bluuebunny/crossref_metadata_2025_split huggingface dataset:
Laryngeal mask airway for ventilation during diagnostic and interventional fibreoptic bronchoscopy in children
Authors: Yazbeck‐Karam Vanda G. , Aouad Marie T. , Baraka Anis S. 
Published: October 2003

SummaryBackground:  The use of the flexible fibreoptic bronchoscope in infants and children has expanded to include both interventional and diagnostic bronchoscopy. The present report utilizes the laryngeal mask airway (LMATM) for ventilation and anaesthesia administration in children during fibreoptic bronchoscopy using an adult bronchoscope.Methods:  The technique was used in 10 children; their age ranged between 1.2 and 5 years. Six of these children had a history of foreign body aspiration and underwent interventional bronchoscopy, while four children underwent diagnostic bronchoscopy. Anaesthesia was induced by facemask using sevoflurane 6–8% followed by the insertion of a LMA size 2 or 2.5. A swivel adapter connected the proximal end of the LMA to the T‐piece anaesthesia system. Anaesthesia was then maintained with spontaneous breathing of sevoflurane 2–4% in oxygen, delivered via the LMA. A flexible adult fibreoptic bronchoscope (outer diameter 4.9 mm) was inserted via the swivel adapter.Results:  The procedure could be accomplished successfully in the 10 patients. However, one child developed laryngospasm that was easily relieved by deepening the level of anaesthesia. In a second child hypoxia and hypercarbia occurred and were relieved by intermittent withdrawal of the fibreoptic bronchoscope.Conclusions:  Laryngeal mask airway is a safe and effective adjunct to fibreoptic bronchoscopy under general anaesthesia in children. Its larger internal diameter compared with a tracheal tube permits the use of relatively large fibreoptic bronchoscope without a significant increase in airway resistance.
Significance of large‐scale sand injectites as long‐term fluid conduits: evidence from seismic data
Authors: Hurst A. , Cartwright J. , Huuse M. , Jonk R. , Schwab A. , Duranti D. , Cronin B. 
Published: October 2003

AbstractSand injectites and related features that are interpreted to have formed by large‐scale, often sudden, fluid escape in the shallow (typically <500 m) crust are readily imaged on modern seismic data. Many of the features have geometrical similarity to igneous dykes and sills and cross‐cut the depositional stratigraphy. Sand injectites may be multiphase and form connected, high‐permeability networks that transect kilometre‐scale intervals of otherwise fine‐grained, low‐permeability strata. North Sea examples often form significant hydrocarbon reservoirs and typically contain degraded, low‐gravity crude oil. Fluid inclusion and stable isotope data from cements in sand injectites record a mixing of aqueous fluids of deep and shallow origin.
Lithology and fluid prediction from amplitude versus offset (AVO) seismic data
Authors: Davies D. J. , Mcinalley A. , Barclay F. 
Published: October 2003

AbstractSeismic reflection data as used in the oil industry is acquired and processed as multitrace data with source‐receiver offsets from a few hundred metres (short offset) to several kilometres (long offset). This set of data is referred to as ‘pre‐stack’. The traces are processed by velocity analysis, migration and stacking to yield a data volume of traces with ‘zero‐offset’. The signal‐to‐noise enhancement resulting from this approach is very significant. However, reflection amplitude changes in the pre‐stack domain may also be analysed to yield enhanced rock physics parameter estimates. Pre‐stack seismic data is widely used to predict lithology, reservoir quality and fluid distribution in exploration and production studies. Amplitude versus offset (AVO) data, especially anomalous signals, have been used for decades as indicators of hydrocarbon saturation and favourable reservoir development. Recently, enhanced quantification of these types of measurement, using seismic inversion techniques in the pre‐stack domain, have significantly enhanced the utility of such measurements. Using these techniques, for example, probability of the occurrence of hydrocarbons throughout the seismic data can be estimated, and as a consequence the many pre‐stack volumes acquired in a three‐dimensional (3D) can be survey, reduced to a single, more interpretable volume. The possibilities of 4D time lapse observation extend the measurements to changes in fluid content (and pressure) with time, and with obvious benefits in establishing the accuracy of dynamic reservoir models and improvements in field development planning. As an illustration, recent results from the Nelson Field (UK North Sea), are presented where we show the method by which probability volumes for oil sands may be calculated. The oil–sand probability volumes for three 3D seismic datasets acquired in 1990, 1997 and 2000 are compared and production effects in these data are demonstrated.
Seismic evidence for fluid migration pathways from an overpressured system in the South China Sea
Authors: Xie X. , Li S. , He H. , Liu X. 
Published: October 2003

