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PubMed1997

Expression, purification, and characterization of a highly soluble N-terminal-truncated form of the neuron-specific membrane-associated phosphoprotein SCG10.

SCG10 is a neuron-specific growth-associated protein with high sequence homology to the ubiquitous phosphoprotein stathmin/Op18. The main structural difference between the two proteins is the 34-amino-acid N-terminal extension of SCG10, which is responsible for the membrane attachment. Full length SCG10 has been purified and shows limited solubility, in contrast to stathmin, which is a highly soluble protein. In order to obtain a more soluble form of SCG10 which would be better suited for biochemical and structural studies, we deleted the N-terminal extension and expressed the C-terminal portion of the protein. Two forms of N-terminal-truncated SCG10 (delta SCG10 and delta SCG10r) were purified to homogeneity in a four-step purification procedure. delta SCG10 starts at amino acid 35 and delta SCG10r at amino acid 48 in the SCG10 sequence, giving proteins of 16,899 and 15,189 kDa, respectively. The truncated SCG10 was highly soluble up to concentrations of 20 mg/ml. The proteins were like the full length SCG10 substrate for serine/threonine protein kinases, including MAP kinase, PKA, and p34cdc2 kinase. With these highly soluble forms of SCG10 biochemical and structural studies of this multiphosphoprotein become feasible.

Amino Acid Sequence↗
PubMed1983

The value of S-100 immunostaining as a diagnostic tool in human malignant melanomas. A comparative study using S-100 and neuron-specific enolase antibodies.

The brain proteins S-100 and neuron-specific enolase have been reported by separate groups to be present in human malignant melanomas. There is no systematic study comparing the occurrence of these proteins in the same tumour specimens. We have examined 33 primary malignant melanomas, including 5 which were amelanotic, and 25 metastatic melanomas using immunohistochemical methods with specific, non-cross-reacting antibodies to S-100 and NSE. We found S-100 immunoreactivity to be present in all cases but one, whereas NSE immunoreaction was very weak and patchy, and present in only 6 cases. S-100 immunoreactivity was not demonstrated in 40 control tumours, either primary or metastatic in skin, including basal- and squamous-cell carcinomas, spindle-cell sarcomas, lymphomas and Merkel cell tumours. All intradermal (n = 4) and compound (n = 1) naevi were positive for S-100, 2 blue naevi showing much less reaction. NSE immunoreactivity was detected in Merkel cell tumours (n = 8), undifferentiated (n = 2) and small cell (n = 1) carcinomas, and all melanocytic naevi. It is suggested therefore that antibody to S-100 is the reagent of choice for demonstration of melanocytic tumours, and may be especially valuable in the diagnosis of amelanotic melanoma or metastatic tumours of doubtful origin where melanoma is suspected.

Fluorescent Antibody Technique↗
PubMed2005

Cerebrospinal fluid neurone-specific enolase in mitochondrial encephalomyopathies.

Whether cerebrospinal fluid (CSF) neurone-specific enolase (NSE) contributes to the diagnosis of mitochondrial encephalomyopathies (MEMs) is unknown. Aim of the present study was thus to assess the validity of CSF-NSE in the diagnosis of MEM. CSF-NSE was determined in 24 controls, aged 28-88 years; and 23 MEM patients, aged 47-81 years. In controls, CSF-NSE was independent of sex (p = 0.849) and age (p = 0.346). Twenty-one MEM patients had clinical CNS involvement and two CNS abnormalities on imaging investigations exclusively. CSF cells were increased in 7, CSF protein in 17, CSF glucose in 1, and CSF lactate in 2 MEM patients. The upper reference limit of CSF-NSE was 14.66 ng/mL. CSF-NSE was elevated in 6 (26%) MEM patients. CSF-NSE was increased in a single MEM patient with subclinical CNS involvement. This study shows that CSF-NSE is elevated in only one quarter of the MEM patients. Determination of CSF-NSE appears to be of minor importance for the assessment of clinical or subclinical CNS involvement in MEM.

Adult↗
PubMed1993

Improvement of the diagnosis of the cause of pleural effusion in patients with lung cancer by simultaneous quantification of carcinoembryonic antigen (CEA) and neuron-specific enolase (NSE) pleural levels.

Carcinoembryonic antigen (CEA) and neuron-specific enolase (NSE) level determinations were carried out by radioimmunoassay in pleural fluid and plasma samples obtained from 24 patients with malignant pleural effusions and 18 patients with non-malignant pleural effusions, and compared to cytological and pathological results. Using a pathological cut-off level of 25 ng/ml for CEA and 8 ng/ml for NSE, we demonstrated that, in the diagnosis of the malignant nature of pleural effusions, the simultaneous quantification of CEA and NSE in pleural fluid possesses better discriminative values than the simultaneous quantification of both markers in plasma or the separate quantification of each marker, in pleural fluid and in plasma.

