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 433 records · Page 24Linked to original sources
PubMed1990

Immunocytochemical demonstration of proopiomelanocortin-derived peptides in pituitary adenomas of the pars intermedia in horses.

Adenomas of the pars intermedia from 19 horses and normal pituitary glands from seven horses were evaluated histologically and immunocytochemically for adrenocorticotropic hormone (ACTH), alpha-melanocyte-stimulating hormone (alpha-MSH), beta-endorphin (beta-END), proopiomelanocortin (POMC), prolactin, neuron specific enolase, and glial fibrillary acidic protein (GFAP). The 26 horses ranged in age from 7 to 31 years. Histologically, all adenomas had a uniform pattern characterized by cords of large columnar cells forming palisades and pseudoacini separated by a delicate fibrovascular stroma. Immunostaining of adenomas derived from the pars intermedia was similar to that of non-neoplastic equine pars intermedia. An immunocytochemical evaluation revealed a diffuse, strong cytoplasmic reaction for POMC, a moderate to strong reaction for alpha-MSH and beta-END, a weak reaction for ACTH, and negative immunostaining for prolactin, GFAP, and neuron specific enolase in the adenomas. The unique clinicopathologic syndrome that develops in horses with pituitary adenomas appears to be the result of an over-production of POMC-derived peptides in addition to space-occupying effects resulting in dysfunction of the hypothalamus and neurohypophysis.

Adenoma↗
PubMed2004

Neuron-specific apolipoprotein e4 proteolysis is associated with increased tau phosphorylation in brains of transgenic mice.

Apolipoprotein E (apoE) is found in amyloid plaques and neurofibrillary tangles (NFTs) in Alzheimer's disease (AD) brains, but its role in their pathogenesis is unclear. Previously, we found C-terminal-truncated fragments of apoE in AD brains and showed that such fragments can cause neurodegeneration and can induce NFT-like inclusions in cultured neuronal cells and in transgenic mice. Here, we analyzed apoE fragmentation in brain tissue homogenates from transgenic mice expressing apoE3 or apoE4 in neurons [neuron-specific enolase (NSE)-apoE] or astrocytes [glial fibrillary acidic protein (GFAP)-apoE] by Western blotting. The C-terminal-truncated fragments of apoE accumulated, in an age-dependent manner, in the brains of NSE-apoE4 and, to a significantly lesser extent, NSE-apoE3 mice; however, no fragments were detected in GFAP-apoE3 or GFAP-apoE4 mice. In NSE-apoE mice, the pattern of apoE fragmentation resembled that seen in AD brains, and the fragmentation was specific for certain brain regions, occurring in the neocortex and hippocampus, which are vulnerable to AD-related neurodegeneration, but not in the less vulnerable cerebellum. Excitotoxic challenge with kainic acid significantly increased apoE fragmentation in NSE-apoE4 but not NSE-apoE3 mice. Phosphorylated tau (p-tau) also accumulated in an age-dependent manner in NSE-apoE4 mice and, to a much lesser extent, in NSE-apoE3 mice but not in GFAP-apoE3 or GFAP-apoE4 mice. Intraneuronal p-tau inclusions in the hippocampus were prominent in 21-month-old NSE-apoE4 mice but barely detectable in NSE-apoE3 mice. Thus, the accumulation of potentially pathogenic C-terminal-truncated fragments of apoE depends on both the isoform and the cellular source of apoE. Neuron-specific proteolytic cleavage of apoE4 is associated with increased phosphorylation of tau and may play a key role in the development of AD-related neuronal deficits.

Aging↗
PubMed1997

Myxoid tissue: its morphology, histochemistry, and relationship with other supporting tissues.

Myxoid tissue was studied in the supporting organ of the cat epiglottis ("epiglottic cartilage"). Under the light microscope, myxoid tissue was characterized by stellate cells placed into an avascular acidic extracellular matrix. This extracellular matrix was alcianophilic at pH = 2.5, reacting with the colloidal iron stain, and staining metachromatically with toluidine blue O at pH = 5.0. Treatment of sections with testicular hyaluronidase abolished these reactions. In addition, staining persisted after methylation/saponification pretreatment, indicating hyaluronic acid as the main acidic component of myxoid extracellular matrix. Under the electron microscope, myxoid extracellular matrix formed flocculent electron dense precipitates. Stellate myxoid cells were characterized by bundles of intermediate (8 nm) cytoplasmic filaments. Myxoid cells were devoid of a basal lamina, contained a few small lipid droplets, and stored some glycogen. Bundles of collagen fibrils, 80-120 nm in diameter, were seen in myxoid areas. Myxoid cells reacted to S-100 protein, glial fibrillary acidic protein, and neuron specific enolase. Moreover, in adult animals, myxoid cells stained for neurofilament protein 200. All these markers were also present in chondrocytes of elastic and fibrous cartilage, indicating a close relationship between myxoid cells and chondrocytes. This was supported by the observation of continuous transitional forms of myxoid tissue into elastic or fibrous cartilage. In 8-week-old kittens, the supporting organ of the epiglottis was found mainly to consist of myxoid tissue with only a few interspersed islets of chondrocytes. It is therefore concluded that myxoid tissue can serve as a precursor of cartilage.

