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At least 109 records · Page 6Linked to original sources
PubMed1994

[Bone marrow granular-cell tumor with histological and immunohistochemical analysis: 1st case in the literature].

Here is described a rare case of a tumour with granular cells, placed in the bone marrow (radius bone) which caused a spontaneous fracture. The tumour has answered positivity to the immuno-histochemical SP 100 and NSE tests. Besides, wide focusing of moderate dysplasia of the granular cells were found, which answered partly in histochemical tests NSE and PS 100. There has been analysed the literature on multi-visceral incidence of this tumoral histotype and on its histogenesis. On the basis of the heterogeneous nature of this tumor, it was thought the name of tumour with granular cells to be more appropriate than myoblastoma.

Azure Stains↗
PubMed1993

Effect of amino acids on the pig muscle enolase.

Fifteen amino acids were used to investigate their effects on the pig muscle enolase. The basic and hydrophobic amino acids decreased the enzyme activity slightly. In the presence of acidic amino acids such as aspartic and glutamic acid the degree of inhibition was higher. One of the most potent inhibitors was cysteine. The presence of amino acids does not change the affinity to the substrate of enolase 2-phosphoglycerate. The possible physiological influence of amino acids on the function of enolase is discussed.

Amino Acids↗
PubMed1992

[Regulation of the activity of neuron-specific enolase by certain endogenous compounds].

The effects of glycolysis metabolites and some amino acids on the activity of bovine brain enolase have been studied. The inhibiting effect of glycolysis metabolites, of which two (2-phosphoglycolate and glyceraldehyde 3-phosphate) may be functionally significant, has been demonstrated. The action mechanisms of these compounds within a range of physiological concentrations as well as the combined effect of glyceraldehyde 3-phosphate and phosphoglyceromutase on enolase activity have been investigated.

Amino Acids↗
PubMed1983

Nervous system-specific enolase in serum as a marker for neuroblastoma.

Serum levels of nervous system-specific enolase (alpha gamma form plus gamma gamma form) were determined in 18 patients with neuroblastoma and in 40 control infants by means of a sandwich enzyme immunoassay method specific to the gamma subunit (or 14-3-2 protein) of enolase isozymes. Levels in patients with neuroblastoma were elevated (mean, 70.3; range, 6.2 to 330.0 ng/mL) when compared with those of control subjects (4.3 +/- 1.7 ng/mL). Most of the patients (6/7), whose serum nervous system-specific enolase level increased more than 100 ng/mL, died within 1 month. Serial measurements in patients with neuroblastoma receiving various therapies have revealed that there was a good correlation between serum nervous system-specific enolase levels and the course of the disease. These results indicate that the nervous system-specific enolase in serum may be a valuable marker for therapeutic monitoring of patients with neuroblastoma, as reported recently in patients with small-cell carcinoma of the lung.

Child↗
PubMed1972

The interaction of catecholamines and adrenal corticosteroids in the induction of phosphopyruvate carboxylase in rat liver and adipose tissue.

Catecholamines induced an increase in the activity of rat adipose tissue and liver phosphopyruvate carboxylases that was maintained for 48h. The response of adipose tissue phosphopyruvate carboxylase was blocked by actinomycin D, corticosteroids and propranolol, whereas corticosteroids and propranolol did not affect the liver enzyme. Cortisol phosphate, like actinomycin D, interfered only with the initiation of the increase in enzyme activity caused by noradrenaline, but not with the process of enzyme accumulation. In contrast, cycloheximide was effective in blocking enzyme induction throughout the course of the catecholamine effect. Adrenocorticotrophic hormone caused a short-term induction of adipose tissue phosphopyruvate carboxylase, which could be blocked by propranolol. Hepatic phosphopyruvate carboxylase, but not the adipose tissue enzyme, was induced by dibutyryladenosine 3':5'-cyclic monophosphate and by glucagon. Both nicotinic acid and nicotinamide decreased the normal induction of adipose tissue phosphopyruvate carboxylase caused by starvation, but only nicotinamide increased the activity of the liver enzyme.

Adipose Tissue↗
PubMed2004

Netrin requires focal adhesion kinase and Src family kinases for axon outgrowth and attraction.

