bluuebunny/crossref_metadata_2025 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

Background:  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

Sand 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

Seismic 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

Overpressured 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

Genetic 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

Because 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

Previously, 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

Recent 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

The 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

The 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

Recombinant, 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

Opioid 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

The 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

In 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.
Antisense peptide nucleic acid‐mediated knockdown of the p75 neurotrophin receptor delays motor neuron disease in mutant SOD1 transgenic mice
Authors: Turner Bradley J. , Cheah Irwin K. , Macfarlane Katherine J. , Lopes Elizabeth C. , Petratos Steven , Langford Steven J. , Cheema Surindar S.
Published: October 2003

Re‐expression of the death‐signalling p75 neurotrophin receptor (p75NTR) is associated with injury and neurodegeneration in the adult nervous system. The induction of p75NTR expression in mature degenerating spinal motor neurons of humans and transgenic mice with amyotrophic lateral sclerosis (ALS) suggests a role of p75NTR in the progression of motor neuron disease (MND). In this study, we designed, synthesized and evaluated novel antisense peptide nucleic acid (PNA) constructs targeting p75NTR as a potential gene knockdown therapeutic strategy for ALS. An 11‐mer antisense PNA directed at the initiation codon, but not downstream gene sequences, dose‐dependently inhibited p75NTR expression and death‐signalling by nerve growth factor (NGF) in Schwann cell cultures. Antisense phosphorothioate oligonucleotide (PS‐ODN) sequences used for comparison failed to confer such inhibitory activity. Systemic intraperitoneal administration of this antisense PNA to mutant superoxide dismutase 1 (SOD1G93A) transgenic mice significantly delayed locomotor impairment and mortality compared with mice injected with nonsense or scrambled PNA sequences. Reductions in p75NTR expression and subsequent caspase‐3 activation in spinal cords were consistent with increased survival in antisense PNA‐treated mice. The uptake of fluorescent‐labelled antisense PNA in the nervous system of transgenic mice was also confirmed. This study suggests that p75NTR may be a promising antisense target in the treatment of ALS.
Caspase cleavage of the amyloid precursor protein modulates amyloid β‐protein toxicity
Authors: Lu Daniel C. , Soriano Salvador , Bredesen Dale E. , Koo Edward H.
Published: October 2003

The amyloid β‐protein precursor (APP) is proteolytically cleaved to generate the amyloid β‐protein (Aβ), the principal constituent of senile plaques found in Alzheimer's disease (AD). In addition, Aβ in its oligomeric and fibrillar forms have been hypothesized to induce neuronal toxicity. We and others have previously shown that APP can be cleaved by caspases at the C‐terminus to generate a potentially cytotoxic peptide termed C31. Furthermore, this cleavage event and caspase activation were increased in the brains of AD, but not control, cases. In this study, we show that in cultured cells, Aβ induces caspase cleavage of APP in the C‐terminus and that the subsequent generation of C31 contributes to the apoptotic cell death associated with Aβ. Interestingly, both Aβ toxicity and C31 pathway are dependent on the presence of APP. Both APP‐dependent Aβ toxicity and C31‐induced apoptotic cell death involve apical or initiator caspases‐8 and ‐9. Our results suggest that Aβ‐mediated toxicity initiates a cascade of events that includes caspase activation and APP cleavage. These findings link C31 generation and its potential cell death activity to Aβ cytotoxicity, the leading mechanism proposed for neuronal death in AD.
Intensive In‐Center Hemodialysis for Children: A Case for Longer Dialysis Duration
Authors: Bell Lorraine , Espinosa Pauline
Published: October 2003

Background:  Children with renal failure need their dialysis time optimized. Although traditional surrogate markers of outcome in pediatric patients have been growth and development, increasing attention is being focused on cardiovascular risk factors, such as hypertension, volume overload, malnutrition, and elevated calcium (Ca) and phosphorus (P) levels. We have previously shown catch‐up growth without growth hormone, in children undergoing long intermittent hemodialysis. Recently we analyzed retrospectively cardiovascular risk factors in patients treated with this regimen.

