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PubMed2005

Serum neuron-specific enolase as a predictor of short-term outcome in children with closed traumatic brain injury.

BACKGROUND: Closed traumatic brain injury (cTBI) is a significant cause of mortality and morbidity in children. The natural course and extent of recovery from cTBI in children are poorly understood. Neuron-specific enolase (NSE), an enzyme detected in serum following structural damage of neuronal brain cells, appears to be a good marker for intracranial injury. However, to the best of the authors' knowledge, the usefulness of NSE as a predictor of disability in children with cTBI has not been reported. OBJECTIVES: To examine the association between posttraumatic serum NSE level and short-term physical disability in children with cTBI. METHODS: This was a retrospective analysis of a prospectively enrolled cohort of children aged 0-18 years with isolated cTBI presenting to the emergency department (ED) within 24 hours of injury, and having a cranial computed tomography (CT) scan as part of the evaluation. The NSE level was obtained at the time of ED evaluation. Physical disability was measured using the Glasgow Outcome Scale (GOS). The GOS score was assigned retrospectively for enrolled patients by a single investigator blinded to NSE level. Patient outcomes were categorized as good (GOS = 5) or poor (GOS < 5). A single radiologist reviewed all cranial CT scans. RESULTS: Ninety eligible subjects with NSE levels were identified; 86 met the enrollment criteria. Seven subjects (8%) had poor outcome. There was a significant difference in NSE levels between the poor and good outcome groups, even within high-risk subgroups. The area under the curve (AUC) for NSE prediction of poor vs. good outcome was 0.83. A serum NSE level of 21.2 ng/dL was 86% sensitive and 74% specific in predicting poor outcome. CONCLUSIONS: It appears that the serum NSE level can be used as a predictor of global short-term physical disability in children following cTBI.

Adolescent↗
PubMed2000

Pro-gastrin-releasing peptide, neuron specific enolase and chromogranin A as serum markers of small cell lung cancer.

BACKGROUND: Small cell lung cancer (SCLC) yields neuroendocrine properties. Pro-gastrin-releasing peptide (ProGRP), neuron specific enolase (NSE) and chromogranin A (CGA) are therefore putative serum markers in this disease. AIM: To assess any difference in the sensitivity-specificity relationship between these neuroendocrine markers regarding various control populations and disease extent. METHOD: A total of 146 patients were prospectively assessed clinically and biologically. Serum marker titrations were performed using commercial immunoradiometric assays (NSE, CGA) or ELISA (ProGRP). Areas under receiver operating characteristic curves (AUC-ROC) were calculated in order to assess the sensitivity-specificity relationship of each marker and to compare marker accuracy. Maximum Youden indices were used to determine marker thresholds able to produce the best overall diagnostic information. RESULTS: Assessing the sensitivity in the SCLC population and the specificity in benign lung disease, ProGRP demonstrated the best sensitivity relationship in as much as its AUC-ROC was significantly greater than the ones calculated using NSE and CGA (respective values, 0.95, 0.89, 0.70; two-tailed Z-test <0.05). The ProGRP threshold value, which offered the best sensitivity-specificity relationship was 53 pg/ml corresponding to a 0.80 sensitivity and a 0.96 specificity. In addition, when specificity was assessed in NSCLC and again the sensitivity in the whole SCLC population, ProGRP continued to demonstrate a greater AUC-ROC in comparison with other markers. Using the 53 pg/ml threshold the specificity of this marker was excellent with no false positives in NSCLC. On the other hand, none of the markers were able to discriminate limited from extensive SCLC as suggested by the fact that AUC-ROC, constructed when sensitivity was defined as a positive test in extensive disease and specificity as a true negative test in limited disease, did not reach the upper left octant (AUC 0.65, 0.71 and 0.63 for ProGRP, NSE and CGA, respectively). CONCLUSION: ProGRP yields the best sensitivity-specificity feature in SCLC, a result deserving further studies designed to evaluate the clinical applicability of this marker.