Although netrins are an important family of neuronal guidance proteins, intracellular mechanisms that mediate netrin function are not well understood. Here we show that netrin-1 induces tyrosine phosphorylation of proteins including focal adhesion kinase (FAK) and the Src family kinase Fyn. Blockers of Src family kinases inhibited FAK phosphorylation and axon outgrowth and attraction by netrin. Dominant-negative FAK and Fyn mutants inhibited the attractive turning response to netrin. Axon outgrowth and attraction induced by netrin-1 were significantly reduced in neurons lacking the FAK gene. Our results show the biochemical and functional links between netrin, a prototypical neuronal guidance cue, and FAK, a central player in intracellular signaling that is crucial for cell migration.

Analysis of Variance↗
PubMed2004

GFAP-expressing progenitors are the principal source of constitutive neurogenesis in adult mouse forebrain.

Establishing the cellular identity in vivo of adult multipotent neural progenitors is fundamental to understanding their biology. We used two transgenic strategies to determine the relative contribution of glial fibrillary acidic protein (GFAP)-expressing progenitors to constitutive neurogenesis in the adult forebrain. Transgenically targeted ablation of dividing GFAP-expressing cells in the adult mouse subependymal and subgranular zones stopped the generation of immunohistochemically identified neuroblasts and new neurons in the olfactory bulb and the hippocampal dentate gyrus. Transgenically targeted cell fate mapping showed that essentially all neuroblasts and neurons newly generated in the adult mouse forebrain in vivo, and in adult multipotent neurospheres in vitro, derived from progenitors that expressed GFAP. Constitutively dividing GFAP-expressing progenitors showed predominantly bipolar or unipolar morphologies with significantly fewer processes than non-neurogenic multipolar astrocytes. These findings identify morphologically distinctive GFAP-expressing progenitor cells as the predominant sources of constitutive adult neurogenesis, and provide new methods for manipulating and investigating these cells.

Analysis of Variance↗
PubMedDate not supplied

Homology of partial primary sequences between alpha-enolase and a suppressive lymphokine from human T cells.

A relationship is described between TS--a human suppressive lymphokine produced by hybridoma T cells--and alpha-enolase from the U937 monocyte human cell line. A strong homology (92%) was observed by comparing the internal amino acid sequences of 6 TS peptides, corresponding to 52 residues, with the complete sequence of alpha-enolase. The molecular masses of these two molecules were found to be of about 47 kDa and both were detected with the same monoclonal antibody to TS. In contrast, no immunosuppressive activity was detected with the purified enolase fraction, whereas TS did not show any enolase activity. A suppressive monokine secreted by U937 cells was found to be unrelated with TS. Theses results suggest that the TS immunosuppressive factor despite its absence of enzyme activity, belongs to the enolase family.

Amino Acid Sequence↗
PubMed1991

Different genomic and metabolic patterns between mass screening-positive and mass screening-negative later-presenting neuroblastomas.

The mass screening of neuroblastoma has been undertaken in Japan by measuring urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) in all infants at the age of 6 months. This program may not only improve the prognosis but also provide important insights into the biology and evolution of human neuroblastoma. The authors studied and discuss the clinical significance of the N-myc oncogene, catecholamine metabolism, and other tumor markers in 43 patients with neuroblastoma who underwent the urinary screening test at 6 months of age. Thirty patients were found by the screening, and 13 were negative at the screening but later had a tumor. In the former group, the tumors were mostly in early stages (Stage I, 12; Stage II, 11; Stage III, seven), no amplification of N-myc was observed, and all patients are alive without disease. Although two patients whose urine at the screening showed elevated VMA and HVA levels and accidentally were not treated for 13 and 17 months, there was no change in the values of VMA and HVA during that time. However, in the latter group, the tumors were mostly in advanced stages (Stage I, one; Stage III, four; Stage IV, eight) and N-myc amplification was observed in seven of 13. Only two of these 13 are alive without disease. The age at diagnosis of the screening-negative group was 23 months compared with 8 months in the patients identified by screening, and the pattern of catecholamine metabolites in the screening-negative group tended to be dopaminergic with a low VMA-HVA ratio, especially in cases with N-myc amplification. These data suggest that the screening-positive patients with neuroblastoma may have favorable characteristics, and the biology of these tumors may be different from that of screening-negative later-presenting tumors. They also suggest that there may be at least two distinct subsets of neuroblastoma. For the early detection of the poor prognostic neuroblastomas, the measurement of urinary dopamine with VMA and HVA at later ages, such as 1 to 2 years, should be considered.

Adrenal Gland Neoplasms↗
PubMed1996

Cloning, nucleotide sequence, and functional expression of the Escherichia coli enolase (eno) gene in a temperature-sensitive eno mutant strain.

