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PubMed1984

Neuron-specific enolase in cerebrospinal fluid: a possible indicator of neuronal damage in kainic acid lesions.

The presence of the neuron specific enolase (NSE) has been tested by sandwich enzyme immunoassay in cerebrospinal fluid (CSF) of rats after intrastriatal injection of various amounts of kainic acid (KA). Incremental release of NSE was observed in CSF for increasing concentrations of injected KA. Still, a significant decrease of NSE striatal content was detected only with the two maximal amounts of KA infused. These data indicate that measurements of NSE in CSF might be a more sensitive index of neuronal damage than the actual assay within the tissue, and also present the advantage of being a non-invasive method of investigation.

Animals↗
PubMed2006

Neuron-specific enolase and tau protein as neurobiochemical markers of neuronal damage are related to early clinical course and long-term outcome in acute ischemic stroke.

OBJECTIVES: Analyses of neuron-specific enolase (NSE) and tau protein in patients with hyperacute ischemic stroke, their association with infarct volume, severity of the neurological deficit, the neurovascular status and functional outcome. PATIENTS AND METHODS: In 66 consecutive patients, serial venous blood samples were taken at 3, 6, 12, 18, 24, 48, 72, 96, and 120 h after stroke onset. The neurovascular status was assessed by repetitive extra- and transcranial duplex sonography. Neurological deficits were quantified by the NIH stroke scale, and functional outcome was assessed with the modified Rankin scale (mRS). RESULTS: After a first rise within 3 h, NSE decreased followed by a secondary increase until Day 5. Tau protein concentrations showed a continuous increase from admission onward. NSE and tau release were highly correlated with severity of neurological deficits and infarct volume (P = 0.001). NSE, but not tau protein, release was associated to the neurovascular status on admission. NSE and tau protein values were significantly correlated with the functional outcome at 3 months (P < 0.001). CONCLUSION: Release kinetics of NSE and tau protein are associated with patients' clinical deficits and infarct volume, and may be used as an additional predictor of the early course and functional outcome.

Aged↗
PubMed1985

Neuron specific enolase: a marker of (small cell) cancers of neuronal and neuroendocrine origin.

Neuron specific enolase (NSE) has been demonstrated to be a marker for tumours of neuroendocrine origin. Serum NSE levels have been shown by several groups to be of help in the identification of advanced small cell lung cancers and neuroblastoma. The lack of sensitivity to small tumour burdens and lack of specificity of small increments above normal restricts the test as a diagnostic aid in early stage disease. The main use would seem to be in the monitoring of chemotherapy and follow up after completing treatment as sequential measurements enable relatively small changes in level to be interpreted.

Carcinoma, Small Cell↗
PubMedDate not supplied

Neuron-specific enolase in cerebrospinal fluid and plasma of patients with acute ischemic brain disease.

The objective of this research was to determine the dynamics of change of neuron-specific enolase concentration in patients with acute ischemic brain disease in cerebrospinal fluid and plasma. The study included 103 patients, their mean age 58-66 years. The control group consisted of 16 patients, of matching age and sex, with radicular lesions of discal origin, subjected to diagnostic radiculography. Concentration of neuron-specific enolase was measured by a flouroimmunometric method. The results showed that the concentration of neuron-specific enolase in cerebrospinal fluid and plasma of patients with brain ischemic disease within first seven days significantly increased compared to the control. The highest increase of concentration was established in brain infarction, somewhat lower in reversible ischemic attack, and the lowest in transient ischemic attack. Maximal concentration was established on the 3rd-4th day upon the brain infarction. Neuron-specific enolase concentration in cerebrospinal fluid and plasma may be an indicator of pathophysiological processes in the acute phase of brain ischemia and is significant in early diagnostics and therapy of the disease.

Acute Disease↗
PubMed2003

Neurone-specific expression and regulation of the pufferfish isotocin and vasotocin genes in transgenic mice.

We used comparative genetics to investigate the location, structure and evolution of the oxytocin and vasopressin gene regulatory regions. The pufferfish, Fugu rubripes, is an attractive vertebrate model for comparison because of its maximal evolutionary distance from mammals and short intergenic regions. To determine whether regulatory DNA is conserved between oxytocin and vasopressin, and their Fugu homologs, isotocin and vasotocin, we generated transgenic mice bearing overlapping Fugu cosmids that contained the isotocin and/or vasotocin genes as well as short isotocin (5 kb) and vasotocin (9 kb) constructs. Our study shows that the Fugu isotocin and vasotocin genes express specifically in the mouse oxytocinergic and vasopressinergic neurones, respectively, and that the cis-regulatory elements which mediate neurone-specific expression are located within the short transgene constructs tested. Thus, the neurone-specific expression of the oxytocin and vasopressin gene families, and the mechanisms mediating the cell-specificity, evolved before the divergence of the fish and mammalian lineages. Salt-loading of transgenic mice induced an increase in abundance of isotocin, but not vasotocin mRNA in the cognate neurones. It appears that either the vasotocin gene does not respond to osmotic perturbations or the vasotocin transgene construct tested lacks osmotic response elements. Comparisons of homologous flanking sequences of the Fugu and mouse genes identified several short matching sequences, which are candidate regulatory elements.

