PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PHOSPHOPYRUVIC ACID”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 685 records · Page 38Linked to original sources
PubMed2003

Enzyme immunoassay of NSE and GFAP as the criterion of dynamic evaluation of the rat blood-brain barrier in perinatal hypoxic ischemic injury of the CNS.

Enzyme immunoassay of the serum neurospecific antigens (gliofibrillar acid protein and neurospecific enolase) was used for evaluation of the resistance of the blood-brain barrier in Wistar rats with perinatal hypoxia and ischemia of the CNS. Perinatal hypoxia and ischemia of the CNS was modeled by two methods: ligation of the common carotid artery in 7-day-old rats followed by 3.5-h hypoxic hypoxia or 15-min anoxic exposure of fetuses isolated via hysterectomy on day 21 of gestation. Enzyme immunoassay of serum gliofibrillar acid protein and neurospecific enolase in control an experimental rat pups was carried out once a week during 3 months. In controls serum levels of gliofibrillar acid protein and neurospecific enolase virtually did not change during postnatal development, while in animals with cerebral hypoxia and ischemia induced in fetuses by both methods serum concentration of neurospecific enolase sharply increased 1 week after the injury and increased on weeks 6 and 10. The content of gliofibrillar acid protein was maximum on week 1 and later considerably varied, the peaks of its concentrations observed on weeks 3 and 8 preceded the increase in neurospecific enolase activity in peripheral blood.

Animals↗
PubMed1996

A DEAD-box RNA helicase in the Escherichia coli RNA degradosome.

The Escherichia coli RNA degradosome is a multi-enzyme complex that contains the exoribonuclease polynucleotide phosphorylase (PNPase) and the endoribonuclease RNase E. Both enzymes are important in RNA processing and messenger RNA degradation. Here we report that enolase and RhlB are two other major components of the degradosome. Enolase is a glycolytic enzyme with an unknown role in RNA metabolism. RhlB is a member of the DEAD-box family of ATP-dependent RNA helicases, which are found in both prokaryotes and eukaryotes. We show that the degradosome has an ATP-dependent activity that aids the degradation of structured RNA by PNPase. Incubation of the degradosome with affinity-purified antibody against RhlB inhibited the ATP-stimulated RNA degradation. These results suggest that RhlB acts by unwinding RNA structures that impede the processive activity of PNPase. RhlB is thus an important enzyme in mRNA turnover.

Adenosine Triphosphatases↗
PubMed2002

Mixed neuronal-glial tumor of the digestive tract: distinctive entity from gastrointestinal stromal tumor?

A 53-year-old-woman presenting with pelvic discomfort was found to have a 9.5 cm tumor located in the wall of the ileon. Light microscopy showed that the tumor was made of fascicles of plump spindle cells and bizarre epithelioid cells. A cuff of lymphoid cells was also present at the tumor margin. The tumor cells strongly expressed tau protein, neuron-specific enolase, protein green product 9.5 and glial fibrillary acid protein (GFAP), but did not show positive immunostaining for S-100 protein, CD34 or CD117. The tumor showed unequivocal ultrastructural evidence of neural differentiation. Skeinoid fibers were scattered throughout the tumor. This is the first mixed neuronal-glial tumor of the digestive tract to be described in the literature. Such histological and immunohistochemical features could be misinterpreted as features of digestive schwannoma. We suggest that this tumor is distinct from gastrointestinal stromal tumors in lacking CD34 and CD117 expression.

Diagnosis, Differential↗
PubMed1993

Catecholaminergic neurons result from intracerebral implantation of embryonal carcinoma cells.

A replication-defective retrovirus was used to introduce the marker gene nlsLacZ into the murine embryonal carcinoma (EC) cell line PCC7-S-aza-R-1009. Undifferentiated EC cells were implanted into the central nervous system of adult rats. One month later, the grafted cells continued to express the nlsLacZ gene. Immunohistochemical analysis demonstrated the presence of EC-derived neurons. These neurons were capable of expressing tyrosine hydroxylase and extended neurites into the host parenchyma. EC-derived glial cells could not be detected. There was no evidence of tumorigenicity. These results demonstrate the utility of EC cells for introduction of exogenous gene products into the central nervous system in experimental models of gene therapy.