Adult↗
PubMed2000

Subtle brain damage cannot be detected by measuring neuron-specific enolase and S-100beta protein after carotid endarterectomy.

OBJECTIVE: To assess whether subtle brain damage after carotid endarterectomy could be detected using serum levels of neuron-specific enolase (NSE) or S-100beta protein. DESIGN: Prospective noninterventional study. SETTING: University hospital. PARTICIPANTS: Twenty-two patients undergoing carotid endarterectomy and 16 patients undergoing repair of abdominal aortic aneurysm. INTERVENTIONS: Serum levels of NSE and S-100beta protein were measured in all patients before surgery and postoperatively at 12, 24, 36, and 48 hours. In patients undergoing carotid endarterectomy, neuropsychologic testing was performed before surgery and postoperatively at discharge from the hospital and after 3 months using a neuropsychologic test battery. MEASUREMENTS AND MAIN RESULTS: Compared with abdominal aortic surgery patients, the preoperative serum concentration of NSE was significantly higher in carotid artery surgery patients. Postoperatively, the NSE serum level decreased significantly after uncomplicated carotid artery surgery, and the level was then similar to that in the aortic surgery patients. Before operation, the S-100beta protein levels were similar in the two groups, but a significant increase was seen in aortic surgery patients postoperatively. Neuropsychologic testing after uncomplicated carotid artery surgery revealed cognitive dysfunction in 2 of 20 (10%) of the patients after 5 days and 3 of 16 (19%) of the patients after 3 months. There was no correlation between the change in cognitive function and the changes in blood levels of either NSE or S-100 protein. CONCLUSIONS: Subtle brain damage after carotid artery surgery could not be detected by measuring blood levels of NSE and S-100beta protein. The NSE level was significantly higher before carotid artery surgery and decreased postoperatively to the level observed in aortic surgery.

Aged↗
PubMed1979

Regulation of the state of phosphorylation of specific neuronal proteins in mouse brain by in vivo administration of anesthetic and convulsant agents.

The effect of drug treatment in vivo on the state of phosphorylation of two specific neuronal proteins, proteins Ia and Ib, has been studied in mouse brain. For this purpose, animals were killed by immersion into liquid nitrogen, and proteins Ia and Ib were extracted by a procedure designed to prevent alterations in their state of phosphorylation. Several anesthetic agents (pentobarbital, chloral hydrate, and urethane) each caused a decrease in the state of phosphorylation of these proteins. Conversely, the convulsant agents pentylenetetrazol and picrotoxin each caused an increase in the state of phosphorylation of these proteins. Neither the anesthetic nor the convulsant agents affected the total amount of these proteins. The results are compatible with a role for proteins Ia and Ib in neuronal function.

Anesthetics↗
PubMed2004

Playing soccer increases serum concentrations of the biochemical markers of brain damage S-100B and neuron-specific enolase in elite players: a pilot study.

PRIMARY OBJECTIVE: To analyse serum concentrations of two biochemical markers of brain tissue damage, S-100B and NSE (neurone-specific enolase), in male soccer players in connection to the game. METHODS: Blood samples were taken in players before and after a competitive game and the numbers of headers and of trauma events during soccer play were assessed. RESULTS: Both S-100B and NSE were significantly raised in serum samples obtained after the game in comparison with the pre-game values (S-100B: 0.118 +/- 0.040 microg L(-1) vs 0.066 +/- 0.025 microg L(-1), p < 0.001; NSE: 10.29 +/- 2.16 microg L(-1) vs 8.57 +/- 2.31 microg L(-1), p < 0.001). Only changes in S-100B concentrations (post-game minus pre-game values) were statistically significantly correlated to the number of headers (r = 0.428, p = 0.02) and to the number of other trauma events (r = 0.453, p = 0.02). CONCLUSION: Playing competitive elite soccer was found to cause increase in serum concentrations of S-100B and NSE. Increases in S-100B were significantly correlated to the number of headers, and heading may accordingly have contributed to these increases.

