bluuebunny/crossref_metadata_2025_split huggingface dataset:
National road casualties and economic development
Authors: Bishai David , Quresh Asma , James Prashant , Ghaffar Abdul 
Published: September 2005

AbstractObjective: This paper explores why traffic fatalities increase with GDP per capita in lower income countries and decrease with GDP per capita in wealthy countries.Methods: Data from 41 countries for the period 1992–1996 were obtained on road transport crashes, injuries, and fatalities as well as numbers of vehicles, kilometers of roadway, oil consumption, population, and GDP. Fixed effects regression was used to control for unobservable heterogeneity among countries.Results: A 10% increase in GDP in a lower income country (GDP/Capita <1600) is expected to raise the number of crashes by 7.9%, the number of traffic injuries by 4.7%, and the number of deaths by 3.1% through a mechanism that is independent of population size, vehicle counts, oil use, and roadway availability. Increases in GDP in richer countries appear to reduce the number of traffic deaths, but do not reduce the number of crashes or injuries, all else equal. Greater petrol use and alcohol use are related to more traffic fatalities in rich countries, all else equal.Conclusion: In lower income countries a rise in traffic‐related crashes, injuries, and deaths accompanies economic growth. At a threshold of around $1500–$8000 per capita economic growth no longer leads to additional traffic deaths, although crashes and traffic injuries continue to increase with growth. The negative association between GDP and traffic deaths in rich countries may be mediated by lower injury severity and post‐injury ambulance transport and medical care. Copyright © 2005 John Wiley & Sons, Ltd.
Efficient allocation of resources to prevent HIV infection among injection drug users: the Prevention Point Philadelphia (PPP) needle exchange program
Authors: Harris Zoë K. 
Published: September 2005

AbstractThe objective of this study is to determine the allocation of resources within a multi‐site needle exchange program (NEP) that achieves the largest possible reduction in new HIV infections at minimum cost. We present a model that relates the number of injection drug user (IDU) clients and the number of syringes exchanged per client to both the costs of the NEP and the expected reduction in HIV infections per unit time. We show that cost‐effective allocation within a multi‐site NEP requires that sites be located where the density of IDUs is highest, and that the number of syringes exchanged per client be equal across sites. We apply these optimal allocation rules to a specific multi‐site needle exchange program, Prevention Point Philadelphia (PPP). This NEP, we find, needs to add 2 or 3 new sites in neighborhoods with the highest density of IDU AIDS cases, and to increase its total IDU client base by about 28%, from approximately 6400 to 8200 IDU clients. The case‐study NEP also needs to increase its hours of operation at two existing sites, where the number of needles distributed per client is currently sub‐optimal, by 50%. At the optimal allocation, the estimated cost per case of HIV averted would be $2800 (range $2300–$4200). Such a favorable cost‐effectiveness ratio derives primarily from PPP's low marginal costs per distributed needle. Copyright © 2005 John Wiley & Sons, Ltd.
Theta rhythm of navigation: Link between path integration and landmark navigation, episodic and semantic memory
Authors: Buzsáki György 
Published: September 2005

AbstractFive key topics have been reverberating in hippocampal‐entorhinal cortex (EC) research over the past five decades: episodic and semantic memory, path integration (“dead reckoning”) and landmark (“map”) navigation, and theta oscillation. We suggest that the systematic relations between single cell discharge and the activity of neuronal ensembles reflected in local field theta oscillations provide a useful insight into the relationship among these terms. In rats trained to run in direction‐guided (1‐dimensional) tasks, hippocampal cell assemblies discharge sequentially, with different assemblies active on opposite runs, i.e., place cells are unidirectional. Such tasks do not require map representation and are formally identical with learning sequentially occurring items in an episode. Hebbian plasticity, acting within the temporal window of the theta cycle, converts the travel distances into synaptic strengths between the sequentially activated and unidirectionally connected assemblies. In contrast, place representations by hippocampal neurons in 2‐dimensional environments are typically omnidirectional, characteristic of a map. Generation of a map requires exploration, essentially a dead reckoning behavior. We suggest that omnidirectional navigation through the same places (junctions) during exploration gives rise to omnidirectional place cells and, consequently, maps free of temporal context. Analogously, multiple crossings of common junction(s) of episodes convert the common junction(s) into context‐free or semantic memory. Theta oscillation can hence be conceived as the navigation rhythm through both physical and mnemonic space, facilitating the formation of maps and episodic/semantic memories. © 2005 Wiley‐Liss, Inc.
Activation of peroxisome proliferator‐activated receptor‐γ by troglitazone (TGZ) inhibits human lung cell growth
Authors: Li Mingyue , Lee Tak W. , Mok Tony S.K. , Warner Timothy D. , Yim Anthony P.C. , Chen George G. 
Published: September 2005

