bluuebunny/crossref_metadata_2025_split huggingface dataset:
4D study of fluid effects on seismic data in the Gullfaks Field, North Sea
Authors: Landrø M. , Strønen L. K. 
Published: October 2003

AbstractThe use of seismic data as a fluid indicator has been investigated on data from a typical North Sea Field (Gullfaks). Examples of qualitative seismic analysis on one single dataset as well as on repeated datasets are shown, clearly demonstrating the usefulness for reservoir description and reservoir management for this field. Quantitative comparisons between expected and measured changes between water‐ and oil‐saturated reservoir rocks are presented. On a single dataset, we found a seismic amplitude increase of 26% between the water zone and the oil zone for the dipping top reservoir horizon. This value was significantly lower than the expected value based on rock physics and simple two‐layer seismic modelling, which was 80%. The discrepancy is attributed to initial oil saturations of probably less than 100%, the relatively high‐noise level in the seismic data, and interference effects with reflectivity from the oil–water contact. For a horizon between a low‐permeable layer (Ness) and a high‐permeable layer (Etive) we find a good quantitative agreement between the observed amplitude increase on the time lapse seismic data (41%) and the predicted amplitude increase from fluid substitution of well logs (40%). The general observation made in this study is that the seismic amplitudes are in good correspondence with the rock physics theory. Furthermore, the seismic fluid effects are visible in good reservoir sands, while heterogeneous sands with higher clay content show a weaker fluid signal on the seismic data.
Seismic constraints on the effects of gas hydrate on sediment physical properties and fluid flow: a review
Authors: Chand S. , Minshull T. A. 
Published: October 2003

AbstractThe formation of gas hydrates in marine sediments changes their physical properties and hence influences fluid flow. Here, we review seismic indicators of gas hydrates and relate these indicators to gas hydrate formation and fluid migration. Analyses of seismic data from sediments containing gas and gas hydrates in a variety of locations have shown that the characteristic bottom‐simulating reflector (BSR), which commonly marks the hydrate phase boundary is caused mainly by the presence of gas beneath the gas hydrate stability zone (GHSZ). The amplitude of the BSR is also dependent on the hydrate concentration and on the porosity of the sediment. The presence of gas hydrate alters the elastic properties of sediments, particularly if it cements sediment grains. However, multifrequency studies in various geological provinces show that any loss of reflectivity or blanking observed within the GHSZ is dependent on both the nature of the sediments and concentration of hydrate present. Gas beneath the BSR may cause amplitude anomalies and may result in bright spots and enhanced reflections. The presence of gas beneath the BSR is the primary cause of observed amplitude versus offset (AVO) anomalies, but the amplitude of these anomalies is also dependent on the amount of cementation brought by the gas hydrates within the GHSZ.Fluid migration appears to play an important role in the formation and dissociation of gas hydrates in both active and passive margin settings. Fluid migration in accretionary prisms influences hydrate accumulation and may therefore control the spatial distribution of BSRs. Fluid migration may influence also the type of hydrate formed by bringing thermogenic gas containing higher order hydrocarbons to the GHSZ from below. Fluid advection may cause local dissociation of gas hydrates by bringing heat from below, thus shifting the gas hydrate phase boundary. Fluid flow within the GHSZ is limited by the formation of hydrate in the pore space, which reduces the permeability of the sediment. Features such as pockmarks, acoustic masking and acoustic turbidity are indirect indicators of fluid flow and identification of these features in seismic sections within and beneath the GHSZ may also suggest the formation of gas hydrate.
Unravelling the petroleum system by enhancing fluid migration paths in seismic data using a neural network based pattern recognition technique
Authors: Ligtenberg J. H. 
Published: October 2003

AbstractUnderstanding the hydrocarbon migration system in the sub‐surface is a key aspect of oil and gas exploration. It is well known that conventional 3D seismic data contains information about hydrocarbon accumulations. Less known is the fact that 3D seismic data also contains information about hydrocarbon migration paths in the form of vertical noise trails. A method has been developed to highlight vertical noise trails in seismic data semi‐automatically, using assemblies of directive multi‐trace seismic attributes and neural network technology. The results of this detection method yield valuable information about the origin of hydrocarbons, about migration paths from source to prospect and about leakage or spillage from these prospects to shallow gas pockets or to the sea bed. Besides, the results reveal the sealing quality of faults, provide information on overpressure and whether prospects are charged or not. All these aspects are useful information for basin modelling studies and for an increased understanding of the petroleum system.
Fe(II)‐induced DNA damage in α‐synuclein‐transfected human dopaminergic BE(2)‐M17 neuroblastoma cells: detection by the Comet assay
Authors: Martin Francis L. , Williamson Sally J. M. , Paleologou Katerina E. , Hewitt Rebecca , El‐Agnaf Omar M. A. , Allsop David 
Published: October 2003