Animals↗
PubMed1988

Immature neural elements in immature teratomas. An immunohistochemical and ultrastructural study.

Immature neural tissue pathobiology in teratomas may have important implications for clinical prognosis, nervous system embryology, and neurological oncology. However, immunohistochemical and ultrastructural examinations of these neoplasms have been scarce. The authors examined immunohistochemically the immature neural elements in nine immature teratomas. Using modified peroxidase-antiperoxidase (PAP) immunoperoxidase (IP) techniques, they evaluated the immunoreactivity to glial fibrillary acidic protein (GFAP), neuron-specific enolase (NSE), neurofilament (NF), chromogranin (CG), and vimentin (VM). All nine teratomas were immunoreactive for both GFAP and NSE, one was reactive for NF, and five (56%) were immunoreactive for vimentin. All cases were nonreactive for chromogranin. In addition, ultrastructural examination (electron microscopic [EM]) was performed on eight of these tumors. By EM examination, both astrocytes and oligodendroglia were identified in varying stages of development. Astrocytes often displayed abundant intermediate filaments. However, primitive undifferentiated cells were also found. Neuronal differentiation included long cell processes with tubules and filaments, vesicles, rare dense-core granules, and synapses. Ependymal differentiation (cilia, microvilli, prominent junctions) was observed in two cases. Pigmented retinal epithelium was seen in one tumor. No ambiguous (hybrid) cells were identified. Cellular interactions usually resembled the relationships found in normal adult brain tissue.

Adolescent↗
PubMed1996

Primary cutaneous Ewing's family sarcoma. Report of a case with immunostaining for glycoprotein p30/32 mic2.

The differential diagnosis of cutaneous small round cell malignancies is a relatively uncommon but recurrent problem that usually requires adjuvant techniques including special histochemical stains, immunohistochemistry (IHC), electron microscopy (EM), and cytogenetics (CG) to arrive at a definite answer. This report describes a case of a primary cutaneous malignancy that, after workup, fulfilled the criteria of extraskeletal Ewing's family sarcoma, which was corroborated by IHC with an antibody to glycoprotein p30/32 mic2 that is highly expressed in these neoplasms. The lesions consisted of a large nodular proliferation of poorly differentiated monotonous small round cells confined to the dermis and subcutaneous tissue. The cells had high nuclear to cytoplasmic (N/C) ratios, scattered prominent nucleoli, and indistinct cytoplasm. A periodic acid-Schiff (PAS) stain with and without diastase demonstrated abundant cytoplasmic glycogen. The glycogen was confirmed with EM, which did not show neurosecretory granules, but extensive sectioning of the tissue blocks demonstrated with light microscopy a single focus with pseudorosette formation. IHC was positive for monoclonal antibody (MAb) O13 to glycoprotein p30/32 mic2 and negative for lymphoid (CD45), neural (S-100, NF, GFAP), neuroendocrine (NSE), and muscle (MSA, desmin) markers. To the best of our knowledge, this is one of few reported cases of primary cutaneous (extraskeletal/extraosseous) Ewing's sarcoma (EEWS) and the first to use IHC with MAb O13, which recognizes the cell surface glycoprotein p30/32 mic2. This case further illustrates the continuum between EEWS and primitive peripheral neuroepithelioma and supports the unifying concept that these two entities are merely subtle morphologic variants of the same malignant neoplasm, which is better designated a Ewing's family sarcoma.

12E7 Antigen↗
PubMed1995

Characterization of IgE-binding epitopes on Candida albicans enolase.

Candida albicans enolase is one of the important allergens in Candida allergy. We isolated and purified 46kDa C. albicans enolase (CAE) from C. albicans and characterized epitopes for IgE antibody by lectin-blotting and enzymatic digestion followed by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting. Lectin blotting and deglycozilation indicated that this protein did not contain polysaccharide side chains. The purified CAE and recombinant fusion protein produced from CAE gene possessed common epitopes for IgE antibody. We estimated IgE binding epitopes on the basis of reported amino acid sequences from the analysis of cDNA encoding CAE. V8 protease digestion of CAE gave six polypeptide fragments (A-F). The N-termini of each fragment were confirmed by amino acid sequence and the C-termini were estimated by molecular weights of each fragment and the specific cutting site of V8 protease. Fragment C (25.0 kDa; F-171-I-399) reacted to 90% IgE antibodies examined, whereas fragments D (21.0 kDa; F-171-I-360), E (16.2 kDa; F-171-D-317) and F (13.0 kDa; A-47-E-170) showed no IgE binding. Our results suggest that epitopes for IgE antibodies exist near the C-terminal of the protein.

