bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quantitative analysis of the expression of glycosylphosphatidylinositol‐anchored proteins during the maturation of different hematopoietic cell compartments of normal bone marrow
Authors: Hernández‐Campo Pilar María , Almeida Julia , Matarraz Sergio , de Santiago María , Sánchez María Luz , Orfao Alberto 
Published: October 2006

AbstractBackground:Glycosylphosphatidylinositol‐anchored proteins (GPI‐AP) are a heterogeneous group of proteins deficiently expressed in patients with paroxysmal nocturnal hemoglobinuria. Up till now, no study has been reported in which the exact patterns of expression of a large number of GPI‐AP are quantitatively evaluated in normal bone marrow (BM) cells classified according to their lineage and maturation stage.Methods:In the present study, we have quantitatively analyzed the expression of eleven different GPI‐AP (CD14, CD16, CD24, CD48, CD52, CD58, CD59, CD66b, CD87, CD109 and CD157) during maturation of the neutrophil, monocytic, erythroid, lymphoid, basophil and plasmacytoid dendritic cells (DC) lineages in normal BM as a frame of reference for the understanding of the abnormal patterns of expression of GPI‐AP observed in the BM of PNH patients.Results:Our results show that expression of most GPI‐AP varies during normal BM maturation, different profiles being frequently observed depending on the cell lineage or the GPI‐AP analyzed.Conclusion:Overall, these results provide a detailed map GPI‐AP expression during normal hematopoietic differentiation, which could serve as a basis for the identification and characterization of changes occurring in PNH. © 2006 International Society for Analytical Cytology
Power flow congestion relief by using customer‐side energy storage systems
Authors: Furusawa Ken , Sugihara Hideharu , Tsuji Kiichiro , Mitani Yasunori 
Published: October 2006

AbstractIn recent years, energy storage systems have increasingly been expected as a means of load leveling of the annual load factor. Of course there is an effect of installing the energy storage systems at the substation. But some customers operate their storage system in an integrated way and it also has an effect of increasing the load factor. In this paper the authors proposed that the energy storage systems on the customer side be used for congestion relief on transmission networks. However, it is not clear which kind of customer has the effect of relieving transmission line congestion. First, this paper assumes the authors determine the optimal configuration of energy equipment including energy storage systems. We propose a new contract whereby electric utility subsidizes a part of the entrance cost of the energy storage systems and customers change the output pattern of energy storage according to the request of the electric utility. This paper evaluates the possibility that the contract gives merit to both the electric utility and the customer. © 2006 Wiley Periodicals, Inc. Electr Eng Jpn, 158(1): 36–45, 2007; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/eej.20299
Cobalt and Nickel Complexes Bearing Pyrazolyliminophosphorane Ligands: Synthesis, Characterisation and Catalytic Ethylene Oligomerisation Behaviour
Authors: Zhang Cheng , Sun Wen‐Hua , Wang Zhong‐Xia 
Published: October 2006

AbstractTreatment of 1‐(2′‐azidophenyl)‐3,5‐dimethylpyrazole (1) with Ph2PR (R = Ph, Me) and (Ph2P)2CH2, respectively, affords the pyrazolyliminophosphoranes 2, 3 and 4. Reaction of 2 or 3 with [NiCl2(dme)] or NiBr2 yields the N,N‐chelate nickel complexes 5–8, and with CoCl2 complexes 9 and 10. Reaction of 4 with [NiCl2(dme)], NiBr2 and CoCl2, respectively, affords the N,N,P‐chelate complexes 11–13. Compounds 2–4 were characterised by 1H, 13C, 31P NMR and IR spectroscopy and elemental analysis, while complexes 5–13 were characterised by IR spectroscopy and elemental analysis. The structures of complexes 5, 9 and 12 were further characterised by single‐crystal X‐ray diffraction techniques. Complexes 5–13 are active catalysts for ethylene oligomerisation upon activation with alkylaluminium derivatives(Et2AlCl, MAO or MMAO). These complexes exhibit good to high catalytic activities (up to 3.54 × 106 g mol–1 h atm for the nickel complexes and 5.48 × 105 g mol–1 h atm for the cobalt complexes). The effects of varying ethylene pressure, temperature and aluminium co‐catalyst/Ni or Co ratios with complexes 5, 9, 11 and 12 are reported. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
The hydrology of northern peatlands as affected by biogenic gas: current developments and research needs
Authors: Rosenberry Donald O. , Glaser Paul H. , Siegel Donald I. 
Published: October 2006

