bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Race Towards Transparency: An Experimental Investigation
Authors: Rossi Marco 
Published: December 2003

To understand the current tendency toward transparency, we studied the effects of accounting disclosure in a laboratory. In our experiment, transparency in the financial accounts of the listed companies improved information efficiency; but, even after checking for fundamentals, the transparency increased the volatility of market prices. Moreover, transparency improved investors’ utility, so that their preference for more certain assets emerged. Therefore, we argue that the current race toward transparency may be better explained by firms’ and markets’ intention to attract household investments rather than to improve market efficiency.(J.E.L.: G92, D44, D81, G12, G28).
Increasing Dependency Ratios, Pensions and Tax Smoothing
Authors: Sadka Efraim , Tanzi Vito 
Published: December 2003

The implication of increasing dependency ratios for pay–as–you–go, defined–benefit pension programmes are examined. Modifications aimed at smoothing contributions while maintaining benefits intact are analysed for both open and closed economies.(J.E.L.: H2, F3, J1).
Pricing Loans Using Default Probabilities
Authors: Turnbull Stuart M. 
Published: December 2003

This paper examines the pricing of loans using the term structure of the probability of default over the life of the loan. We describe two methodologies for pricing loans. The first methodology uses the term structure of credit spreads to price a loan, after adjusting for the difference in recovery rates between bonds and loans. In loan origination, it is common practice to estimate the probability of default for a loan over a specified time horizon and the loss given default. The second methodology shows how to incorporate this information into the arbitrage free pricing of a loan. We also show how to derive an estimate of the credit spread due to liquidity risk. For both methodologies, we show how to calculate a break–even credit spread, taking into account the fee structure of a loan and the costs associated with the term structure of marginal economic capital. The break–even spread is the minimum spread for the loan to be EVA neutral in a multi–period setting.(J.E.L.: G12, G33).
Macroeconomic News and the Euro/Dollar Exchange Rate
Authors: Galati Gabriele , Ho Corrinne 
Published: December 2003

This paper investigates to what extent daily movements in the euro/dollar rate were driven by news about the macroeconomic situation in the USA and the euro area during the first two years of EMU. We examine whether market participants reacted to news in different ways depending on whether the news came from the USA or from the euro area, and whether the news was good or bad. Furthermore, we investigate whether traders’ reaction to news has changed over time. We find that macroeconomic news has a statistically significant correlation with daily movements of the euro against the dollar. However, this relationship exhibits considerable time variation. There are indications of asymmetric response, but to different extents at different times. Our results also provide evidence that the market seemed to ignore good news and remain fixated on bad news from the euro area, as often claimed in market commentaries, but only for some time. Finally, we find evidence that the impact of macroeconomic news on the euro/dollar rate was stronger when news switches from good to bad or vice versa.(J.E.L.: F31).
Formaldehyde-Detoxifying Role of theTetrahydromethanopterin-Linked Pathway in
Methylobacteriumextorquens
AM1
Authors: Marx Christopher J. , Chistoserdova Ludmila , Lidstrom Mary E. 
Published: December 2003

ABSTRACT

The
facultative methylotroph
Methylobacterium extorquens
AM1
possesses two pterin-dependent pathways for C
1
transfer
between formaldehyde and formate, the tetrahydrofolate
(H
4
F)-linked pathway and the tetrahydromethanopterin
(H
4
MPT)-linked pathway. Both pathways are required for
growth on C
1
substrates; however, mutants defective for the
H
4
MPT pathway reveal a unique phenotype of being inhibited
by methanol during growth on multicarbon compounds such as succinate.
It has been previously proposed that this methanol-sensitive phenotype
is due to the inability to effectively detoxify formaldehyde produced
from methanol. Here we present a comparative physiological
characterization of four mutants defective in the H
4
MPT
pathway and place them into three different phenotypic classes that are
concordant with the biochemical roles of the respective enzymes. We
demonstrate that the analogous H
4
F pathway present in
M.
extorquens
AM1 cannot fulfill the formaldehyde detoxification
function, while a heterologously expressed pathway linked to
glutathione and NAD
+
can successfully substitute for
the H
4
MPT pathway. Additionally, null mutants were generated
in genes previously thought to be essential, indicating that the
H
4
MPT pathway is not absolutely required during growth on
multicarbon compounds. These results define the role of the
H
4
MPT pathway as the primary formaldehyde oxidation and
detoxification pathway in
M. extorquens
AM1.
Development ofa Physical and Genetic Map of the VirulentWolbachiaStrainwMelPop
Authors: Sun Ling V. , Riegler Markus , O'Neill Scott L. 
Published: December 2003

