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PubMed1991

Changes of neuron-specific enolase concentration in plasma after cardiac arrest and resuscitation.

The concentration of neuron-specific enolase (NSE) was measured in plasma of 18 patients after cardiac arrest and resuscitation (14 nonsurvivors and 4 survivors). In all patients, the NSE concentration was significantly higher in comparison to reference values. The highest concentration was measured in nonsurvivors. Time-course investigation in the first 24 h after cardiac arrest was performed in five patients. Two nonsurvivors and one survivor of the five patients showed a significant rise, and a NSE peak concentration of 42.7 micrograms/L, 13.6 micrograms/L, and 10.5 micrograms/L, respectively, was found 10-19 h after cardiac arrest.

Brain Ischemia↗
PubMed1999

Serum levels of neuron-specific enolase and s-100 protein after single tonic-clonic seizures.

Serum neuron-specific enolase (s-NSE) and s-100 protein (s-100) are sensitive markers of various brain diseases. We investigated both of these markers in nine patients within 5 min, 6 h, 12 h, and 48 h after a single tonic-clonic seizure. The mean peak s-NSE level was significantly higher after 5 min (11.97 +/- 8.56 microg/l) and 48 h (10.31 +/- 8.92 microg/l, P < 0.05) than the levels of seizure-free, age-matched controls. Five patients had increased s-NSE levels regarding the upper limit of normal as mean + 3 SD. s-100 was not detected either in controls or epileptic patients. These data indicate that s-NSE in contrast to s-100 may be an in vivo marker after generalized seizures in some patients.

Adult↗
PubMed1983

Serum neuron-specific enolase: a serum marker for nonfunctioning pancreatic islet cell carcinoma.

The isoenzyme, neuron-specific enolase (NSE) was evaluated as a serum marker for nonfunctioning pancreatic islet cell carcinoma. Serum NSE was measured by radioimmunoassay in 6 patients with islet cell cancer and in 22 healthy adults. Mean serum NSE in control subjects was 5 ng/ml (range 3.2 to 8.4 ng/ml). Three of six patients had clearly elevated serum NSE with values that ranged from 22 to 44 ng/ml. One patient had an equivocally elevated serum NSE of 9.2 ng/ml while receiving chemotherapy. When relapse occurred, the NSE level increased to 44 ng/ml. One of two patients with normal serum NSE had undergone radical pancreatectomy and had no evidence of disease when studied. Elevated serum NSE returned to normal limits after removal of all gross tumor in the only patient from whom a preoperative measurement was obtained. Results of this preliminary study suggest that serum NSE levels can aid in the diagnosis and monitoring of the course of nonfunctining islet cell carcinoma.

Adenoma, Islet Cell↗
PubMed1990

Expression of the neuron-specific glycoprotein GP50 by granule cell cultures.

The expression and properties of the neuron-specific glycoprotein, GP50, by neonatal rat granule cells grown in primary tissue culture were studied using the monoclonal antibody MabSM-GP50. GP50 was expressed by granule cells in culture but not by astrocytes or PC12 cells that had been induced to differentiate with nerve growth factor. Immunocytochemical staining of granule cell cultures demonstrated that immunoreactivity was concentrated in the cell body. Although the amount of GP50 increased slowly throughout the culture period the maximum level of expression in vitro was markedly lower than that observed in cerebellum of the comparable age. Radiolabelling of cell surface proteins by lactoperoxidase-catalyzed iodination demonstrated that GP50 was expressed on the surface of granule cells. Following phase-partitioning of granule cells in the presence of Triton X-114, 75% of GP50 was found to be present in the detergent phase, indicating that it is an integral membrane protein. Sucrose density gradient centrifugation of Triton X-100 extracts of granule cells resolved GP50 into two components with sedimentation coefficients of 3.6S and 7.3S. The 3.6S species (Mr 42,000 Da) accounted for greater than 80% of the total, indicating that GP50 is present predominantly in a monomeric form within the membrane. These properties are similar to those of GP50 expressed in P12 cerebellum but contrast with the behavior of GP50 from mature brain, in which the 7.3S, hydrophilic form is the predominant species. The results suggest that the mature expression of GP50 may be dependent upon the histotypic pattern of development which occurs in vivo.

