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At least 631 records · Page 35Linked to original sources
PubMed1998

Hypothalamic hamartoma: report of a case with unusual histologic features.

A rare case of hypothalamic hamartoma with unusual radiologic and histopathological features is described, possibly the first of its type in English literature. A 1.5-year-old female child presented with precocious puberty. MR scan of the brain revealed a pedunculated hypothalamic mass, most of which was isointense with normal brain on T1- and T2-weighted images. However, a sizeable component of the lesion was hyperintense on T1-weighted images, suggestive of adipose tissue. Microscopically, the lesion was a hamartoma composed of an admixture of neuroectodermal elements, namely glial cells, neurons, and nerve bundles along with mesenchymal elements in the form of fibroadipose tissue.

Brain Diseases↗
PubMedDate not supplied

Characteristics of human medulloblastoma cell line TE-671 under different growth conditions in vitro: a morphological and immunohistochemical study.

The human medulloblastoma cell line, TE-671, was studied in vitro both in monolayer culture and in a three-dimensional culture system using gelfoam as the supporting matrix. Flow cytometry studies of cells grown in monolayer culture revealed a unimodal, tetraploid DNA content. Most cells in both in vitro systems contained neuron-specific enolase (NSE), actin, and tubulin, while only occasional cells or cell clusters contained the 68,000 molecular weight subunit of neurofilaments (NF mol. wt 68,000) or microtubule-associated protein 2 (MAP-2). In monolayer culture, long cellular processes containing NSE, NF mol. wt 68,000 and MAP-2, which were present at 2 days, were nearly absent by 7 days. All antigens were present at 4 days in the organ culture system; by 72 days, cells still stained positively for NF mol. wt 68 000 and MAP-2, but staining for NSE, actin, and beta-tubulin was diminished as compared to 4 days. Retinoic acid (RA) in the 13-cis isomer form at 10(-6) M was applied to monolayer cultures at day 1 for 6 days and to gelfoam cultures at day 1 for 28 days. RA did not significantly alter cell proliferation up to 7 days in vitro and did not appreciably affect cellular expression of NSE, NF mol. wt 68 000, MAP-2, beta-tubulin, or actin in either system. By electron microscopy, most cells grown under different culture conditions with or without RA treatment appeared to be undifferentiated and polygonal, with occasional cytoplasmic annulate lamellae. The immunohistochemical and ultrastructural features reported indicate that the TE-671 medulloblastoma line is composed primarily of primitive neuroepithelial cells with a limited potential for neuronal differentiation. This differentiation was not promoted by RA or by an in vitro system known to favour differentiation in a number of human and animal nervous system tumours. The findings suggest that the cells of the TE-671 line lack either receptors for retinoic acid or the capacity to respond to bound retinoic acid.

Actins↗
PubMed2004

The peptide sequence Arg-Glu-Arg, present in the amyloid precursor protein, protects against memory loss caused by A beta and acts as a cognitive enhancer.

Amino acid sequences containing the palindromic tripeptide RER, matching amino acids 328-330 of the amyloid precursor protein APP, when injected intracerebrally prior to or just after training, protect against memory loss induced by amyloid-beta (A beta) in a one-trial passive avoidance task in the young chick. RER also acts as a cognitive enhancer, strengthening memory for a weak version of the task. N-terminal acylation of RER protects it against rapid degradation, and AcRER is effective in restoring memory if administered peripherally. Biotinylated RER binds to chick neuronal perikarya in an APP-displaceable manner via 66 and approximately 110 kDa neuronal cell membrane proteins. We suggest that RER binding is likely to exert effects on memory retention via receptor-mediated events that include activation of second messenger pathways. These findings suggest that RER and its derivatives may offer a novel approach to enhancing the neuroprotective effects of APP and alleviating the effects of memory loss in the early stages of Alzheimer's disease.

Amnesia↗
PubMed2004

Intraocular delivery of BDNF following visual cortex lesion upregulates cytosolic branched chain aminotransferase (BCATc) in the rat dorsal lateral geniculate nucleus.