AbstractOverpressured systems and intense, anomalously hot fluid expulsion in the Yinggehai Basin of the South China Sea offer an opportunity to understand the history of fluid flow and the process of hydrocarbon accumulation in overpressured environments. Fluid migration pathways from overpressured compartments in the basin are largely controlled by the distribution of faults and fractures. Episodic opening of these faults are related to the dynamics of an overpressured system and tectonic movements during basin evolution. At the crests of diapiric structures, fluid expulsion is seismically imaged as chimney‐ or plume‐like features, low to middle seismic amplitudes, and intermittently chaotic and blank reflecting seismic facies. These fluid pathways are controlled by vertical faults, which commonly penetrate overpressured and overlying normally pressured zones. Fluid expulsion is also observed near the main faults, such as the No. 1 Fault at the north‐eastern margin of the basin. Investigation by sidescan sonar on onshore and offshore Hainan Island indicates that there are more than 100 gas seepages adjacent to the No. 1 Fault. Migration pathways in the diapiric structures are controlled by three types of fault and fracture. Penetrative faults formed by dextral strike‐slip movement of the Red River faults commonly occur in the centre of the diapirs, and may have been a triggering factor for the diapirism, and controlled their distribution. Hydrofractures occur in certain mud‐rich layers and may have been generated by hydraulic fracturing. Radial normal faults occur at the top of diapirs and were formed by the intrusive process. These fluid migration pathways played an important role in regional hydrocarbon accumulation.
Coupling gene chip analyses and rat genetic variances in identifying potential target genes that may contribute to neuropathic allodynia development
Authors: Valder Carolina R. , Liu Jan‐Jan , Song Yan‐Hua , Luo Z. David 
Published: October 2003

AbstractGenetic factors and nerve injury‐induced changes of gene expression in sensory neurons are potential contributors to tactile allodynia, a neuropathic pain state manifested as hypersensitivity to innocuous mechanical stimulation. To uncover genes relevant to neuropathic allodynia, we analyzed gene expression profiles in dorsal root ganglia (DRG) of spinal nerve‐ligated Harlan and Holtzman Sprague Dawley rats, strains with different susceptibilities to neuropathic allodynia. Using Affymetrix gene chips, we identified genes showing differential basal‐level expression in these strains without injury‐induced regulation. Of more than 8000 genes analyzed, less than 180 genes in each strain were regulated after injury, and 19–22% of that was regulated in a strain‐specific manner. Importantly, we identified functionally related genes that were co‐regulated post injury in one or both strains. In situ hybridization and real‐time PCR analyses of a subset of identified genes confirmed the patterns of the microarray data, and the former also demonstrated that injury‐induced changes occurred, not only in neurons, but also in non‐neuronal cells. Together, our studies provide a global view of injury plasticity in DRG of these rat stains and support a plasticity‐based mechanism mediating variations in allodynia susceptibility, thus providing a source for further characterization of neuropathic pain‐relevant genes and potential pathways.
Marked disparity between age‐related changes in dopamine and other presynaptic dopaminergic markers in human striatum
Authors: Haycock John W. , Becker Laurence , Ang Lee , Furukawa Yoshiaki , Hornykiewicz Oleh , Kish Stephen J. 
Published: October 2003

AbstractBecause age‐related changes in brain dopaminergic innervation are assumed to influence human disorders involving dopamine (DA), we measured the levels of several presynpatic DAergic markers [DA, homovanillic acid, tyrosine hydroxylase (TH), aromatic l‐amino acid decarboxylase (AADC), vesicular monoamine transporter 2 (VMAT2), and dopamine transporter (DAT)] in post‐mortem human striatum (caudate and putamen) from 56 neurologically normal subjects aged 1 day to 103 years. Striatal DA levels exhibited pronounced (2‐ to 3‐fold) post‐natal increases through adolescence and then decreases during aging. Similarly, TH and AADC increased almost 100% during the first 2 post‐natal years; however, the levels of TH and, to a lesser extent, AADC then declined to adult levels by approximately 30 years of age. Although VMAT2 and DAT levels closely paralleled those of TH, resulting in relatively constant TH to transporter ratios during development and aging, a modest but significant decline (13%) in DAT levels was observed in only caudate during aging. This biphasic post‐natal pattern of the presynaptic markers suggests that striatal DAergic innervation/neuropil appears to continue to develop well past birth but appears to become overelaborated and undergo regressive remodeling during adolescence. However, during adulthood, a striking discrepancy was observed between the loss of DA and the relative preservation of proteins involved in its biosynthesis and compartmentation. This suggests that declines in DA‐related function during adulthood and senescence may be explained by losses in DA per se as opposed to DAergic neuropil.
Amyloid β‐protein (Aβ)1–40 protects neurons from damage induced by Aβ1–42 in culture and in rat brain
Authors: Zou Kun , Kim Daesung , Kakio Atsuko , Byun Kyunghee , Gong Jian‐Sheng , Kim Jaewoo , Kim Myeungju , Sawamura Naoya , Nishimoto Sei‐ichi , Matsuzaki Katsumi , Lee Bonghee , Yanagisawa Katsuhiko , Michikawa Makoto 
Published: October 2003