Biomarkers, Tumor↗
PubMed1995

Cerebrospinal fluid concentration of neuron-specific enolase in diagnosis of Creutzfeldt-Jakob disease.

Neuron-specific enolase (NSE) is among the biochemical markers in cerebrospinal fluid reported to be useful in the differential diagnosis of Creutzfeldt-Jakob disease from other dementing illnesses. In a group of 58 patients with definite and probable Creutzfeldt-Jakob disease, NSE concentrations (median 94.0, interquartile range 256 ng/mL) were significantly higher (p < 0.001) than in 26 control patients (9.5, 15.5 ng/mL). At a cut-off of 35 ng/mL an optimum sensitivity of 80% with a specificity of 92% for the diagnosis of Creutzfeldt-Jakob disease by NSE in cerebrospinal fluid was obtained.

Aged↗
PubMed1985

Evaluation of a radioimmunoassay for neuron specific enolase in small cell lung cancer.

A radioimmunoassay for neuron specific enolase (NSE), a marker of neuroendocrine differentiation, has been evaluated in small cell lung cancer (SCLC). In untreated patients 25/38 (68%) with localized SCLC had raised blood levels of NSE (greater than 13 ng ml-1), in extensive disease 34/39 (87%) patients had raised NSE levels. In patients with non-small cell lung cancer (NSCLC) the serum levels were raised in 16/94 (17%). In extensive tumours of non-pulmonary origin NSE levels were increased in 24/116 (20%) patients. Longitudinal studies indicated a good correlation between the response to chemotherapy and fall of NSE levels. Tumour progression was accompanied by a rising NSE in 25/29 patients, with doubling times of 7-90 days. In patients with progression with a normal NSE the recurrence was a NSCLC. Cerebral metastases occurring as the only recurrence during clinical complete remission were not accompanied by a rise of NSE. Serum NSE levels provides a valuable monitor for SCLC during and after chemotherapy.

Carcinoma, Small Cell↗
PubMed1996

Serum neurone-specific enolase as an indicator of stroke volume.

Serum neurone-specific enolase (NSE) and computerized tomography (CT) stroke volume were compared in patients admitted within 24 h of an acute stroke. Serum samples were obtained on admission and daily for the next 4 days. Of 163 patients, CT scans revealed 25 with intracerebral haemorrhages, one haemorrhagic infarct and 83 measurable acute infarcts. The serum NSE levels of those with infarcts was significantly higher than in those with haemorrhages at 48 (P = 0.0003) and 72 h (P = 0.04). The maximum serum NSE value tended to occur later in those with large infarcts (P = 0.0035). There was a significant correlation between infarct volume and serum NSE at 48 h (r = 0.27, P = 0.015) and 96 h (r = 0.27, P = 0.015) and with the maximum serum NSE over the 4 days (r = 0.36, P = 0.001). There was no significant correlation between haemorrhage volume and NSE. In conclusion, serum NSE may be a useful marker of infarct volume in studies of therapy in acute stroke. Sampling for NSE should continue, at least in those with large infarcts, for longer than 4 days. Serum NSE cannot be used to distinguish between haemorrhage and infarction in patients with an acute stroke.

Adult↗
PubMed2006

Prediction of neurological outcome after cardiopulmonary resuscitation by serial determination of serum neuron-specific enolase.

AIMS: Data on the diagnostic accuracy of neuron-specific enolase (NSE) as marker of hypoxic brain damage are conflicting. The purpose of this prospective observational cohort study was to explore the prognostic value of serum NSE after cardiopulmonary resuscitation (CPR) and to define the most sensitive cutoff value with a specificity of 100% for the prediction of persistent coma. METHODS AND RESULTS: Serum NSE concentrations were serially determined in 227 consecutive unconscious patients after CPR who were classified according to the best Glasgow-Pittsburgh cerebral performance categories (CPC, 1-4) achieved within 6 months follow-up. Sixteen patients were excluded due to incomplete NSE data and 34 due to death under analgesia sedation. The prevalence of poor neurological outcome (persistent coma, CPC 4) in our 177 analysed patients was 33%. At a specificity of 100%, a peak NSE concentration above 80 ng/mL predicted persistent coma with a sensitivity of 63%, a positive predictive value of 100%, a negative predictive value of 84%, and a predictive accuracy of 88%. CONCLUSION: A peak serum NSE concentration exceeding 80 ng/mL is a highly specific but only moderately sensitive marker for a poor neurological outcome after CPR.

Adolescent↗
PubMed1994

Neuron-specific enolase as a tumor marker in metastatic melanoma.