Visual cortex ablation in newborn rats determines the almost complete degeneration of neurons in the dorsal lateral geniculate nucleus (dLGN), as a consequence of the axotomy of the geniculo-cortical fibres. Death of dLGN neurons is massive and rapid, and occurs by apoptosis. We recently showed that exogenous administration of the neurotrophin brain-derived neurotrophic factor (BDNF) in the eye prevents the degeneration of dLGN neurons occurring after visual cortex lesion in newborn rats. To elucidate the molecular mechanisms of BDNF-mediated neuroprotection, we sought to identify novel genes regulated by BDNF in the rat dLGN after visual cortex lesion. By using mRNA fingerprinting, we isolated a cDNA fragment upregulated in the dLGN of lesioned rats treated with BDNF. This cDNA fragment shared 100% homology with the rat cytosolic branched chain aminotransferase (BCATc), a key enzyme of glutamate metabolism. Quantitative reverse transcription-polymerase chain reaction and in situ hybridization confirmed that BCATc mRNA is markedly overexpressed by exogenous supply of BDNF to axotomized dLGNs. Immunohistochemical analysis showed that upregulation of BCATc in the dLGN of lesioned rats treated with BDNF takes place in astrocytes. These results suggest that modulation of glutamate metabolism by astrocytes might play an important role in BDNF-mediated survival of axotomized dLGN neurons.

Animals↗
PubMedDate not supplied

Perchloroethylene-induced reduction in glial and neuronal cell marker proteins in rat brain.

Rats were exposed to continuous inhalation of 300 and 600 p.p.m. of perchloroethylene for 4 and 12 weeks. Exposure to 600 p.p.m. for 4 to 12 weeks resulted in a slower increase in brain weight. Brain region weights, total proteins and DNA were decreased in frontal cerebral cortex and brain stem but not in hippocampus after exposure to 600 p.p.m. for 12 weeks. Four marker proteins were measured to monitor the specific neurotoxic effects of perchloroethylene: S-100 protein and glial fibrillary acidic protein as glial cell markers and neurone specific enolase and neurofilament 68 kD polypeptide as neuronal markers. The concentrations of glial and neuronal cytoskeletal proteins (glial fibrillary acidic protein and neurofilament 68 kD polypeptide) were reduced in frontal cerebral cortex. The total tissue contents of glial proteins (S-100 protein and glial fibrillary acidic protein) were decreased in all 3 brain regions investigated (frontal cerebral cortex, hippocampus and brain stem). Neurone specific enolase was unchanged by perchloroethylene exposure. These results indicate that exposure to perchloroethylene reduces the number of brain cells, possibly glial cells, and interferes with the metabolism of cytoskeletal elements in both glial and neuronal cells.

Administration, Inhalation↗
PubMed1993

Nonculture methods for diagnosis of disseminated candidiasis.

Two of the nonculture approaches to the diagnosis of DC, enzymatic-fluorometric determination of serum D-arabinitol and detection of marker antigens in antigenemia (enolase and CWMP), have been commercialized and have shown promise in limited clinical trials. These approaches are not new but are the culmination of efforts made over 10 or more years. Clearly, further fine-tuning of both metabolite and antigen detection is needed to simplify the methods and to improve their sensitivity and specificity so that they will be valuable in guiding clinical treatment decisions. An alternative approach, detection of DC by DNA amplification methods such as PCR, is a special case of a compelling technology and one that is capable of standardization across microbial genera. The availability of simplified PCR diagnostic methods for DC remains a tantalizing prospect. Nevertheless, the development of methods to release DNA from very small numbers of Candida organisms in the blood in a form that is sufficiently free of inhibitors of PCR will require further intensive effort. The maturation of these converging laboratory approaches to nonculture diagnosis of DC leads to more optimism about the eventual use of these methods in clinical laboratories.

Antigens, Fungal↗
PubMed2006

Microcirculatory dysfunction in the brain precedes changes in evoked potentials in endotoxin-induced sepsis syndrome in rats.