Animals↗
PubMed1996

Increased serum levels of neuron-specific enolase in epileptic patients and after electroconvulsive therapy--a preliminary report.

Serum neuron-specific enolase (NSE) levels were studied by an enzymo-immunoassay method in 2 groups of patients: a group of epileptic patients, and a group of patients with refractory major depression after electroconvulsive therapy (ECT). In patients without organic neurological disease (n = 274) the mean serum NSE level (+/- S.D.) was 8.4 +/- 3.4 micrograms/l. No correlation with sex or age was observed. No significant difference was observed between epileptic patients without seizure or major electroencephalogram (EEG) abnormality, and a reference group. Significant increases were observed in 32 samples collected from patients with interictal EEG without spikes and waves before the 7th day after a seizure, in whom mean NSE was 21.5 +/- 9.4 micrograms/l, and in 26 samples from 4 patients without seizures but with spikes and waves in the interictal EEG, whose mean NSE was 20.6 +/- 11.5 micrograms/l. The increases of serum NSE levels in epileptic patients seem therefore to be linked to seizures and/or to EEG abnormalities. The consequences of these observations for the survey of epileptic patients, and for the diagnosis of cerebral tumors (mainly neuroblastoma) or for monitoring treatment after surgical resection, are discussed. In only 1 patient out of 6, an increase in serum NSE levels was observed with a peak about 12 h after ECT. No significant correlation with the ECT features (length of seizures, one- or two-sided electrodes) was observed.

Adult↗
PubMed1987

Appearance and development of neuron-specific enolase immunoreactivity in organotypic cultures of mouse embryo otocysts.

The appearance of neuron-specific enolase (NSE) immunoreactivity was studied in sensory and vestibular ganglion cells during the development of mouse embryo otocysts grown in vitro from the 13th gestation day. NSE appeared sequentially in the ganglion and sensory cell populations of the inner ear with a pattern that paralleled their successive maturation. Comparison with NSE immunoreactivity profile during in vivo development shows that NSE appears earlier during organotypic in vitro maturation.

Animals↗
PubMed1988

Early detection of response in small cell bronchogenic carcinoma by changes in serum concentrations of creatine kinase, neuron specific enolase, calcitonin, ACTH, serotonin and gastrin releasing peptide.

Creatine kinase (CK-BB), neuron specific enolase (NSE), ACTH, calcitonin, serotonin and gastrin releasing peptide (GRP) were measured in serum or plasma before and immediately after initiation of treatment in patients with small cell lung cancer (SCC). Pretherapeutic elevated concentrations of CK-BB were found in 82% of extensive disease patients and in 50% of patients with local disease. NSE was raised in 72% with extensive disease versus 14% of patients with local disease. Calcitonin and ACTH were raised in 27% and 28%, respectively, in all patients without significant difference between extensive and local disease patients. Serotonin was generally overall elevated in 10% and GRP in 7% but elevations were seen only in patients with extensive disease. Out of the four most frequently elevated substances at least one marker was elevated in 80% of all the patients, including 91% in extensive stage patients and 71% in limited stage patients. Frequent initial monitoring of the substances showed an increase in the concentrations of pretherapeutic elevated CK-BB and NSE on day 1 or 2 followed by a sharp decrease within 1 week. These changes were correlated to objective clinical response determined within 4-8 weeks. The results indicate that serum CK-BB and NSE are potential markers for SCC at the time of diagnosis and that changes in the concentrations during the first course of cytostatic therapy are promising as biochemical tests for early detection of response to chemotherapy.

Adrenocorticotropic Hormone↗
PubMed1992

Neuron-specific enolase reduction in irradiated salivary glands of the rat--an immunohistochemical study.