Methods:  Patients starting dialysis between 1997 and 2001 and on dialysis at least 6 months were evaluated. Charts were reviewed for Ca, P, parathyroid hormone (PTH), albumin, hemoglobin and blood pressure levels, Ca intake, blood pressure medications, dialysis time, and clearance and ultrafiltration rates. Means were calculated for 6‐ month intervals, up to 36 months.

Results:  Mean equilibrated dialyzer Kt/V

urea

ranged from 1.9 to 2.1, and mean weekly dialysis time for oliguric patients varied from 14.8 to 16.3 hr, with average hourly ultrafiltration rates from 0.3 to 0.4 L. Mean values for P and Ca × P were below 1.8 mM and 4.4 mmol 2/L2, respectively. Mean hemoglobin levels were 115 to 126 g/L, albumin 39 to 41 g/L, and PTH 156 to 231 pg/mL. Most patients had normal predialysis blood pressures.

Conclusions:  In this pediatric cohort, intensive center hemodialysis was associated with excellent growth, nutrition, Ca, P, and anemia control and reasonable blood pressure values. Large multicenter studies are needed to better determine optimal dialysis therapy for children.
Hepatitis B Virus Vaccine Response in Hemodialysis: Baseline Patient Characteristics
Authors: Chin Andrew I.
Published: October 2003

Background:  Hepatitis B virus (HBV) vaccination is recommended for all individuals with renal failure. Nevertheless, the response rate for this vaccine in hemodialysis (HD) patients is low, ranging from 50% to 80%. The goal of this study was to determine patient characteristics at the initiation of HD that influence HBV vaccine response.

Methods:  Patients new to HD in an urban population in the United States were retrospectively examined. Analyzed patients were HBV antibody and antigen negative and hepatitis C virus antibody negative at the start of HD, who received HBV recombinant vaccine. Nonresponse was defined as failure to seroconvert (>10 UI/L) after six deltoid intramuscular injections of vaccine. Response was defined as a lasting seroconversion (at least two consecutive positive titers) with ≤6 injections. Demographic, laboratory, and kinetic modeling data were examined.

Results:  A total of 33 nonresponders and 64 responders were identified. Univariate analysis demonstrated that nonresponders were older (59 vs. 51 years), had a higher prevalence of diabetes mellitus (DM) (70 vs. 39%), had lower serum albumin levels (3.2 vs. 3.3 g/dL), and had higher dry weights (84 vs. 71 kg) than responders at HD start. In addition, nonresponders had lower normalized protein catabolic rates (0.74 vs. 0.85 g/kg/day) and lower (single‐pool) spKt/V

urea

values (0.95 vs. 1.19). Nonresponders had lower serum creatinine levels than responders, despite the greater dry weights. In a multiple logistic analysis model, the presence of DM, age ≥ 55 years, body weight ≥80 kg, and normalized protein catabolic rate ≤0.75 g/kg/day were associated with HBV vaccination nonresponse. At the end of the vaccination period, nonresponders versus responders continued to have lower serum albumin (3.5 vs. 3.8 g/dL) and creatinine levels (7.8 vs. 10.0 mg/dL) and spKt/V

urea

(1.27 vs. 1.39).

Conclusion:  Hepatitis B vaccine nonresponders on HD are older, are more likely to have DM, are more malnourished, and have lower spKt/Vurea than responders. Nonresponders may also have a different body composition with a lower ratio of lean to total body mass.
Relation between Access‐Related Infection and Preinfection Serum Albumin Concentration in Patients on Chronic Hemodialysis
Authors: Adeniyi Oladipo A. , Tzamaloukas Antonios H.
Published: October 2003

Background:  Hemodialysis (HD) access‐related infection is a major cause of morbidity and mortality in HD patients. We tested whether hypoalbuminemia is a risk factor for HD access infection and whether mortality of HD catheter infection is affected by removal of the infected catheter.

Methods:  We analyzed the records of 87 patients on chronic HD who were hospitalized for HD access‐related infection. We obtained data on age, sex, preinfection serum albumin level, comorbidities, complications, infecting organism, type of infection, mode of management, and mortality. We compared preinfection serum albumin levels in 79 patients with HD access infection with the serum albumin levels of 198 control patients on chronic HD without HD access infection admitted to the hospital during the same time for other reasons. In the HD catheter infection subgroup, we compared mortalities between patients treated with catheter removal plus antibiotics as the primary mode of management and those treated initially with antibiotics alone.