AbstractPeroxisome proliferator‐activated receptor‐gamma (PPAR‐γ) is a member of the nuclear hormone receptor superfamily of ligand‐activated transcription factors and a crucial regulator of cellular differentiation. PPAR‐γ ligands have been demonstrated to inhibit growth of several cancer cells. In this study, two human lung cancer cells (NCI‐H23 and CRL‐2066) and one human lung normal cell (CRL‐202) were used for the experiments. The results showed that in consistence with the loss of viability, troglitazone (TGZ) induced apoptosis of CRL‐2066 and NCI‐H23 cells but not CCL‐202 cells. TGZ upregulated PPAR‐γ expression in all the three lung cell lines, especially in the cancer cells. In association of the time‐dependent inhibition of the cell proliferation, TGZ downregulated the expression of Bcl‐w and Bcl‐2 but activated extracellular signal‐regulated kinase (ERK)1/2 and p38, suggesting that the growth‐inhibitory effect of TGZ is associated with the reduction of Bcl‐w and Bcl‐2 and the increase of ERK1/2 and p38 activation. SAPK/JNK activation assay showed a decreased activity in all the three cell lines tested after TGZ treatment. It was also demonstrated that TGZ could activate PPAR‐γ transcriptionally. We conclude that TGZ inhibits growth of human lung cancer cells via the induction of apoptosis and the inhibition of cell growth, at least in part, in a PPAR‐γ‐relevant manner. The mechanism of TGZ is associated with the activation of ERK and p38, the reduction of SAPK/JNK activity, and the alteration of Bcl‐w and Bcl‐2. © 2005 Wiley‐Liss, Inc.
Mitochondrial mechanism of oxidative stress and systemic hypertension in hyperhomocysteinemia
Authors: Tyagi Neetu , Moshal Karni S. , Ovechkin Alexander V. , Rodriguez Walter , Steed Mesia , Henderson Brooke , Roberts Andrew M. , Joshua Irving G. , Tyagi Suresh C. 
Published: September 2005

AbstractFormation of homocysteine (Hcy) is the constitutive process of gene methylation. Hcy is primarily synthesized by de‐methylation of methionine, in which s‐adenosyl‐methionine (SAM) is converted to s‐adenosyl‐homocysteine (SAH) by methyltransferase (MT). SAH is then hydrolyzed to Hcy and adenosine by SAH‐hydrolase (SAHH). The accumulation of Hcy leads to increased cellular oxidative stress in which mitochondrial thioredoxin, and peroxiredoxin are decreased and NADH oxidase activity is increased. In this process, Ca2+‐dependent mitochondrial nitric oxide synthase (mtNOS) and calpain are induced which lead to cytoskeletal de‐arrangement and cellular remodeling. This process generates peroxinitrite and nitrotyrosine in contractile proteins which causes vascular dysfunction. Chronic exposure to Hcy instigates endothelial and vascular dysfunction and increases vascular resistance causing systemic hypertension. To compensate, the heart increases its load which creates adverse cardiac remodeling in which the elastin/collagen ratio is reduced, causing cardiac stiffness and diastolic heart failure in hyperhomocysteinemia. J. Cell. Biochem. © 2005 Wiley‐Liss, Inc.
Regulation of GTP cyclohydrolase I gene transcription by basic region leucine zipper transcription factors
Authors: Sarraj Jude Al , Vinson Charles , Han Jiahuai , Thiel Gerald 
Published: September 2005