Neuron-specific enolase (NSE) has been shown by some investigators to be a useful tumor marker for melanoma, but the relationship between NSE and tumor burden has not been extensively studied. We therefore examined NSE levels in 240 patients of whom 169 had no clinical evidence of disease (NED) and 71 had metastatic disease. There was no statistically significant difference in NSE levels in patients with NED compared with metastatic disease as well as those with high tumor burden compared with low or intermediate tumor burden. In addition, the mean absolute values of NSE, despite a slight elevation with tumor burden, were within the normal range (< 20 ng/ml). Our data suggest that NSE levels measured by the method used in our study are of no benefit in melanoma.

Biomarkers, Tumor↗
PubMed1982

A developmental study of neuron-specific enolase in rat adrenal medulla.

The levels of neuron-specific enolase (NSE) in rat adrenal medulla increase with age. A sharp increase was observed until the age of 15 days. At this time, the NSE level dropped slightly, followed by a gradual increase until the rats were 1 year old. The adrenal medullary NSE levels in males were higher than those observed in females. The difference was seen from 32 days of age, but was not statistically significant until 1 year. This study indicates that NSE can be used as a marker for differentiation in adrenal medulla, as it is used in the central nervous system and in neuroblastoma and pheochromocytoma cells.

14-3-3 Proteins↗
PubMed1995

Neuron-specific enolase is increased after nonconvulsive status epilepticus.

Serum neuron-specific enolase (s-NSE), a marker of brain injury and acute seizures, was increased in 2 patients with nonconvulsive SE. Neither patient had an acute neurologic insult other than nonconvulsive SE (NCSE) accounting for s-NSE changes. Increase in s-NSE provides further in vivo evidence of transient brain injury after NCSE.

Adult↗
PubMed1989

Establishment and evaluation of a radioimmunoassay for neuron-specific enolase. A marker for small cell lung cancer.

Neuron-specific enolase (NSE) was purified from human brain to a specific activity of 91 U/mg with no demonstrable impurities. The enzyme has a molecular weight of 96,000, consists of two subunits of 47,000, and has an isoelectric point at pH 4.5. A radioimmunoassay based on antibody raised in sheep was established. The assay has a sensitivity of 2 micrograms/l, and an interassay coefficient of variation of 6.4% at 10 micrograms/l. The reference limit was defined as 10 micrograms/l, as found in sera from a population of 389 persons. Of 50 untreated patients with small cell lung cancer (SCLC), 70% had NSE levels above 10 micrograms/l. None of 170 patients with non-SCLC neoplasms had elevated enzyme levels.

Adult↗
PubMed1998

Status epilepticus increases CSF levels of neuron-specific enolase and alters the blood-brain barrier.

Neuron-specific enolase (NSE) is a sensitive marker of brain damage in stroke, global ischemia, and coma. Serum NSE is also correlated with the duration and outcome of status epilepticus (SE). CSF-NSE levels have not been previously reported in SE. We report the CSF concentrations of NSE in 11 patients with cryptogenic/remote symptomatic SE. CSF obtained within 24 hours of SE showed increased concentrations of NSE in 9 of 11 patients. The mean CSF-NSE for the group was elevated compared with the levels for normal control subjects (30.8 +/- 18.33 versus 10.76 +/- 3.08 ng/mL; p = 0.002). Further, CSF-NSE levels were elevated compared with simultaneous serum levels in the same group of patients (p = 0.01). In addition, the CSF/serum albumin ratio (QAlb), a measure of the integrity of the blood-brain barrier, was increased in SE patients compared with control individuals (33.4 versus 4.79 x 10(-3); p = 0.0001). An increase of QAlb correlated with CSF-NSE (rs = 0.66, p = 0.04) and serum NSE levels (rs = 0.83, p = 0.004). CSF-NSE is a promising in vivo marker for brain injury after SE.

Adult↗
PubMed1987

[Clinical evaluation of serum neuron-specific enolase levels in patients with lung cancer].

Serum neuron-specific enolase (NSE) levels were studied in 105 patients with malignant neoplasms (lung cancer 38, others 67), 13 patients with various benign diseases and 7 healthy adults. The mean serum NSE level in adult control subjects was 7.4 +/- 0.8 ng/ml, and cut off level was decided 10 ng/ml. Serum NSE levels were elevated in 14/38 (37%) of patients with lung cancer and in 14/67 (21%) of patients with the other malignant neoplasms. In patients with benign diseases, serum NSE level was elevated only in one patient with pituitary adenoma. In 7 patients with small cell lung cancer, the positive rate was higher (86%) than in those with non-small cell lung cancer (26%), and serum NSE levels were higher than 25 ng/ml except one case. There was no correlation between serum NSE and CEA (carcinoembryonic antigen) levels in patients with small cell lung cancer, also in patients with lung cancer. The measurement of serum NSE level seemed to be useful for diagnosis in patients with small cell lung cancer.