Results:  Preadmission serum albumin level was lower in the HD access infection group (2.4 ± 0.6 g/dL) than in the control group (3.2 ± 0.6 g/dL, P < 0.0001). Logistic regression identified preadmission serum albumin level as a strong independent predictor of HD access infection. In a logistic regression model, with age, sex, HIV status, diabetes, and type of HD vascular access (excluding arterovenous fistula) as the covariates, the odds ratio of HD access infection was 9.8 (95% confidence interval [CI] 4.9–19.7) for a serum albumin level ≤ 3.0 g/dL (P < 0.0001), 10.4 (95% CI 4.97–21.6) for a serum albumin level ≤ 2.5 g/dL (P < 0.0001), and 28.0 (95% CI 5.8–135.9) for a serum albumin level ≤ 2.0 g/dL (P < 0.0001). Case mortality was 25.0% (4/16) in patients with tunneled HD catheter infection initially treated with antibiotics alone and 2.8% (2/71) in those treated with catheter removal plus antibiotics at the time of presentation (P = 0.0096).

Conclusion:  Hypoalbuminemia is associated with increased risk of HD access infection. Treatment of HD access infection with antibiotics alone is associated with increased risk of death.
Air‐Bubble Method of Locking Central‐Vein Catheters for Prevention of Hub Colonization: A Pilot Study
Authors: Twardowski Zbylut J. , Reams Garry , Prowant Barbara F. , Moore Harold L. , Van Stone John C.
Published: October 2003

Background:  The major source of catheter‐associated bacteremia is contamination of the catheter hub during connection–disconnection procedures. A new method of catheter locking has been developed wherein anticoagulant is injected first, followed by a 0.1‐mL air bubble and 0.9 mL of bactericidal solution. The anticoagulant is then located at the catheter tip and the bactericidal solution is located at the catheter hub. The air bubble prevents mixing of the two solutions. The bactericidal solution was acidified concentrated saline (ACS). The 27% saline solution has a pH of 2.0. ACS was chosen because it is theoretically harmless if injected in the amount used to lock the catheter lumens. The goals of this pilot study were to determine whether the new method of catheter locking is easy to perform with available syringes and whether eventual injection of the experimental solution is well tolerated.

Methods:  Ten patients were randomly assigned, either to heparin lock (5 patients, 62 treatments) or air‐bubble method (5 patients, 56 treatments). In the control group, the catheters were locked with heparin, 5000 U/mL. In the experimental group, the catheters were locked with heparin, air bubble, and ACS. Altogether, the lumens were overfilled by 0.2 mL.

Results:  Compared to the routine method, the experimental method required a 1‐ to 2‐min‐longer procedure time. There were no errors in proper sequence of injections into the lumina. There were no episodes of bacteremia related to hub contamination in either group. In the air‐bubble group, there was one case of bacteremia associated with purulent drainage from the exit and the same organism in both cultures. In three instances in each group, the locking solution could not be aspirated and was injected without any subjective symptoms or objective signs.

Conclusion:  We conclude that the air‐bubble method of locking central‐vein catheters is easy to perform. In three instances of air‐bubble and ACS injection, there were no adverse effects. A full‐scale prospective randomized study is feasible and warranted.
Lipoprotein (a) in Chronic Renal Failure: Effect of Maintenance Hemodialysis
Authors: Kalra Om Prakash , Khaira Ambar , Gambhir Jasvinder Kaur , Agarwal Sunil , Bhargava Satish Kumar
Published: October 2003

Background:  Coronary artery disease accounts for significant morbidity and mortality in patients with chronic kidney disease (CKD). Besides the higher prevalence of traditional risk factors, several uremia‐related factors may play a role in accelerated atherosclerosis, such as elevated levels of lipoprotein (a) (Lp(a)). The effect of maintenance hemodialysis (MHD) on Lp(a) levels is not well understood. The present work was carried out to study the Lp(a) levels in Stage 4 and Stage 5 CKD patients as well as the effect of MHD on Lp(a) levels in patients with Stage 5 CKD.