ABSTRACTWe report here the construction of a physical and genetic map of the virulentWolbachiastrain,wMelPop. This map was determined by ordering 28 chromosome fragments that resulted from digestion with the restriction endonucleasesFseI,ApaI,SmaI, andAscI and were resolved by pulsed-field gel electrophoresis. Southern hybridization was done with 53Wolbachia-specific genes as probes in order to determine the relative positions of these restriction fragments and use them to serve as markers. Comparison of the resulting map with the whole genome sequence of the closely related benignWolbachiastrain,wMel, shows that the two genomes are largely conserved in gene organization with the exception of a single inversion in the chromosome.
XopC and XopJ, Two Novel Type III Effector Proteinsfrom
Xanthomonas campestris
pv.vesicatoria
Authors: Noël Laurent , Thieme Frank , Gäbler Jana , Büttner Daniela , Bonas Ulla 
Published: December 2003

ABSTRACT

Pathogenicity
of the gram-negative plant pathogen
Xanthomonas campestris
pv.
vesicatoria depends on a type III secretion (TTS) system which
translocates bacterial effector proteins into the plant cell. Previous
transcriptome analysis identified a genome-wide regulon of putative
virulence genes that are coexpressed with the TTS system. In this
study, we characterized two of these genes,
xopC
and
xopJ
. Both genes encode
Xanthomonas
outer proteins
(Xops) that were shown to be secreted by the TTS system. In addition,
type III-dependent translocation of both proteins into the plant cell
was demonstrated using the AvrBs3 effector domain as a reporter. XopJ
belongs to the AvrRxv/YopJ family of effector proteins from plant and
animal pathogenic bacteria. By contrast, XopC does not share
significant homology to proteins in the database. Sequence analysis
revealed that the
xopC
locus contains several features that
are reminiscent of pathogenicity islands. Interestingly, the
xopC
region is flanked by 62-bp inverted repeats that are also
associated with members of the
Xanthomonas avrBs3
effector
family. Besides
xopC
, a second gene of the locus, designated
hpaJ
, was shown to be coexpressed with the TTS system.
hpaJ
encodes a protein with similarity to transglycosylases
and to the
Pseudomonas syringae
pv. maculicola protein
HopPmaG. HpaJ secretion and translocation by the
X. campestris
pv. vesicatoria TTS system was not detectable, which is consistent with
its predicted Sec signal and a putative function as transglycosylase in
the bacterial
periplasm.
FarRRegulates thefarAB-Encoded Efflux Pump ofNeisseriagonorrhoeaevia an MtrR RegulatoryMechanism
Authors: Lee E.-H. , Rouquette-Loughlin C. , Folster J. P. , Shafer W. M. 
Published: December 2003

ABSTRACTThefarABoperon ofNeisseria gonorrhoeaeencodes an efflux pump which mediates gonococcal resistance to antibacterial fatty acids. It was previously observed that expression of thefarABoperon was positively regulated by MtrR, which is a repressor of themtrCDE-encoded efflux pump system (E.-H. Lee and W. M. Shafer, Mol. Microbiol. 33:839-845, 1999). This regulation was believed to be indirect since MtrR did not bind to thefarABpromoter. In this study, computer analysis of the gonococcal genome sequence database,lacZreporter fusions, and gel mobility shift assays were used to elucidate the regulatory mechanism by which expression of thefarABoperon is modulated by MtrR in gonococci. We identified a regulatory protein belonging to the MarR family of transcriptional repressors and found that it negatively controls expression offarABby directly binding to thefarABpromoter. We designated this regulator FarR to signify its role in regulating thefarABoperon. We found that MtrR binds to thefarRpromoter, thereby repressingfarRexpression. Hence, MtrR regulatesfarABin a positive fashion by modulatingfarRexpression. This MtrR regulatory cascade seems to play an important role in adjusting levels of the FarAB and MtrCDE efflux pumps to prevent their excess expression in gonococci.
Competence-Induced Cells ofStreptococcuspneumoniaeLyse Competence-Deficient Cells of the SameStrain duringCocultivation
Authors: Steinmoen Hilde , Teigen Aina , Håvarstein Leiv Sigve 
Published: December 2003