AbstractLewy bodies in the brains of patients with Parkinson's disease (PD) contain aggregates of α‐synuclein (α‐syn). Missense mutations (A53T or A30P) in the gene encoding α‐syn are responsible for rare, inherited forms of PD. In this study, we explored the susceptibility of untransfected human dopaminergic BE(2)‐M17 neuroblastoma cells, cells transfected with vector only, or cells transfected with wild‐type α‐syn, A30P α‐syn or A53T α‐syn to Fe(II)‐induced DNA damage in the form of single‐strand breaks (SSBs). DNA SSBs were detected following 2‐h treatments with various concentrations of Fe(II) (0.01–100.0 μm), using the alkaline single cell‐gel electrophoresis (‘Comet’) assay and quantified by measuring comet tail length (CTL) (μm). Fe(II) treatment induced significant increases in CTL in cells transfected with A30P α‐syn or A53T α‐syn, even at the lowest concentrations of Fe(II) tested. In comparison, untransfected cells, vector control cells or cells transfected with wild‐type α‐syn exhibited increases in SSBs only when exposed to concentrations of 1.0 μm Fe(II) and above. Even when exposed to higher concentrations (10.0–100.0 μm) of Fe(II), untransfected cells, vector control cells or cells transfected with wild‐type α‐syn were less susceptible to DNA‐damage induction than cells transfected with A30P α‐syn or A53T α‐syn. Incorporation of DNA‐repair inhibitors, hydroxyurea and cytosine arabinoside, enhanced the sensitivity of DNA damage detection. Susceptibility to Fe(II)‐induced DNA damage appeared to be dependent on α‐syn status because cells transfected with wild‐type α‐syn or A53T α‐syn were equally susceptible to the damaging effects of the mitochondrial respiratory chain inhibitor rotenone. Overall, our data are suggestive of an enhanced susceptibility to the toxic effects of Fe(II) in neuroblastoma cells transfected with mutant α‐syn associated with inherited forms of PD.
Stroke‐induced progenitor cell proliferation in adult spontaneously hypertensive rat brain: effect of exogenous IGF‐1 and GDNF
Authors: Dempsey Robert J. , Sailor Kurt A. , Bowen Kellie K. , Türeyen Kudret , Vemuganti Raghu 
Published: October 2003

AbstractProgenitor cells in the dentate gyrus of hippocampus (DG) and the subventricular zone of lateral ventricles (SVZ) generate new neurons throughout the life of mammals. Cerebral ischemia increases this basal progenitor cell proliferation. The present study evaluated the time frame of proliferation, length of survival and the phenotypes of the new cells formed after transient middle cerebral artery occlusion (MCAO) in adult spontaneously hypertensive rats. Compared to sham controls, ischemic rats showed a significantly higher number of newly proliferated cells (as defined by BrdU immunostaining) in both the DG (by fourfold, p < 0.05) and the SVZ (by twofold, p < 0.05). DG showed increased proliferation only in the first week of reperfusion and 49% of the cells formed in this period survived to the end of third week. Whereas, SVZ showed a continuous proliferation up to 3 weeks after MCAO, but the cells formed survived for less than a week. In both DG and SVZ, at the end of the first week of reperfusion, majority of the BrdU‐positive (BrdU+) cells were immature neurons (DCX positive). In the DG, 28% of the cells formed in the first week after MCAO mature into neurons (NeuN positive). The ischemic cortex and striatum showed several BrdU+ cells which were ED‐1 positive microglia/macrophages. At 1 week of reperfusion, MCAO‐induced progenitor cell proliferation in the ipsilateral DG was significantly increased by i.c.v. infusion of IGF‐1 (by 127 ± 14%, p < 0.05) and GDNF (by 91 ± 5%, p < 0.05), compared to vehicle. In the growth factor treated rats subjected to transient MCAO, several BrdU+ cells formed in the first week survived up to the third week.
Mass spectrometric investigation of the neuropeptide complement and release in the pericardial organs of the crab, Cancer borealis
Authors: Li Lingjun , Kelley Wayne P. , Billimoria Cyrus P. , Christie Andrew E. , Pulver Stefan R. , Sweedler Jonathan V. , Marder Eve 
Published: October 2003