AbstractTetrahydrobiopterin is an essential cofactor for the phenylalanine, tyrosine and tryptophan hydroxylases, and the family of nitric oxide synthases. The initial and rate‐limiting enzyme in the biosynthesis of tetrahydrobiopterin is GTP cyclohydrolase I. The proximal promoter of the human GTP cyclohydrolase I gene contains the sequence motif 5′‐TGACGCGA‐3′, resembling a cAMP response element (CRE). The objective of this study was to analyze the regulation of GTP cyclohydrolase I gene transcription by basic region leucine zipper (bZIP) transcription factors. A constitutively active mutant of the cAMP response element binding (CREB) protein strongly stimulated GTP cyclohydrolase I promoter activity, indicating that the CRE in the context of the GTP cyclohydrolase I gene is functional. Likewise, GTP cyclohydrolase I promoter/luciferase gene transcription was stimulated following nuclear expression of the catalytic subunit of cAMP‐dependent protein kinase. Constitutively active mutants of activating transcription factor 2 (ATF2) and c‐Jun additionally stimulated GTP cyclohydrolase I promoter activity, but to a lesser extent than the constitutively active CREB mutant. The fact that stress‐activated protein kinases target the GTP cyclohydrolase I gene was corroborated by expression experiments involving p38 and MEKK1 protein kinases. We conclude that signaling pathways involving either the cAMP‐dependent protein kinase or stress‐activated protein kinases converge to the GTP cyclohydrolase I gene. Hence, enzymatic reactions that require tetrahydrobiopterin as cofactor are therefore indirectly controlled by signaling cascades involving the signal‐responsive transcription factors CREB, c‐Jun, and ATF2. J. Cell. Biochem. © 2005 Wiley‐Liss, Inc.
FGF and FGFR signaling in chondrodysplasias and craniosynostosis
Authors: Marie P.J. , Coffin J.D. , Hurley M.M. 
Published: September 2005

AbstractThe first experimental mouse model for FGF2 in bone dysplasia was made serendipitously by overexpression of FGF from a constitutive promoter. The results were not widely accepted, rightfully drew skepticism, and were difficult to publish; because of over 2,000 studies published on FGF‐2 at the time (1993), only a few reported a role of FGF‐2 in bone growth and differentiation. However, mapping of human dwarfisms to mutations of the FGFRs shortly, thereafter, made the case that bone growth and remodeling was a major physiological function for FGF. Subsequent production of numerous transgenic and targeted null mice for several genes in the bone growth and remodeling pathways have marvelously elucidated the role of FGFs and their interactions with other genes. Indeed, studies of the FGF pathway present one of the best success stories for use of experimental genetics in functionally parsing morphogenetic regulatory pathways. What remains largely unresolved is the pleiotropic nature of FGF‐2. How does it accelerate growth in one cell then stimulate apoptosis or retard growth for another cell in the same type of tissue? Some of the answers may come through distinguishing the FGF‐2 protein isoforms, made from alternative translation start sites, these appear to have substantially different functions. Although we have made substantial progress, there is still much to be learned regarding FGF‐2 as a most complex, enigmatic protein. Studies of genetic models in mice and human FGFR mutations have provided strong evidence that FGFRs are important modulators of osteoblast function during membranous bone formation. However, there is some controversy regarding the effects of FGFR signaling in human and murine genetic models. Although significant progress has been made in our understanding of FGFR signaling, several questions remain concerning the signaling pathways involved in osteoblast regulation by activated FGFR. Additionally, little is known about the specific role of FGFR target genes involved in cranial bone formation. These issues need to be addressed in future in in vitro and in vivo approaches to better understand the molecular mechanisms of action of FGFR signaling in osteoblasts that result in anabolic effects in bone formation. J. Cell. Biochem. © 2005 Wiley‐Liss, Inc.
Characterization of putative cis‐regulatory elements that control the transcriptional activity of the human Oct4 promoter
Authors: Yang Heung‐Mo , Do Hyun‐Jin , Oh Jong‐Hyun , Kim Jin‐Hoi , Choi Sang‐Yun , Cha Kwang‐Yul , Chung Hyung‐Min , Kim Jae‐Hwan 
Published: September 2005

