Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Changes in piglet auditory brainstem response amplitudes without increases in serum or cerebrospinal fluid neuron-specific enolase. 148 Apr 52

Enolase isozymes (alpha enolase and gamma enolase) in the extracts of adrenal tumours (phaeochromocytoma, adenoma of primary aldosteronism and Cushing's syndrome, and neurinoma) were determined by means of enzyme immunoassay systems. The mean +/- SEM, respectively, of alpha and gamma enolase levels were 2.5 +/- 0.37 microgram/mg protein and 3.2 +/- 0.69 micrograms/mg protein for 9 phaeochromocytomas, 15.2 +/- 3.1 microgram/mg protein and 0.65 +/- 0.18 microgram/mg protein for three adenomas with primary aldosteronism, 10.8 +/- 3.0 micrograms/mg protein and 0.23 +/- 0.02 micrograms/mg protein for five adenomas causing Cushing's syndrome, and 3.8 +/- 0.88 micrograms/mg protein and 0.30 +/- 0.15 micrograms/mg protein for three neurinomas. Thus, the gamma enolase concentration in the extract of phaeochromocytoma was higher than that of other adrenal tumours. The serum level of gamma enolase was determined in 36 patients with adrenal tumours and 26 normal controls by radioimmunoassay. The mean +/- SEM for gamma enolase level was 5.4 +/- 0.3 ng/ml in normal controls, 9.1 +/- 0.9 ng/ml for 10 patients with phaeochromocytoma, 6.3 +/- 0.3 ng/ml for 11 with primary aldosteronism, 5.5 +/- 0.4 ng/ml for 11 with Cushing's syndrome, and 5.1 +/- 0.7 ng/ml for four with neurinoma. Thus, patients with phaeochromocytoma had a significantly higher serum gamma enolase levels than did those with tumours derived from adrenal cortex and normal controls. In patients with phaeochromocytoma, serum gamma enolase levels showed a significant positive correlation with urinary adrenaline levels (P less than 0.05), and after resection the elevated level of gamma enolase fell significantly (P less than 0.05) and returned to normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Determination of enolase isozymes in various adrenal gland tumours. 365 76

Neuron-specific enolase (NSE) is a neuronal form of the glycolytic enzyme enolase, which was first found in extracts of brain tissue, and was later shown to be present in APUD (amine precursor uptake and decarboxylation) cells and neurons of the diffuse neuroendocrine system but not in other peripheral cells. 90 neuroendocrine neoplasias (APUDomas) (including islet-cell tumours, phaeochromocytomas, medullary thyroid carcinomas, oat-cell tumours, and APUDomas of the gut, pancreas, and lung) reacted strongly with antisera to NSE. In addition, large amounts of the enzyme were found by radioimmunoassay in the tumours (mean 1626 +/- 479 SEM ng of NSE/mg protein), whereas control non-endocrine neoplasias contained less than 15 ng NSE/mg protein. Thus NSE, a specific enzyme produced in the neural and endocrine systems, was found to be produced in considerable quantities by all types of APUDomas but not in any non-endocrine tumours. NSE seems to be a useful and easily detected marker which may be used to distinguish endocrine from nonendocrine neoplasias. Clinical detection of endocrine tumours is difficult and such tumours are often missed. Use of NSE as a marker may avoid this.
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PMID:Neuron-specific enolase is produced by neuroendocrine tumours. 611 74

The aim of this study was to compare immunoreactivities for substance P with other enteric neuropeptides and GAP-43, a general marker for enteric nerves, in normal human colon and in different stages of ulcerative colitis. Tissue samples from normal colon and regions of ulcerative colitis colon were obtained at surgery and immunostained for substance P, vasoactive intestinal polypeptide (VIP), somatostatin, calcitonin gene-related peptide (CGRP), enkephalin, galanin, GAP-43, and neuron-specific enolase (NSE). Visual examination and semiquantitative analysis revealed a clear increase in the immunoreactivity for substance P in ulcerative colitis, whereas no differences were observed in the distribution of the other peptides. Therefore, quantitative analysis was performed only for substance P immunoreactivity in the lamina propria, circular muscle layer, and myenteric ganglia. In the lamina propria, the score of total intensity of substance P immunoreactivity was 0.55 +/- 0.15 (mean +/- SEM) in normal colon, 1.30 +/- 0.35 (p = 0.087) in least affected colon, and 2.22 +/- 0.28 (p < 0.001) in moderately affected colon, whereas no significant differences were observed in immunoreactivities for GAP-43. Similar results were obtained for the mean substance P- or GAP-43-immunoreactive area. In the circular muscle layer, the number, density, total intensity, and perimeter of substance P- and GAP-43-immunoreactive fibers were essentially similar in normal colon, and in mild or moderately affected colon. We conclude that ulcerative colitis does not change the density of gut innervation as a whole. However, the density of substance P-containing nerves is specifically increased, probably due to increased peptide synthesis leading to better visibility of the fibers.
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PMID:Quantitative comparison of growth-associated protein-43 and substance P in ulcerative colitis. 1137 21

In the treatment of severe traumatic brain injury (TBI), the choice of fluid and osmotherapy is important. There are practical and theoretical advantages to the use of hypertonic saline. S100B, neuron-specific enolase (NSE), and myelin-basic protein (MBP) are commonly assessed biomarkers of brain injury with potential utility as diagnostic and prognostic indicators of outcome after TBI, but they have not previously been studied in the context of fluid resuscitation. This randomized controlled trial compared serum concentrations of S100B, NSE, and MBP in adult severe TBI patients resuscitated with 250 mL of 7.5% hypertonic saline plus 6% dextran70 (HSD; n = 31) versus 0.9% normal saline (NS; n = 33), and examined their relationship with neurological outcome at discharge. Blood samples drawn on admission (<or=3 h post-injury), and at 12, 24, and 48 h post-resuscitation were assayed by ELISA for the selected biomarkers. Serial comparisons of biomarker concentrations were made by ANOVA, and relationships between biomarkers and outcome were assessed by multiple regression. On admission, mean (+/-SEM) S100B and NSE concentrations were increased 60-fold (0.73 +/- 0.08 microg/L) and sevenfold (37.0 +/- 4.8 microg/L), respectively, in patients resuscitated with NS, compared to controls (0.01 +/- 0.01 and 6.2 +/- 0.6, respectively). Compared with NS resuscitation, S100B and NSE were twofold and threefold lower in HSD-treated patients and normalized within 12 h. MBP levels were not significantly different from controls in either treatment arm until 48 h post-resuscitation, when a delayed increase (0.58 +/- 0.29 microg/L) was observed in NS-treated patients. Biomarkers were elevated in the patient group showing an unfavorable outcome. HSD-resuscitated patients with favorable outcomes exhibited the lowest serum S100B and NSE concentrations, while maximal levels were found in NS-treated patients with unfavorable outcomes. The lowest biomarker levels were seen in survivors resuscitated with HSD, while maximal levels were in NS-resuscitated patients with fatal outcome. Pre-hospital resuscitation with HSD is associated with a reduction in serum S100B, NSE, and MBP concentrations, which are correlated with better outcome after severe TBI.
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PMID:Resuscitation with hypertonic saline-dextran reduces serum biomarker levels and correlates with outcome in severe traumatic brain injury patients. 1963 68