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At least 145 records · Page 8Linked to original sources
PubMed1997

Serum neuron-specific enolase as early predictor of outcome after cardiac arrest.

OBJECTIVE: To examine the prognostic value of serum neuron-specific enolase for early prediction of outcome in patients at risk for anoxic encephalopathy after cardiac arrest. DESIGN: Prospective study. SETTING: Coronary intensive care unit of the University of Heidelberg. PATIENTS: Forty-three patients (66.8 +/- 12.7 [SD] yrs, range 33 to 85) who had had either primary or secondary cardiac arrest, followed by cardiopulmonary resuscitation (CPR). INTERVENTIONS: Serial blood samples and clinical examinations. MEASUREMENTS AND MAIN RESULTS: Serum neuron-specific enolase concentrations were determined after CPR on 7 consecutive days. Twenty-five patients remained comatose and subsequently died; 18 patients survived the first 3 months and had no relevant functional deficit at 3-month follow-up. Neuron-specific enolase concentrations were correlated with neurologic outcome. Concentrations of >33 ng/mL predicted persistent coma with a high specificity (100%) and a positive predictive value of 100%. Overall sensitivity was 80%, with a negative predictive value of 78%. Serum concentrations of neuron-specific enolase exceeded this cutoff value no more than 3 days after cardiac arrest in 95% of patients in whom these concentrations had exceeded 33 ng/mL. CONCLUSIONS: In patients who have been resuscitated after cardiac arrest, serum neuron-specific enolase concentrations of >33 ng/mL predict persistent coma with a high specificity. Values below this cutoff level do not necessarily indicate complete recovery, because this method has a sensitivity of 80%.

Adult↗
PubMed1984

Immunohistochemical localization of neuron-specific enolase in the human hypophysis and pituitary adenomas.

Neuron-specific enolase (NSE) was localized, using the immunoperoxidase technique, in the cytoplasm of the five adenohypophyseal hormone-secreting cell types, and in nerve fibers of the pars nervosa of the human pituitary. Crooke's hyaline material was negative. Neuron-specific enolase was found in all pituitary adenoma types; there was no correlation between degree of granularity or differentiation of tumor cells and intensity of NSE immunopositivity. One hypothalamic hamartoma was positive for NSE; a craniopharyngioma and a neurohypophyseal granular cell tumor were not. Neuron-specific enolase was present in peptide hormone-producing endocrine cells outside the pituitary and in their tumors; the majority of other tumors were negative for NSE, although one breast carcinoma, one ovarian cystadenocarcinoma, and one lymphoma were positive for NSE. In control studies, absorption of NSE antisera with growth hormone abolished immunoreactivity; there was no immunologic cross-reaction demonstrable by radioimmunoassay.

Adenoma↗
PubMed2004

Identification of thermosensory and olfactory neuron-specific genes via expression profiling of single neuron types.

Most C. elegans sensory neuron types consist of a single bilateral pair of neurons, and respond to a unique set of sensory stimuli. Although genes required for the development and function of individual sensory neuron types have been identified in forward genetic screens, these approaches are unlikely to identify genes that when mutated result in subtle or pleiotropic phenotypes. Here, we describe a complementary approach to identify sensory neuron type-specific genes via microarray analysis using RNA from sorted AWB olfactory and AFD thermosensory neurons. The expression patterns of subsets of these genes were further verified in vivo. Genes identified by this analysis encode 7-transmembrane receptors, kinases, and nuclear factors including dac-1, which encodes a homolog of the highly conserved Dachshund protein. dac-1 is expressed in a subset of sensory neurons including the AFD neurons and is regulated by the TTX-1 OTX homeodomain protein. On thermal gradients, dac-1 mutants fail to suppress a cryophilic drive but continue to track isotherms at the cultivation temperature, representing the first genetic separation of these AFD-mediated behaviors. Expression profiling of single neuron types provides a rapid, powerful, and unbiased method for identifying neuron-specific genes whose functions can then be investigated in vivo.

Amino Acid Sequence↗
PubMedDate not supplied

S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum: markers of cell damage in human central nervous system.