AbstractRecent research indicates that accumulation and release of biogenic gas from northern peatlands may substantially affect future climate. Sudden release of free‐phase gas bubbles into the atmosphere may preclude the conversion of methane to carbon dioxide in the uppermost oxic layer of the peat, resulting in greater contribution of methane to the atmosphere than is currently estimated. The hydrology of these peatlands also affects and is affected by this process, especially when gas is released suddenly and episodically. Indirect hydrological evidence indicates that ebullitive gas releases are relatively frequent in some peatlands and time‐averaged rates may be significantly greater than diffusive releases. Estimates of free‐phase gas contained in peat have ranged from 0 to nearly 20% of the peat volume. Abrupt changes in the volume of gas may alter hydraulic gradients and movement of water and solutes in peat, which in turn could alter composition and fluxes of the gas. Peat surfaces also move vertically and horizontally in response to accumulation and release of free‐phase gas. Future research should address the distribution, temporal variability, and relative significance of ebullition in peatlands and the consequent hydrological responses to these gas‐emission events. Copyright © 2006 John Wiley & Sons, Ltd.
Promutagen activation with mammalian and avian S9 liver microsomes
Authors: Tometsko Andrew M. , Sheridan Kathleen M. , DeTraglia Michael C. 
Published: October 2006

AbstractMetabolic activation activity of Aroclor 1254 induced rat liver microsomes (S9) were compared with uninduced microsomes obtained from beef, pig, sheep and chicken liver. Using the Ames Salmonella typhimurium mutagenesis assay (strains TA98 and TA100), in conjunction with benzo(a)pyrene and 2‐aminoanthracene, the highest promutagen activation levels were obtained with chicken liver S9. The S9 from the other domestic animals gave results which were close to those of the induced rat S9 values. Enhanced promutagen activation activity was observed with chicken S9 following freeze drying and reconstitution of the S9 preparation.
Deposition and clearance of inhaled diesel exhaust particles in the respiratory tract of fischer rats
Authors: Chan T. L. , Lee P. S. , Hering W. E. 
Published: October 2006

AbstractThe fate of inhaled diesel particles was determined in male Fischer 344 rats using radioactive tracers of 131Ba and 14C. Test animals were exposed in a ‘nose‐only’ inhalation chamber for 40–45 min to diluted diesel exhaust generated from diesel engines burning type 2D diesel fuel containing either 131Ba labelled barium dodecylbenzene sulfonate or 14C labelled n‐hexadecane. Immediately after exposure, the deposition efficiency of inhaled diesel particles in the respiratory tract was determined to be 15 ± 6% by external gamma counting of 131Ba and 17 ± 2% by liquid scintillation counting of 14C in the lung tissue samples. Elimination of the particles was observed by measuring the 131Ba activity in which 40% of the initial deposition was excreted in the feces via the GI tract in 4 days. The long‐term retention was determined with the 14C tag in the insoluble ‘core’ of the diesel particles. Two distinct phases of clearance were evident in the experimental data collected up to 105 days. Clearance half‐times of 1 day and 62 days were found for mucociliary and alveolar clearance, respectively. A small fraction of the particles, about 6% of the initial deposition, was found in the mediastinal lymph nodes after 28 days. This demonstrated that the lymphatic system was also involved in the removal of diesel particles from the pulmonary airways.
Aryl hydrocarbon hydroxylase activity induced by injected diesel particulate extract vs inhalation of diluted diesel exhaust
Authors: Chent K‐C. , Vostal J. J. 
Published: October 2006

AbstractThe effects of long‐term inhalation of diluted diesel exhaust on aryl hydrocarbon hydroxylase activity (AHH) and cytochrome P‐450 content in lung and liver microsomes were investigated in male Fischer‐344 rats and compared with repeated parenteral administration of organic solvent extracts of hydrocarbons adsorbed on the diesel particulate surface during the combustion process. The animals were exposed to concentrations of 750 μg m−3 or 1500 μg m−3 of diesel particulates from a 5.7L GM diesel engine 20 h per day, 5 1/2 days per week for up to 9 months or treated by repeated IP injections of diesel particulate extract (dissolved in corn oil) from the same engine at several dose levels for 4 days. No significant effects of long‐term inhalation exposure were observed in liver microsomal AHH activity. A slight decrease in lung microsomal AHH activity was found in rats following 6 months of exposure to diesel exhaust at the particulate concentration of 1500 μg m−3. The total mass of particles deposited in the lung during the inhalation exposure was estimated and an equivalent dose of extractable hydrocarbons was administered intraperitoneally; no increase in AHH activity was observed in the lung or liver microsomes. In contrast, 1.4‐to 9‐fold increases in AHH activity were observed in liver and lung microsomes of rats pretreated by intraperitoneal doses 10‐50 times larger than the most conservative estimate of the deposited lung burden. No changes in cytochrome P‐450 content were observed in the microsomes of rat liver after inhalation or injection treatment studies. The data indicate that hydrocarbons adsorbed on inhaled diesel particles are not effective as enzyme inducers primarily due to their absence in quantities necessary for enzyme induction which is further potentiated by the lack of their availability for distribution in the body.
Effect of diesel particulate exposure on adenylate and guanylate cyclase of rat and guinea pig liver and lung
Authors: Schneider David R. , Felt Barbara T. 
Published: October 2006