Adult↗
PubMed2001

Neuron-specific enolase serum levels after controlled cortical impact injury in the rat.

The aim of this study was to investigate the time course and the correlation of neuron-specific enolase (NSE) serum levels to the severity of traumatic brain injury in rats. Sixty-five male Wistar rats were subjected to severe cortical impact injury (100 PSI, 2 mm deformation). Blood samples were drawn directly after trauma and after 1, 6, 12, 24, and 48 h in the trauma group. In the sham operated levels animals samples were drawn directly after craniotomy and after 6 and 48 h. Additionally, NSE serum levels after controlled cortical impact at different levels of severity samples (45 PSI, 75 PSI; 2 mm deformity) were compared to sham-operated animals. The severity of the injury was not validated histopathologically. NSE serum levels were estimated with a commercially available enzyme immunoassay (LIA mat Sangtec). The control animals showed a NSE serum level of 8.82 microg/L (mean, n = 10) and the injured animals demonstrated a time-dependent release of NSE into the serum. The highest NSE serum values were detected 6 h after trauma (31.5 microg/L mean, n = 10). In addition, we found a close relationship between NSE serum levels and the severity of traumatic brain injury in the cortical impact model. NSE serum levels reflect in a time-dependent manner the severity of brain trauma induced by cortical impact model in rat.

Animals↗
PubMed2003

Neuron specific enolase concentration is increased in serum and decreased in platelets of patients with active systemic sclerosis.

OBJECTIVE: To determine frequency, origin, and clinical associations of elevated serum neuron specific enolase (NSE) in systemic sclerosis (SSc). METHODS: Serum was obtained from 75 patients with SSc, 20 systemic lupus erythematosus, 8 polymyositis, 10 idiopathic interstitial lung disease, and 10 healthy volunteers. NSE status was determined in serum (in all individuals) and in platelet lysate (in volunteers and 30 patients with SSc). RESULTS: Elevated serum NSE (mean 22.6 ng/ml, range 12.1-68.2 ng/ml) was observed in 26 patients with SSc (34.6%). Those with diffuse SSc had higher serum NSE than those with limited disease (16.5 +/- 13.4 vs 9.6 +/- 5.0 ng/ml, p = 0.006). No association was found between serum NSE and lung or esophagus involvement. Patients with long-standing disease had lower serum NSE than those with early disease (10.8 +/- 7.3 vs 16.1 +/- 13.6 ng/ml, p = 0.05). Serum NSE was 19.4 +/- 13.0 ng/ml in patients with total skin score (TSS) > 20, 8.3 +/- 2.1 ng/ml in patients with TSS < 5, and 6.0 +/- 3.1 ng/ml in volunteers (p = 0.01). NSE platelet lysate concentration was 3.6 +/- 2.9 ng/ml in patients with TSS > 20, 12.4 +/- 4.1 ng/ml in those with TSS < 5, and 14.1 +/- 6.5 ng/ml in healthy individuals (p < 0.001). Volunteers and SSc patients with low TSS had comparable S/PL-NSE index (serum/platelet lysate NSE concentration) (0.42 +/- 0.16 and 0.75 +/- 0.33, respectively), both lower than SSc patients with high TSS (7.45 +/- 5.57) (p < 0.001). CONCLUSION: Elevated serum NSE was observed in one-third of SSc patients but not in other autoimmune rheumatic diseases. The inverse relationship between serum and platelet lysate NSE concentration suggests platelet activation as the origin of high serum NSE in SSc. NSE S/PL was the best discriminatory variable between healthy volunteers and SSc patients as well as between patients with high and low TSS. High serum NSE and high NSE-S/PL index seemed to be associated with SSc disease activity. Further work is warranted to investigate a possible role for this marker in assessing disease activity and therapy response.

Adult↗
PubMedDate not supplied

[Neuron-specific enolase in ophthalmology].

Tissue location and biochemical aspects of the enolase, enzyme belonging to the glycolytic pathway, are presented. Embryological applications of the dimer gamma-gamma (Neuronal Specific Enolase) as a biological marker of the neuroectodermal derivatives is discussed. The authors stress the clinical importance of the NSE in the early detection of tumors.