Adipose Tissue↗
PubMed1989

Differentiation in medulloblastomas and other primitive neuroectodermal tumours.

Fifty-four cases of primitive neuroectodermal tumour (PNET) including 47 medulloblastomas, were examined for evidence of neuronal and glial differentiation, using antibodies to neuron-specific enolase (NSE), neurofilament protein (NF), and glial fibrillary acidic protein (GFAP). In 30 of the cases, antibodies to vimentin, alphafetoprotein, cytokeratin, epithelial membrane antigen and lymphoid markers were also used. Most of the 47 medulloblastomas in the group were NSE positive but NF negative; about half were GFAP positive and three of them were positive for both neuronal markers and for GFAP. Vimentin was demonstrated in four cases and was not always co-expressed with GFAP. Medulloblastomas were negative for all the other markers. Supratentorial PNETs were sometimes positive with neuronal markers but were GFAP negative. The cell specificity of these markers and the interpretation of immunocytochemical findings are discussed in relation to differentiation potential in primitive neuroectodermal tumours.

Adolescent↗
PubMed1990

The human genome contains a single processed pseudogene for alpha enolase located on chromosome 1.

We have isolated and characterized human genomic clones containing an alpha enolase pseudogene which lacks introns and has the hallmarks of having been generated by reverse transcription. Two in-frame termination codons renders its coding region incapable of producing a functional protein. An Alu-like sequence is present in the region homologous to the 3' untranslated of the alpha enolase mRNA. Comparison of the two sequences shows that the pseudogene diverged from its functional counterpart about 14 million years ago and interestingly it is the only alpha enolase pseudogene present in the human genome. Chromosomal mapping locates the processed pseudogene to human chromosome 1, the same chromosome where the functional gene has been mapped.

Base Sequence↗
PubMed1988

A hypothesis for myeloschisis: overgrowth and reopening. An experimental study.

A hypothesis for embryopathogenesis of myeloschisis is described on the basis of experimental studies analyzing the stage specificity and immunohistochemical/histological characteristics of the exposed neural tissue (placode). Myeloschisis developed in six fetuses among 205 chick embryos treated in various stages with teratogens including ethylnitrosourea, and anticonvulsant and antipyretic agents. All but one case (with associated cephalothoracopagus) demonstrated myeloschisis in the thoracic region with a lamina defect of two and three levels. No fetus was exposed to a teratogen prior to or within Hamburger and Hamilton stage 12 (45 to 49 hours postincubation), when the neuropore closes. Immunohistochemical studies of chick myeloschisis clearly indicated that neuron-specific enolase-positive elements were extremely active only in the overgrown placode, corresponding to the histological findings with Kluver-Barrera's special stain. These findings were compared with observations in a case of myeloschisis in a human neonate. The results of this study imply the possibility of another mechanism for the embryopathogenesis of myeloschisis: namely, the overgrowth and reopening hypothesis.

Animals↗
PubMedDate not supplied

Immunohistochemical diagnosis of a totally necrotic retinoblastoma: a clinicopathologic case.

An 8-month-old girl underwent enucleation of her right eye because of a calcified retrolental white mass filling the entire vitreous cavity. The conventional histological examination revealed a totally necrotic unidentifiable tumor, with scattered foci of calcification. In addition, we found two islands of viable small round cells, suspected to be retinoblastoma cells, which were located in the optic nerve behind the lamina cribrosa. These cells stained positively for neuron-specific enolase (NSE), but not for glial-fibrillary-acidic-protein (GFAP), supporting the diagnosis of retinoblastoma. Because one of the latter foci of viable tumor cells was located at the cut end of the optic nerve, the baby was treated by external beam irradiation.

Eye Neoplasms↗
PubMed1998

[A clinical and pathological study of cerebellar medulloblastoma in adult patients].

OBJECTIVE: In order to study the clinicopathological characteristics, histogenesis and prognosis of medulloblastoma in the adult patients. METHODS: Altogether 27 patients of medulloblastoma admitted form 1974-1995 were reviewed. RESULTS: In all of the cases, age ranged from 16 to 55, (average 25.8 years) with 21 tumors localized in the cerebellar vermis, and 6 tumors in the cerebellum. Among them, 12 cases were completely while 14 cases were subtotally removed and biopsy was done in only one case. In the 21 patients to be followed up, 7 survived for 2.5-17 years after the operation, and 14 died. The average survival period was 41.6 months. One year survival rate was 71.4%, five years and ten years survival rates were 14.3% respectively. Regarding to the histological types, 14 cases were considered to be classic and 13 cases were desmoplastic by histological classification. CONCLUSION: Medulloblastoma keeps still the ability of differentiation to neurons and astrocytes confirmed by electronmicroscopy and immunohistochemical staining for Syn, NSE and GFAP. Factors considered responsible to the prognosis included age, tumor location, various therapeutic measurements and the histological classification.