AbstractAn examination of the effects of 250 or 1500 μg m−3 concentrations of diesel particulate from diesel exhaust on the activity of adenylate or guanylate cyclase was undertaken using liver and lung tissue of rats and guinea pigs. These membrane and cytosolic enzymes were selected to screen for functional or regulatory alterations in these tissues. The studies for adenylate cyclase used the microsomal membrane fraction of each tissue; for guanylate cyclase, the microsomal membrane and supernate fractions were used. Basal and fluoride‐stimulated adenylate cyclase activity were measured. Basal and sodium azide‐stimulated guanylate cyclase activity were also determined. The basal activity of rat liver adenylate cyclase is generally unchanged throughout 52 weeks of diesel exposure. Stimulated adenylate cyclase shows an age‐related decrease for all animal treatments throughout the study. Changes in enzyme activity occurred at 12 weeks and 52 weeks after 1500 μg m−3 exposure. Soluble stimulated guinea pig lung guanylate cyclase was first increased (6 weeks) and then decreased (24 weeks) by diesel exposure. At 52 weeks, there was no change. The data suggest the following trends: (1) an increased basal adenylate cyclase in the rat lung; (2) an age‐related decrease in adenylate cyclase activity in rat liver, and (3) a biphasic exposure‐related response of soluble guanylate cyclase for the guinea pig lung during the first 24 weeks, but no change at 52 weeks. In general, however, these studies suggest that diesel exposure does not substantially alter either of these intracellular regulating enzymes.
A rapid in vitro assay for carcinogenicity of chemical substances in mammalian cells utilizing an attachment‐independence endpoint 2 – assay validation
Authors: Traul Karl A. , Takayama K. , Kachevsky V. , Hink R. J. , Wolff J. S. 
Published: October 2006

AbstractIn vitro carcinogenesis assays, in mammalian cells, are proving to be a necessary part of batteries of in vitro tests for detecting potential mutagens/carcinogens. The selection of which particular test to use requires an evaluation of test reliability, repeatability, sensitivity and degree of validation. Validation is particularly important because it is an integral part of the other criteria. Attachment independence is a common characteristic of transformed cells and is often used in follow‐up testing to confirm transformation. In an earlier report we described a transformation assay, the Survival Assay, which measures the acquisition of attachment independence. The Rauscher leukemia virus‐infected rat embryo target cells are treated with test compound for 72 h. Cells are then transferred to petri dishes containing a bottom layer of agar/medium. After 6 days the viable cell numbers of treated and control cultures are compared. We report here the results of testing 77 additional compounds in this assay; 73 of these were tested under code. Since definitive Carcinogenicity data were not available for 18 of the test compounds, it is not possible to list specific correlations with in vivo test results. None the less the assay correctly identified 44 of the 49 carcinogens and 7 of the 10 noncarcinogens in the list. The noncarcinogen status of two of the latter is, however, open to question. Thus the Survival Assay appears to provide information rapidly as to the potential carcinogenicity of a test material, even when subjected to validation testing with coded compounds.
Identification of 2‐Nitrofluorene in diesel exhaust particulates
Authors: Xu X. B. , Nachtman J. P. , Rappaport S. M. , Wei E. T. , Lewis S. , Burlingame A. L. 
Published: October 2006

AbstractDiesel exhaust particulates contain mutagens which are direct‐acting in the Ames test. A dichloromethane extract of these particulates was separated by liquid chromatography and analyzed by high resolution gas chromatography/high resolution mass spectrometry (HRGC/HRMS). 2‐Nitrofluorene, a known carcinogen and direct mutagen, was positively identified by comaxima of ion fragments and retention time on the gas chromatograph.
The inhibitory action of dithiocarbamates and carbon disulphide on malondialdehyde formation resulting from lipid peroxidation in rat liver microsomes
Authors: Freundt K. J. , Römer K. G. , Kamal A. M. 
Published: October 2006