Neuron-specific enolase (NSE) in the salivary glands of normal and irradiated rats was studied by immunohistochemical methods. The normal salivary gland of Sprague-Dawley rats (465 g) showed positive staining for NSE in striated ducts and granular convoluted tubule (GCT) cells. A single radiation, TDF (time, dose, fractionation factor) 100 and 200 (18.82 Gy and 27.97 Gy, respectively) was done, and 4 groups (1, 2, 3 and 4 weeks after radiation) of 5 rats each were used. Irradiated salivary glands indicated a remarkable reduction of NSE staining in GCT cells and a reduction but to a lesser degree in the striated duct of the submandibular gland. Immunohistochemical deposition of NSE was not changed in the sublingual glands of irradiated rats. The reduction of NSE immunodeposition was irradiation dose dependent.

Animals↗
PubMed1999

Neuron-specific enolase levels in the cerebrospinal fluid of neurologically healthy children.

Levels of neuron-specific enolase (NSE) levels in the cerebrospinal fluid (CSF) of children without neurological disease were assessed. CSF samples were obtained from 37 subjects aged between 1 month and 13 years. All subjects had undergone lumbar puncture for diagnostic purposes, and were subsequently shown not to be suffering any form of neurological disease. NSE levels in CSF were determined by an enzyme immunoassay method. NSE level ranged from below the detection limit to 4.8 ng/ml (1.52+/-1.01 ng/ml). The present results may be useful as a basis for defining reference levels of NSE in CSF in post-neonatal children.

Adolescent↗
PubMed1985

Immunocytochemical demonstration of neuron-specific enolase (NSE) in human lung cancers.

An anti-serum against human neuron-specific enolase (NSE), raised in sheep, has been characterized and used for immunocytochemical localization of NSE in paraffin sections of normal tissues and lung cancers. Of the small cell carcinomas (SCC), 69 out of 99 (70%) cases stained with the anti-serum. Maltreated biopsies showed a lower frequency of positive staining (19/39), indicating the importance of well-preserved biopsies. There was no clear difference in the staining between the oat cell and intermediate cell type of SCC. A majority (14 out of 21) of the non-SCC:s (large cell, adenocarcinoma and squamous cell carcinoma) were also stained by the anti-serum. Generally, this staining was weak and it could be blocked by preabsorption of the anti-serum by purified NSE. It is concluded that NSE expression, in conjunction with traditional histology, serves as a useful but not exclusive marker for SCC.

Adenocarcinoma↗
PubMed1990

Mutation of serine 41 in the neuron-specific protein B-50 (GAP-43) prohibits phosphorylation by protein kinase C.

The neuron-specific, calmodulin-binding protein B-50 (also known as GAP-43, F1, or neuromodulin) is an endogenous substrate of protein kinase C (PKC). PKC exclusively phosphorylates Ser residues in B-50. As potential phosphorylation sites for PKC, Ser41, Ser110, and Ser122 were indicated, of which Ser41 is contained in the sequence ASF, which matches with the sequence of a synthetic PKC substrate. N-terminally 35S-labeled B-50, produced from cDNA, was subjected to digestion with Staphylococcus aureus V8 protease (SAP). Consecutively, 35S-labeled 28- and 15-kDa fragments were formed, similar to those after digestion of 32P-labeled B-50. In a previous study, we showed that the 32P-labeled 15-kDa SAP fragment contains all 32P radioactivity. The present data indicate that it contains the N-terminus of B-50 as well. The 15-kDa fragment, with a calculated length ranging from amino acid residue 1 to 65, contains only one potential PKC phosphorylation site, at Ser41. Mutagenesis of Ser41 into Thr or Ala resulted in recombinant B-50 products with mobilities on two-dimensional electrophoresis similar to those of the nonmutated recombinant B-50 and the rat brain B-50. Only [Ser41]B-50 was phosphorylated by PKC, whereas [Thr41]- or [Ala41]B-50 did not show any phosphorylation at the positions indicated on the immunoblots. This leads us to the conclusion that Ser41 is the sole phosphorylation site for PKC in vitro.

Animals↗
PubMed1993

Neuron-specific enolase: a serum tumor marker in renal cell carcinoma?

In previous reports, neuron-specific enolase (NSE) has been considered to be a useful tumor marker in renal cell carcinoma (RCC). This led us to perform a prospective clinical trial in this field. NSE was checked as a tumor marker for diagnosis and monitoring of patients with RCC. We report on 55 patients and their NSE level before and after radical nephrectomy and correlated the serum level of NSE to immunohistological staining and clinical stage of nephrectomy specimens. In contrast to other researchers, our results on NSE as a tumor marker in RCC are disappointing.

