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At least 631 records · Page 35Linked to original sources
PubMed1989

Immunocytochemical reactivity of breast cancer tissue with antibodies to neuron-specific enolase and an adenocarcinoma-associated glycolipid antigen.

The immunocytochemical reactivity of breast cancers to antibodies raised against neuron-specific enolase (NSE), carcinoembryonic antigen (CEA) and an adenocarcinoma-associated glycolipid antigen (IR-14) was studied in relation to the long-term outcome of the neoplastic disease. The patients whose tumours exhibited reactivity with the IR-14 and anti-NSE antibodies had a considerably better 5-year and long-term survival than those without such reactivity. Assessment of DNA-ploidy of the tumour cells was also relevant for long-term prognosis, immunohistochemistry giving additional prognostic information among aneuploid tumours. Reactivity with polyclonal CEA antibodies was of no prognostic value. It is suggested that tumours carrying the IR-14 reactive epitope, which was originally isolated from circulating antigen-antibody complexes, might evoke a favourable immune response and thus improve the survival of the patient.

Adult↗
PubMed1988

Immunohistochemical observation of S-100 protein and neuron specific enolase in the tumour cells of granular cell tumour.

An immunohistochemical technique for the detection of S-100 protein, neuron specific enolase (NSE), carcinoembryonic antigen (CEA) and muramidase (lysozyme) was applied to a case of the granular cell tumour. S-100 protein was detected both in the nuclei and cytoplasma of the granular cells, and NSE was weakly positive in their cytoplasms. CEA and lysozyme were negative in the tumour cells. Our results supports the concept that granular cell tumours are derived from Schwann cells.

Adult↗
PubMed2003

Serum neuron-specific enolase in children with febrile seizures: time profile and prognostic implications.

Compared to publications of elevated levels of neuron-specific enolase (NSE) in adult patients with single seizures or epilepsy, data in children are rare. We studied serial NSE serum concentrations in children after febrile convulsions (FC). In addition, the predictive value of NSE levels in serum for recurrence of FC or further development of epilepsy was determined. Serum NSE levels were determined at (1) 0-2 h, (2) 6-8 h and (3) 20-24 h after a first or second FC in children aged 4 months to 6 years. Eighty-two patients (35 female, 47 male) aged four months to 5.7 years were included. Seventy-one children had generalized, and seven focal FC. The seizures in the remaining four patients could not be properly classified. During the follow-up of 14-28 months 13 patients had at least one more FC and in five epilepsy due to recurrent afebrile seizures was diagnosed. There was no statistically significant elevation of NSE concentration in the group of children with FC or the group with recurrent FC or epilepsy. The comparison of the NSE values at different times after FC did not show any significant differences either. It seems from our results that NSE activity cannot be used as a predictor for possible brain damage caused by FC and that it is not of predictive value considering further FC or development of epilepsy. We cannot confirm the published results of the elevation of NSE serum levels in adults with single seizures or status epilepticus.

Child, Preschool↗
PubMed2003

Comparison between mono- and bi-exponential models for reaction kinetics in the immunoradiometric assay of neuron-specific enolase.

This paper studies the kinetics of the antigen-antibody reactions involved in the analytical determination of neuron-specific enolase (NSE) by means of radiometric immunoassay (IRMA). For the global process, kinetics were found to be dependent on analyte and labelled antibody concentrations, such dependence fitting with the models described in previous papers. Viscosity results clearly indicate its negative influence on the direct reaction rate. Ionic strength shows noticeable but not too relevant effects, which suggests that the variation caused by the glycerol addition is not due to the influence of the dielectric constant of the solutions used. The effect of temperature shows activation parameters similar to the viscous flow energy of water, which suggests diffusion control for the global process. The analysis of the kinetic data of the experiences conducted can be explained by admitting that the antigen-antibody binding takes place through two different binding site types.

Immunoradiometric Assay↗
PubMed1990

Serum neuron-specific enolase as a marker of small-cell carcinoma of the esophagus.

We monitored the changes in serum neuron-specific enolase (NSE) level in two patients with esophageal small-cell carcinoma (SCC) during the course of treatment by chemotherapy or surgery, with radiation. Serum NSE levels at diagnosis were 18.5 and 58.0 ng/ml. In both cases, after treatment the serum NSE level decreased to within normal range (less than 10.0 ng/ml), concurrent with reduction in the size of the tumor. However, with relapse of the disease, the serum NSE increased to 24.3 and 200.0 ng/ml, respectively. One patient died of lung and skin metastases 4 months after surgery; the other, who developed brain metastasis, was treated again with chemotherapy by the same regimen. The serum NSE level decreased to 13.0 ng/ml, and the symptoms improved. These results indicate that there is a correlation between serum NSE level and remission or relapse of the disease after treatment in patients with SCC of the esophagus, as with SCC of the lung.