Biomarkers↗
PubMed2006

In vivo identification of a 107-base pair promoter element mediating neuron-specific expression of mouse gonadotropin-releasing hormone.

To identify regions of the mouse GnRH (mGnRH) promoter that mediate tissue-specific gene expression, transgenic mice have been generated with fragments of mGnRH promoter fused to the luciferase reporter gene. In this manuscript, we examine transgenic mice, generated with -356/+28 bp and -249/+28 bp of the mGnRH gene. Both fragments of mGnRH promoter target ovarian expression of the luciferase transgene, but neuronal luciferase activity is detected only in the mice bearing the -356-bp fragment, suggesting that the DNA sequences essential for directing neuron-specific expression of the GnRH gene are located between -356 and -249 bp. Two consensus binding sites for Otx2 were identified in this promoter region and were confirmed to be functional. EMSAs demonstrated specific binding of Otx2 to the mGnRH promoter, and overexpression of Otx2 increased transcriptional activity of the mGnRH promoter in transient transfection studies. When both Otx2 binding sites were eliminated, overexpression of Otx2 had no effect. GnRH mRNA expression in immortalized GnRH-secreting cell lines was also found to correlate with Otx2 expression. In addition, transgenic mice, bearing the 356 fragment of the mGnRH gene in which the Otx2 binding sites were eliminated, have significantly lower luciferase activity in the neonatal brain compared with mice generated with intact Otx2 binding sites. Luciferase activity was, however, still present in the ovary. Our findings provide evidence that Otx2 may have a critical role in directing tissue-specific expression of the mGnRH gene to the neuron, but not the ovary.

Animals↗
PubMed1981

Increased levels of neuron-specific enolase in PC12 pheochromocytoma cells as a result of nerve growth factor treatment.

Treatment of PC12 pheochromocytoma cells with nerve growth factor (NGF) resulted in increased levels of neuron-specific enolase (NSE). Neither insulin, growth hormone, cytochrome c, nor sodium butyrate increased NSE levels. Epidermal growth factor (EGF) did increase NSE levels, although not to the same extent as NGF. As little as 1 ng/ml NGF induced the maximal increase in NSE. As PC12 cells increased in density, the NSE levels increased even in untreated cells.

Adrenal Gland Neoplasms↗
PubMed1992

Neuronal specificity of the alpha 7 nicotinic acetylcholine receptor promoter develops during morphogenesis of the central nervous system.

A transient transfection assay has been developed to analyse promoter activity in neuronal cells freshly dissociated from the chick central nervous system. The assay enabled us to identify cis-acting regulatory elements within the 5'-flanking region of the alpha 7 nicotinic acetylcholine receptor gene. In differentiated retina, regulatory elements direct reporter gene expression to a small subset of neurons which has been identified as ganglion cells, i.e. to the population of neurons in which alpha 7 transcripts were localized by in situ hybridization. However, these promoter elements exhibit ubiquitous activity in undifferentiated neural cells and in mesodermal stem cells. Our study supports the idea that alpha 7 regulatory elements acquire their neuronal specificity in the course of embryogenesis.

Amino Acid Sequence↗
PubMed1991

Increases of neuron-specific enolase, S-100 protein, creatine kinase and creatine kinase BB isoenzyme in CSF following intraventricular catheter implantation.

In 15 patients without acute brain injury the concentrations of Neuron-specific Enolase (NSE), S-100 Protein (S-100), Creatine Kinase (CK), and Creatine Kinase BB isoenzyme (CK-BB) in ventricular cerebrospinal fluid (CSF) were measured immediately after lateral ventricle cannulation for diagnostic or treatment purposes. From patients who were treated with a shunt another CSF sample was obtained one week after shunt implantation by puncture of the antechamber of the valve. The CSF concentrations of NSE, S-100, CK and CK-BB after cannulation were found to be of the same order as found in patients with severe head injury, stroke or subarachnoid haemorrhage. One week after shunt implantation the concentrations of S-100, CK and CK-BB had returned to normal levels in almost all patients, while the NSE concentrations remained elevated. These findings indicate that the sampling procedure may result in contamination of CSF with NSE, S-100, CK and CK-BB and they should be taken into account in the prognostic evaluation of enzyme concentrations after brain injury.

