Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intoxication with gamma-hydroxybutyrate (GHB) is associated with coma, seizure, and death; treatment of overdoses is symptomatic. Previous studies in our laboratory have demonstrated that L-lactate and pyruvate treatment can increase the renal clearance of GHB and increase its elimination in rats, suggesting that GHB may undergo renal reabsorption mediated by monocarboxylic acid transporters (MCTs). The goals of this study were to characterize the renal transport of GHB in rats and to determine the role of MCT in its renal transport. Brush-border membrane (BBM) and basolateral membrane (BLM) vesicles were isolated from rat kidney cortex, and the uptake of L-lactate and GHB was characterized. L-Lactate and GHB undergo both pH- and sodium-dependent transport in BBM vesicles and pH-dependent transport in BLM vesicles. A simple Michaelis-Menten equation best described the pH-dependent uptake of GHB in BBM (Km, 8.0 +/- 1.8 mM; Vmax, 838 +/- 45 pmol/mg/s) and in BLM vesicles (Km, 10.5 +/- 2.6 mM; Vmax, 806 +/- 253 pmol/mg/s). mRNA of MCT1 and MCT2 was determined in rat kidney cortex using reverse transcriptase-polymerase chain reaction; using Western blot, the protein expression of MCT1 was present mainly in BLM vesicles, with weak expression in BBM vesicles, whereas that of MCT2 was exclusively in BLM vesicles. Studies with rat MCT1 gene-transfected MDA-MB231 cells demonstrated that GHB was a substrate of MCT1. The data suggest that rat MCT1 may represent an important transporter for GHB in renal tubule cells. This investigation provides evidence for the importance of MCTs in the reabsorption of the monocarboxylic acids l-lactate and GHB in the kidney.
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PMID:Transport of gamma-hydroxybutyrate in rat kidney membrane vesicles: Role of monocarboxylate transporters. 1670 23

We sought to determine the changes in brain interleukin-1beta (IL-1beta) following the coadministration of norfloxacin (25 mg/kg, i.p.) with biphenylacetic acid (100 mg/kg, p.o.) in rats. Norfloxacin provoked clonic convulsions in rats treated concomitantly with biphenylacetic acid, a major metabolite of the nonsteroidal anti-inflammatory drug fenbufen. Seizure activity was analyzed by EEG monitoring. Behavioral changes were also monitored. IL-1beta expressions in the prefrontal cortex and hippocampus at different time intervals were studied by reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The epileptiform discharges appeared in all the rats, accompanied with limb twitching and clonic-tonic seizures after administration of norfloxacin coadministered with biphenylacetic acid. Norfloxacin plus biphenylacetic acid-induced convulsions rapidly and transiently enhanced IL-1beta mRNA in the prefrontal cortex and hippocampus. IL-1beta mRNA expression in the prefrontal cortex and hippocampus was detected as soon as 30 min after norfloxacin injection, and decayed to control levels by 6 h. ELISA analysis revealed significant increase of the IL-1beta protein in the prefrontal cortex and hippocampus at 2 h and 6 h. Administration of either norfloxacin or biphenylacetic acid alone did not elicit convulsions and increase in IL-1beta mRNA and protein expressions. The results suggest that the increased IL-1beta expressions in the prefrontal cortex and hippocampus induced by norfloxacin with biphenylacetic acid relate to seizure activities, and that these brain regions play pivotal roles in norfloxacin-induced convulsions.
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PMID:Changes in brain interleukin-1beta following the coadministration of norfloxacin with biphenylacetic acid in rats. 1682 9

Neurocysticercosis is a parasitic infection of the human central nervous system caused by the cestode Taenia solium. The most common clinical manifestations of neurocysticercosis are seizures. Taenia crassiceps cysticercosis in mice has been used as an experimental model for T. solium cysticercosis. Granulomas surrounding murine cysticerci have striking immunopathological resemblance to human neurocysticercosis; early stage granulomas were able to induce seizures in a rodent model. To assess the role of proinflammatory cytokines in early stage granulomas, we isolated RNA from murine cysticercal granulomas and checked for cytokine expression by reverse transcriptase-polymerase chain reaction (RT-PCR) and/or ribonuclease (RNase) protection assays. Cytokine expression was compared with histological stages. Interleukin (IL)-1alpha, IL-1beta, IL-1 receptor antagonist, and tumor necrosis factor (TNF-alpha) were the major cytokines detected in all granulomas. Signals for IL-12, IL-18, and IL-6 RNA were not consistently detected and, when detected, were barely demonstrable. Expression of migration inhibitory factor (MIF), IL-6, IL-1alpha, TNF-alpha, and IL-18 was not significantly different between early and late-stage granulomas. Expression of IL-1beta, IL-1 receptor antagonist, and IL-12 p40 were higher in late, compared with early, stages. Thus, we demonstrated a broad range of cytokines in these granulomas. However, we did not document preferential expression of any proinflammatory cytokines in early stage granulomas. Thus, proinflammatory cytokines are not responsible for the seizures in the rodent model of neurocysticercosis.
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PMID:Proinflammatory cytokines in granulomas associated with murine cysticercosis are not the cause of seizures. 1699 90