Animals↗
PubMed1986

Identification and characterization of neuron-specific and developmentally regulated gene transcripts in the chick embryo spinal cord.

Clones corresponding to neuron-specific and developmentally regulated messenger RNA species in the chick have been isolated from a complementary DNA library prepared using polyadenylated RNA from 7-day embryonic spinal cord. The library was initially screened by differential complementary DNA hybridization procedures for clones identifying polyadenylated RNAs present in embryonic spinal cord but absent from or at low abundance in liver tissue. A high proportion of selected recombinant plasmids were found to identify different RNA species which, although present in 14-day embryonic spinal cord, could not be detected in a corresponding region of the developing chick CNS that is devoid of neuronal cell bodies, the optic nerve. The neuron-specific assignment of these mRNAs within the developing neuroectoderm was confirmed using bulk-isolated neuronal and glial-enriched cell fractions from 7-day embryonic spinal cord. In addition, several distinctive patterns of developmentally regulated expression of neuron-specific messenger RNA species have been observed in the chick spinal cord. The studies lay a foundation for detailed examination of the regional and temporal distribution and control of neuronal gene expression in the chick spinal cord during embryogenesis.

Animals↗
PubMed1985

Determination of urine neuron-specific enolase levels in neuroblastoma patients.

Urine levels of neuron-specific enolase were determined in 3 neuroblastoma patients (1 in an advanced state and 2 in remission), 25 control children, 37 control adults and 4 children with hematuria by means of the double-antibody inhibition radioimmunoassay specific to the gamma subunit of enolase isozymes. The levels of neuron-specific enolase mean +/- S.D. ng/creatinine mg in an advanced neuroblastoma patient were elevated (1.25 +/- 0.29 before or after treatment and range 1.61-74.2 during treatment) when compared with those of control subjects (0.51 +/- 0.26 in children and 0.36 +/- 0.17 in adults). The levels in 2 neuroblastoma patients in remission were within normal range. Urine samples with hematuria were not used for the assay.

Central Nervous System Diseases↗
PubMed1988

[Determination of serum neuron-specific enolase in bronchial tumors of neuroendocrine origin].

Neurone-specific enolase, a serum marker of neuroendocrine tumours has been determined in small-cell anaplastic bronchial carcinomas, in typical and atypical carcinoid. The marker presents good sensitivity in small-cell tumours and in atypical carcinoids, while blood levels are within normal limits in cases of typical carcinoid. The low serum levels of neurone-specific enolase found in typical carcinoid suggest a failure of the enzyme to express itself in the circulation owing to the poor or lack of cellular necrosis.

Biomarkers, Tumor↗
PubMed2000

Predictive value of S-100beta and neuron-specific enolase serum levels for adverse neurologic outcome after cardiac surgery.

OBJECTIVES: The aim of this study was to evaluate the time course of S-100beta and neuron-specific enolase serum levels after cardiac surgery and their clinical relevance in predicting postoperative adverse neurologic outcomes; the 2 proteins are only released in peripheral blood in association with nervous system lesions. METHODS: We neurologically assessed 190 consecutive patients undergoing elective cardiac operations for coronary artery bypass (n = 147), valve replacement (n = 29), or both (n = 14), before as well as after the operation. Postoperative outcome was classified as type I (uncomplicated), type II (confusion, agitation, disorientation, or epileptic seizures), or type III (stroke, stupor, or coma). Levels of S-100beta and neuron-specific enolase were evaluated in venous blood samples drawn preoperatively and then daily in the first 5 postoperative days. RESULTS: Levels of S-100beta and neuron-specific enolase differed significantly among the 3 groups (type III > type II > type I) throughout the postoperative period and had a diagnostic specificity and specificity of 89% and 79%, respectively, in identifying patients with type III outcome. S-100beta (but not neuron-specific enolase) levels were identified as significant independent predictors for type II and III outcomes (odds ratio 16.2, P <.0004). The same was true for duration of cardiopulmonary bypass (odds ratio 1.02, P <.006). CONCLUSIONS: Serum levels of S-100beta are reliable markers for adverse neurologic outcomes after cardiac surgery.

Biomarkers↗
PubMed2003

[Postburn change in the plasma level of neuron specific enolase in burned patients with cerebral malfunction].