Amino Acid Sequence↗
PubMed1993

Chondroid syringoma with hyaline cell change.

Four cases of chondroid syringoma containing large numbers of hyaline or plasmacytoid cells are described. Three cases occurred in the hand and one in the foot. Hyaline cells are commonly seen in mixed tumours and myoepitheliomas of salivary glands and rarely in chondroid syringomas. The hyaline-cell change in three of the cases initially caused diagnostic difficulties and the possibility of sarcoma was raised in two cases. In addition to the characteristic hyaline cells, the presence of tubulo-glandulo-ductal structures, benign squamous epithelium and myxochondroid stroma aided diagnosis. Immunohistochemically, the hyaline cells exhibited positivity for vimentin, cytokeratin, S-100 protein, carcino-embryonic antigen, focal glial fibrillary acidic protein (3 cases), neuron-specific enolase (3 cases) and focal alpha-smooth muscle actin (2 cases). Occasional cells were Ber EP4 positive (2 cases). In some cells, a striking peripheral ring-like positivity for cytokeratin and S-100 protein was noted. Ultrastructurally, desmosomes, varying numbers of tonofibrils and non-bundling intermediate filaments were seen. Scanty fine filaments with vague focal densities were detected in some cells. Our studies suggest that the hyaline cells represent modified epithelial as well as myoepithelial cells. One of our cases also exhibited collagenous spherulosis.

Actins↗
PubMed2005

Molecular profiles of mRNA levels in laser capture microdissected murine hippocampal regions differentially responsive to TMT-induced cell death.

Using a chemical-induced model of dentate granule (DG) cell death, cDNA microarray analysis was used to identify gene profiles from the laser-captured microdissected (LCM) hippocampal DG cell region versus the CA pyramidal cell layer (CA) from 21-day-old male CD1 mice injected with trimethyltin hydroxide (TMT; 3.0 mg/kg, i.p.). At 6 h post-TMT, lectin + microglia displaying a reactive morphology were in contact with active caspase 3+ neurons. By 18 h, amoeboid microglia and signs of phagocytosis, and a mild astrocytic response were present in the DG. There was no evidence of IgG extravasation in the hippocampus, or cell death and glial reactivity in the CA. Atlas 1.2K Clontech array detected 115 genes changed in the hippocampus with TMT and included genes associated with immediate-early responses, calcium homeostasis, cellular signaling, cell cycle, immunomodulation and DNA repair. Early responses localized to LCM DG samples consisted of elevations in inflammatory factors such as tumor necrosis factor-alpha and receptors, as well as MIP1alpha, CD14, CD18, and a decrease in factors associated with calcium buffering. By 18 h, in the DG, changes occurred in transcripts associated with apoptosis, cell adhesion, DNA repair, cell proliferation and growth. In the CA, a differential level of elevation was seen in CD86 antigen, zinc finger protein 38 and DNA damage inducible transcript 3. A significant number of genes was decreased at these early time points in both hippocampal regions.

Animals↗
PubMed2006

A ubiquitin ligase HRD1 promotes the degradation of Pael receptor, a substrate of Parkin.