The development of a radioimmunoassay for S-100 protein is described. This method was used in combination with a recently developed radioimmunoassay for neuron-specific enolase in cerebrospinal fluid and serum from 47 patients with cerebral infarction, transient ischemic attack, intracerebral hemorrhage, subarachnoid hemorrhage, and head injury. In cerebrospinal fluid, increased concentrations of both S-100 and neuron-specific enolase were found after large infarcts, whereas after small infarcts and transient ischemic attacks, only neuron-specific enolase increased. The increased concentrations of S-100 and/or neuron-specific enolase were noted 18 hours to 4 days after cerebral infarction and transient ischemic attacks. Cerebrospinal fluid concentrations of these proteins also reflected the severity of the disease in patients with intracerebral hematoma, subarachnoid hemorrhage, or head injury. Temporal changes in serum S-100 and neuron-specific enolase concentrations reflected the clinical course in 4 patients. In stroke patients, the S-100 and neuron-specific enolase concentrations may reflect the extent of brain damage and could be useful in selecting patients with major stroke for more aggressive treatment during the acute phase.

Cerebrovascular Disorders↗
PubMed2003

A neuron-specific EGF family protein, NELL2, promotes survival of neurons through mitogen-activated protein kinases.

NELL2 is a neuron-specific thrombospondin-1-like extracellular protein containing six epidermal growth factor-like domains. NELL2 is highly expressed in the hippocampus and cerebral cortex. Although the involvement of NELL2 in neural functions has been inferred from its expression and biochemical profiles, biological roles of NELL2 remain uncertain. We evaluated the survival effect of NELL2 using primary cultured neurons from fetal rat brain following treatment with a recombinant NELL2 protein. NELL2 increased survival of neurons from the hippocampus and cerebral cortex. We further examined the protective effect of NELL2 from oxygen-glucose deprivation- and beta-amyloid-induced neuronal death, and found that NELL2 did not protect neurons from these insults. To understand signaling properties underlying the survival effect, we studied activation of mitogen-activated protein kinases (MAPKs) by NELL2. Treatment of primary cultured cells from the hippocampus with NELL2 enhanced phosphorylation of c-jun N-terminal kinase (JNK), whereas phosphorylation of extracellular signal-regulated kinase (ERK) was decreased by NELL2 treatment. NELL2-enhanced survival of hippocampal neurons was completely blocked by SP600125, an anthrapyrazolone inhibitor of JNK, while treatment of MEK (MAPK/ERK kinase) inhibitors per se enhanced survival of neurons similar to NELL2 treatment. These results suggest that NELL2 promotes survival of neurons by modulating MAPK activities.

Amyloid beta-Peptides↗
PubMed1987

Monoclonal antibodies to human neuron-specific enolase reveal heterogeneity of the enzyme in neurons of the central nervous system.

Three monoclonal antibodies to human neuron-specific enolase (NSE) were used to survey the human brain and spinal cord for immunoreactivity. Two of the antibodies (EB and CF) recognized the same population of cells and cell processes. Reactivity was restricted to myelinated axons, basket cell bodies and processes, and a small population of pyramidal cell bodies in the visual cortex. The third antibody (AD) reacted with some, but not all, of the neuronal cell bodies in cerebral cortex, hippocampus, midbrain, and spinal cord. Many neurons did not react with any of the antibodies. The epitope recognized by AD was trypsin-sensitive, while those recognized by EB and CF were not. These studies suggest that NSE may have multiple conformational or structural forms which are segregated between the cell body and axon.

Animals↗
PubMed1998

Quantitative analysis of mRNA expression of neuron-specific growth-associated genes in rat primary neurons by competitive RT-PCR.

The reverse transcriptase-polymerase chain reaction (RT-PCR) application is a sensitive method for detecting gene expression in tissues where the message level is a very small percentage of the total RNA and where only small amounts of sample are available such as in primary cultured hippocampal neurons. Based on a previously developed quantitative competitive RT-PCR strategy, mRNA expression and regulation of the neuron-specific growth-associated genes T alpha1 alpha-tubulin (T alpha1), microtubule-associated protein-2 (MAP-2) and growth-associated protein-43 (GAP-43), all of which have been proposed as putative markers of neurite growth during development and regeneration, were quantitated. This protocol, in combination with morphological evaluation of neurite outgrowth, may provide a useful tool for quantitation of neurite outgrowth during differentiation and regeneration in cultured neurons and may also be applied to detect the expression of other genes where the levels of message are low and in other tissues where small quantities of RNA are available.