ABSTRACTSeveral streptococcal species are able to take up naked DNA from the environment and integrate it into their genomes by homologous recombination. This process is called natural transformation. InStreptococcus pneumoniaeand related streptococcal species, competence for natural transformation is induced by a peptide pheromone through a quorum-sensing mechanism. Recently we showed that induction of the competent state initiates lysis and release of DNA from a subfraction of the bacterial population and that the efficiency of this process is influenced by cell density. Here we have further investigated the nature of this cell density-dependent release mechanism. Interestingly, we found that competence-induced pneumococci lysed competence-deficient cells of the same strain during cocultivation and that the efficiency of this heterolysis increased as the ratio of competent to noncompetent cells increased. Furthermore, our results indicate that the lysins made by competent pneumococci are not released into the growth medium. More likely, they are anchored to the surface of the competent cells by choline-binding domains and cause lysis of noncompetent pneumococci through cell-to-cell contact.
Legume Symbiotic Nitrogen Fixation byβ-Proteobacteria Is Widespread inNature
Authors: Chen Wen-Ming , Moulin Lionel , Bontemps Cyril , Vandamme Peter , Béna Gilles , Boivin-Masson Catherine 
Published: December 2003

ABSTRACT

Following
the initial discovery of two legume-nodulating
Burkholderia
strains (L. Moulin, A. Munive, B. Dreyfus, and C.
Boivin-Masson, Nature 411:948-950, 2001), we identified as
nitrogen-fixing legume symbionts at least 50 different strains of
Burkholderia caribensis
and
Ralstonia
taiwanensis
, all belonging to the β-subclass of
proteobacteria, thus extending the phylogenetic diversity of the
rhizobia.
R. taiwanensis
was found to represent
93% of the
Mimosa
isolates in Taiwan, indicating thatβ
-proteobacteria can be the specific symbionts of a legume. The
nod
genes of rhizobial β-proteobacteria
(β-rhizobia) are very similar to those of rhizobia from theα
-subclass (α-rhizobia), strongly supporting the
hypothesis of the unique origin of common
nod
genes. Theβ
-rhizobial
nod
genes are located on a 0.5-Mb plasmid,
together with the
nifH
gene, in
R
.
taiwanensis
and
Burkholderia phymatum
.
Phylogenetic analysis of available
nodA
gene sequences
clustered β-rhizobial sequences in two
nodA
lineages
intertwined with α-rhizobial sequences. On the other hand, theβ
-rhizobia were grouped with free-living nitrogen-fixingβ
-proteobacteria on the basis of the
nifH
phylogenetic
tree. These findings suggest that β-rhizobia evolved from
diazotrophs through multiple lateral
nod
gene
transfers.
TheStreptomyces coelicolorPolynucleotide PhosphorylaseHomologue, and Not the Putative Poly(A) Polymerase, CanPolyadenylateRNA
Authors: Sohlberg Björn , Huang Jianqiang , Cohen Stanley N. 
Published: December 2003

ABSTRACTA protein containing a nucleotidyltransferase motif characteristic of poly(A) polymerases has been proposed to polyadenylate RNA inStreptomyces coelicolor(P. Bralley and G. H. Jones, Mol. Microbiol.40:1155-1164, 2001). We show that this protein lacks poly(A) polymerase activity and is instead a tRNA nucleotidyltransferase that repairs CCA ends of tRNAs. In contrast, aStreptomyces coelicolorpolynucleotide phosphorylase homologue that exhibits polyadenylation activity may account for the poly(A) tails found in this organism.
Differencesin Genetic and Transcriptional Organization of theglpTQOperons betweenHaemophilus influenzaeType b andNontypeableStrains
Authors: Song Xin-Ming , Janson Håkan 
Published: December 2003

ABSTRACTTheglpTQoperon ofHaemophilus influenzaetype b (Hib) and nontypeableH. influenzae(NTHi) strains is highly conserved, except for a 1.4-kbglpTQintergenic region that was found in most Hib strains. The presence of this intergenic region results in divergentglpTQtranscriptional profiles for Hib and NTHi where Hib strains appear to have evolved an alternative promoter forglpQexpression. Based on the intergenic region's low G+C content, we speculate that this DNA fragment was acquired by lateral transfer.
Environmental Fate of Gallium Arsenide Semiconductor Disposal
Authors: Uryu Tsutomu , Yoshinaga Jun , Yanagisawa Yukio 
Published: November 2003