Although the diagnosis is rarely confirmed, enteroviruses are a common cause of meningitis. Coxsackie B is responsible for more than half of the cases of aseptic meningitis in infants less than 3 months old, but is less common as a cause of neurological disease in older persons. In addition to aseptic meningitis, Coxsackie B has been reported to cause a wide range of other neurological disorders, albeit rarely. The authors report a young adult with persistent Coxsackie B encephalitis that was heralded by focal seizures and evolved to intractable coma with multifocal myoclonus. The diagnosis was established by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) on tissue obtained at brain biopsy. Cerebrospinal fluid (CSF) viral cultures and PCR were negative for enteroviruses. This case highlights unusual features of a persistent infection that could easily have been mistaken for a neurodegenerative or other noninfectious process. It also emphasizes the importance of performing brain biopsy on individuals with neurological disease of obscure nature.
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PMID:Persistent Coxsackie B encephalitis: Report of a case and review of the literature. 1716 66

Enteroviruses have been implicated as a cause of low Apgar scores in conjunction with perinatal seizures and respiratory insufficiency. Using in-situ reverse transcriptase polymerase chain reaction (in-situ PCR), Nuovo et al detected enterovirus in up to 86% of placentas from perinates exhibiting these symptoms. In-situ PCR has been the only method employed to assess for the presence ofenterovirus in this specific patient population. The purpose of our study was to use PCR amplification of enterovirus from extracted RNA to confirm these observations. RNA was extracted from 26 placentas of infants with low Apgar scores, perinatal seizures, and respiratory insufficiency. Each extraction was positive for beta-actin RNA, which confirmed that the integrity of RNA was maintained in the sample. Enterovirus RNA was not detected in any of the cases. Our results indicate that enterovirus is not present in placentas from neonates with the combination of low Apgar scores, respiratory insufficiency, and seizures, as previously reported.
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PMID:Enterovirus is not present in placentas from cases of perinatal depression using polymerase chain reaction analysis. 1880 15

A 29-year-old female green-winged macaw (Ara chloropterus) was presented for acute pelvic limb lameness. On physical examination the bird was found to be mildly dehydrated with paraparesis and proprioceptive deficits of the pelvic limbs. Antemortem diagnostics included a complete blood count and plasma biochemistry panel, fecal Gram and Ziehl-Neelsen acid fast stains, plasma heavy metal concentrations, reverse transcriptase (RT)-PCR testing for West Nile virus (WNV) RNA and PCR testing for Chlamydophila psittaci DNA from choanal/cloacal swabs, and survey radiography. Abnormal findings included a heterophilic leukocytosis, elevated kidney and muscle enzyme values, and a positive RT-PCR result for West Nile viral RNA. Although the bird showed some improvement with supportive care, on the fourth day it began having seizures and was euthanatized. There were no abnormal findings detected on gross necropsy; however, histopathology revealed mononuclear inflammatory cell infiltration in multiple organs including brain, heart, and pancreas. WNV antigen and RNA were detected using immunohistochemistry and RT-PCR in various tissues including brain, pancreas, and spleen. WNV was successfully isolated from brain, pancreas, spleen, and liver. To our knowledge, this is the first report characterizing WNV disease in a green-winged macaw and one of few reports of this disease in a psittacine bird.
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PMID:West Nile virus infection in a green-winged macaw (Ara chloropterus). 2040 19

Disruption of E3 ubiquitin ligase activity in immature zebrafish mind bomb mutants leads to a failure in Notch signaling, excessive numbers of neurons, and depletion of neural progenitor cells. This neurogenic phenotype is associated with defects in neural patterning and brain development. Because developmental brain abnormalities are recognized as an important feature of childhood neurological disorders such as epilepsy and autism, we determined whether zebrafish mutants with grossly abnormal brain structure exhibit spontaneous electrical activity that resembles the long-duration, high-amplitude multispike discharges reported in immature zebrafish exposed to convulsant drugs. Electrophysiological recordings from agar immobilized mind bomb mutants at 3 d postfertilization confirmed the occurrence of electrographic seizure activity; seizure-like behaviors were also noted during locomotion video tracking of freely behaving mutants. To identify genes differentially expressed in the mind bomb mutant and provide insight into molecular pathways that may mediate these epileptic phenotypes, a transcriptome analysis was performed using microarray. Interesting candidate genes were further analyzed using conventional reverse transcriptase-PCR and real-time quantitative PCR, as well as whole-mount in situ hybridization. Approximately 150 genes, some implicated in development, transcription, cell metabolism, and signal transduction, are differentially regulated, including downregulation of several genes necessary for GABA-mediated signaling. These findings identify a collection of gene transcripts that may be responsible for the abnormal electrical discharge and epileptic activities observed in a mind bomb zebrafish mutant. This work may have important implications for neurological and neurodevelopmental disorders associated with mutations in ubiquitin ligase activity.
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PMID:Spontaneous seizures and altered gene expression in GABA signaling pathways in a mind bomb mutant zebrafish. 2094 12