OBJECTIVE: To explore the relationship between the change in neuron specific enolase (NSE) and brain malfunction in burned patients. METHODS: The serum samples of 11 burned patients with brain dysfunction were collected for the development of the serum level of neuron specific enolase with radioimmunoassay, and the correlation between condition of systemic inflammation and the levels of neuron specific enolase was assessed. RESULTS: The level of NSE in burn patients with cerebral malfunction was obviously higher than that in control, and the level was correlated with the systemic inflammation. CONCLUSION: The change in the level of serum NSE could reflect the damage degree of central nervous system to some extent.

Adult↗
PubMed1986

Neuron-specific gamma-enolase derived from human glioma.

Neuron-specific gamma-enolase in human neurogenic tumors, including gliomas, transplanted gliomas, and permanent human glioma cell lines, was studied quantitatively, using newly established enzyme immunoassay methods, together with immunostaining of the tissue and cell preparations. A significantly high level of gamma-enolase was found in some glioblastomas, astrocytomas and oligodendrogliomas as well as medulloblastomas. Glioblastomas transplanted into mice and cultured cell lines derived from the same origins, as well as the permanent human glioma cell lines, also contained gamma-enolase, although the contents were low compared with findings in the original tumor tissues. Immunohistochemically, gamma-enolase stained intensely in the glioblastomatous cells. Serum gamma-enolase concentrations in some patients with gliomas and those of all the transplanted mice were enhanced. The serum gamma-enolase levels in the mice correlated well with size of the transplanted tumor tissues. These results indicate that neuron-specific gamma-enolase is produced in some neurogenic tumors of nonneuronal origin, therefore, serum gamma-enolase may be a useful biomarker for monitoring the extent of disease in patients with gliomas.

Animals↗
PubMed1988

Immunohistochemical characterization of a set of monoclonal antibodies to human neuron-specific enolase.

This paper describes the immunohistochemical staining properties of four monoclonal antibodies (MAbs) (CF, EB, AD, and KB) which had been previously shown to be specific for purified neuron-specific enolase (NSE) by a solid-phase radioimmunoassay. In this study, the authors immunostained a spectrum of normal and neoplastic neuronal, "neuroendocrine," and nonneuronal tissues fixed in formalin and embedded in paraffin. Positivity was generally restricted to normal neuronal structures and neuronal tumors, including adrenal neuroblastoma, ganglioneuroblastoma, olfactory neuroblastoma, pheochromocytoma, carotid body paraganglioma, duodenal gangliocytic paraganglioma, and teratoma with neuroepithelial components. Three staining patterns of the normal or neoplastic neuronal structures were observed: two MAbs (CF and EB) stained predominantly the nerve fibers (axoplasm); one (AD) stained predominantly the cell bodies (perikaryon); and one (KB) stained both the axoplasm and the perikaryon. "Neuroendocrine" tumors such as pulmonary small cell carcinoma, pancreatic islet cell tumor, thyroid medullary carcinoma, and carcinoid tumors from various locations showed a variable staining pattern. Tumor cells undergoing mitotic division were usually positive regardless of type. Normal structures other than neuronal or "neuroendocrine," including normal glial cells, were negative. The authors also studied a range of glial cell tumors with MAbs CF and AD as well as with Dako polyclonal antiserum to NSE. The results showed that CF stained the axonal fibers in the normal white matter surrounding these tumors; it did not stain the tumor cells or the perikarya of neurons in the surrounding normal gray matter. AD stained the glioma cells as well as the perikarya and dendrites of neurons in the surrounding normal gray matter; it did not stain the axonal fibers in the surrounding normal white matter. By contrast, the polyclonal antiserum stained all of these structures. The high degree of staining specificity of the MAbs should prove them to be valuable in immunohistochemical diagnosis of tumors as well as in further understanding the role of NSE in neuronal differentiation.

Adrenal Glands↗
PubMed1993

Immunohistochemistry of neurone specific enolase with gamma subunit specific anti-peptide monoclonal antibodies.

AIMS: To investigate the application in immunohistochemistry of gamma-subunit specific anti-peptide monoclonal antibodies to human neurone specific enolase (NSE); and to determine their reactivity with formalin fixed, wax embedded sections of normal tissue and neuroendocrine tumours. METHODS: Immunohistochemical staining was performed on sections of formalin fixed, wax embedded tissue with two monoclonal antibodies (NSE-P1 and NSE-P2) raised against different synthetic peptides specific for the gamma subunit of human enolase (neurone specific enolase). RESULTS: Both antibodies gave strong immunostaining in normal tissues and cells known to contain NSE. There was no immunoreactivity in tissues containing either the alpha alpha or beta beta isozymes of enolase. The reactivity of the antibodies with a range of neuroendocrine tumours was also studied and both antibodies gave strong immunostaining of tumour cells in the different tumours. CONCLUSIONS: The use of synthetic peptides from defined regions of a molecule as immunogenes provides antibodies of high specificity. These monoclonal antibodies to NSE are ideally suited for immunohistochemical studies and they should be particularly useful in histopathology as they react with epitopes which are resistant to formalin fixation and wax embedding.