AbstractPreviously, we found that amyloid β‐protein (Aβ)1–42 exhibits neurotoxicity, while Aβ1–40 serves as an antioxidant molecule by quenching metal ions and inhibiting metal‐mediated oxygen radical generation. Here, we show another neuroprotective action of nonamyloidogenic Aβ1–40 against Aβ1–42‐induced neurotoxicity in culture and in vivo. Neuronal death was induced by Aβ1–42 at concentrations higher than 2 μm, which was prevented by concurrent treatment with Aβ1–40 in a dose‐dependent manner. However, metal chelators did not prevent Aβ1–42‐induced neuronal death. Circular dichroism spectroscopy showed that Aβ1–40 inhibited the β‐sheet transformation of Aβ1–42. Thioflavin‐T assay and electron microscopy analysis revealed that Aβ1–40 inhibited the fibril formation of Aβ1–42. In contrast, Aβ1–16, Aβ25–35, and Aβ40–1 did not inhibit the fibril formation of Aβ1–42 nor prevent Aβ1–42‐induced neuronal death. Aβ1–42 injection into the rat entorhinal cortex (EC) caused the hyperphosphorylation of tau on both sides of EC and hippocampus and increased the number of glial fibrillary acidic protein (GFAP)‐positive astrocytes in the ipsilateral EC, which were prevented by the concurrent injection of Aβ1–40. These results indicate that Aβ1–40 protects neurons from Aβ1–42‐induced neuronal damage in vitro and in vivo, not by sequestrating metals, but by inhibiting the β‐sheet transformation and fibril formation of Aβ1–42. Our data suggest a mechanism by which elevated Aβ1–42/Aβ1–40 ratio accelerates the development of Alzheimer's disease (AD) in familial AD.
A novel ubiquitin‐specific protease, synUSP, is localized at the post‐synaptic density and post‐synaptic lipid raft
Authors: Tian Qing Bao , Okano Akira , Nakayama Kohzo , Miyazawa Shoko , Endo Shogo , Suzuki Tatsuo 
Published: October 2003

AbstractRecent reports suggest an important role for protein ubiquitination in synaptic plasticity. We cloned, from the rat brain, a novel gene that encoded an ubiquitin‐specific protease (USP), and termed this protein synaptic ubiquitin‐specific protease (synUSP, GenBankTM Accession no. AB073880). The homologous human gene was mapped to a locus on chromosome 1p36.12. The deduced synUSP protein consisted of 1036 amino acids, and possessed an ubiquitin‐like domain at the C‐terminus, Cys‐ and His‐boxes, leucine zipper motifs, and six amino acid‐repeats of L/ILCPHG. The protein possessed de‐ubiquitinating activity toward a model substrate, as expected from its sequence. The protein of 125 kDa was present in the rat brain; in particular, it was enriched in the post‐synaptic density and the dendritic lipid raft fractions. The immunostaining of cortical neurons confirmed the post‐synaptic localization. The mRNA for synUSP was localized to dendrites, as well as somas, of neuronal cells. Thus, both the mRNA and the protein were localized in the post‐synaptic compartments. These results suggest a regulatory mechanism for the ubiquitin‐related system at the post‐synaptic sites.
Induction by β‐bungarotoxin of apoptosis in cultured hippocampal neurons is mediated by Ca2+‐dependent formation of reactive oxygen species
Authors: Shakhman Olena , Herkert Matthias , Rose Christine , Humeny Andreas , Becker Cord‐Michael 
Published: October 2003