BACKGROUND: During sepsis progression microcirculatory dysfunction precedes macrocirculatory failure, partly explaining the occurrence of early organ dysfunction. The matter concerning microcirculatory dysfunction in the brain under septic conditions is less clear. We investigated the integrity of the activation flow coupling during sepsis progression in a rat model of septic shock. METHODS: Chloralose-anesthetized rats (n = 30) were subjected to electric forepaw stimulation. Over the somatosensory cortex electrical activity and hemodynamic responses were recorded with surface electrodes and laser Doppler. After baseline recordings, vehicle, 1 or 5 mg/kg lipopolysaccharide (LPS) from Escherichia coli was given intravenously, and activation flow coupling, blood pressure and blood gases were investigated at regular time points up to 270 min. In the end lactate, glucose, neuron-specific enolase (NSE) and S-100B protein levels were measured. RESULTS: Besides stable data from the control group, all LPS-treated rats developed signs of septic shock, which were more pronounced in the 5 mg/kg LPS group. Cerebral hyperemia occurred and was similar between the sepsis groups despite lower blood pressure levels in the 5 mg/kg LPS group. While the activation flow coupling remained intact in the 1 mg/kg LPS group, an uncoupling occurred in the 5 mg/kg group. First, the evoked flow velocity responses dropped 60 min after sepsis induction before the somatosensory amplitudes also decreased 120 min later. From similar NSE levels we suggest a functional rather than structural deficit explaining the difference in evoked potentials. CONCLUSIONS: For the first time we demonstrate microcirculatory dysfunction in the activation flow coupling of the brain. Inappropriate blood supply of neurons might explain the disturbance of neuronal function.

Animals↗
PubMed2006

Differentiation and neurological benefit of the mesenchymal stem cells transplanted into the rat brain following intracerebral hemorrhage.

Spontaneous intracerebral hemorrhage (ICH) is often a fatal event. In a patient who survives the initial ictus, the resulting hematoma within brain parenchyma can trigger a series of events that lead to secondary insults and severe neurological deficits. Great efforts have been focused on searching for new approaches to help patients recover neurological function after ICH. Previous studies indicate that mesenchymal stem cells (MSCs) grafted into the ischemic rat brain can improve neurological function. However, there is no report regarding whether MSCs can be used in the same way to improve the neurological function after ICH. We generated the ICH model by injecting collagenase VII into rat brain. Subsequently, 5-bromo-2-deoxyuridine (BrdU)-labeled mesenchymal stem cells were delivered into the brain through carotid artery, cervical vein or lateral ventricle. The distribution and differentiation of MSCs were investigated by methods of immunohistochemistry. We found that MSCs were able to differentiate into neural cells in vitro as well as in the rat brain after ICH. The injected MSCs were able to migrate into hippocampus, blooding foci and ipsilateral cortex. In the hippocampus, MSCs differentiated into neurons; but in surrounding bleeding foci, they differentiated into neurons and astrocytes. In the ipsilateral cortex, MSCs differentiated into neurons, astrocytes and oligodendrocytes. Notably, the motor function of the rats in the carotid artery (CA) group and the lateral ventricle (LV) group improved significantly. Collectively, our study indicates that MSCs are able to differentiate into neural cells in the rat brain after ICH and can significantly improve motor function.

Animals↗
PubMed1999

Screening for multiple endocrine neoplasia type 1 and hormonal production in apparently sporadic neuroendocrine tumors.

Screening was performed in 130 consecutive patients with apparently sporadic neuroendocrine tumors (NET) to assess the prevalence of multiple endocrine neoplasia type 1 (MEN1) and hormonal production. Screening for MEN1 included measurement of serum calcium and PTH [PTH-(1-84)], gastrin, PRL, and insulin-like growth factor type I (IGF-I) levels. MEN1 genetic testing was performed in patients with two components of the MEN1 syndrome. Screening for hormonal production included measurement of serum neuron-specific enolase (NSE), calcitonin (CT), glycoprotein alpha-subunit (GP alpha), hCG beta-subunit (free hCG beta), and somatostatin levels. Twenty-four-hour urinary free cortisol (UFC) and 5-hydroxyindolacetic acid (5-HIAA) determinations were also performed. Four patients had hyperparathyroidism, none of whom had pituitary or familial disease. Hyperprolactinemia was compatible with a pituitary disease in one patient. No acromegalic feature or any increase in IGF-I was found. Hypergastrinemia, compatible with an associated pancreatic NET, was found in one patient. Genetic screening of the MEN1 gene was performed in five of the six patients with two components of the MEN1 syndrome. A nonsense mutation (Arg108stop) was identified in the tumor of one patient. Elevated NSE, 5-HIAA, CT, GP alpha, free hCG beta, SMS, and nonsuppressible UFC were found in 47%, 46%, 14%, 19%, 12%, 3%, and 6% of NET patients, respectively. Production of CT, GP alpha, and free hCG beta was highly related to the primary site: all but two of these secretions originated in foregut NET. 5-HIAA secretion was found in 27% of foregut-derived and 85% of midgut-derived NET. In conclusion, MEN1 is a rare event in patients presenting with apparently sporadic NET. It occurred mainly in foregut NET and should be screened for by serum calcium and PTH-(1-84) measurements. Routine hormonal measurements should depend on the primary site. NSE, 5-HIAA, CT, and alphaGP should be routinely measured in foregut-derived NET; only serum NSE and 5-HIAA measurements are recommended in midgut-derived NET.