AbstractThe crustacean stomatogastric ganglion (STG) is modulated by both locally released neuroactive compounds and circulating hormones. This study presents mass spectrometric characterization of the complement of peptide hormones present in one of the major neurosecretory structures, the pericardial organs (POs), and the detection of neurohormones released from the POs. Direct peptide profiling of Cancer borealis PO tissues using matrix‐assisted laser desorption/ionization (MALDI) time‐of‐flight (TOF) mass spectrometry (MS) revealed many previously identified peptides, including proctolin, red pigment concentrating hormone (RPCH), crustacean cardioactive peptide (CCAP), several orcokinins, and SDRNFLRFamide. This technique also detected corazonin, a well‐known insect hormone, in the POs for the first time. However, most mass spectral peaks did not correspond to previously known peptides. To characterize and identify these novel peptides, we performed MALDI postsource decay (PSD) and electrospray ionization (ESI) MS/MS de novo sequencing of peptides fractionated from PO extracts. We characterized a truncated form of previously identified TNRNFLRFamide, NRNFLRFamide. In addition, we sequenced five other novel peptides sharing a common C‐terminus of RYamide from the PO tissue extracts. High K+ depolarization of isolated POs released many peptides present in this tissue, including several of the novel peptides sequenced in the current study.
Selective γ‐hydroxybutyric acid receptor ligands increase extracellular glutamate in the hippocampus, but fail to activate G protein and to produce the sedative/hypnotic effect of γ‐hydroxybutyric acid
Authors: Castelli M. Paola , Ferraro Luca , Mocci Ignazia , Carta Francesca , Carai Mauro A. M. , Antonelli Tiziana , Tanganelli Sergio , Cignarella Giorgio , Gessa Gian Luigi 
Published: October 2003

AbstractTwo γ‐hydroxybutyric acid (GHB) analogues, trans‐γ‐hydroxycrotonic acid (t‐HCA) and γ‐(p‐methoxybenzyl)‐γ‐hydroxybutyric acid (NCS‐435) displaced [3H]GHB from GHB receptors with the same affinity as GHB but, unlike GHB, failed to displace [3H]baclofen from GABAB receptors. The effect of the GHB analogues, GHB and baclofen, on G protein activity and hippocampal extracellular glutamate levels was compared. While GHB and baclofen stimulated 5′‐O‐(3‐[35S]thiotriphospate) [35S]GTPγS binding both in cortex homogenate and cortical slices, t‐HCA and NCS‐435 were ineffective up to 1 mm concentration. GHB and baclofen effect was suppressed by the GABAB antagonist CGP 35348 but not by the GHB receptor antagonist NCS‐382. Perfused into rat hippocampus, 500 nm and 1 mm GHB increased and decreased extracellular glutamate levels, respectively. GHB stimulation was suppressed by NCS‐382, while GHB inhibition by CGP 35348. t‐HCA and NCS‐435 (0.1–1000 µm) locally perfused into hippocampus increased extracellular glutamate; this effect was inhibited by NCS‐382 (10 µm) but not by CGP 35348 (500 µm). The results indicate that GHB‐induced G protein activation and reduction of glutamate levels are GABAB‐mediated effects, while the increase of glutamate levels is a GHB‐mediated effect. Neither t‐HCA nor NCS‐435 reproduced GHB sedative/hypnotic effect in mice, confirming that this effect is GABAB‐mediated. The GHB analogues constitute important tools for understanding the physiological role of endogenous GHB and its receptor.
Membrane receptors for oestrogen in the brain
Authors: Beyer Cordian , Pawlak Justyna , Karolczak Magdalena 
Published: October 2003