Antibodies, Monoclonal↗
PubMed1988

Complete amino acid sequence of the neurone-specific gamma isozyme of enolase (NSE) from human brain and comparison with the non-neuronal alpha form (NNE).

The complete amino acid sequence (433 residues) of the human neurone-specific gamma isozyme of enolase (NSE) has been determined by a combination of direct amino acid sequencing and nucleotide sequencing of cloned cDNA. Substantial amino acid sequence of the non-neuronal alpha form of the enzyme was also obtained which agreed almost entirely with the indirect cDNA sequence. Comparison of the two human sequences shows no insertions or deletions, but 72 replacements. Comparison of the human gamma form with the corresponding isozyme from the rat shows only 7 replacements (compared to 27 changes between the human and rat alpha isozymes). We have identified regions of sequence difference between the human alpha and gamma forms that are mainly hydrophilic in character (residues 271-285, 298-316 and 416-433). These residues are on the surface of the three-dimensional structure and could be useful as immunogens to produce antibodies specific for the neurone-specific form.

Amino Acid Sequence↗
PubMed1995

Transduction of foreign regulatory sequences by a replication-defective herpes simplex virus type 1: the rat neuron-specific enolase promoter.

Herpes simplex virus type 1 (HSV-1) can transduce genes into non-proliferating cells such as neurons that are refractory to other means of gene transfer. We have been interested to examine the potential usefulness of HSV-1 as a gene transfer vehicle to analyze neuron-specific regulatory sequences. In this study, we have used a replication-defective HSV-1-based vector deleted for the essential immediate early gene 3 (IE3) to transduce a 1.8 kb promoter fragment from the rat neuron-specific enolase gene (nse) linked to the firefly luciferase reporter gene (luc). It has previously been shown that the same promoter fragment is capable of directing neuron-specific expression of a linked reporter gene in transgenic mice. As an internal control for infection and gene expression, we also inserted the chloramphenicol acetyltransferase (cat) gene driven by the SV40 early promoter/enhancer into the thymidine kinase locus of the same vector. We infected (i) non-neuronal BHK-C13 cells which do not express the endogenous nse gene, (ii) differentiated and non-differentiated pheochromocytoma PC12 cells as well as (iii) N1E-115 neuroblastoma cells, all of which do express endogenous nse. All three cell types produced luciferase upon infection, indicating that the same nse promoter fragment that has previously been shown to be regulated in a cell-specific manner in transgenic mice, was not regulated cell type-specifically in the context of the HSV-1 genome.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

A neuron-specific enhancer of the Drosophila dopa decarboxylase gene.

At least two cis-regulatory elements are necessary for correct neuron-specific expression of the Drosophila melanogaster dopa decarboxylase gene, Ddc. In addition to a previously described proximal element located approximately 60 bp upstream of the mRNA start site, we have now characterized a distal approximately 600-bp DNA fragment, extending from -1019 to -1623 bp, which possesses enhancer-like properties and is essential for normal neuron-specific expression. Immunofluorescent labeling of neurons expressing deleted Ddc genes indicates that this region contains both general neuronal regulatory elements and cell-specific elements that selectively affect Ddc expression in either dopaminergic or serotonergic neurons. These selective effects can be correlated with the removal of sequence elements that are protected from DNase digestion by factors present in embryonic nuclear extracts. Several of these elements are also homologous to sequences located upstream of the evolutionarily diverged Ddc gene of Drosophila virilis. These results suggest that the neuron-specific expression of Ddc results from the combined action of several factors binding within this distal enhancer region.

Animals↗
PubMed1986

[Significance of neuron-specific enolase (NSE) in the diagnosis of bronchial carcinomas and neuroendocrine tumors].

The diagnostic significance of neuron-specific enolase in serum was examined in 54 patients with bronchial carcinoma and in 28 with neuroendocrine tumors. Control groups were 42 patients with epithelial and 39 with nonepithelial malignant neoplasms as well as 40 patients with benign pulmonary diseases. The sensitivity of neuron-specific enolase in small-cell bronchial carcinoma was 60% and increased to 87.5% in advanced stages ("extensive disease"). On the other hand, non-specific enolase showed an increase in only 13.8% of patients with other than small-cell bronchial carcinoma. The proportion of false-positive enolase values in non-malignant pulmonary diseases was 5%. Some endocrinal tumors (e.g. tumors of the APUD cell system) showed pathological serum concentrations in 7.1% of the cases only. 37.5% of epithelial malignant neoplasms had enhanced levels, but only 5.1% in nonepithelial neoplasms. Small-cell bronchial carcinoma is most probably present in patients with bronchial carcinoma and neuron-specific enolase serum concentrations above 25 micrograms/l.

Adenocarcinoma↗