It has been proposed that in autosomal recessive juvenile parkinsonism (AR-JP), a ubiquitin ligase (E3) Parkin, which is involved in endoplasmic reticulum-associated degradation (ERAD), lacks E3 activity. The resulting accumulation of Parkin-associated endothelin receptor-like receptor (Pael-R), a substrate of Parkin, leads to endoplasmic reticulum stress, causing neuronal death. We previously reported that human E3 HRD1 in the endoplasmic reticulum protects against endoplasmic reticulum stress-induced apoptosis. This study shows that HRD1 was expressed in substantia nigra pars compacta (SNC) dopaminergic neurons and interacted with Pael-R through the HRD1 proline-rich region, promoting the ubiquitylation and degradation of Pael-R. Furthermore, the disruption of endogenous HRD1 by small interfering RNA (siRNA) induced Pael-R accumulation and caspase-3 activation. We also found that ATF6 overexpression, which induced HRD1, accelerated and caused Pael-R degradation; the suppression of HRD1 expression by siRNA partially prevents this degradation. These results suggest that in addition to Parkin, HRD1 is also involved in the degradation of Pael-R.

Animals↗
PubMed1999

Enolase is present in the cell wall of Saccharomyces cerevisiae.

Non-covalently attached or soluble cell wall proteins of Saccharomyces cerevisiae were extracted using a high pH/2-mercaptoethanol procedure and were separated for peptide sequencing using 2D-PAGE. A partial N-terminal sequence of a major protein spot was obtained and showed high identity with enolase gene products. Western blotting with an anti-enolase antibody confirmed that enolase was present in the cell wall extract. Biotinylation of cells prior to protein extraction with a membrane impermeable biotinylating agent confirmed that the detection was not owing to cell lysis during extraction. Transmission immunoelectron microscopy showed enolase to be present in the cell wall. Enolase contains no known secretion signal that would localize it to the cell wall. Thus S. cerevisiae must have further mechanisms for targeting proteins to the cell wall.

Amino Acid Sequence↗
PubMed2004

Mucinous adenocarcinoma with neuroendocrine differentiation of the mandibular ramus: report of a case.

A rare case of mucinous adenocarcinoma with neuroendocrine differentiation of the mandibular ramus is presented. The patient, an 80-year-old man, was referred to our hospital with chief complaint of swelling and pain in the left buccal mucosa. CT and MRI examination showed an osteolytic tumor mass occupying the upper region of the left mandibular ramus. Macroscopically, the excised tumor was a relatively well-defined, solid mass with diffuse bone resorption, measuring 3 cm x 3.2 cm x 3 cm. Microscopical examination showed that the tumor forming glandular structures with abundant mucous production and high cellular atypia. Immunohistochemical studies demonstrated the positive reactivities for pan-keratin, cytokeratin 7, vimentin,alpha-amylase, alpha-smooth muscle actin, neuron-specific enolase, glial fibrillary acid protein, calcitonin, and somatostatin in tumor cells. These findings suggested that the tumor was originated from heterotopic or misplaced salivary gland in the mandible.

Actins↗
PubMed2006

Increased cerebrospinal fluid and serum levels of S100B in first-onset schizophrenia are not related to a degenerative release of glial fibrillar acidic protein, myelin basic protein and neurone-specific enolase from glia or neurones.

OBJECTIVE: To assess levels of glial fibrillar acidic protein (GFAP), myelin basic protein (MBP), neurone-specific enolase (NSE) and S100B in patients with first-onset schizophrenia. METHOD: We investigated CSF and serum samples from 12 patients with first-onset schizophrenia and from 17 control subjects by ELISA (GFAP, MBP) or immunoluminometric sandwich assays (NSE, S100B). RESULTS: Patients with schizophrenia had significantly higher levels of S100B in CSF (p = 0.004; 2.73 (SD 0.80) v 1.92 (0.58) microg/l) and serum (p = 0.032; 0.09 (0.03) v 0.08 (0.02) microg/l) in comparison with those in the matched control group. No diagnosis-dependent differences of protein concentration were seen for GFAP, MBP and NSE. DISCUSSION: Our finding of increased levels of S100B in patients with schizophrenia without an indication for significant glial (GFAP, MBP) or neuronal (NSE) damage may be interpreted as indirect evidence for increased active secretion of S100B during acute psychosis.

Adolescent↗
PubMed2002

AMPA antagonist ZK200775 in patients with acute ischemic stroke: possible glial cell toxicity detected by monitoring of S-100B serum levels.