AbstractOestrogen is important for the development of neuroendocrine centres and other neural networks including limbic and motor systems. Later in adulthood, oestrogen regulates the functional performance of different neural systems and is presumably implicated in the modulation of cognitive efficiency. Although still a matter of controversial discussion, clinical and experimental studies point at a potential neuroprotective role of oestrogen. Concerning the concept of cellular oestrogen action, it is undisputed that it comprises the binding and activation of nuclear receptors. The last decades have, however, immensely broadened the spectrum of steroid signalling within a cell. Novel steroid‐activated intracellular signalling mechanisms were described which are usually termed ‘non‐classical’ or ‘non‐genomic’. The brain appears to be a rich source of this new mode of oestrogen action. Studies from the past years have pinpointed non‐classical oestrogen effects in many CNS regions. All available data support the view that non‐classical oestrogen action requires interactions with putative membrane binding sites/receptors. In this article, we aim at compiling the most recent findings on the nature and identity of membrane oestrogen receptors with respect to the brain. We also attempt to turn readers attention to the coupling of these ‘novel’ receptors to distinct intracellular signalling pathways.
15‐Deoxy‐Δ12,14‐prostaglandin J2regulates the functional state and the survival of microglial cells through multiple molecular mechanisms
Authors: Bernardo Antonietta , Ajmone‐Cat Maria Antonietta , Levi Giulio , Minghetti Luisa 
Published: October 2003

AbstractWe have previously reported that rat primary microglial cultures express the nuclear receptor peroxisome proliferator‐activated receptor‐γ (PPAR‐γ) and that several functions associated with the activation of these cells, including nitric oxide (NO) and tumor necrosis factor‐α synthesis, are down‐regulated by 15‐deoxy‐Δ12,14‐prostaglandin J2(15d‐PGJ2) and ciglitazone, two specific PPAR‐γ agonists. Here we demonstrate that microglial cells not only express a functionally active PPAR‐γ, but also synthesize large amounts of 15d‐PGJ2upon stimulation with lipopolysaccharide (LPS). In addition, we show that, although 15d‐PGJ2and ciglitazone were equally effective in reducing microglial activation when used at 1–5 µmconcentrations, 15d‐PGJ2, but not of ciglitazone, reduced PGE2production at low concentration (0.1 µm) and induced a time‐dependent microglial impairment and apoptosis at high concentration (10 µm). Interestingly, the inhibition of PGE2production was achieved mainly through the inhibition of cycloxygenase‐2 enzymatic activity, as the expression of this enzyme and that of the microsomal isoform of PGE synthase remained unaltered. These findings suggest that 15d‐PGJ2affects the functional state and the survival of activated microglia through mechanisms only in part dependent on PPAR‐γ and that the concentration of 15d‐PGJ2is crucial in determining the particular microglial function affected.
Primary cortical neuronal cultures reduce cellular energy utilization during anoxic energy deprivation
Authors: Munns Shane E. , Meloni Bruno P. , Knuckey Neville W. , Arthur Peter G. 
Published: October 2003

AbstractIt has been widely hypothesized that neurons reduce cellular energy use in response to periods of energy deprivation. To test this hypothesis, we measured rates of energy use under normoxia and anoxia in immature (6 days in vitro) and mature (13 days in vitro) neuronal cultures. During anoxic incubation immature and mature cultures reduced cellular energy use by 80% and 45%, respectively. Reduced cellular energy use dramatically affected ATP depletion in neuronal cultures under anoxia. Intracellular ATP stores were expected to deplete within 3 min of anoxia. However, ATP was maintained at decreased but stabilized concentrations for at least 3 h. The capacity of neuronal cultures to reduce cellular energy use during anoxia correlated with their sensitivity towards simulated ischemia. Immature cultures, with the largest capacity to reduce cellular energy use, survived simulated ischemia 2.5 times longer than mature cultures. The addition of glutamate receptor antagonists to mature cultures further decreased cellular energy use during anoxia and significantly extended their survival time under simulated ischemia. This study verifies that primary cortical neuronal cultures reduce cellular energy use during energy deprivation. Additionally, we show that maturation of glutamate receptor activity increases non‐depressible energy demand in neuronal cultures.
Identification of Tau and MAP2 as novel substrates of Rho‐kinase and myosin phosphatase
Authors: Amano Mutsuki , Kaneko Takako , Maeda Akio , Nakayama Masanori , Ito Masaaki , Yamauchi Takashi , Goto Hideyuki , Fukata Yuko , Oshiro Noriko , Shinohara Azusa , Iwamatsu Akihiro , Kaibuchi Kozo 
Published: October 2003