Aged↗
PubMed1994

Transitional cell carcinoma of the renal pelvis and its expression of p53 protein, c-erbB-2 protein, neuron-specific enolase, Phe 5, chromogranin, laminin and collagen type IV.

Expression of p53 protein, c-erbB-2 protein, neuron-specific enolase (NSE), Phe 5, chromogranin, laminin and collagen type IV was studied by immunohistochemistry in formalin-fixed and paraffin-embedded specimens from 20 patients with renal pelvic carcinoma. Positive membrane-bound c-erbB-2 staining was not found in any case. Two tumors stained for p53 protein. Focal immunoreactivity for laminin was present in 55% and for collagen type IV in 80%. 25% of the cases were NSE positive. None of the tumors stained for Phe 5 or chromogranin. The results were compared with the clinical outcome and the immunohistological findings of p53 protein and c-erbB-2 protein in 13 cases of bladder carcinoma in the same patient group. Four of the thirteen bladder cancer specimens, but only 2 of the 20 renal pelvic cancer specimens, expressed p53 protein. As for renal pelvic carcinoma, c-erbB-2 protein was not expressed in bladder carcinoma. We conclude that p53 gene abnormalities may be of importance in the development of carcinoma in the renal pelvis and urinary bladder, but c-erbB-2 protein expression does not play a major role.

Adult↗
PubMed1989

Pleural fluid neuron-specific enolase. A useful diagnostic marker for small cell lung cancer pleurisy.

We studied the value of pleural fluid neuron-specific enolase as a possible diagnostic marker for pleurisy of small cell lung cancer by using enzyme immunoassay. Pleural fluid NSE levels in 12 patients with carcinomatous pleurisy due to small cell lung cancer were compared with those in 37 patients with carcinomatous pleurisy due to non-small cell lung cancer and 39 patients with tuberculous pleurisy. The pleural fluid NSE level was elevated in nine of 12 (75 percent) patients with SCLC. However, only two of 37 (5 percent) patients with NSCLC and two of 39 (5 percent) patients with tuberculous pleurisy had an elevated pleural fluid NSE level. Moreover, none of ten SCLC patients with cytology-negative pleural effusions showed elevated pleural fluid NSE level. Thus, determination of pleural fluid NSE levels seems to be an effective means to differentiate carcinomatous pleurisy due to SCLC from that due to NSCLC, tuberculous pleurisy and cytology-negative pleural effusion in SCLC.

Carcinoma, Non-Small-Cell Lung↗
PubMed1999

[Creutzfeldt-Jakob disease: diagnostic value of protein 14-3-3 and neuronal specific enolase assay in cerebrospinal fluid].

We studied the diagnostic value of detecting protein 14-3-3 and of assaying neuronal specific enolase (NSE) in the cerebrospinal fluid of 150 patients with suspected sporadic Creutzfeldt-Jakob disease registered in an epidemiology research program between 1991 and 1996. Sensitivity and specificity of these two tests were high. This study confirms results reported earlier and authorizes a new definition of Creutzfeldt-Jakob disease which gives protein 14-3-3 the same diagnostic value as EEG recordings for classifying sporadic cases.

14-3-3 Proteins↗
PubMed2005

[Effects of propofol and isoflurane on serum neuron-specific enolase level in surgical patients with acute craniocerebral trauma: a comparative study].

OBJECTIVE: To investigate changes in serum neuron-specific enolase (NSE) concentration in patients before, during and after surgery for acute craniocerebral trauma, and examine the effects of propofol and isoflurane on these changes. METHODS: Ten patients scheduled for urinary operation without cerebral injury were enrolled in the control group. Thirty patients with acute cerebral trauma were randomly allocated to propofol group (n=15) and isoflurane group (n=15). Serum concentrations of NSE before surgery, 2 h after the surgery began, and after completion of surgery were measured in all the patients by enzyme-linked immunoadsorbent assay. Glasgow scores of patients with cerebral trauma were also estimated and recorded. RESULTS: Serum concentration of NSE in patients with cerebral trauma were significantly higher than those in the control group before the surgery (P<0.01). The Glasgow score was inversely correlated with serum NSE concentration (r=-0.494, P<0.01). Serum NSE level after completion of surgery was significantly lower in propofol group than in isoflurane group (P<0.05). NSE levels at 2 h after the initiation of the surgery and after the completion of surgery were higher than those before the surgery. CONCLUSIONS: Serum NSE concentration increases in patients with acute cerebral injury in parallel to the severity of brain damage. Application of propofol by intravenous pumping can reduce the increase in serum NSE, alleviate cerebral injury, and protect the brain tissues of patients undergoing surgery for acute craniocerebral trauma.