Brain Damage, Chronic↗
PubMed2001

S-100B and neuron-specific enolase in serum of mild traumatic brain injury patients. A comparison with health controls.

OBJECTIVES: The aim of the study was to determine whether serum concentrations of neuron-specific enolase (NSE) and S100-B in mild traumatic brain injury (MTBI) patients are higher than in serum of healthy controls. MATERIAL AND METHODS: Blood samples from 104 MTBI patients were taken shortly after the trauma for measurement of S-100B and NSE in serum. In 92 healthy persons these markers were also measured. Marker concentrations in serum of patients and controls were compared. In the patient group the relation between serum-marker concentrations and clinical symptoms and signs, that occurred shortly after the traumatic event, were evaluated. RESULTS: Median NSE concentration was only slightly higher in patients (9.8 microg/l; 10 to 90 percentile range 6.9 to 14.3 microg/ l) than in controls (9.4 microg/l; 6.3 to 13.3 microg/l). Median S-100B concentration was significantly higher in patients (0.25 microg/l; 0.00 to 0.68 microg/l) than in controls (0.02 microg/l; 0.00 to 0.13 microg/l). An association was found between S-100B concentrations and vomiting in patients. CONCLUSIONS: S-100B is a useful marker for brain damage in MTBI patients and seems to be associated with the presence of vomiting after the trauma.

Adolescent↗
PubMed2004

Sputum carcinoembryonic antigen, neuron-specific enolase and cytokeratin fragment 19 levels in lung cancer diagnosis.

OBJECTIVE: The aim of the present study was to examine the impact of sputum carcinoembryonic antigen (CEA), neuron-specific enolase (NSE) and cytokeratin fragment 19 (CYFRA 21-1) levels in lung cancer diagnosis and to compare the diagnostic usefulness of sputum assays with that of serum assays. METHODOLOGY: Forty-seven patients with lung cancer and 62 with benign lung disease were studied. Tumour marker levels in sputum (sp.) and serum (ser) were measured by immunoradiometric assays. RESULTS: Sputum and serum tumour marker levels were significantly higher in lung cancer than in benign disease. When the specificity was 95%, the sensitivity was 57%, 43%, 36%, 30%, 28% and 19%, for spCEA, serCYFRA 21-1, spCYFRA 21-1, serCEA, serNSE, and spNSE, respectively. Bayesian analysis showed that the best predictive values correspond to spCEA and serCYFRA 21-1. The maximum overall gain was obtained in pretest probability of 0.35 for both spCEA and serCYFRA 21-1, with predictive values of 84% and 80% for spCEA and serCYFRA 21-1, respectively. CONCLUSION: Sputum tumour marker levels were no more useful than the serum levels in lung cancer diagnosis. SpCEA offered the best predictive values but these were still not sufficiently satisfactory for spCEA to be proposed for routine use.

Adult↗
PubMed1987

201Tl/67Ga uptake ratio in small cell carcinoma of the lung: with special reference to serum neuron-specific enolase and prognosis.

201Tl/67Ga crude uptake ratio (CUR) was measured in 12 patients with small cell carcinoma of the lung (SCCL); it was further compared with serum neuron-specific enolase (NSE) and the actual survival times. A significant inverse correlation was observed between CUR and serum NSE (r = 0.610; p less than 0.05); CUR also correlated with actual survival time (r = 0.605; p less than 0.05). Oat cell-type SCCL having a low CUR and highly raised serum NSE, showed a poorer prognosis than the other subtype which has a high CUR whose serum NSE was not raised as much as in oat cell-type SCCL. This preliminary study suggests that 201Tl/67Ga uptake ratio is a possible prognostic indicator of SCCL.