Animals↗
PubMed1985

Identification of neuron-specific enolase and nonneuronal enolase in human and rat brain on two-dimensional polyacrylamide gels.

The location of the enzymes neuron-specific enolase and nonneuronal enolase on two-dimensional gels generated from tissue samples obtained from fresh human and rat cortex has been identified. This identification is based upon the following criteria: comigration on polyacrylamide gels with the appropriate purified protein and staining on nitrocellulose protein blots of human and rat cortex using antibodies specific for each protein. The results show that our preparation of neuron-specific enolase from rat and human brain is highly pure, as only one spot is obtained on two-dimensional gels. Further, the antiserum to neuron-specific enolase is highly specific, as it reacts only with neuron-specific enolase on nitrocellulose blots derived from two-dimensional gels of cortical tissue. The location of these proteins is of interest because it positively identifies two major brain proteins on two-dimensional polyacrylamide gels of fresh cortical tissue. This information will be useful in a variety of future studies aimed at both identifying specific proteins on two-dimensional gels and observing the effects of experimental manipulations on brain and other neuronal proteins.

Animals↗
PubMed1991

Serum neurone specific enolase (NSE) levels as an indicator of neuronal damage in patients with cerebral infarction.

A radioimmunoassay has been developed and used to measure serum neurone specific enolase (NSE) concentrations in 24 patients, following cerebral infarction. A significant correlation between cerebral infarct volume and maximum serum NSE concentration was observed (P = 0.047). Serum NSE was also assayed at times 24, 48, 72 and 96 h post ictus. At 72 h a significant correlation existed between serum NSE levels and infarct volume (P = 0.012), and levels appeared to be approaching statistical significance at 48 h (P = 0.067). No correlation existed at 24 and 96 h. In addition serum concentrations of NSE were compared to clinical outcome as determined by the Glasgow Outcome Score. Using the Mann-Whitney U test, there was no significant difference in maximum NSE level between patients graded 1-3 on the Glasgow Outcome Score and those graded 4 and 5. However, further studies are required on a larger population to more completely assess this. NSE may prove to be a useful marker of neuronal damage in the study of stroke, with particular application in the assessment of treatment.

Adult↗
PubMed1995

The significance of neuron specific enolase levels in cerebrospinal fluid and serum after experimental traumatic brain damage.

In the posttraumatic period, measurement of neural tissue enzymes in serum and cerebrospinal fluid gives quantitative information about the severity of the head injury. In our study, we evaluated the relationship between the serum and cerebrospinal fluid levels of neuron specific enolase and the severity of trauma. Head traumas at different severity were applied experimentally (Mild 0.038 N, Moderate 0.057 N, Severe 0.3 N). Serum and cerebrospinal fluid levels of neuron specific enolase were measured in trauma and control groups of rats. Only in the severe trauma group, the neuron specific enolase levels of cerebrospinal fluid were significantly increased. There was no statistically significant difference between the groups when serum neuron specific enolase levels were evaluated. Our data leads us to conclude that trauma, causing significant neural damage, results in an increase in cerebrospinal fluid neuron specific enolase levels, however the serum neuron specific enolase levels do not seem to run parallel with that increase.

Animals↗
PubMed1985

Ultrastructural immunocytochemical localization of neuron-specific enolase in parafollicular cells of the rat thyroid.

Using pre- and post-embedding procedures, neuron-specific enolase and calcitonin were localized in rat thyroid parafollicular cells by light and electron microscopy. Peroxidase-antiperoxidase (PAP), biotin-avidin (ABC) and protein A--colloidal gold techniques were used. In paraffin sections neuron-specific enolase was demonstrated in all calcitonin-storing parafollicular cells in rats aging 1 to 180 days. The post-embedding procedure failed to detect neuron-specific enolase in ultrathin sections, but the enzyme could be demonstrated using a preembedding procedure. Neuron-specific enolase was localized exclusively within the cytosol of parafollicular cells, while calcitonin was localized within secretory granules applying either post- or pre-embedding incubation techniques.