AbstractThe component of the venom of the Taiwanese banded krait Bungarus multicinctus, β‐bungarotoxin (β‐BuTx), acts as an extremely potent inducer of neuronal apoptosis when applied to rat hippocampal cultures. While induction of cell death is dependent on toxin binding to voltage‐activated K+ channels and subsequent internalization, the pro‐apoptotic signals triggered by picomolar concentrations of β‐BuTx are not understood. Following toxin binding, a dramatic increase in intracellular Ca2+ became detectable after 30 min, and in reactive oxygen species (ROS) after 3–4 h. Conversely, Ca2+ chelators, radical quenchers and antioxidants efficiently antagonized β‐BuTx induced apoptosis. As shown for the antioxidant 2,3‐dihydroxybenzoic acid, analysis by matrix assisted laser desorbtion‐time of flight (MALDI–TOF) mass spectrometry excluded the protective effects to be due to reductive cleavage of the toxic β‐BuTx dimer. Inhibitors of the intracellular antioxidant defence system enhanced neuronal susceptibility to β‐BuTx, supporting the essential role of ROS in β‐BuTx‐initiated apoptosis. Cell damage was accompanied by an accumulation of markers of oxidative cell stress, phospholipid hydroxyperoxides and the lipid peroxidation product, malonyl dialdehyde. These observations indicate that β‐BuTx‐induced cell death resulted from an intracellular signalling cascade involving subsequent stages of a dramatic rise in free Ca2+, the accumulation of ROS, membrane lipid peroxidation and, finally, apoptosis.
Co‐ordinated expression of 5‐HT2C receptors with the NCX1 Na+/Ca2+ exchanger in histaminergic neurones
Authors: Sergeeva O. A. , Amberger B. T. , Eriksson K. S. , Scherer A. , Haas H. L. 
Published: October 2003

AbstractThe different roles of Na+/Ca2+ (NCX) exchangers and Na+/Ca2+/K+ (NCKX) exchangers in regulation of the ionic homeostasis in neurones are poorly understood. We have previously shown that serotonin excites histaminergic tuberomamillary (TM) neurones by activation of 5‐HT2C‐receptors and Na+/Ca2+ exchange. With the help of single‐cell RT–PCR (sc‐RT–PCR) we have now determined the coexpression pattern of different subtypes of NCX and NCKX with serotonin receptors. The majority of TM neurones express NCX1, NCX2 and NCKX3. Serotonin 2C receptor–mRNA was detected in 70% while 5‐HT2A mRNA was found in only 10% of TM neurones. In all neurones expressing the 5‐HT2C receptor NCX1–mRNA was present. Double immunostaining revealed the presence of the NCX1 protein in histidine decarboxylase‐positive neurones. In the majority of TM neurones one or two out of five isoforms, NCX1.4, NCX1.5, NCX1.7, NCX1.14, NCX1.15, were detected by cDNA sequencing and/or by restriction analysis. The alternative splicing region is important for the Ca2+ sensitivity and presumably for the modulation of NCX1 function by second messengers. We conclude that several exchanger‐subtypes can be coexpressed in single neurones and that TM cells are heterogeneous with respect to their calcium homeostasis regulation.
Potent activation of dopamine D3/D2 heterodimers by the antiparkinsonian agents, S32504, pramipexole and ropinirole
Authors: Maggio Roberto , Scarselli Marco , Novi Francesca , Millan Mark J. , Corsini Giovanni U. 
Published: October 2003