Adolescent↗
PubMed2000

[Expression of S-100 proteins and intermediate filament proteins in pleomorphic adenoma].

OBJECTIVE: To observe immunohistochemical expression of S-100A1, S-100A2, S-100A4, S-100A6, S-100B, K8.12, KL1, Vimentin, GFAP and NSE in pleomorphic adenoma of salivary gland, and to evaluate the differential localization of S-100 proteins and biological behaviour of neoplastic myoepithelial cells. METHODS: 23 cases of normal salivary gland and 60 cases of pleomorphic adenoma were embedded, in paraffin and were routinely diagnosed on the basis of hematoxylin and eosin-stained sections. Serial sections at 4 microns from the paraffin embedded blocks were used for the immunohistochemical studies. RESULTS: Normal salivary glands had positive immunoreactivity for S-100A families, K8.12 and KL1 in the ductal cells, while S100B, GFAP and NSE were observed in peripheral nerve fibers innervating the gland. In pleomorphic adenomas, luminal tumor cells in duct-like structures had positive immunoreactivity for S-100A subfamilies and keratin. Nonluminal tumor cells had positive immunoreactivity for S-100B, as well as Vimentin, keratins detected by monoclonal K8.12 and KL1, GFAP and NSE. CONCLUSIONS: These findings may suggest that the neoplastic myoepithelial cells contain Ca2+ binding proteins which may have a role in the regulation of calcium ions or calcium signaling mechanisms in the modulation of extracellular matrix deposition in pleomorphic adenoma which may in turn affect the extracellular matrix synthesis as well as histomorphology of the tumor.

Adenoma, Pleomorphic↗
PubMed1992

C-reactive protein (CRP) peptides inactivate enolase in human neutrophils leading to depletion of intracellular ATP and inhibition of superoxide generation.

The nature and the biochemical mechanism of inhibition of neutrophil membrane-associated oxidative metabolism by two synthetic peptides p77-82 and p201-206 (amino acid sequences Val-Gly-Gly-Ser-Glu-Ile and Lys-Pro-Gln-Leu-Trp-Pro respectively, from the primary amino acid sequence of C-reactive protein) have been ascertained. Preincubating neutrophils for 15 min with 50 microM of p77-82 or p201-206 resulted in superoxide generation by opsonized zymosan stimulated neutrophils being inhibited by 34 +/- 2% (P less than 0.005) and 29 +/- 2% (P less than 0.005) respectively. With a 60-min preincubation period 6.25 microM of p77-82 or p201-206 was effective in inhibiting this superoxide generation by 12 +/- 2% (P less than 0.01) and 10 +/- 1% (P less than 0.01) respectively. Neither peptide inhibited neutrophil arachidonic acid release, transmembrane potential or transductional events preceding superoxide generation. Inhibition of neutrophil functions was found to be due to the ability of each peptide (50 microM) following a 15-min preincubation period to inhibit both neutrophil glycolysis and ATP generation by approximately 30%. The inhibition of ATP generation and glycolysis in neutrophils is attributable to the ability of these peptides to inhibit uncompetitively the glycolytic enzyme enolase. Using purified enolase the relative Ki values for p77-82 and p201-206 were 27 and 19 microM respectively. Inhibition of neutrophil function by the peptides is concluded to be due to effective interference of neutrophil energy metabolism.

Adenosine Triphosphate↗
PubMedDate not supplied

Immunohistochemical characterization of pineocytomas.

The immunoreactivity of a panel of poly- and monoclonal antibodies raised against different neuronal and glial antigens, was studied in paraffin-embedded specimens of five pineocytomas. Antibodies against neuron-specific enolase (NSE), S-100 protein, neurofilaments protein (NFP), glial fibrillar acidic protein (GFAP), myelin basic protein (MBP), Synaptophysin (SYN) and vimentin were used. NSE immunoreactivity was detectable in nearly all tumoral cells. S-100 expression was present in all tumors, but a significant variation in the number of S-100 positive cells was noted in the different specimens; they ranged from 3% of S-100 positive cells in some areas of case 1, to 30% in other areas of case 4. The number of GFAP-positive cells detected in four of the five tumors was minimal. In the remaining tumor, 10% to 14% the positively GFAP antisera-stained cells could be seen in some areas; this tumor was considered a pineocytoma with astrocytic differentiation. MBP immunoreactivity was found in isolated cells only in one tumor. Neurofilaments or vimentin expression could not be found in tumoral cells. Synaptophysin was studied in two tumors (cases 4 and 5). Both tumors showed a fine granular neuropil pattern of immunoreactivity, but only in isolated cells of case 5, occasional cytoplasmic positivity could be determined. Based upon our results we can conclude that NSE and synaptophysin are markers that may be applied in the diagnosis of pineocytomas. Further, our results support the hypothesis that the tumoral cells in these neoplasms are of neuroendocrine origin.