Adult↗
PubMed2004

Glial and neuronal proteins in serum predict outcome after severe traumatic brain injury.

OBJECTIVE: To study the ability of glial (glial fibrillary acidic protein [GFAP] and S100b) and neuronal (neuron specific enolase [NSE]) protein levels in peripheral blood to predict outcome after severe traumatic brain injury. METHODS: Eighty-five patients with severe traumatic brain injury (admission Glasgow Coma Score [GCS] < or = 8) were included. Blood samples taken at the time of hospital admission were analyzed for S100b, GFAP, and NSE. Data collected included demographic and clinical variables. Outcome was assessed using the Glasgow Outcome Scale (GOS) at 6 months post injury. RESULTS: The median serum levels of S100b, GFAP, and NSE were raised 18.3 fold (S100b), 4.6 fold (GFAP), and twofold (NSE) compared to normal reference values. S100b, GFAP, and NSE serum levels correlated significantly with the injury severity score and CT findings but not with age, sex, or GCS. S100b, GFAP, and NSE levels were significantly higher in patients who died or had a poor outcome 6 months post injury than in those who were alive or had good outcome. S100b level >1.13 microg/L was the strongest predictor of death with 100% discrimination, but GFAP (>1.5 microg/L) and NSE (>21.7 microg/L) levels also strongly predicted death (adjusted odds ratios 5.82 [for GFAP] and 3.91 [for NSE]). S100b, GFAP, and NSE all strongly predicted poor outcome (adjusted odds ratios 5.12 [S100b], 8.82 [GFAP], and 3.95 [NSE]). CONCLUSIONS: These results suggest that determination of serum levels of glial and neuronal proteins may add to the clinical assessment of the primary damage and prediction of outcome after severe traumatic brain injury.

Adolescent↗
PubMed2001

Nerve cell markers in ossifying fibromyxoid tumour of soft parts.

Reported herein are two benign ossifying fibromyxoid tumors (OFMTs) of the soft tissues in axilla and terminal phalanx respectively. Both cases on immunohistochemistry (IHC) showed reactivity for vimentin, S-100 protein and glial fibrillary acidic protein (GFAP) antibodies. In addition, a focal/diffuse strong positivity for neurofilament (NF) and neuron specific enolase (NSE) was observed. Electron microscopy in one instance revealed abundant intermediate filaments, primitive cell junctions and a focally present external lamina. In the light of nerve cell differentiation of these tumors and the similarity of IHC profile and EM features of OFMT to a poorly differentiated malignant peripheral nerve sheath tumor (MPNST); it is suggested that OFMT is a variably differentiated PNST rather than a simple Schwannian neoplasm as is believed.

Adult↗
PubMed1991

Do astroglial cells participate in the process of human spinal cord myelination?

The material comprised spinal cord segments C8 or Th1 of 6 human fetuses aged from 16-17 up to 34 weeks and 6 infants aged from one day to 3 years. On formalin-fixed, paraffin-embedded sections, peroxidase-antiperoxidase Sternberger's et al. (1970) method for visualization of astrocytic proteins (S-100 and GFAP), myelin basic protein (MBP) and neuron specific enolase (NSE), was used. Parallelly to the increasing immunoreactivity to MBP, more S-100 and GFAP-positive cells were observed. Immunoreactivity to S-100 was more distinct in astrocytic perikarya, whereas, in GFAP reaction immunostaining of astrocytic processes was more pronounced. It is very difficult to explain why reactivity of astrocytes appears during myelination.

Age Factors↗
PubMed1989

A cell line derived from non-neoplastic human neuroretinal cells.