Methods:  The study subjects included 15 patients with Stage 4 CKD, 15 patients with Stage 5 CKD, and 15 age‐ and sex‐matched healthy controls. Plasma Lp(a) was measured by ELISA in all the subjects at the time of entry into the study and after 4 weeks of MHD in patients with Stage 5 CKD. Patients on MHD were dialyzed two to three times weekly for 4 hr during each session.

Results:  Mean Lp(a) levels were significantly higher in patients with CKD than in control patients. In patients with Stage 4 CKD, the Lp(a) level was 34.0 ± 19.5 mg/dL, whereas in Stage 5 CKD the level was 49.0 ± 30.9 and in healthy controls it was 22.2 ± 16.4. In patients with Stage 5 CKD, 4 weeks of MHD led to a significant fall in Lp(a) levels by 23.6% (P < 0.001).

Conclusions:  The results of this study show that increases in Lp(a) levels start early during the course of CKD and become more pronounced with increased severity of disease. Initiation of MHD lowers Lp(a) levels and may have a long‐term beneficial effect on cardiovascular morbidity and mortality.
Impact of Predialysis Care on Clinical Outcomes
Authors: Yeoh Hock H. , Tiquia Herbert S. , Abcar Antoine C. , Rasgon Scott A. , Idroos Mohamed L. , Daneshvari Sam F.
Published: October 2003

Introduction:  A structured predialysis multidisciplinary team program is beneficial in improving quality of life in patients with end‐stage renal disease (ESRD). Educating pre‐ESRD patients about their disease is vital in their care. Patients who can identify signs and symptoms of impending problems can seek help and avoid complications that may lead to hospital admissions. Our dialysis center offers two predialysis classes in a structured format. The first class is for those patients with mild to moderate renal disease, whereas the second class is for those with advanced renal disease who are expected to need dialysis in 3 to 6 months. The patients are followed by a multidisciplinary team once they are enrolled in our chronic kidney disease program.

Methods:  We retrospectively reviewed all the charts of patients who started dialysis at our center between 1997 and 2000. We identified 68 patients who participated in the predialysis education program and 35 patients who did not because of late referral or refusal to participate. We compared these two groups over a 100‐day period (10 days before initial dialysis and 90 days after), for hospitalizations, emergency room (ER) visits, and dialysis access placement. Patients' comorbid conditions, complications, and length of hospitalizations were extracted from the medical records.

Results:  The 68 patients who completed the predialysis program had an average age of 60.3 years, a total of 96 hospital days, and 39 ER visits. Average length of hospital stay for these patients was 1.4 days. Three patients (4.4%) required placement of temporary catheters for the initial dialysis. Fifty‐one percent of these patients had diabetes mellitus. The 35 patients of average age of 54.9 years who did not go through the program had 347 total hospital days and 39 ER visits. Average length of hospitalization was 9.9 days. Thirteen patients (37%) required temporary catheters for initial dialysis. This group included 16 patients (45.7%) with diabetes.

Conclusion:  Patients who participated in a multidisciplinary predialysis education program had fewer complications, ER visits, and hospitalizations. They also had fewer temporary catheter placements, shorter hospital stays, and reduced costs associated with initial dialysis.
Evolution of Home Hemodialysis Monitoring Systems
Authors: Diaz‐Buxo Jose A. , Schlaeper Christian , VanValkenburgh Denise
Published: October 2003

Systems for monitoring hemodialysis patients at home have evolved during the past 30 years. They consist of hardware and software to record dialysis events from the home hemodialysis machine and transmit them to a server, which in turn sends the data to a remote central monitoring center. Most of the parameters monitored are related to machine function and events. At present, the only commonly monitored patient vital functions are pulse and blood pressure. The early systems used direct telephone lines and modem for telecommunication. The use of Internet links reduces the cost of the service and provides fast and safe transmission of the data. The actual value of these monitoring systems, the need for additional monitoring options, indications for specific groups of patients dialyzing at home, and acceptance by patients, physicians, and regulators will require further evaluation.
Helicobacter‐induced Gastritis in Mice Not Expressing Metallothionein‐I and II*
Authors: Tran Cuong D. , Huynh Hien , Van Den Berg Maartje , Van Der Pas Mechtelt , Campbell M. A. Fiona , Philcox Jeffrey C. , Coyle Peter , Rofe Allau M. , Butler Ross N.
Published: October 2003