Biomarkers, Tumor↗
PubMed2005

Serum biomarkers for experimental acute spinal cord injury: rapid elevation of neuron-specific enolase and S-100beta.

OBJECTIVE: We evaluated whether serum levels of neuron-specific enolase (NSE) and S-100beta protein are biomarkers for traumatic injury in an animal model of spinal cord injury (SCI). METHODS: Enzyme-linked immunosorbent assay serum measurements of NSE and S-100beta and assays of serum protein were compared at 6 and 24 hours after a graded contusive SCI (150 or 200 kdyn IH impactor injury (Infinite Horizons, L.L.C., Lexington, KY) or sham laminectomy at T9 in 30 female Sprague-Dawley rats. Serum from control animals was also analyzed. RESULTS: Increases in serum levels of NSE were observed for 200-kdyn (3.1-fold, P < 0.001) and 150-kdyn (2.3-fold, P < 0.001) injury groups at 6 hours after injury, which decreased by 73.7% (P < 0.001) and 65.2% (P < 0.001) at 24 hours after SCI, respectively; the levels were still greater than in sham animals (P < 0.001, P = 0.001). The 200- and 150-kdyn injury groups were not different at either time point. S-100beta serum levels increased at 6 hours in the 200-kdyn injury group (P < 0.05), and no differences from sham levels were seen at 24 hours. No differences in total protein concentrations were observed between the injury and control groups. CONCLUSION: Present data suggest that NSE and S-100beta serum levels may be useful experimental tools for the acute measurement of tissue loss after SCI. Despite significant shortcomings, NSE and S-100beta serum measurements in acute SCI patients with clinically defined functional deficits should allow comparisons with well-characterized SCI animal models. Future efforts to develop biomarkers that predict functional outcomes in the acute phase should focus on axon-specific proteins as markers of secondary axonal loss and regeneration.

Acute Disease↗
PubMed1986

Urine neuron-specific enolase and its clinical implication in patients with neuroblastoma.

Urine levels of neuron-specific enolase (NSE) were determined in 6 patients with neuroblastoma, in 72 controls and in 5 infants with hematuria by means of a double-antibody inhibition radioimmunoassay method. Urine levels (NSE ng/creatinine mg) in 2 patients with advanced neuroblastoma were elevated (3.03 +/- 0.28 (S.D.)), when compared with those of 4 patients with neuroblastoma in remission (0.65 +/- 0.26 (S.D.], 10 healthy neonates (1.26 +/- 0.42 (S.D.)), 25 healthy infants (0.51 +/- 0.26 (S.D.)), and 37 healthy adults (0.37 +/- 0.17 (S.D.)). Urine levels in 4 infants with microhematuria and an infant with macrohematuria were 1.62 +/- 0.10 (S.D.) and 33.83, respectively. Serial measurements in 3 patients with neuroblastoma receiving various therapies have revealed that there was a good correlation between urine NSE level and the response to therapy. These results indicate that NSE in urine may be a valuable marker for monitoring the effectiveness of therapy in patients with neuroblastoma.

Child, Preschool↗
PubMed1989

[Diagnostic value of neuron specific enolase (NSE) in the cerebrospinal fluid of malignant brain tumor with intrathecal metastasis].

Neuron specific enolase (NSE) in the cerebrospinal fluid (CSF) and serum of 54 cases of brain tumors, in the tumor tissues of 10 brain tumors and in the cyst fluids of 7 brain tumors was measured by radioimmunoassay with NSE measurement kit (Eiken Chemistry co.) NSE values in the cerebrospinal fluid of 35 malignant brain tumors showed abnormal increase higher than 10 ng/ml in 17 cases (about 50%) of them, whereas all of benign cases were lower than 10 ng/ml. The means and standard deviations of NSE in the cerebrospinal fluid of malignant tumors were 20.63 +/- 20.78 ng/ml in the astrocytoma grade 3 and 4, 19.73 +/- 15.5 ng/ml in the medulloblastoma and 12.4 +/- 8.9 ng/ml in the germ cell tumor. NSE values in the CSF of 12 brain tumors with intrathecal metastasis were 28.0 +/- 18.9 ng/ml (mean +/- SD) showing about three times as much as those without intrathecal metastasis. There was significant difference between these groups (p less than 0.01). All cyst fluids including in 7 cases of brain tumors demonstrated high values of NSE even if they were benign tumor and their NSE values in CSF were normal. NSE values of brain tumor tissues had no correlation with malignancy, but were higher in the periphery of the tumors than in the center. NSE values of CSF in brain tumors might be changed in relation with the improvement or deterioration on clinical state and CT. It might be suggested that the measurement of NSE in the CSF had significance as a monitor of therapeutic efficacy and prognosis for the brain tumors.

