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At least 433 records · Page 24Linked to original sources
PubMed1996

Neuron-specific enolase is increased after single seizures during inpatient video/EEG monitoring.

Neuron-specific enolase (NSE) is a marker of brain injury after acute neurologic insults. We report changes in serum NSE (s-NSE) in 25 patients (15 with epilepsy and 10 patients with nonepileptic events) during continuous inpatient video/EEG monitoring. s-NSE was significantly increased as compared with baseline and normal controls after the first ictal event in the epileptic group, especially in patients with secondarily generalized tonic-clonic seizures (p = 0.01), but s-NSE was not increased in patients with nonepileptic events. These preliminary data indicate that s-NSE may be increased after complex partial seizures--and generalized tonic-clonic seizures (GTCS).

Adult↗
PubMed2004

Neuron-specific enolase-producing leiomyosarcoma of the mesentery.

A case of neuron-specific enolase (NSE)-producing leiomyosarcoma arising in the mesentery of a 62-year-old female is presented. Preoperatively, serum level of NSE was markedly elevated. A well-defined but unencapsulated tumor measuring 14 x 12 x 9 cm was histologically characterized by a fascicular or herring-bone arrangement of atypical spindle or oval tumor cells with vesicular cigar-shaped nuclei, inconspicuous nucleoli and abundant clear to brightly eosinophilic cytoplasm. Immunohistochemically, the tumor was positive for vimentin, alpha-smooth muscle actin, muscle actin, desmin, and gamma-NSE. Postoperatively, serum level of NSE decreased to within normal range. The NSE levels were, however, elevated again as metastatic lesions in the liver had enlarged. The patient died of the liver metastases 10 months after surgery. Serum NSE level can be a useful index of tumor extent and for monitoring treatment of some patients with leiomyosarcoma.

Fatal Outcome↗
PubMed1994

Measurement of the serum tumor marker neuron-specific enolase in patients with benign pulmonary diseases.

Serum concentrations of neuron-specific enolase (NSE) were measured in 135 patients with benign pulmonary diseases who also underwent a clinical, laboratory, and radiologic evaluation. Eleven percent of the patients as a whole and 27.3% of those who were tuberculous had abnormal serum levels of NSE. Significant differences in NSE levels were observed among the six diagnostic groups evaluated (p = 0.002). Males had higher levels than females (p = 0.003), and patients infected with the human immunodeficiency virus (HIV) had higher NSE levels than those not infected (p = 0.0026). Patients with alveolar infiltrates or an interstitial pattern on chest X-ray had higher NSE levels than those with normal radiographs (p = 0.003 and p = 0.01, respectively). In fact, only 3.6% of the patients with normal radiographs had above-normal levels of NSE. Direct damage to the neural or neuroendocrine lung cells or some degree of local hypoxia is likely to play a role in the increase in NSE in these patients. The small number and degree of abnormal values of NSE observed in this study make it unlikely that an underlying benign lung disease will substantially modify the interpretation of an increased NSE value in patients with lung cancer. However, care should be taken in interpreting a moderately abnormal NSE value in the cancer patient in the presence of lung infiltrates such as obstructive pneumonitis.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Circulating neuron-specific enolase in medullary thyroid cancer.

The utility of determining circulating neuron-specific enolase (NSE) in medullary thyroid carcinoma was assessed in 25 patients followed up for a mean period of 45.6 months. In 5 patients tested before any treatment serum NSE concentrations were in the normal range. After total thyroidectomy abnormally high serum NSE concentrations (more than 9.8 ng/ml) were found in 1/3 patients with normal calcitonin (CT) in remission, in 2/10 with elevated CT levels but no evidence of disease and in 9/12 with elevated CT levels and documented metastases. The mean (+/- SD) NSE value in this last group was 12.0 +/- 12.6 ng/ml, significantly higher than in the other groups (p less than 0.005). The time course of serum NSE in patients with long follow-up seems to indicate that serum NSE rises when a large tumor mass is present and usually parallels the pattern of circulating CT. Effective treatment of the metastases is usually followed by reduction of serum NSE. Thus, serum NSE can serve as an additional humoral marker for medullary thyroid carcinoma, its elevation being associated with important metastatic involvement and with a poor prognosis of the tumor.

Adolescent↗
PubMed1990

[Diagnostic usefulness of the determination of serum neuron-specific enolase in small cell bronchial carcinoma].