BACKGROUND AND PURPOSE: S-100B and neuron-specific enolase (NSE) serum concentrations can be used as peripheral markers of glial cell and neuronal damage, respectively. We investigated these markers in a clinical trial with the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) antagonist ZK200775 in acute ischemic stroke patients. METHODS: In a multicenter, double-blind, randomized, placebo-controlled phase 2 trial, 61 ischemic stroke patients were treated with either placebo or active drug in a dose-finding design. Twenty-five patients received placebo, 12 patients received a total dose of 262.5 mg in 48 hours (dose group 1), and 13 patients received a total dose of 525 mg in 48 hours (dose group 2). Eleven patients received a total dose of 105 mg over a period of 6 hours (dose group 3; reduction of total dose and infusion time because of adverse events in group 2). Serum concentrations of S-100B and NSE were analyzed with the use of a monoclonal sandwich immunoluminometric assay. Neurological outcome was assessed with the National Institutes of Health Stroke Scale (NIHSS). RESULTS: In group 2 there was a significant transient worsening in the mean NIHSS score 48 hours after the start of treatment. The mean increase was 11 points. This was due to reduction of consciousness (stupor and coma) in 8 of 13 patients. Neurological deterioration in group 2 was associated with a higher increase of S-100B concentrations, but not of NSE concentrations, than in the placebo group. The trial was stopped prematurely for safety reasons. CONCLUSIONS: The AMPA antagonist ZK200775 transiently worsened the neurological condition in patients with acute ischemic stroke. Our results suggest that in addition to neuronal dysfunction, glial cell toxicity may have occurred. It may be useful to introduce monitoring of serum markers of brain damage in phase 2 trials with glutamate receptor antagonists.

Acute Disease↗
PubMed1987

Immunohistochemical demonstration of keratin in canine neuroepithelioma.

Morphological features and immunoreactivity for cytokeratin (CK), glial fibrillary acidic protein (GFAP) and neuron-specific enolase (NSE) of three canine neuroepitheliomas and three canine ependymomas were investigated. Neuroepitheliomas were in three German shepherds as intradural-extramedullary solitary masses, with spinal cord displacement between T10 and L2. Histologically, they contained tubules and acini, lined by epithelial cells with focal squamous metaplasia, rosette-like structures, and polygonal to spindle-shaped cells between tubules. Acini were empty or filled with a homogeneous, eosinophilic periodic acid-Schiff (PAS)-positive material. Mitotic indices varied from low to moderate. Ependymomas occurred in the third (two cases) and fourth ventricle in adult boxers. Histologically, they were composed of cells with an ill-defined, scant amphophilic cytoplasm, with a central round euchromatic nucleus; cells formed pseudorosettes, with a central fibro-vascular stroma. Neuroepitheliomas stained for CK, but ependymomas did not. Both failed to stain for GFAP, NSE, or phosphotungstic acid hematoxylin (PTAH). Thus, antibodies to cytokeratin are useful to distinguish neuroepitheliomas from ependymomas.

Animals↗
PubMed2005

Human marrow stromal cell treatment provides long-lasting benefit after traumatic brain injury in rats.

OBJECTIVE: This study was designed to investigate the effects of human bone marrow stromal cell (hMSC) administration in rats for 3 months after traumatic brain injury (TBI). METHODS: Adult male Wistar rats (n = 60) were injured with controlled cortical impact and divided into four groups. The three treatment groups (n = 10 each) were injected with 2 x 10, 4 x 10, and 8 x 10 hMSCs, respectively, intravenously, whereas the control group (n = 30) received phosphate-buffered saline. All injections were performed 1 day after injury into the tail veins of rats. Neurological functional evaluation of animals was performed before and after injury by use of Neurological Severity Scores. Animals were sacrificed 3 months after TBI, and brain sections were stained by immunohistochemistry. RESULTS: Statistically significant improvement in functional outcome was observed in all three treatment groups compared with control values (P < 0.05). This benefit was visible 14 days after TBI and persisted until 3 months (end of trial). There was no difference in functional outcome among the three treatment groups. Histological analysis showed that hMSCs were present in the lesion boundary zone at 3 months with all three doses tested. CONCLUSION: hMSCs injected in rats after TBI survive until 3 months and provide long-lasting functional benefit. Functional improvement may be attributed to stimulation of endogenous neurorestorative functions such as neurogenesis and synaptogenesis.

Animals↗