Animals↗
PubMed1994

CSF neuron-specific enolase after methohexital activation during electrocorticography.

We report changes in CSF and serum neuron-specific enolase (NSE) before and after methohexital infusion during electrocorticography in three patients undergoing epilepsy surgery. NSE is a critical enzyme for energy metabolism that accounts for 1.5% of all soluble brain protein and is an accepted marker of neuronal injury. CSF NSE rose three- to fourfold from baseline within 60 minutes after methohexital activation. Serum NSE was unchanged. This report supports evidence that CSF NSE rises acutely after induction of epileptiform activity and suggests that CSF NSE is a marker of seizure activity.

Biomarkers↗
PubMed1999

Time course of neurone-specific enolase and S-100 protein release during and after coronary artery bypass grafting.

Serum neurone-specific enolase (NSE) and S-100 protein are well established as markers of cerebral injury, and have been used as markers of neuronal and glial cell damage, respectively, after cardiac surgery with cardiopulmonary bypass (CPB), but the speed of their increase during CPB has not been studied. Therefore, we have investigated the time course of NSE and S-100 release during and after CPB. We studied 18 adult patients undergoing elective coronary artery bypass grafting (CABG). Standard hypothermic (32 degrees C) pulsatile bypass with membrane oxygenation was used. Blood samples were obtained at induction, before bypass, before rewarming, at the end of rewarming, 10 min, 1 h and 8 h after bypass and 1, 2 and 3 days after surgery. NSE and S-100 were assayed using immunoradiometric assay kits (Sangtec Medical). NSE and S-100 release followed similar time courses. Both increased sharply during bypass, reached peak concentrations at the end of rewarming (mean 25.55 (SEM 2.79) and 1.65 (0.23) microgram litre-1, respectively), had decreased significantly by the end of operation and returned to pre-bypass concentrations by the second day after surgery. No patient developed a major neurological deficit. When using NSE and S-100 assays to study cerebral dysfunction in relation to CPB, postoperative samples miss peak (end-bypass) concentrations, and studies should be designed to include intraoperative samples.

Adult↗
PubMed2004

Regulation of the neuron-specific Ras GTPase-activating protein, synGAP, by Ca2+/calmodulin-dependent protein kinase II.

synGAP is a neuron-specific Ras GTPase-activating protein found in high concentration in the postsynaptic density fraction from mammalian forebrain. Proteins in the postsynaptic density, including synGAP, are part of a signaling complex attached to the cytoplasmic tail of the N-methyl-d-aspartate-type glutamate receptor. synGAP can be phosphorylated by a second prominent component of the complex, Ca(2+)/calmodulin-dependent protein kinase II. Here we show that phosphorylation of synGAP by Ca(2+)/calmodulin-dependent protein kinase II increases its Ras GTPase-activating activity by 70-95%. We identify four major sites of phosphorylation, serines 1123, 1058, 750/751/756, and 764/765. These sites together with other minor phosphorylation sites in the carboxyl tail of synGAP control stimulation of GTPase-activating activity. When three of these sites and four other serines in the carboxyl tail are mutated, stimulation of GAP activity after phosphorylation is reduced to 21 +/- 5% compared with 70-95% for the wild type protein. We used phosphosite-specific antibodies to show that, as predicted, phosphorylation of serines 765 and 1123 is increased in cultured cortical neurons after exposure of the neurons to the agonist N-methyl-d-aspartate.

Animals↗