Adolescent↗
PubMed1991

[Determining the level of the tumor marker--neuron-specific enolase in patients with neoplastic and non-neoplastic diseases].

Radioimmunoassay was employed to measure serum levels of neuron-specific enolase (NSE) in 38 lung cancer patients, 20 patients with noncancer pulmonary lesions and 10 healthy donors. An average NSE level (92.8 +/- 18.7 micrograms/l) in small cell carcinoma (10 patients) was significantly higher (p less than 0.01) than in control, nonmalignant pulmonary diseases, squamous cell and adenocarcinoma. Sensitivity and specificity of the tumor marker to small cell carcinoma reached 80 and 95%, respectively. NSE serum test may serve an additional tool in differential diagnosis of small cell carcinoma of the lung.

Adult↗
PubMed1986

[Clinical investigation of neuron-specific enolase, squamous cell carcinoma-related antigen and carcinoembryonic antigen in carcinoma of the lung].

Serum levels of neuron-specific enolase (NSE), squamous cell carcinoma-related antigen (SCC antigen) and carcinoembryonic antigen (CEA) were measured in 53 untreated patients with carcinoma of the lung. The positive rates of serum NSE were 17.0% in all patients with lung cancer, 53.8% in small cell carcinoma, 6.7% in adenocarcinoma, 5.0% in squamous cell carcinoma and 0% in large cell carcinoma; 0% in stage I, 14.3% in stage III and 26.7% in stage IV. The positive rates of serum SCC antigen were 45.3% overall, 70.0% in squamous cell carcinoma, 40.0% in adenocarcinoma, 23.1% in small cell carcinoma and 0% in large cell carcinoma; 42.9% in stage I, 57.1% in stage III and 46.7% in stage IV. In comparison with serum CEA, serum NSE and SCC antigen were much more specific in small cell carcinoma and squamous cell carcinoma, respectively. Moreover, serum levels of NSE and SCC antigen changed in parallel with the clinical course during the treatments. In conclusion, serum NSE and SCC antigen were considered to be very useful markers of lung cancer, especially of small cell carcinoma and squamous cell carcinoma, respectively.

Adenocarcinoma↗
PubMed1990

Neuron-specific enolase (NSE)-like and neurofilament protein (NFP)-like immunoreactivities in the rat dorsal root ganglia and sciatic nerve.

The presence of neuron-specific enolase (NSF) and neurofilament proteins (NFP) immunoreactivities (IR) was investigated in dorsal root ganglia (DRG) of adult rats at cervical, thoracic, lumbar and sacral levels. All neurons display NSE-like IR with a variable intensity of immunostain which is not related to the neuronal size. Conversely, the antibody against all three proteic subunits of NFP no labelled the primary sensory neurons, whereas the intraganglionic axons and dorsal root of spinal nerves result positives. In the sciatic nerve the immunoreactivity was similar for NSE- and NFP-like IR. No regional differences were found among the different levels of DRG for NSE-like IR. The present results demonstrate heterogeneity in the neurons of the rat. DRG for NSE-like IR, and differences between sensory neurons and fibers in the distribution of NFP-like IR.

Animals↗
PubMed1988

Cerebrospinal fluid neuron-specific enolase is decreased in multi-infarct dementia, but unchanged in Alzheimer's disease.

Cerebrospinal fluid (CSF) levels of neuron-specific enolase (NSE) were measured in 22 patients with probable Alzheimer's disease and in 35 patients with multi-infarct dementia, and in 15 controls. CSF NSE in patients with Alzheimer's disease did not differ from those in controls. In patients with multi-infarct dementia without recent vascular events CSF NSE was lower than in controls or in Alzheimer patients. This finding is in accord with the prevailing opinion that vascular dementia is caused by multiple infarcts and not by continuous neuronal ischaemia.

Aged↗
PubMed1996

Serum neuron-specific enolase, carnosinase, and their ratio in acute stroke. An enzymatic test for predicting outcome?

BACKGROUND AND PURPOSE: Few admission variables adequately predict neuronal damage and prognosis in individual patients after stroke. Therefore, there is a need for a reliable non-invasive surrogate measure of clinical outcome. METHODS: We have developed a surrogate measure of stroke outcome using the ratio of serum neuron-specific enolase (NSE) to human serum carnosinase (HSC) in 124 patients with acute ischemic or hemorrhagic stroke and 61 matched control subjects. Serum NSE is known to rise and HSC to fall after neuronal injury such as cerebral ischemia. RESULTS: Serum NSE levels were significantly higher and HSC levels lower in the patient group. The NSE/HSC ratio was elevated in patients with stroke: median (semiquartile) hemorrhages, 0.072 (0.033); infarcts, 0.039 (0.026); and control subjects, 0.019 (0.014), P = .0001. Patients with a primary intracerebral hemorrhage had nonsignificantly higher ratios than those with an infarct (P = .082). The NSE/HSC ratio was significantly associated with 90-day outcome measured in two out of three disability and handicap scales: modified Barthel Index (rs = -.34, P = .001), modified Rankin Scale (rs = .30, P = .002), and Lindley Score (rs = .19, P = .057). Patients who died or were institutionalized had higher ratios than those who were discharged home: 0.069 (0.043) versus 0.038 (0.024), P = .011. Correlations between the NSE/HSC ratio and outcome were comparable to those between patient age or consciousness level on admission and clinical outcome. CONCLUSIONS: We believe that measurement of NSE, HSC, or their ratio may be useful in the assessment of patients with acute stroke with respect to diagnosis and prediction of clinical outcome.