The aim of this study was to determine the clinical characteristics of children demonstrating neurological complications with pandemic influenza (H1N1). We reviewed the medical and laboratory records of all children who were hospitalized with neurological symptoms and who had proven influenza virus infection by reverse transcriptase-polymerase chain reaction on nasal and throat swabs. Eight children aged between 10 months and 7 years had neurological complications due to pandemic influenza (H1N1) and five of them were female. Four of them were previously healthy; there was chronic renal failure (CRF) in one and neurologic disease in three patients. Seven of them had seizure and altered consciousness. Seven of them were followed in pediatric intensive care units. We performed lumbar puncture in four patients and their cerebrospinal fluid examinations showed pleocytosis in one and no cell in three specimens. Neuroimaging was performed in four patients and three of them had abnormalities. We diagnosed aseptic meningitis in one, acute disseminated encephalomyelitis (ADEM) in one, acute necrotizing encephalopathy (ANE) in one, meningoencephalitis in one, and status epilepticus in four patients. All patients were treated with oseltamivir and antiepileptic drugs. One patient with CRF died; four previously healthy patients recovered fully, and three patients who had neurologic disorder returned to their previous neurological status. In conclusion, during pandemic influenza (H1N1) infection, neurological complications may be seen in addition to the respiratory infection. The type of neurological involvement may be variable such as triggering seizure, aseptic meningitis, encephalitis, ADEM, and ANE. Neurological complications frequently recover fully especially in previously healthy children, but sometimes a severe clinical course occurs.
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PMID:Neurological complications of pandemic influenza (H1N1) in children. 2111 Feb 4

Disruption of calcium homeostasis in epileptic cells is characterized by both short- and long-term perturbations of Ca(2+) buffering systems. Along with the Na(+)/Ca(2+) exchanger, the plasma membrane Ca(2+)-ATPase (PMCA) plays an important role in excitable cells. The involvement of PMCAs in epileptogenesis has primarily been studied in brief intervals after various stimuli; however, the specific contribution of this molecule to epileptogenesis is not yet fully understood. Our aim has been to investigate whether PMCA expression in the chronic stages of epilepsy is altered. Through an interdisciplinary approach, involving whole-cell recordings and real-time reverse transcriptase-polymerase chain reaction, we have shown that epileptic neurons in our preparation consistently show changes in electrical properties during the period of chronic epilepsy. These changes included increased spike frequency, altered resting membrane potential and changes in passive membrane properties. Following these observations, which indicate an altered excitability in the epileptic cells studied, PMCA mRNA transcripts were studied. It was found that while PMCA1 transcripts are significantly increased one month following the pilocarpine epileptogenic stimulus, PMCA3, an isoform important in excitable tissues, was significantly, decreased. These findings suggest that, in the long-term, a slow PMCA (PMCA1) plays a role in the reestablishment of a new calcium homeostasis attained by epileptic cells. Overall, this phenomenon points out the fact that in seizure disorders, changes that take place in the balance of the different molecules and their isoforms in charge of maintaining neuronal calcium homeostasis, are fundamental in the survival of affected cells.
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PMID:Analysis of plasma membrane Ca2+-ATPase gene expression during epileptogenesis employing single hippocampal CA1 neurons. 2144 70

We describe an 8-year-old boy admitted because of prolonged seizures during norovirus gastroenteritis without any signs of encephalopathy. Blood tests were normal and cerebrospinal fluid examination resulted negative for both bacteria and viruses. A reverse transcriptase polymerase chain reaction revealed norovirus RNA in a stool sample. A cerebral computed tomography turned out to be normal whereas subsequent cerebral magnetic resonance imaging showed transitory signal abnormalities consistent with vasogenic edema. The post-ictal electroencephalogram revealed normal background activity with sporadic left posterior delta waves. The child was discharged after 10 days with an unremarkable physical examination. A cerebral magnetic resonance imaging and an electroencephalogram after 1 month were both negative. We report a new case of benign infantile convulsions due to norovirus gastroenteritis with neuroradiological abnormalities to the pertinent literature in order to improve knowledge about this disorder and increase the possibility of clarifying its pathogenesis.
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PMID:Norovirus gastroenteritis and seizures: an atypical case with neuroradiological abnormalities. 2193 82


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