Adolescent↗
PubMed2003

Cerebellar liponeurocytoma: a case report and review of the literature.

Cerebellar liponeurocytoma has recently been recognised by the 2000 World Health Organisation classification of tumours of the central nervous system as a distinct clinicopathologic entity. To our knowledge, 18 cases have been reported so far, under different names, such as "lipomatous medulloblastoma, lipidized medulloblastoma, neurolipocytoma, medullocytoma and lipomatous glioneurocytoma". The new classification included cerebellar liponeurocytoma in the category of glioneuronal tumours grade I or II because of its favourable clinical behaviour. The origin and nature of the lipomatous component have been matter of debate and make this tumour entity puzzling. We describe a new case of liponeurocytoma removed from the left cerebellar hemisphere of a 38-year-old-woman. The patient showed unspecific signs of intracranial hypertension and symptoms suggesting a posterior fossa lesion.

Adult↗
PubMed1991

Giant epignathus. A case report.

We report the successful treatment of a 2.8 kg female infant born with a giant epignathus, and we present our current prenatal and neonatal recommendations for managing this problem. We recommend that the delivery be done by cesarean section, that an adjacent operating room be ready for the baby, and that a neonatologist, anesthesiologist, and pediatric surgeon be standing by. The term epignathus now commonly applies to a teratoma protruding from a newborn's mouth. The survival of these otherwise normal children has been very low. We discuss the perinatal, neonatal, and operative care necessary to improve survival, as evidenced by the case presented.

Biomarkers, Tumor↗
PubMed1987

Immunocytochemical and electrophysiological differentiation of rat cerebellar granule cells in explant cultures.

We have used a combination of immunocytochemical and electrophysiological measurements to monitor the differentiation of cerebellar granule cells in vitro. We present immunocytochemical evidence showing that several characteristic features of developing rat cerebellar tissue were retained in postnatal explant cultures. Most notably the cultures expressed radiating GFAP-positive (Bergmann) glia processes, proliferating NSE-negative neuroblasts, and migrating NSE-positive granule cells. The latter were subdivided into 3 developmental stages--i.e., immature, intermediate, and mature granule cells, based upon cell differences in location from the explant, intensity of NSE staining, excitability, and the amplitude of voltage-dependent conductances. Immature cells were identifiable during the first week in culture and were located up to 140 micron from the explant. These cells stained lightly for NSE and displayed conductances of insufficient magnitude to generate action potentials. Intermediate cells were present after 1-2 weeks in culture and were located up to 500 micron from the explant. These cells were also NSE positive and were characterized by the presence of soma action potentials. Intermediate cells displayed 3 large voltage-dependent conductances: a transient, TTX-sensitive inward current; a delayed, TEA-sensitive outward current; and a transient, 4AP-sensitive outward current. Mature cells were present after 1 month in culture and, like intermediate cells, were no more than 500 micron from the explant. However, mature cells stained more intensely for NSE, and the somata of these cells were devoid of voltage-dependent conductances (although axonal currents were usually present). These results indicate that granule cells undergo a stereotypic sequence of differentiation in postnatal explant cultures. These stages may correspond to developmental changes in granule cells during migration into the (internal) granular cell layer in vivo.

4-Aminopyridine↗
PubMed1995

Markers of neurotoxicity: from behavior to autoantibodies against brain proteins.

Evidence of potentially neurotoxic exposures may be obtained in peripheral indicator media, but molecular or cellular evidence of neurotoxic effects has not been as readily available, primarily because the nervous system of living humans is beyond the reach of direct measures. Although there is limited evidence that molecular changes in the blood can provide information about neurotoxicity, several new approaches are being investigated. One is that the immune system may preserve evidence of damage to the nervous system. Debris from damaged cells in the nervous system may present as antigens, giving rise to autoantibodies, which may be detectable in blood for a long time after injury. Progress will depend on more control experiments and clarification of confounding variables. Validation of new molecular markers must go hand in hand with documentation of impaired function, most commonly measured as behavioral or neurophysiological changes. These noninvasive markers will be measured with greater sensitivity and precision, thanks to innovative computer technology. The practical advantages of the new markers may be as important as their contribution to our understanding of the mechanisms by which the nervous system defends against chemical insult.

Autoantibodies↗