The plasma level of neuron-specific enolase (NSE) was measured in 55 patients with small cell bronchial carcinoma (SCC) with cytohistological confirmation to evaluate its diagnostic usefulness. As a control group, 132 patients with non-small cell bronchial carcinoma, 81 with non-neoplastic disease and 37 healthy individuals were used. The sensitivity of the test was 84% with a specificity of 79% when values below 13 ng/mg were considered as normal. To achieve a specificity of 95% and 99% cutoff values had to be increased to 25 and 50 ng/ml, respectively, and then the sensitivity was reduced to 51% and 38%. There were false positive findings in the three control groups, although they were more common (28%) and had higher values in patients with widespread disease the sensitivity was significantly higher (p less than 0.005) than in those with limited disease. Carcinoembryonic antigen, which was measured with comparative purposes, had a lower sensitivity. In our area, a NSE level over 50 ng/ml is closely correlated with the diagnosis of SCC, whereas values over 13 ng/ml select a wider group of individuals where most patients with this type of carcinoma are included.

Adenocarcinoma↗
PubMedDate not supplied

[Neuron-specific enolase in pleural effusions of various etiologies].

The concentration of neuron-specific enolase (NSE) was measured in the serum and pleural fluid of 42 patients with pleural effusions of different etiology. High levels (above 13.0 micrograms/l) of NSE in pleural fluid of 9 patients with malignant disease were observed (sensitivity 57%). However, pleural fluid NSE levels were also increased in 14 with non-malignant diseases (specificity 45%). Increased pleural fluid NSE activity is not specific for malignancy.

Adult↗
PubMed1988

The expression of S-100 protein and neuron-specific enolase in meningiomas.

The distribution of S-100 protein and neuron-specific enolase (NSE) was examined in 19 meningiomas using the peroxidase-antiperoxidase (PAP) immunohistochemical technique. Positive cytoplasmic staining for NSE was observed in 16 tumors, and comparable staining for S-100 protein was observed in eight tumors. The finding of S-100 protein and NSE immunoreactivity in fibroblastic, meningiotheliomatous, and transitional meningiomas raises the possibility that these morphologically distinct neoplasms derive from a common pluripotential cell capable of differentiation along diverse paths.

Biomarkers, Tumor↗
PubMed1995

Neuron-specific enolase in patients with acute ischemic stroke and related dementia.

Neuron-specific enolase (NSE) levels of cerebrospinal fluid (CSF) were measured in 39 patients with ischemic stroke and 15 controls. There was a significant increase of CSF NSE in acute ischemic stroke patients as compared with the controls. The altered CSF NSE levels correlated well with the infarct size in CT scan. The CSF NSE levels were higher in 6-multiinfarct dementia (MID) patients who were diagnosed after 6-month follow-up than those in 22 non-MID patients of this series. Our research supports the view that CSF NSE can be a useful biochemical marker for brain ischemia. The importance of CSF NSE in the study of dementia related to ischemic stroke is worth further studies.

Aged↗
PubMed1988

Developmental changes of neuron-specific enolase and neurofilament proteins in primary neural culture.

The expression of neuron-specific enolase (NSE) and neurofilament (NF) proteins in primary dissociated cell cultures derived from 14-day-old fetal rat diencephalon was studied by immunocytochemistry and quantitative western-blot techniques. Both neuronal marker proteins, NSE and NF, can be detected as early as day 2 in vitro. They show pronounced quantitative increases during the time period studied (12 days), the relative change being highest during the first few days in vitro (DIV). The molar ratio of the medium weight NF to the heavy NF polypeptide is 9.1 after 2 DIV and 2.6 after 12 DIV. Phosphorylation of the heavy NF polypeptide increases steadily during cultivation. Comparison of these results to in vivo data reported in the literature suggests that, qualitatively, neuronal development in vitro follows the pattern observed in vivo, but at an accelerated pace.

Animals↗
PubMed2004

Sensory neuron-specific receptor activation elicits central and peripheral nociceptive effects in rats.

The sensory neuron-specific G protein coupled receptors (SNSRs) have been described as a family of receptors whose expression in small diameter sensory neurons in the trigeminal and dorsal root ganglia suggests an implication in nociception. To date, the physiological function(s) of SNSRs remain unknown. Hence, the aim of the present study was to determine the effects of rat SNSR1 activation on nociception in rats. The pharmacological characterization of rat SNSR1 was initially performed in vitro to identify a specific ligand, which could be used subsequently in the rat for physiological testing. Among all ligands tested, gamma2-MSH was the most potent at activating rat SNSR1. Structure-activity relationship studies revealed that the active moiety recognized by rat SNSR1 was the C-terminal part of gamma2-MSH. The radiolabeled C-terminal part of gamma2-MSH, gamma2-MSH-6-12, bound with high affinity to membranes derived from rat skin and spinal cord, demonstrating the presence of receptor protein at both the proximal and distal terminals of dorsal root ganglia. To investigate the physiological role of SNSR, specific ligands to rat SNSR1 were tested in behavioral assays of pain sensitivity in rats. Selective rat SNSR1 agonists produced spontaneous pain behavior, enhanced heat and mechanical sensitivity when injected intradermally, and heat hypersensitivity when injected centrally, consistent with the localization of rat SNSR1 protein at central and peripheral sites. Together, these results clearly indicate that the SNSR1 plays a role in nociception and may provide novel therapeutic opportunities for analgesia.