AbstractThe dithiocarbamates (DTCs) disulfiram, thiram, diethyldithiocarbamate and dimethyldithiocarbamate on the equimolar base inhibited to the same extent both the lipid peroxidation (LPO) induced by ascorbic acid (non‐enzymatic) and that stimulated by an NADPH‐regenerating system with CCl4 admixture (enzymatic). Lipid peroxidation measurements were made in terms of malondialdehyde (MDA) formation in rat liver microsomes, or in the 9000 × g supernatant. The inhibitory action of tetramethylthiuram monosulphide was considerably weaker. Carbon disulphide (CS2) inhibited the enzymatic and non‐enzymatic stimulated microsomal LPO by 4 orders less than the DTCs. In parallel with the inhibition of MDA formation, oxidative destruction of microsomal cytochrome P‐450 was delayed with increasing concentrations of the DTCs. A well‐correlated, non‐linear, semi‐logarithmic relation was found for the concentration‐activity relationship for all DTCs and CS2. As the DTCs inhibited LPO both in heat‐denatured and freshly prepared microsomes, it can be deduced that the DTCs intervene in a non‐enzymatic oxidation phase of the LPO. The DTC inhibitory action is attributed to a radical‐trap mechanism since LPO that has already been initiated was inhibited with the DTCs. However, more inhibitor is required to trap the radicals the later the DTC administration takes place.
The acute toxicity and teratogenicity of cadmium in the pregnant rat
Authors: Samarawickrama G. P. , Webb M. 
Published: October 2006

AbstractUntil the 16th day of gestation the intravenous LD50 of Cd2+ in the pregnant Wistar‐Porton rat is higher, but not significantly different from that (1.8 mg Cd2+ per kg body weight) in nulliparous females. At 20 days it is 1.1 mg Cd2+ kg per body weight. This decrease is related to the rapid increase in weight of the conceptuses in late gestation and to the retention of most of the dose in the maternal compartment. If the dose is based on body weight at conception, the LD50for the 20‐day pregnant rat (1.6 mg Cd2+ per kg body weight) and non‐gravid female do not differ significantly. Nevertheless, after the same Cd2+ dose, hepatic and renal Cd2+ concentrations are less in the pregnant than in the non‐pregnant animal. The Cd2+ concentrations, therefore, do not determine the liver and kidney damage, which is restricted to the pregnant rat. Placentae also accumulate Cd2+ and placental haemorrhage follows the injection of the appropriate Cd2+ LD50 on day 12–20 of gestation. In those animals that die between 16 and 30 h after dosing, haemorrhage and death appear to be correlated. Renal damage, therefore, probably results from haemorrhagic shock. It is not dependent on the transfer of protein‐bound Cd2+ from the necrotic placentae to the kidney. Between the 8th and 15th day of gestation, Cd2+ (1.25 mg per kg body weight) is highly teratogenic. Hydrocephalus is the most frequent abnormality when the dose is given between the 8th and 12th day. Other malformations include eye defects, gastroschiasis and umbilical hernia.
Limitations on the uptake of mercury vapour by human erythrocytes in a closed exposure system
Authors: Halbach Stefan 
Published: October 2006

AbstractPrevious in vitro studies using the exposure of suspensions of normal human erythrocytes to mercury vapour (Hg°) in Warburg vessels revealed a broad variation of the cellular Hg uptake in the presence of hydrogen peroxide and furnished evidence for an oxidation of Hg° by the catalase‐H2O2 pathway. This report describes the uptake of Hg° in the same exposure system as it depends on haematocrit, H2O2 supplementation and exposure time. The results indicate that the uptake of vapour by the whole suspensions was virtually independent of haematocrit and of the H2O2 supplementation at high rates of H2O2 infusion, whereas at low rates it was directly proportional to the amount of peroxide added. Since the retention of mercury by the medium is negligible, the haemoglobin‐related (specific) uptake is inversely proportional to the haematocrit at high rates of H2O2 infusion. These results are consistent with the conclusion that the incorporation of Hg° by erythrocytes is controlled by two processes: transfer of vapour to the cells and enzymic oxidation. The net rate of uptake is limited by the oxidizing capacity at low, and by the vapour transfer at high H2O2 supplementation. As a practical consequence of these findings the spread of the specific uptakes reported in the literature is considerably reduced if the values observed when transfer becomes rate limiting are related to the haematocrit.
Bendiocarb poisoning in birds and a dog
Authors: Humphreys D. J. , Stodulski J. B. J. 
Published: October 2006