AbstractRho‐kinase and myosin phosphatase are implicated in the phosphorylation‐state of myosin light chain downstream of Rho, which is thought to induce smooth muscle contraction and stress fibre formation in non‐muscle cells. Here, we found that microtubule‐associated proteins, Tau and MAP2, interacted with the myosin‐binding subunit (MBS) of myosin phosphatase, and were the possible substrates of both Rho‐kinase and myosin phosphatase. We determined the phosphorylation sites of Tau (Thr245, Thr377, Ser409) and MAP2 (Ser1796) by Rho‐kinase. We also found that Rho‐kinase phosphorylated Tau at Ser262 to some extent. Phosphorylation by Rho‐kinase decreased the activity of Tau to promote microtubule assembly in vitro. Substitutions of Ala for Ser/Thr at the phosphorylation sites of Tau (Tau‐AAA) did not affect the activity to promote microtubule assembly, while substitutions of Asp for Ser/Thr (Tau‐DDD), which are expected to mimic the phosphorylation‐state of Tau, slightly reduced the activity. When Tau, or mutated forms of Tau, were expressed in PC12 cells, followed by treatment with cytochalasin D, they promoted extension of the cell process in a cytochalasin‐dependent manner. However, Tau‐DDD showed the weaker activity in this capacity than wild‐type Tau or Tau‐AAA. These results suggest that the phosphorylation‐state of these residues of Tau affects its activity both in vitro and in vivo. Thus, it is likely that the Rho‐kinase/MBS pathway regulates not only the actin‐myosin system but also microtubule dynamics.
Polarized actin bundles formed by human fascin‐1: their sliding and disassembly on myosin II and myosin V in vitro
Authors: Ishikawa Ryoki , Sakamoto Takeshi , Ando Toshio , Higashi‐Fujime Sugie , Kohama Kazuhiro 
Published: October 2003

AbstractFascin‐1 is a putative bundling factor of actin filaments in the filopodia of neuronal growth cones. Here, we examined the structure of the actin bundle formed by human fascin‐1 (actin/fascin bundle), and its mode of interaction with myosin in vitro. The distance between cross‐linked filaments in the actin/bundle was 8–9 nm, and the bundle showed the transverse periodicity of 36 nm perpendicular to the bundle axis, which was confirmed by electron microscopy. Decoration of the actin/fascin bundle with heavy meromyosin revealed that the arrowheads of filaments in the bundle pointed in the same direction, indicating that the bundle has polarity. This result suggested that fascin‐1 plays an essential role in polarity of actin bundles in filopodia. In the in vitro motility assay, actin/fascin bundles slid as fast as single actin filaments on myosin II and myosin V. When myosin was attached to the surface at high density, the actin/fascin bundle disassembled to single filaments at the pointed end of the bundle during sliding. These results suggest that myosins may drive filopodial actin bundles backward by interacting with actin filaments on the surface, and may induce disassembly of the bundle at the basal region of filopodia.
GABAC receptor agonist suppressed ammonia‐induced apoptosis in cultured rat hippocampal neurons by restoring phosphorylated BAD level
Authors: Yang Li , Omori Kyoko , Omori Koichiro , Otani Hitomi , Suzukawa Junko , Inagaki Chiyoko 
Published: October 2003

AbstractAmmonia‐induced apoptosis and its prevention by GABAC receptor stimulation were examined using primary cultured rat hippocampal neurons. Ammonia (0.5–5 mm NH4Cl) dose‐dependently induced apoptosis in pyramidal cell‐like neurons as assayed by double staining with Hoechst 33258 and anti‐neurofilament antibody. A GABAC receptor agonist, cis‐4‐aminocrotonic acid (CACA, 200 µm), but not GABAA and GABAB receptor agonists, muscimol (10 µm) and baclofen (50 µm), respectively, inhibited the ammonia (2 mm)‐induced apoptosis, and this inhibition was abolished by a GABAC receptor antagonist (1,2,5,6‐tetrahydropyridin‐4‐yl)methylphosphinic acid (TPMPA, 15 µm). Expression of all three GABAC receptor subunits was demonstrated in the cultured neurons by RT‐PCR. The ammonia‐treatment also activated caspases‐3 and ‐9 as observed in immunocytochemistry for PARP p85 and western blot. Such activation of the caspases was again inhibited by CACA in a TPMPA‐sensitive manner. The anti‐apoptotic effect of CACA was blocked by inhibitors for MAP kinase kinase and cAMP‐dependent protein kinase, PD98059 (20 µm) and KT5720 (1 µm), suggesting possible involvement of an upstream pro‐apoptotic protein, BAD. Levels of phospho‐BAD (Ser112 and Ser155) were decreased by the ammonia‐treatment and restored by coadministration of CACA. These findings suggest that GABAC receptor stimulation protects hippocampal pyramidal neurons from ammonia‐induced apoptosis by restoring Ser112‐ and Ser155‐phospho‐BAD levels.