The entire Escherichia coli eno gene was cloned by functional complementation of a newly isolated temperature-sensitive enolase mutant and its nucleotide sequence determined. The deduced amino acid sequence is homologous to other known prokaryotic or eukaryotic enolases and amino acid residues, assumed to be involved in substrate or cofactor binding and catalysis, were found to be strictly conserved among all enolase proteins. Expression of the eno gene under the control of the lac promoter/operator resulted in an IPTG-inducible production of enzymatically active enolase in wild-type and enolase mutant strains.

Amino Acid Sequence↗
PubMed1999

Unexpected divergence of enzyme function and sequence: "N-acylamino acid racemase" is o-succinylbenzoate synthase.

A protein identified as "N-acylamino acid racemase" from Amycolaptosis sp. is an inefficient enzyme (kcat/Km = 3.7 x 10(2) M-1 s-1). Its sequence is 43% identical to that of an unidentified protein encoded by the Bacillus subtilis genome. Both proteins efficiently catalyze the o-succinylbenzoate synthase reaction in menaquinone biosynthesis (kcat/Km = 2.5 x 10(5) and 7.5 x 10(5) M-1 s-1, respectively), suggesting that this is their "correct" metabolic function. Their membership in the mechanistically diverse enolase superfamily provides an explanation for the catalytic promiscuity of the protein from Amycolaptosis. The adventitious promiscuity may provide an example of a protein poised for evolution of a new enzymatic function in the enolase superfamily. This study demonstrates that the correct assignment of function to new proteins in functional and structural genomics may require an understanding of the metabolism of the organism.

Actinobacteria↗
PubMed2006

Nucleus accumbens lesions decrease sensitivity to rapid changes in the delay to reinforcement.

Both humans and non-humans discount the value of rewards that are delayed or uncertain, and individuals that discount delayed rewards at a relatively high rate are considered impulsive. To investigate the neural mechanisms that mediate delay discounting, the present study examined the effects of excitotoxic lesions of the nucleus accumbens (NAC) on discounting of reward value by delay and probability. Rats were trained on delay (n=24) or probability discounting (n=24) tasks. Following training, excitotoxic lesions of the NAC were made by intracranial injections of 0.5 microl 0.15 M quinolinic acid (n=12) or vehicle (n=12) aimed at the NAC (AP +1.6, ML +/-1.5, DV -7.1). NAC lesions did not alter performance in animals tested with a constant delay (4s) or probability (0.4) of reinforcement. However, when tested with between session changes in the delay (0, 1, 2, 4, and 8s) of reinforcement, the lesioned rats had flatter discount curves than the sham group, indicating that they were less sensitive to frequent changes in the delay to reward. In contrast, the NAC lesions did not affect discounting of probabilistic rewards. NAC lesions impaired the ability to adapt to frequent between session changes in the delay to reward but did not increase or decrease discounting when the delay was held constant across sessions. NAC lesions may disrupt the ability of the animals to predict the timing of delayed rewards when the delay to reward is changed frequently.

Animals↗
PubMed1994

Activity-dependent plasticity of inhibitory and excitatory amino acid transmitter systems in cultured rat cerebral cortex.

Chronic suppression of spontaneous bioelectric activity in cultures of dissociated fetal rat cerebral cortex increases neuronal cell death and results in electrophysiological changes which indicate an altered balance between excitatory and inhibitory neurotransmission in culture. To delineate whether alterations in neurotransmitter release could underlie this imbalance, we investigated the effects of chronic tetrodotoxin (TTX) treatment on the content and release of glutamate, aspartate and gamma-aminobutyric acid (GABA) in culture. Chronic TTX treatment decreased the content of all amino acids investigated. However, only GABA was decreased relative to the neuronal marker NSE (neuron-specific enolase), indicating a disproportionate loss of GABA production following chronic silencing. Depolarization-induced release of GABA, glutamate and aspartate increased about 10-fold between 7 and 21 days in control cultures. Chronic TTX treatment significantly increased the depolarization-induced release of glutamate and aspartate at 7 days in vitro relative to control levels. At all ages it caused a two-fold increase in the ratio of evoked excitatory amino acid release to that of GABA. These observations suggest that chronic silencing of developing neocortex cell cultures increases the ratio of excitatory to inhibitory synaptic activity either by differential cell death or by reduced synaptic efficiency, on which a decrease in GABA neurotransmission appears to play a major role. Since similar mechanisms may be involved in activity-dependent plasticity in vivo, these cultures provide a useful model to analyse this phenomenon at the cell biological and molecular level.

Animals↗