Background.  Helicobacter pylori a primary cause of gastritis and peptic ulcer disease, is associated with increased production of reactive oxygen species within the gastric mucosa. Metallothionein (MT), a low‐molecular‐weight, cysteine‐rich, metal‐binding ligand, has been shown to sequester reactive oxygen species and reduce tissue damage. This study investigates the role of MT in H. pylori‐induced gastritis in mice.

Materials and Methods.  Control (MT+/+) and MT‐null (MT–/–) mice were inoculated with either 1 × 108H. pylori or H. felis, and were infected for 4, 8 and 16 weeks or 8 weeks, respectively. H. pylori load was determined by culture. Myloperoxidase activity and MT levels were also determined.

Results.  The stomachs of H. felis‐infected mice were more severely inflamed than those of H. pylori‐infected mice. H. felis‐induced gastritis was more severe (p = .003) in MT–/– than in MT+/+ mice. MT–/– mice also had higher (60%; p < .05) H. pylori loads than MT+/+ mice 4 weeks after infection but not 8 or 16 weeks after infection. Myloperoxidase activity with H. pylori was similar between MT+/+ and MT–/– mice. Thirty‐three per cent greater (p < .05) myloperoxidase activity was observed in MT–/– than in MT+/+ mice infected with H. felis. In MT+/+ mice infected with H. pylori, liver MT was increased by 33 and 39% (p < .05) at 8 and 16 weeks, respectively, whereas gastric MT increased by 46% (p < .05) at 4 weeks and declined to baseline levels at 8 and 16 weeks.

Conclusions.  Mice lacking MT are more susceptible to H. pylori colonization and gastric inflammation, indicating that MT may be protective against H. pylori‐induced gastritis.
Inhibition of Helicobacter pylori‐induced Nuclear Factor‐kappa B Activation and Interleukin‐8 Gene Expression by Ecabet Sodium in Gastric Epithelial Cells
Authors: Kim Jung Mogg , Kim Joo Sung , Jung Hyun Chae , Oh Yu‐Kyoung , Kim Nayoung , Song In Sung
Published: October 2003

Background.  Helicobacter pylori stimulates nuclear factor‐kappa B (NF‐κB) activation and chemokine interleukin‐8 (IL‐8) expression in gastric epithelial cells. Ecabet sodium (ecabet), a locally acting antiulcer drug, is known to have anti‐H. pylori activity. However, there is little understanding of how ecabet induces anti‐inflammatory activity in gastric epithelial cells infected with H. pylori. The aim of this study was to investigate the effects of ecabet on IL‐8 gene expression and NF‐κB activation in human gastric epithelial cells infected with H. pylori.

Materials and Methods.  After Hs746T, MKN‐45, or SNU‐5 gastric epithelial cell lines had been infected with cagA+cytotoxin+H. pylori in the presence of ecabet, IL‐8 mRNA expression was assessed by quantitative reverse transcription–polymerase chain reaction, and IL‐8 secretion was measured by enzyme‐linked immunosorbent assay. NF‐κB and inhibitory kappa B‐alpha (IκBα) signals were assayed by electrophoretic mobility shift assay and Western blot, respectively. The activation of NF‐κB and IL‐8 reporter genes was determined by luciferase assay.

Results.  Ecabet showed no antimicrobial activiy against Gram‐positive or ‐negative bacteria. However, ecabet inhibited transcription of the IL‐8 gene and secretion of IL‐8 by gastric epithelial cells infected with H. pylori at a concentration of 5 µg/ml. Moreover, ecabet inhibited the activation of NF‐κB and the degradation of IκBα in gastric epithelial cells in response to H. pylori infection. In addition, the NF‐κB signal inhibited by ecabet was comprised predominantly of heterodimers of p65/p50.

