbic seizures.
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PMID:[Experimental complex partial seizure and its possible clinical application]. 218 69

Diabetic and sickle retinopathy have features in common--for example, venous dilatation, microaneurysms, and capillary closure preceding neovascularisation. Bearing in mind that haemoglobin in poorly controlled diabetes is abnormal and that extremely low oxygen tensions (known to cause sickling) exist in the healthy cat retina, we wished to explore the possibility that diabetic blood, like that of sickle cell disease, may become more viscous when deoxygenated. To do this we measured whole blood viscosity, under oxygenated and deoxygenated conditions, of 23 normal persons, 23 diabetic patients without retinopathy, and 34 diabetic patients with retinopathy. The shear rate used was 230 s-1, which is similar to that thought to prevail in the major retinal veins. The viscosity of blood from normal persons, corrected for packed cell volume, did not change significantly on deoxygenation: mean 4.54 (SD 0.38) cps, versus, 4.57 (0.39) paired t test, p = 0.66. Similarly the blood from diabetics without retinopathy showed no change: 4.42 (0.45) versus 4.42 (0.30), p = 0.98; whereas the blood from patients with retinopathy changed from 4.82 (0.48) to 4.95 (0.63), p = 0.027. The hypoxic viscosity ratio (deoxygenated divided by oxygenated viscosity) correlated with total serum cholesterol (r = 0.44, p = 0.018) but not with HbA1, serum glucose, triglycerides, or age. A disproportionate increase in venous viscosity relative to arterial viscosity would lead to increased intraluminal and transmural pressure and therefore exacerbate leakage across capillary walls.
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PMID:Hypoxic viscosity and diabetic retinopathy. 237 52

We used positron emission tomography with 18F-2-deoxy-D-glucose to study the effect of carbamazepine on local cerebral metabolic rate for glucose (lCMRGlc) in 9 patients with complex partial seizures. Twenty regions of interest were evaluated. Seven control patients had serial scans without a drug change. Metabolic rates were significantly (p less than 0.05) lower in patients on carbamazepine in 6 of 20 regions of interest (3 left cerebral hemisphere, 3 right). Mean lCMRGlc was 7.4 +/- 2.0 mg/min/100 in patients on carbamazepine and 8.8 +/- 2.5 in patients off carbamazepine (p less than 0.00005; cutoff level for 180 comparisons: 0.00027). The mean (+/- SEM) difference in lCMRGlc between scans was 12 +/- 2%. No significant changes in lCMRGlc on serial scans were detected in any of the 20 regions for the control group. The mean (+/- SEM) variation for control regions of interest was 1 +/- 1%. This study showed that carbamazepine depresses cerebral glucose metabolism as much as phenytoin does, but much less than phenobarbital does. The difference in effect on lCMRGlc may be related to drug mechanisms of action, as well as to effects on memory, learning, mood, and behavior.
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PMID:The effect of carbamazepine on cerebral glucose metabolism. 277 94

Neurochemical studies in animal models of epilepsy have demonstrated the importance of multiple neurotransmitters and their receptors in mediating seizures. The role of opiate receptors and endogenous opioid peptides in seizure mechanisms is well developed and is the basis for measuring opiate receptors in patients with epilepsy. Patients with complex partial seizures due to unilateral temporal seizure foci were studied by positron emission tomography using 11C-carfentanil to measure mu-opiate receptors and 18F-fluoro-deoxy-D-glucose to measure glucose utilization. Opiate receptor binding is greater in the temporal neocortex on the side of the electrical focus than on the opposite side. Modeling studies indicate that the increase in binding is due to an increase in affinity or the number of unoccupied receptors. No significant asymmetry of 11C-carfentanil binding was detected in the amygdala or hippocampus. Glucose utilization correlated inversely with 11C-carfentanil binding in the temporal neocortex. Increased opiate receptors in the temporal neocortex may represent a tonic anticonvulsant system that limits the spread of electrical activity from other temporal lobe structures.
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PMID:Mu-opiate receptors measured by positron emission tomography are increased in temporal lobe epilepsy. 283 32


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