AbstractRecombinant, human dopamine D3 and D2 receptors form functional heterodimers upon co‐expression in COS‐7 cells. Herein, actions of the antiparkinsonian agents, S32504, ropinirole and pramipexole, at D3/D2L heterodimers were compared to their effects at the respective monomers and at split, chimeric D3trunk/D2tail and D2trunk/D3tail receptors: the trunk incorporated transmembrane domains (TDs) I–V and the tail TDs VI and VII. In binding assays with the antagonist [3H]nemonapride, all agonists were potent ligands of D3 receptors showing, respectively, 100‐, 18‐ and 56‐fold lower affinity at D2L receptors, mimicking the selective D3 receptor antagonist, S33084 (100‐fold). At D3trunk/D2tail receptors, except for ropinirole, all drugs showed lower affinities than at D3 sites, whereas for D2trunk/D3tail receptors, affinities of all drugs were higher than at D2L sites. The proportion of high affinity binding sites recognized by S32504, pramipexole and ropinirole in membranes derived from cells co‐expressing D3 and D2L sites was higher than in an equivalent mixture of membranes from cells expressing D3 or D2L sites, consistent with the promotion of heterodimer formation. In contrast, the percentage of high and low affinity sites (biphasic isotherms) recognized by S33084 was identical. Functional actions were determined by co‐transfection of a chimeric adenylyl cyclase (AC)‐V/VI insensitive to D3 receptors. Accordingly, D3 receptor‐transfected cells were irresponsive whereas, in D2L receptor‐transfected cells, agonists suppressed forskolin‐stimulated cAMP production with modest potencies. In cells co‐transfected with D3 and D2L receptors, S32504, ropinirole and pramipexole potently suppressed AC‐V/VI with EC50s 33‐, 19‐ and 11‐fold lower than at D2L receptors, respectively. S32504 also suppressed AC‐V/VI activity at split D3trunk/D2tail and D2trunk/D3tail chimeras transfected into COS‐7 cells. In conclusion, antiparkinson agents behave as potent agonists at D3/D2‘heterodimers’, though any role in their actions in vivo remains to be demonstrated.
The first and third intracellular loops together with the carboxy terminal tail of the δ‐opioid receptor contribute toward functional interaction with Gα16
Authors: Chan Anthony S. L. , Law Ping Y. , Loh Horace H. , Ho Peter N. N. , Wu Wai‐Man , Chan Joy S. C. , Wong Yung H. 
Published: October 2003

AbstractOpioid peptides exert their regulatory effects on both central and pheripheral nervous systems via multiple opioid receptors that are linked to seemingly identical sets of guanine nucleotide‐binding regulatory proteins (G proteins). In contrast to the μ‐opioid receptor, the δ‐opioid receptor can efficiently stimulate phospholipase C via G16. We used a series of μ/δ‐opioid receptor chimeras to examine the involvement of intracellular receptor domains in the recognition of G16. After ascertaining that the chimeras can bind opioid ligands with high affinity and elicit inhibition of adenylyl cyclase, COS‐7 cells were cotransfected with cDNAs encoding Gα16 and a μ/δ‐opioid receptor chimera and assayed for [d‐Ala2,d‐Leu5]enkephalin‐induced stimulation of phospholipase C. Our results indicate that (i) the carboxy terminal tail of the δ‐opioid receptor is necessary but insufficient for conferring coupling to Gα16, (ii) the third inner loop together with the carboxy terminal tail of the δ‐opioid receptor can provide sufficient contact domains for Gα16, and (iii) the first inner loop of the δ‐opioid receptor, in particular Leu80, as well as the fifth transmembrane domain and/or the third extracellular loop may also contribute in defining the fidelity of interaction between the δ‐opioid receptor and Gα16. These results indicate that efficient coupling of the δ‐opioid receptor to Gα16 requires the participation of most of the intracellular regions, including the first intracellular loop.
In through the out door: nuclear localization of the regulators of G protein signaling
Authors: Burchett Scott A. 
Published: October 2003

AbstractThe regulators of G protein signaling (RGS) are an extraordinary class of diverse multifunctional signaling proteins best known for their potent capacity to down‐regulate the activity of Gα subunits at the plasma membrane. In certain circumstances, some RGS proteins undergo translocation to the nucleus or plasma membrane from the cytoplasm. Translocation demonstrates a potentially dynamic alternative mechanism for Gα subunit or effector regulation. The nuclear localization of the regulators of G protein signaling proteins further suggests these proteins possess even greater functional heterogeneity than that envisioned previously, as regulators of transcription and cell cycle control.
Acetylcholinesterase level and molecular isoforms are altered in brain of Reelin Orleans mutant mice
Authors: Salud García‐Ayllón M. , Seguí Dolores , Perales Mercedes , López‐Hurtado Edith , Prieto Jorge J. , Sáez‐Valero Javier 
Published: October 2003

AbstractIn this study we examined changes in acetylcholinesterase (AChE) pattern in the brain of adult Reelin Orleans (RelnOrl) homozygous mutant mice. The AChE histochemistry firstly revealed an abnormal distribution of AChE‐positive cells in several areas of the reeler brain, including cortices; the strongest labelling was observed in cerebellum and hippocampus when compared with controls. Biochemical determinations demonstrated an increase of 80–90% in AChE specific activity from cerebellar and hippocampal extracts. We also report that the AChE tetrameric form (G4) was selectively increased in the RelnOrl brain. The relationship between AChE and Reelin and suggested morphogenetic functions are also discussed.