Conclusions.  Ecabet inhibited H. pylori‐induced IL‐8 gene transcription and secretion by suppressing the NF‐κB signal. This inhibition might be one pathway by which ecabet exerts its anti‐inflammatory effect on H. pylori‐induced gastric inflammation.
Placental Acquisition of Maternal Specific IgG and Helicobacter pylori Colonization in Infancy
Authors: Bunn James E. G. , Thomas Julian E. , Harding Marilyn , Coward W. Andrew , Weaver Lawrence T.
Published: October 2003

Background.  Colonization with Helicobacter pylori generally occurs in infancy, and the microorganism is often acquired from close family members. Rate of infant colonization may be affected by maternal immune status.

Methods.  To investigate the potential protective effect of anti‐H. pylori immunoglobulin G (IgG) acquired via the placenta, 65 mothers and their infants were studied from the infant's birth for 1 year. Circulating IgG antibodies were measured by enzyme‐linked immunosorbent assay (ELISA) in cord blood and every 8 weeks. Immunoblotting was performed on sera from infants with significant increases in IgG levels. Rate of infant H. pylori colonization was measured by 13C urea breath tests every 4 weeks from the age of 12 weeks.

Results.  Maternal and infant cord blood specific IgG levels were correlated (R2 = .747, p < .001). Infant H. pylori specific IgG fell 5‐fold compared to maternal levels over the first 6 months of life, and rose subsequently in many cases, with the development of novel immunoblot patterns. There were no significant associations between the age at first positive urea breath test and maternal or infant cord specific H. pylori IgG levels.

Conclusions.  Transplacentally acquired specific IgG antibody does not protect infants from colonization by H. pylori.
Design Progress of the Ultracompact Integrated Heart Lung Assist Device—Part 1: Effect of Vaned Diffusers on Gas‐Transfer Performances
Authors: Tsukiya Tomonori , Tatsumi Eisuke , Nishinaka Tomohiro , Katagiri Nobumasa , Takewa Yoshiaki , Ohnishi Hiroyuki , Oshikawa Mitsuo , Shioya Kyoko , Mizuno Toshihide , Taenaka Yoshiyuki , Takano Hisateru , Kitamura Soichiro
Published: October 2003

Abstract: The integrated heart lung assist device (IHLAD) has been developed to overcome the problems of currently available extracorporeal membrane oxygenation devices. The integrated structure of a centrifugal blood pump and cylindrical bundle of polyolefin hollow‐fibers has allowed a remarkably compact size for the device. This study deals with the design change of the IHLAD that added to the vaned diffuser between the impeller of the centrifugal pump and the hollow‐fiber bundle with a view to enhancing the gas‐transfer performance. Ex vivo gas‐transfer performance tests were carried out, as well as hydrodynamic characteristics and hemolysis test using fresh goat blood. The oxygen transfer rate was generally improved, and the carbon dioxide removal rate was slightly improved. Intolerable amount of hemolysis (index of hemolysis= 0.177) was caused by the IHLAD, which must be resolved by improving the design in the future.
Studies of Turbulence Models in a Computational Fluid Dynamics Model of a Blood Pump
Authors: Song Xinwei , Wood Houston G. , Day Steven W. , Olsen Don B.
Published: October 2003

Abstract: Computational fluid dynamics (CFD) is used widely in design of rotary blood pumps. The choice of turbulence model is not obvious and plays an important role on the accuracy of CFD predictions. TASCflow (ANSYS Inc., Canonsburg, PA, U.S.A.) has been used to perform CFD simulations of blood flow in a centrifugal left ventricular assist device; a k‐ɛ model with near‐wall functions was used in the initial numerical calculation. To improve the simulation, local grids with special distribution to ensure the k‐ω model were used. Iterations have been performed to optimize the grid distribution and turbulence modeling and to predict flow performance more accurately comparing to experimental data. A comparison of k‐ω model and experimental measurements of the flow field obtained by particle image velocimetry shows better agreement than k‐ɛ model does, especially in the near‐wall regions.