Animals↗
PubMed1998

Neuron-specific enolase: reference values in cord blood.

With foetal sonography prenatal detection of tumours has become more frequent. To evaluate and treat these infants it is necessary to identify the tumour postnatally. Elevated neuron-specific enolase is a biochemical marker of neuroblastoma. Since conditions during birth may influence neuron-specific enolase concentration in foetal serum, specific reference values in cord blood are required. Cord blood samples were taken from 192 healthy term newborns and concentration of neuron-specific enolase was measured by enzyme immunoassay (EIA). Median neuron-specific enolase concentration in the reference group was 8.0 micrograms/l and the 5th-95th percentiles were 4.8-19.4 micrograms/l. No differences between male and female newborns were detected (p = 0.13). Measurement of neuron-specific enolase in cord blood, in comparison with our reference values, offers an early postnatal possibility of confirming the diagnosis of neuroblastoma.

Biomarkers, Tumor↗
PubMed2001

Neuron-specific expression of therapeutic proteins: evaluation of different cellular promoters in recombinant adenoviral vectors.

In order to achieve neuron-restricted expression of antiapoptotic proteins, cellular promoters were investigated for their expression profiles in the context of adenoviral vectors. Both the synapsin 1 gene and the tubulin alpha1 gene promoters were strictly neuron specific in cocultures of primary neurons with their essential feeder cells. The neuron-specific enolase gene promoter exhibited only weak activity in cultured hippocampal neurons and was not neuron specific in preparations of cerebellar granule cells. By attaining virtually 100% transduction efficiency we were able to generate "quasi-transgenic" primary neuron cultures using both differentiated and completely undifferentiated hippocampal neurons. In a functional assay, we used the synapsin promoter to evaluate the effect of Bcl-X(L) overexpression on potassium-withdrawal-induced apoptosis of cerebellar granule neurons. We found nearly complete inhibition of caspase-9 and -3 activation and apoptosis, indicating a major role for mitochondrial pathways in this paradigm of neuronal cell death. The excellent suitability of the synapsin promoter as a strong panneuronal promoter was further demonstrated by its restricted neuronal activity in various brain regions of adult rats in vivo.

Adenoviridae↗
PubMed1986

Development profile of neuron-specific enolase in human gut and its implications in Hirschsprung's disease.

The most widely held view on the pathogenesis of Hirschsprung's disease as an arrest of neuroblast migration in the gut was based on the hypothesis of a single craniocaudal gradient of development of enteric neurons. Recent experimental studies in animals, however, have revived a contradictory hypothesis of a dual gradient of neuronal development; such data are not available in humans. To test these hypotheses in humans, we studied the pylorus, ileum, and colon of 28 fetuses with gestational ages of 9-21 wk, using immunohistochemical localization of neuron-specific enolase, a specific neuronal marker indicative of differentiation. Development of the enteric nervous system was shown to be most advanced in the pylorus, less so in the colon, and least so in the ileum. The findings support the hypothesis of a dual gradient of neuronal development proceeding from both ends to the middle of the gut in midtrimester human fetuses and suggest that the pathogenesis of Hirschsprung's disease needs to be reconsidered.

Colon↗
PubMed1986

Determination of serum neuron-specific enolase by differential immunocapture.

A new method for the determination of serum neuron-specific enolase is presented. It consists of two steps: first, an immunocapture of gamma-subunit containing isoenzymes by absorption on immobilized anti-gamma antibodies; second, bioluminescence assay of enolase activities in untreated control samples and in the supernates of antibody treated samples. Total and alpha alpha activities are obtained, from which the neuron-specific enolase activity (alpha gamma + gamma gamma) can then be calculated by difference. As compared to the procedures currently in use, the immunocapture method is very rapid (30 min) and is more suitable for small series of determinations as needed in clinical chemistry applications. Reference interval values for serum found by this method agree with published data. When tested with samples from patients suffering from neuroblastoma or small cell lung cancer, it confirms the specific elevations in neuron-specific enolase activity previously described for these cancers, using other analytical approaches.