Acute Disease↗
PubMed1992

Changes in piglet auditory brainstem response amplitudes without increases in serum or cerebrospinal fluid neuron-specific enolase.

We studied the relationship between changes in auditory brainstem responses (ABR) and serum and cerebrospinal fluid levels of neuron-specific enolase (NSE) in hyperbilirubinemic 2- to 8-d-old piglets. Infusion of a stabilized solution of bilirubin resulted in serum bilirubin levels of 571.1 +/- 48.8 mumol/L (mean +/- SEM) after 6 h. ABR were obtained at baseline and then hourly until the piglets were killed. We measured peak amplitudes and latencies for waves I-V, as well as latency for the post-V trough. Changes in amplitudes and latencies were analyzed as slopes because of heterogeneous variances. Over time, a significant reduction was observed in peak II-V amplitudes of bilirubin-infused piglets, but not in those of corresponding controls. No change was observed in latencies. NSE was analyzed by RIA. Serum NSE remained stable throughout the experiment (means 5.1-6.6 micrograms/L) and did not differ between the groups. Cerebrospinal fluid NSE values also remained stable, and no differences that could be ascribed to hyperbilirubinemia were detected. We conclude that hyperbilirubinemia induced significant changes in piglet ABR amplitudes without concomitant evidence of severe neuronal compromise, as might have been indicated by significant increases in serum and/or cerebrospinal fluid NSE levels. This provides further support to the clinical impression that early ABR changes during hyperbilirubinemia may be reversible.

Animals↗
PubMed1983

Isolation of PGP 9.5, a new human neurone-specific protein detected by high-resolution two-dimensional electrophoresis.

Protein gene product (PGP) 9.5 is a new brain-specific protein originally detected by high-resolution two-dimensional electrophoresis of the soluble proteins of human brain and other organs. We have purified this protein from human brain and raised a rabbit antihuman PGP 9.5 antiserum. The protein has a monomer molecular weight of approximately 27,000 and is present in brain at concentrations at least 50 times greater than in other organs. Immunoperoxidase labelling has localised PGP 9.5 to neurones in the human cerebral cortex with no evidence of staining of glial elements. PGP 9.5 is estimated to be present in brain at concentrations of 200-500 micrograms/g wet weight and represents a major protein component of neuronal cytoplasm. This new neurone-specific cytoplasmic marker may prove useful in studies of neuronal development and in the detection of neuronal damage in disease of the nervous system.

Brain Chemistry↗
PubMed2004

Deletion of the neuron-specific protein delta-catenin leads to severe cognitive and synaptic dysfunction.

Delta-catenin (delta-catenin) is a neuron-specific catenin, which has been implicated in adhesion and dendritic branching. Moreover, deletions of delta-catenin correlate with the severity of mental retardation in Cri-du-Chat syndrome (CDCS), which may account for 1% of all mentally retarded individuals. Interestingly, delta-catenin was first identified through its interaction with Presenilin-1 (PS1), the molecule most frequently mutated in familial Alzheimer's Disease (FAD). We investigated whether deletion of delta-catenin would be sufficient to cause cognitive dysfunction by generating mice with a targeted mutation of the delta-catenin gene (delta-cat(-/-)). We observed that delta-cat(-/-) animals are viable and have severe impairments in cognitive function. Furthermore, mutant mice display a range of abnormalities in hippocampal short-term and long-term synaptic plasticity. Also, N-cadherin and PSD-95, two proteins that interact with delta-catenin, are significantly reduced in mutant mice. These deficits are severe but specific because delta-cat(-/-) mice display a variety of normal behaviors, exhibit normal baseline synaptic transmission, and have normal levels of the synaptic adherens proteins E-cadherin and beta-catenin. These data reveal a critical role for delta-catenin in brain function and may have important implications for understanding mental retardation syndromes such as Cri-du-Chat and neurodegenerative disorders, such as Alzheimer's disease, that are characterized by cognitive decline.

Analysis of Variance↗