Adenocarcinoma↗
PubMedDate not supplied

Neuron-specific enolase (gamma enolase, gamma-gamma dimer) expression in Hodgkin's disease and large cell lymphomas.

BACKGROUND: The presence of gamma-enolase, gamma gamma dimer, or neuron-specific enolase (NSE) has been demonstrated in miscellaneous tumors, including malignant lymphomas. Up to now these results have been interpreted as non-specific, although NSE can be expressed by normal B and T lymphoid cells at a particular stage of differentiation. The aim of the present study was to investigate the expression of NSE in a large series of malignant lymphomas, including Hodgkin's disease, in relation to morphology and immunophenotype. MATERIALS AND METHODS: Frozen and paraffin embedded sections from 16 cases of Hodgkin's disease (4 lymphocyte predominance, nodular; 4 mixed cellularity; 6 nodular sclerosis; 2 lymphocyte depletion) and 35 cases of non-Hodgkin's lymphomas were investigated in order to evaluate the expression of NSE, its specificity and correlation to immunophenotype or other immunological cell markers. Among the non-Hodgkin's lymphomas, there were 9 Anaplastic Large Cell (CD30+) Lymphomas; 2 Peripheral Large T-Cell Lymphomas; 22 Diffuse Large B-Cell Lymphomas and 2 Primary Mediastinal Large B-Cell Lymphomas. RESULTS: In Hodgkin's disease, NSE showed a diffuse cytoplasmic reaction in CD30+ Reed-Sternberg cells, whereas the "popcorn" (L&H) cells of lymphocyte predominance, nodular variant cases, were always negative. Among the non-Hodgkin's lymphomas, NSE positivity was found only in lymphomas expressing CD30. All the other cases were negative. No relationship was found between NSE and B- or T-immunophenotype. CONCLUSIONS: Our results suggest that a link between NSE and CD30 expression exists in malignant lymphomas. However, at the moment this has not been sufficiently investigated and is subject to speculation.

Antibodies, Monoclonal↗
PubMedDate not supplied

[Usefulness of determining the level of neuron-specific enolase (NSE) in the cerebrospinal fluid as a biochemical indicator of the extent of cerebral ischemic stroke. Experimental study of the rat model of stroke].

Changes of neuron-specific enolase (NSE) in cerebrospinal fluid after experimental ischaemic stroke caused by middle cerebral artery occlusion in rat were studied. High enzyme levels were found between the second and seventh day after artery occlusion and they correlated well with the extension of infarct seen in histology. NSE levels in cerebrospinal fluid are sensitive and reliable markers of brain tissue damage during the acute phase of ischaemic stroke.

Animals↗
PubMed2000

Olf-1, a neuron-specific transcription factor, can activate the herpes simplex virus type 1-infected cell protein 0 promoter.

Herpes simplex virus type 1 (HSV-1) establishes a life-long latent infection in sensory neurons of infected individuals. Infected cell protein 0 (ICP0) is important for productive infection and reactivation from latency. Thus, activation of ICP0 expression in neurons is likely to be important for reactivation from latency. In a mouse neuroblastoma cell line, ICP0 promoter activity is high compared with other strong viral promoters. In contrast, promoter activity is low in non-neuronal cells. DNase I footprinting assays indicated that three distinct motifs in the ICP0 promoter are bound by nuclear factors. One of these motifs contains a binding site for a novel helix-loop-helix olfactory neuron-specific transcription factor (Olf-1). Gel shift assays and supershift assays using an Olf-1-specific antibody demonstrated that mouse neuroblastoma cells express Olf-1, which is bound to the Olf-1-like site in the ICP0 promoter. Deletion of the putative Olf-1 motif reduced ICP0 promoter activity more than 5-fold in mouse neuroblastoma cells and prevented trans-activation by an Olf-1 expression vector. We hypothesize that the Olf-1-binding site activates ICP0 promoter activity in neurons during reactivation from latency.

Animals↗