Adult↗
PubMed1992

Serum neuron-specific enolase in various pathological conditions.

Quantitative determination of neuron-specific enolase in the serum was performed by RIA method in 18 neurological patients and in 22 patients with pulmonary diseases. The data confirmed that the specificity of this marker is not absolute for the detection both of the nature and of the seat of origin of the disease. Further problems are posed in patients which simultaneously suffer from endocrine, nervous and pulmonary abnormality.

Adolescent↗
PubMed1996

[Electrophoretic determination of aqueous and serum neuron-specific enolase (NSE) in the diagnosis of retinoblastoma].

OBJECTIVE: Neuron-specific enolase (NSE) or isoenzymes containing gamma-enolase are considered valuable in the diagnosis of tumors of neuroectodermal origin. METHOD: We used rapid electrophoretic method on cellulose acetate plate to determine the patterns of enolase isoenzymes in the 21 aqueous humor and 23 serum specimens from 23 patients with retinoblastoma (Rb) and 21 aqueous and 25 serum specimens from 25 control cases to evaluate NSE in the diagnosis of RB. The assay allowed assessment of all three major isoenzymes (alpha alpha, alpha gamma, and gamma gamma), and NSE relative activity and its percentage in the total relative activity of the three enolase isoenzymes were assessed by means of a fluorometer. RESULTS: Aqueous from all patients with Rb contained alpha alpha, alpha gamma, and gamma gamma isoenzymes and presented strong positive, the positive rate of NSE being 100% and its relative activity accounting for 45 +/- 9% of the total relative activity of the 3 enolase isoenzymes; no enolase was detectable in the control aqueous with cataract, glaucoma and Coats's diseases (4 cases), but in two patients with traumatic hyphema alpha alpha band, while the sera faint alpha gamma and gamma gamma presented in the aqueous. The control serum contained only an alpha alpha band, while the sera from patients with RB contained alpha alpha, alpha gamma and gamma gamma bands in 18 of 23 specimens, the positive rate being 78.2%, and only alpha alpha bands in the rest 5 specimens (21.8%). In the patients with Rb, the NSE relative activity and its percentage in the total relative activity of the 3 isoenzymes in serum (36 +/- 9%) were significantly lower than that in aqueous. CONCLUSION: The amounts of NSE significantly in both serum and aqueous from patients with Rb, and the immunoelectrophoretic assay for determination of enolase patterns is valuable in the diagnosis and differential diagnosis of Rb. In addition, the method is rapid, simple and requires only a little among (< 5 microliters) of sample.

Aqueous Humor↗
PubMed2006

A retinoic acid-Hox hierarchy controls both anterior/posterior patterning and neuronal specification in the developing central nervous system of the cephalochordate amphioxus.

Retinoic acid (RA) mediates both anterior/posterior patterning and neuronal specification in the vertebrate central nervous system (CNS). However, the molecular mechanisms downstream of RA are not well understood. To investigate these mechanisms, we used the invertebrate chordate amphioxus, in which the CNS, although containing only about 20,000 neurons in adults, like the vertebrate CNS, has a forebrain, midbrain, hindbrain, and spinal cord and is regionalized by RA-signaling. Here we show, first, that domains of genes with expression normally limited to diencephalon and midbrain are generally not affected by altered RA-signaling, second, that contrary to previous reports, not only Hox1, 3, and 4, but also Hox2 and Hox6 are collinearly expressed in the amphioxus CNS, and third, that collinear expression of all these Hox genes is controlled by RA-signaling. Finally, we show that Hox1 is involved in mediating both the role of RA-signaling in regionalization of the hindbrain and in specification of hindbrain motor neurons. Thus, morpholino knock-down of the single amphioxus Hox1 mimics the effects of treatments with an RA-antagonist. This analysis establishes RA-dependent regulation of collinear Hox expression as a feature common to the chordate CNS and indicates that the RA-Hox hierarchy functions both in proper anterior/posterior patterning of the developing CNS and in specification of neuronal identity.

Animals↗
PubMed1988

Serum neuron-specific enolase in senile dementia of the Alzheimer type.

The level of neuron-specific enolase (NSE), a glycolytic enzyme localized in neurons, was measured in the serum of patients with senile dementia of the Alzheimer type (SDAT). No difference was observed between NSE levels in SDAT and in healthy elderly controls of the same age range. No correlation was found between NSE levels and severity of the cognitive deficits. There was a marginally significant negative correlation between age and NSE, younger patients having higher NSE levels. The present results suggest that serum NSE is not a useful biological marker in the senile form of the dementia of the Alzheimer type.

Aged↗