AbstractAn incident involving the poisoning of sparrows, blackbirds and a dog in the garden of a block of flats in London is described. An aluminium foil tray and bread recovered from the garden were shown to contain the carbamate insecticide bendiocarb. The gastrointestinal tract contents of the birds contained a cholinesterase‐inhibiting material which behaved in the same manner as bendiocarb on thin layer chromatography. The clinical signs shown by the dog and the presence of bendiocarb in the bread it consumed are consistent with it having died as a result of bendiocarb poisoning. The use of concentrated preparations containing this material for the illegal killing of urban birds has not been described previously. The source of the preparation used, which is not freely available to the public, was not established.
Actions of avermectin B1a on the γ‐aminobutyric AcidA receptor and chloride channels in rat brain
Authors: Abalis Ibrahim M. , Eldefrawi Amira T. , Eldefrawi Mohyee E. 
Published: October 2006

AbstractThe interaction of avermectin B1a (AVM) with the γ‐aminobutyric acid (GABA) receptor of rat brain was studied using radioactive ligand binding and tracer ion flux assays. Avermectin potentiated the binding of [3H]flunitrazepam and inhibited the binding of both [3H]muscimol and [35S]t‐butylbicyclo‐phosphorothionate to the GABAA receptor. Inhibition of muscimol binding by AVM suggested competitive displacement. Two kinds of 36chloride (Cl) flux were studied. The 36Cl efflux from preloaded microsacs was potentiated by AVM and was highly inhibited by the Cl‐channel blocker 4,4′‐diisothiocyano‐2,2′‐stilbenedisulfonic acid (DIDS). However, it was not potentiated by GABA nor was it sensitive to the convulsants picrotoxin or bicuculline. On the other hand, 36Cl‐influx measurement in a different microsac preparation of rat brain was very sensitive to GABA and other GABA‐ergic drugs. Avermectin induced 36Cl influx into these microsacs in a dose–dependent manner, but to only 35% of the maximal influx induced by GABA. The AVM‐induced 36Cl influx was totally blocked by bicuculline. It is suggested that AVM opens the GABAA‐receptor Cl channel by binding to the GABA recognition site and acting as a partial receptor agonist, and also opens a voltage–dependent Cl channel which is totally insensitive to GABA but is very sensitive to DIDS.
Antagonistic effect of magnesium chloride on the nickel chloride–induced inhibition of DNA replication in chinese hamster ovary cells
Authors: Conway Kathleen , Sen Pramila , Costa Max 
Published: October 2006

AbstractThe degree of inhibition of semiconservative DNA replication induced by nickel chloride (NiCl2) was analyzed by radiolabeled‐thymidine incorporation alone or with cesium chloride (CsCl) density gradient centrifugation. The onset and duration of this Ni2+‐induced inhibition was time‐ and concentration‐ dependent, but the degree of inhibition was not. A maximal reduction in the rate of DNA synthesis was observed within the first hour of treatment with 2.5 mM NiCl2, which was the highest noncytotoxic concentration utilized. After six hours, 500 μM and 1 mM as well as 2.5 mM NiCl2 all produced the same 50% to 60% reduction in [3H]‐thymidine incorporation into DNA. The inhibitory effect of nickel ions on DNA synthesis was reversible. The rate of DNA synthesis following a 500 μM or 1 mM NiCl2 treatment began to increase after washout of nickel, but a six‐hour exposure of cells to 2.5 mM NiCl2 produced a sustained 50% to 60% suppression of DNA synthetic activity for at least 36 hours. At all concentrations of NiCl2 used in this study, some inhibition of DNA synthesis persisted for at least 48 hours, but by 72 hours after treatment, the rate of [3H]‐thymidine incorporation was actually 10% above the control. Examination of autoradiographic slides of cells treated with 2.5 mM NiCl2 for six hours demonstrated a 60% reduction of silver grains, but there was no preferential reduction in the quantity of grains in the nucleolus or any other region. Cesium chloride density gradient analysis of the replication of nucleolar DNA in cells treated with 2.5 mM nickel supported the autoradiographic findings. The inhibitory effect of NiCl2 on DNA replication was prevented by the addition of magnesium chloride (MgCl2) to cells maintained in a simple salts/glucose medium (SGM). This effect did not appear to be due to an antagonism of the cellular uptake of nickel by Mg2+, since the maximally effective dose of Mg2+ reduced 63Ni2+ uptake by no more than 25% while the inhibition of replication was completely reversed.