Animals↗
PubMedDate not supplied

Neuron-specific enolase and embryology of the trabecular meshwork of the rat eye: an immunohistochemical study.

Neuron-specific enolase (NSE) is a unique form of the glycolytic enzyme enolase found exclusively in neurons and neuroendocrine tissues. Immunohistochemical techniques in which antineuron-specific enolase antibodies are used have made it possible to map out derivatives of the neural crest in humans. By using affinity-purified antibodies against NSE, we investigated whether the contribution of the neural crest cells to the development of the anterior ocular structures in the rat is similar to that in man. We found that filtration structures in rats show morphologically striking similarities with the analogous region of the human eye. Hence, the rat eye, with certain reservations, is a suitable model for experimental studies on ocular diseases that are characterized by chamber angle anomalies or congenital glaucoma.

Animals↗
PubMed1994

Repeated electroconvulsive shock selectively increases the expression of the neuron specific enolase in piriform cortex.

The effect of repeated electroconvulsive shock (ECS) on the activities of the three enolase isoenzymes present in rat brain: neuron specific enolase (NSE), non-neuronal enolase (NNE) and the hybrid enolase was investigated in piriform cortex. The activities were estimated on isoenzymes separated by agarose gel electrophoresis. Whereas the specific activities of NNE and hybrid enolase were unchanged in piriform cortex or ECS-treated rats the specific activity of NSE was increased by 16.3 percent (P < 0.02). The brain enolase isoenzymes are dimers of alpha- and gamma-enolase subunits. The calculated ratio between the gamma-subunit present in both NSE and hybrid enolase and the alpha-subunits present in both NNE and hybrid enolase was increased by 11.7 percent in piriform cortex of ECS-treated rats (P < 0.05). Previously, it has been shown that the gamma-subunit is only expressed in neurons whereas the alpha-subunit is expressed in both neurons and glial cells. The selectively increased expression of the enolase gamma-subunit in ECS-treated rats might either reflect an increased transcription of a whole group of neuronal genes or rather the trophic role of NSE in ECS-enhanced synaptic remodelling of the rat brain.

Animals↗
PubMed1998

Immunohistochemical study of neuron-specific enolase in human brains from forensic autopsies.

Immunohistochemistry using anti-human neuron-specific enolase (NSE) mouse monoclonal antibody was performed in human brains from autopsy cases, which enabled us to assess the neuronal damage besides hematoxylin and eosin or Klüver-Barrera stain. Neurons in cerebral neocortex which showed necrotic changes such as prominent cytoplasmic vacuolization or cellular shrinkage with nuclear pyknosis showed a tendency to be less stained by anti-NSE antibody. Anti-NSE immunostaining was statistically significantly less in the neocortex from CO intoxication than from other causes of death, although morphological necrotic changes were less observed in CO intoxication. Hippocampal CA1 neurons clearly lost NSE immunoreactivity with the progression of necrotic changes. Neurons in CA2 were statistically significantly better stained by anti-NSE antibody than in CA1, 3, and 4. Cerebellar Purkinje cells were poorly stained by anti-NSE antibody, whereas neurons in cerebellar dentate nucleus and inferior olive in medulla oblongata were better stained. Anti-NSE immunostaining was lost in the injured areas of the cerebral neocortex while neurons in the intact areas were better stained in brain injury. These results indicate that anti-NSE immunostaining of neurons could reflect vital reaction and could be useful in evaluating neuronal damage in the hippocampal CA1 region or brain injury.

Adolescent↗
PubMedDate not supplied

Neuron-specific enolase, S-100 protein, myelin basic protein and lactate in CSF in dementia.

The pattern of injury of the specific cell structures of the central nervous system (CNS) is different in the various types of the dementia syndrome. We challenged the hypothesis that this could be reflected in specific patterns of brain-specific proteins in the cerebrospinal fluid (CSF). The neuron-specific enolase (NSE), S-100, myelin basic protein (MBP) and lactate levels were retrospectively analyzed in the CSF of 159 patients with various types of dementia. A previous study from our department demonstrated age-related reference values for the brain-specific proteins in the CSF. The present study affirmed the strikingly high NSE and S-100 values in the CSF of patients with autopsydiagnosed Creutzfeld-Jacob disease: NSE, S-100 and MBP levels in the CSF of patients with various other types of dementia, and controls, did not differ significantly. Therefore we concluded that a single determination of CSF concentrations of these brain-specific proteins were of little value in the differential diagnosis of the dementia syndrome. In the diagnosis of normal pressure hydrocephalus increased levels of CSF lactate may be helpful.