SummaryThis article describes a methodology for the quantitative assessment of the environmental fate of gallium and arsenic from the disposal of mobile phones containing gallium arsenide (GaAs) semiconductors, using data from Japan.The product lifetime of mobile phones is short, and the recycling systems for such phones are currently underdeveloped. As a result, many mobile phones are disposed of via incineration and landfilling. The disposal of GaAs semiconductors could lead to some releases of gallium and arsenic to air and water. The methodology presented here begins with an estimation of the cumulative number of disposed mobile phones, using a logistic curve. Then, thermodynamic simulation and laboratory experiments are carried out to assess how much gallium and arsenic may be released into the environment. Using this method, the cumulative number of mobile phones disposed of in Japan is calculated to be 610 million by 2010. Distribution among air emissions, the leachate, and the insoluble residue (in landfilled incinerator ash) was determined to be 4.20 × 10‐2%, 1.58 × 10‐1%, and 99.8% for gallium, and 2.00 × 10‐1%, 19.5%, and 80.3% for arsenic, respectively. For phones that are disposed of directly in landfills, it is estimated that nearly 100% of the gallium and arsenic exists as the insoluble residue. We suggest that, in the conditions present in Japan, disposal of mobile phones directly into the landfill is preferable to the incineration with subsequent landfill of ash with respect to gallium and arsenic emissions into the environment. The proposed methodology may be adapted for the assessment of the environmental fate of problematic substances from the disposal of similar products.
A novel mechanism of complement-independent clearance of red cells deficient in glycosyl phosphatidylinositol–linked proteins
Authors: Jasinski Marek , Pantazopoulos Panagiotis , Rother Russell P. , van Rooijen Nico , Song Wen-Chao , Molina Hector , Bessler Monica 
Published: December 2003

AbstractParoxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia characterized by the increased sensitivity of red blood cells (RBCs) to complement, leading to intravascular hemolysis and hemoglobinuria. PNH is due to the expansion of a cell clone that has acquired a mutation in the PIGA gene. Mice with targeted Piga gene inactivation genetically mimic the human disease and have phosphatidylinositol glycan class A-negative (PIGA-) RBCs with a reduced half-life in circulation. Although PIGA-RBCs are hypersensitive to complement in vitro, their complement sensitivity in vivo is barely detectable. Here we show that the shortened survival of PIGA- RBCs is independent of complement either by using inhibitory C5 antibodies or by transfusion into C5-, C4-, C3-, or factor B-deficient mice. Splenectomy or high-dose cortisone treatment had no effect on the shorter survival of PIGA- RBCs. However, treatment with liposome-encapsulated clodronate, an agent that depletes macrophages in vivo, normalized the half-life of PIGA- RBCs. This indicates that the shortened survival of PIGA- RBCs is due to a novel pathway of PIGA- RBC clearance that is mediated by macrophages, but occurs independently of complement. Future investigations will show whether this novel pathway of PIGA- RBC destruction identified in mice may also operate in patients with PNH. (Blood. 2004;103:2827-2834)
Correction of hypercoagulability and amelioration of pulmonary arterial hypertension by chronic blood transfusion in an asplenic hemoglobin E/β-thalassemia patient
Authors: Atichartakarn Vichai , Chuncharunee Suporn , Chandanamattha Pakorn , Likittanasombat Khanchit , Aryurachai Katcharin 
Published: December 2003

AbstractChronic transfusion of packed red blood cells, in addition to other ongoing treatment with warfarin, acetyl salicylic acid, desferrioxamine, and other supportive measures, was given to a splenectomized hemoglobin E/β-thalassemia woman with pulmonary arterial hypertension (PHT). Serial measurements of plasma thrombin-antithrombin III complex (TAT) levels and right-sided cardiac catheterization were used to monitor changes after treatment. Reduction of plasma TAT levels from 7.5 to 3.8 μg/L (normal, 3 ± 2.4 μg/L), pulmonary vascular resistance (PVR) from 553.8 to 238.6 dyne.sec.cm-5 (normal, 67 ± 30 dyne.sec.cm-5), and mean pulmonary arterial pressure from 51 to 32 mm Hg (normal, 9 to 19 mm Hg) occurred in tandem. Normalization of blood hypercoagulability as reflected in plasma TAT level by chronic blood transfusion was the likely basis for improvement of increased PVR, being secondary to thrombotic pulmonary arteriopathy and subsequently PHT. (Blood. 2004;103: 2844-2846)
CD200 is a novel p53-target gene involved in apoptosis-associated immune tolerance
Authors: Rosenblum Michael D. , Olasz Edit , Woodliff Jeffery E. , Johnson Bryon D. , Konkol Marja C. , Gerber Kimberly A. , Orentas Rimas J. , Sandford Gordon , Truitt Robert L. 
Published: December 2003