Adult↗
PubMed2002

Cloning and characterization of the 5'-flanking region of the rat neuron-specific Class III beta-tubulin gene.

The promoter regions of several neuron-specific structural proteins (e.g. neurofilaments, peripherin, Talpha1-tubulin) have revealed potential regulatory elements that could contribute to the choice of a neuronal phenotype during development. We initiated study of the 5'-flanking region of the rat Class III neuron-specific beta-tubulin gene (betaIII-tubulin) because this gene is expressed at the time of terminal mitosis only in neurons and thus its promoter should be an excellent tool for studying neuron-specific gene expression during the transition from proliferative progenitor cell to early neuronal differentiation. We identified the minimal promoter region needed to drive expression of the betaIII-tubulin gene. This minimal region contains multiple putative binding sites for the transcription factors SP1 and AP2, as well as a central nervous system enhancer regulatory element and an E-box. A primer extension analysis identifies a single transcription start site. We highlight several putative regulatory elements that may modulate the expression of the betaIII-tubulin gene in a stage- and tissue-specific manner. In addition, we show that the first 490 bp of the promoter are sufficient to regulate betaIII-tubulin gene expression during neuronal differentiation of PCC7 cells.

5' Flanking Region↗
PubMed2004

Correlation between serum level of neuron-specific enolase and long-term functional outcome after acute cerebral infarction: prospective study.

OBJECTIVE: To determine the value of measuring serum levels of neuron-specific enolase in predicting extent of disease and short- and long-term functional outcome after acute cerebral infarction. DESIGN: Prospective study. SETTING: Neurology departments at two university teaching hospitals, Shanghai. PATIENTS: Thirty-eight patients who presented for acute cerebral infarction between October 1998 and October 2000 were divided into two groups: those whose infarction extended to the cerebral cortex in the carotid artery region (cortical group) and those with an infarction in the subcortical carotid artery region (subcortical group). MAIN OUTCOME MEASURES: Using a solid-phase enzyme immunoassay, we measured serum levels of neuron-specific enolase on admission and on days 2, 3, and 15. Infarct volume was measured by computed tomography on day 5. The Activities of Daily Living scale was used to assess the clinical outcome at 1-, 3-, and 6-month follow-up after onset. RESULTS: Mean (standard deviation) serum neuron-specific enolase levels were significantly higher among patients with acute cerebral infarction than among controls (18.48 [16.61] ng/mL versus 9.00 [2.70] ng/mL; P<0.001). The neuron-specific enolase level was also higher in the cortical group than in the subcortical group (33.54 [29.71] ng/mL versus 15.97 [5.91] ng/mL; P<0.01). Levels peaked after 2.11 (0.86) days and correlated positively with the infarct volume (r=0.81; P<0.01) and negatively with clinical outcome at 1 month (r= -0.37; P<0.05), 3 months (r= -0.45; P<0.01), and 6 months (r= -0.65; P<0.001), as assessed on the Activities of Daily Living scale. CONCLUSION: Serum neuron-specific enolase levels after cerebral infarction may be a useful marker to predict infarct volume and short- or long-term functional outcome.

Activities of Daily Living↗
PubMed1986

Neuron-specific enolase in retinoblastoma. An immunohistochemical study.

Forty-six retinoblastoma specimens were studied for the presence of neuron-specific enolase (NSE) in the tumour cells and in the remaining morphologically normal retina. The laboratory method was a sensitive immunohistochemical peroxidase staining procedure, and normal ocular nerves were used as positive controls. Neuron-specific enolase was found in perikarya and cell processes in all layers of morphologically normal appearing neuroretina, but not in Müller's cells. All but two of the retinoblastomata studied contained positively staining tumour cells, whereas stromal cells remained constantly negative. Many Flexner-Wintersteiner rosettes stained positively as well. The proportion of retinoblastoma cells expressing neuron-specific enolase seemed to be greater in small tumours, in bilateral cases, and in tumours that contained rosettes. The presence of neuron-specific enolase in tumour cells seems to favour a neuronal or neuroectodermal origin for retinoblastoma, but it should be noted that this marker has recently been found in several non-neuronal and non-neuroectodermal malignant neoplasms.

Eye Neoplasms↗