We have derived a cell line from an epiretinal membrane excised surgically from a premature female infant born at a gestational age of 25 weeks, and who developed stage 5 retinopathy of prematurity. The cell line, which in early passages appeared immunocytochemically to contain cells with both neuronal and glial characteristics, has been maintained in culture for 14 months at the time this manuscript was submitted, and has survived 20 passages. The cells have a diploid, human karyotype, with most cells possessing 46 normal appearing chromosomes, including 44 autosomes and two X-chromosomes. Morphologically, the cell line at early passages consisted of polygonal cells and also of cells possessing long, spindly branching processes. These two cell types were cloned. Nearly 100% of the cells of both morphologic types in mixed cultures stained immunocytochemically for neuron-specific enolase (NSE), a neuronal marker, and approximately 5-10% of the cells in mixed cultures (including about 50% of the cells with the spindly morphology, that were less prevalent in mixed cultures) stained for glial fibrillary acid protein (GFAP), a glial marker. We have not performed "double-label" immunocytochemistry, but it was evident from the proportion of cells that stained with each marker that many cells must contain both GFAP and NSE. At least 50% of the cells in most of the early cultures were positive for keratin, while all were (and remain) negative for muscle actin. No cells are found that are immunocytochemically positive for factor VIII, a vascular endothelial cell marker. These cultured cells have also been studied immunocytochemically for their production of extracellular matrix substances. The cultures are immunocytochemically positive for type IV (but not type I) collagen, laminin and fibronectin. In later passages, cells of both clones lost their immunocytochemical positivity for GFAP and NSE, and all became positive for keratin. Cells of both clones also developed a similar, polygonal morphology, lacking long processes. By electron microscopy, many of the cells were seen to possess nonmotile cilia, with a 9 + 0 pattern of microtubule doublets. This cell line may be useful for studies of human retinal cell development and metabolism, and responses to pathological processes.

Cell Division↗
PubMed1987

Chemical modification of histidine, tyrosine, tryptophan and cysteine residues in carp (Cyprinus carpio) muscle enolase.

Enolase from carp (Cyprinus Carpio) muscle was modified by diethylpyrocarbonate, tetranitromethane, N-bromosuccinimide and 5,5'-dithiobis(2-nitrobenzoic acid). The extent and rate of modification and its effect on the enzyme activity were determined. Modification of histidine, tyrosine and tryptophan residues caused complete inactivation of the enzyme; Mg2+ as well as 2-phosphoglycerate markedly altered the rates of modification and inactivation. The above-mentioned amino acid residues seem to be essential for the functioning of muscle enolases. Modification of cysteine residues had no effect on the enolase activity.

Amino Acids↗
PubMed1981

The amino acid sequence of yeast enolase.

Automatic sequencing of yeast enolase and of its chemically and enzymatically produced peptide fragments has established the sequence of 416 of the 436 residues in the enolase subunits. The missing segments have been provided from results from sequencing the DNA of the yeast enolase genes (Holland, M. J., Holland, J. P., Thill, G. P., and Jackson, K. A. (1981) J. Biol. Chem. 256, 1385-1395). The reported enolase sequence thus represents the results of two completely independent studies, which yielded identical results for 404 of the 436 residues, and which on re-examination are consistent with the reported sequence in all but nine positions. The availability of the entire yeast enolase sequence has permitted a reassessment of structure-function parameters available for the enzyme, and some implications of the sequence information on the secondary, tertiary, and quarternary structure and on the active site components of yeast enolase have been summarized and discussed.

Amino Acid Sequence↗
PubMed1993

Practical applications of some antibodies labelling the human retina.

Eight enucleated eyes were promptly fixed in 10% formalin and processed for light microscopy. Employing the ABC technique, we used antibodies against neuron-specific enolase (NSE), synaptophysin (SY), neurofilament (NF), glial fibrillary acidic protein (GFAP), keratins, LEU-7 and S-100 protein. Using NSE we found immunoreactivity in all sensory layers except the outer segments of photoreceptors which were nonreactive. SY showed a striking immunoreactivity of the synaptic regions (outer plexiform and inner plexiform layers). NF labelled the axons of the ganglion cells. GFAP stained perivascular glial cells and Müller cells only in areas of peripheral microcystoid degeneration. Keratin was non-reactive in all layers. LEU-7 showed that all layers were moderately reactive while the Müller cell processes and the outer limiting membrane were strongly immunoreactive. S-100 protein stained the perivascular glial cells in the nerve fiber layer. We conclude that NSE and LEU-7 are helpful markers for most layers of the sensory retina; GFAP and LEU-7 clearly outline Müller cells and GFAP immunoreacts with astrocytes; NF is specific for axons and SY labels vividly the synaptic regions.

Adult↗