Aged↗
PubMed1999

The neuron-specific K-Cl cotransporter, KCC2. Antibody development and initial characterization of the protein.

The neuron-specific K-Cl cotransporter (KCC2) is hypothesized to function as an active Cl- extrusion pathway important in postsynaptic inhibition mediated by ligand-gated anion channels, like gamma-aminobutyric acid type A (GABAA) and glycine receptors. To understand better the functional role of KCC2 in the nervous system, we developed polyclonal antibodies to a KCC2 fusion protein and used these antibodies to characterize and localize KCC2 in the rat cerebellum. The antibodies specifically recognized the KCC2 protein which is an approximately 140-kDa glycoprotein detectable only within the central nervous system. The KCC2 protein displayed a robust and punctate distribution in primary cultured retinal amacrine cells known to form exclusively GABAAergic synapses in culture. In immunolocalization studies, KCC2 was absent from axons and glia but was highly expressed at neuronal somata and dendrites, indicating a specific postsynaptic distribution of the protein. In the granule cell layer, KCC2 exhibited a distinct colocalization with the beta2/beta3-subunits of the GABAA receptor at the plasma membrane of granule cell somata and at cerebellar glomeruli. KCC2 lightly labeled the plasma membrane of Purkinje cell somata. Within the molecular layer, KCC2 exhibited a distinctly punctate distribution along dendrites, indicating it may be highly localized at inhibitory synapses along these processes. The distinct postsynaptic localization of KCC2 and its colocalization with GABAA receptor in the cerebellum are consistent with the putative role of KCC2 in neuronal Cl- extrusion and postsynaptic inhibition.

Animals↗
PubMed2000

Cerebrospinal fluid purine metabolite and neuron-specific enolase concentrations after febrile seizures.

If febrile seizures cause significant compromise of neuronal metabolism (whether permanent or reversible), this should be reflected in an increase in the cerebrospinal fluid concentrations of neuron-specific enolase (NSE) and/or adenosine triphosphate (ATP) breakdown products. In the present study, AMP, IMP, inosine, adenosine, guanosine, adenine, guanine, hypoxanthine, xanthine, uric acid and NSE concentrations were determined in the cerebrospinal fluid of 90 children 1 h after febrile seizure (73 simple febrile seizures (SFS); 17 complex febrile seizures (CFS)), and in a control group of 160 children. There was no statistically significant difference between the SFS group and the control group for any of the substances determined, suggesting that SFS neither significantly depletes neuronal ATP concentration, nor significantly increases NSE concentration; thus, SFS do not appear to constitute a threat to neuronal integrity. However, patients with CFS showed significantly lower IMP concentrations and significantly higher adenine concentrations than controls, and significantly higher AMP concentrations than SFS patients; these results suggest that CFS may affect energy metabolism in the brain. However, NSE concentrations were normal in the cerebrospinal fluid of both SFS and CFS patients, suggesting that neither type of seizure causes significant neuronal damage, at least early after the seizure.

Adenosine Monophosphate↗
PubMed1995

A neuron-specific isoform of brain ankyrin, 440-kD ankyrinB, is targeted to the axons of rat cerebellar neurons.

Two isoforms of brain ankyrin, 440- and 220- kD ankyrinB, are generated from the same gene by alternative splicing of pre-mRNA. The larger isoform shares the same NH2-terminal and COOH-terminal domains to the smaller isoform and contains, in addition, a unique inserted domain of about 220-kD in size (Kunimoto, M., E. Otto, and V. Bennett. 1991. J. Cell Biol. 115:1319-1331). Both Isoforms were expressed in primary cerebellar cells in a manner similar to that in vivo; the larger isoform appeared first when axogenesis is actively conducted and the smaller isoform came up later. 440-kD ankyrinB was localized in the axons of cerebellar neurons both in vivo and in vitro using an antibody raised against the insert region, while 220-kD isoform was rather localized in the cell bodies and dendrites of neurons by a specific antibody prepared using a synthetic peptide corresponding to the splice site as antigen. Astroglia cells also expressed 220-kD ankyrinB but not the 440-kD isoform. These results indicate that 440-kD ankyrinB is a neuron-specific isoform targeted to the axons and its unique inserted domain is essential for the targeting.

Animals↗