AbstractDuring apoptotic cell death, biochemical processes modify self-proteins and create potential autoantigens. To maintain self-tolerance in the face of natural cell turnover, the immune system must prevent or control responses to apoptosis-associated autoantigens or risk autoimmunity. The molecular mechanisms governing this process remain largely unknown. Here, we show that expression of the immunoregulatory protein CD200 increases as murine dendritic cells (DCs) undergo apoptosis. We define CD200 as a p53-target gene and identify both p53- and caspase-dependent pathways that control CD200 expression during apoptosis. CD200 expression on apoptotic DCs diminishes proinflammatory cytokine production in response to self-antigens in vitro and is required for UVB-mediated tolerance to haptenated self-proteins in vivo. Up-regulation of CD200 may represent a novel mechanism, whereby immune reactivity to apoptosis-associated self-antigens is suppressed under steady state conditions. (Blood. 2004;103: 2691-2698)
Antibody blockade or mutation of the fibrinogen γ-chain C-terminus is more effective in inhibiting murine arterial thrombus formation than complete absence of fibrinogen
Authors: Jiroušková Markéta , Chereshnev Igor , Väänänen Heikki , Degen Jay L. , Coller Barry S. 
Published: December 2003

AbstractAn elevated plasma fibrinogen level is a risk factor for thrombotic cardiovascular disease, but which of fibrinogen's functions is responsible for the increased risk is unknown. To define better the contribution of fibrinogen to large vessel thrombus formation, we studied carotid artery thrombosis in wild-type mice, mice lacking fibrinogen (fbg–/–), mice treated with 7E9 (a blocking antibody to the fibrinogen γ-chain C-terminus), and mice expressing a mutant fibrinogen (γΔ5) that lacks the γ-chain platelet-binding motif QADGV. In control mice, thrombus formation resulted in occlusion in 8 ± 2 minutes (mean ± SD). In fbg–/– mice, thrombi grew to large sizes, but then they abruptly embolized, confirming previous observations by others in an arteriolar thrombus model. In contrast, mice treated with 7E9 and γΔ5 mice developed only small, nonoclusive mural thrombi and embolization was limited. These findings reveal that a fibrinogen antibody, 7E9, or a fibrinogen mutant retaining clotting function, can limit thrombus formation more effectively than the complete absence of fibrinogen. We hypothesize that the smaller thrombi in these animals result from the ability of fibrin to bind and sequester thrombin and/or the ability of the altered fibrinogen molecules, which cannot recruit platelets, to bind to and passivate the surface.
GW654652, the pan-inhibitor of VEGF receptors, blocks the growth and migration of multiple myeloma cells in the bone marrow microenvironment
Authors: Podar Klaus , Catley Laurence P. , Tai Yu-Tzu , Shringarpure Reshma , Carvalho Pedro , Hayashi Toshiaki , Burger Renate , Schlossman Robert L. , Richardson Paul G. , Pandite Lini N. , Kumar Rakesh , Hideshima Teru , Chauhan Dharminder , Anderson Kenneth C. 
Published: December 2003

AbstractPrevious studies have shown that the multiple myeloma (MM) cell line and MM patient cells express high-affinity vascular endothelial growth factor (VEGF) receptor-1 or Fms-like tyrosine kinase-1 (Flt-1) but not VEGF receptor-2 or Flk-1/kinase insert domain-containing receptor (Flk-1/KDR) and that VEGF triggers MM cell proliferation through a mitogen-activated protein kinase (MAPK)-dependent pathway and migration through a protein kinase C (PKC)-dependent pathway. The present study evaluates the efficacy of the small molecule tyrosine-kinase inhibitor GW654652, which inhibits all 3 VEGF receptors with similar potency. We show that GW654652 acts directly on MM cells and in the bone marrow microenvironment. Specifically, GW654652 (1-10 μg/mL) inhibits, in a dose-dependent fashion, VEGF-triggered migrational activity and cell proliferation of MM cell lines that are sensitive and resistant to conventional therapy. As expected from our previous studies of VEGF-induced signaling and sequelae in MM cells, GW654652 blocked VEGF-induced Flt-1 phosphorylation and downstream activation of AKT-1 and MAPK-signaling cascades. Importantly, GW654652 also inhibits interleukin-6 and VEGF secretion and proliferation of MM cells induced by tumor cell binding to bone marrow (BM) stromal cells. The activity of a pan-VEGF receptor inhibitor against MM cells in the BM milieu, coupled with its lack of major toxicity in preclinical mouse models, provides the framework for clinical trials of this drug class to improve patient outcome in MM. (Blood. 2004;103:3474-3479)