AbstractOctamer‐binding transcription factor‐4 (Oct4), a member of the POU domain transcription factors, is crucial for both early embryonic development and the maintenance of stem cell pluripotency. The human Oct4 (hOct4) 5′ upstream sequence contains four conserved regions (CR1, 2, 3, 4) that are homologous in the murine. In this study, we constructed a series of deletion mutants of the hOct4 5′ upstream region and identified cis‐regulatory elements that may be important determinants for the transcriptional activity of the hOct4 promoter. Our studies showed that CR2, 3, and 4 each acted as positive cis‐regulatory elements in hOct4 promoter activity. We also newly identified a putative negative cis‐acting element located between CR1 and CR2. In addition, the sequence −380/−1 at CR1 that contains a GC box was sufficient to provide the minimal promoter activity. Site‐directed mutagenesis and electrophoretic mobility shift assays revealed the GC box located in the −380/−1 region may play a critical role in controlling the transcriptional activity of hOct4 by the direct binding of Sp1 or Sp3 transcription factors to the GC box. An overexpression study showed that Sp1 and Sp3 positively and negatively regulate hOct4 promoter activity. Thus, the hOct4 promoter upstream region contains multiple regulatory elements, one of which, the GC box, may be an important cis‐regulatory element that regulates the transcription of the hOct4 promoter by the binding of Sp family transcription factors. © 2005 Wiley‐Liss, Inc.
On the heating of inductively coupled resonators (stents) during MRI examinations
Authors: Busch Martin , Vollmann Wolfgang , Bertsch Thomas , Wetzler Rainer , Bornstedt Axel , Schnackenburg Bernhard , Schnorr Jörg , Kivelitz Dietmar , Taupitz Matthias , Grönemeyer Dietrich 
Published: September 2005

AbstractStents that have been implanted to preserve the results of vascular dilatation are frequently affected by in‐stent restenosis, which ideally should be followed up by a noninvasive diagnostic modality. Active MRI stents can enable this kind of follow‐up, while normal metallic stents can not. The prototype stents investigated in this study were designed as electric resonating circuits without a direct connection to the MR imager, and function as inductively coupled transmit coils. The model of a long solenoid coil is used to describe the additional power loss caused by such resonators. The theoretically estimated temperature increase is verified by measurements for different resonators and discussed for worst‐case conditions. The RF power absorption of an active resonator is negligible compared to the total power absorbed during MRI. The local temperature increase observed for prototypes embedded in phantoms is in a range that excludes direct tissue damage. However, ruptures in the conducting structure of a resonator can cause hot spots, which may establish a high local temperature. This hazard can be reduced by designing resonators with a low quality (Q) factor or by setting the circuit slightly off resonance; however, this would lower the nominal amplification for which the resonator was designed. Magn Reson Med, 2005. © 2005 Wiley‐Liss, Inc.
A direct Schur–Fourier decomposition for the efficient solution of high‐order Poisson equations on loosely coupled parallel computers
Authors: Trias F. X. , Soria M. , Pérez‐Segarra C. D. , Oliva A. 
Published: September 2005

AbstractIn this paper a parallel direct Schur–Fourier decomposition (DSFD) algorithm for the direct solution of arbitrary order discrete Poisson equations on parallel computers is proposed. It is based on a combination of a Direct Schur method and a Fourier decomposition and allows to solve each Poisson equation almost to machine accuracy using only one communication episode. Thus, it is well suited for loosely coupled parallel computers, that have a high network latency compared with the CPU performance. Several three‐dimensional direct numerical simulations (DNS) of wall‐bounded turbulent incompressible flows have been carried out using the DSFD algorithm. Numerical examples illustrating the robustness and scalability of the method on a PC cluster with a conventional 100 Mbits/s network are also presented. Copyright © 2005 John Wiley & Sons, Ltd.
Effective removal of albumin from serum
Authors: Colantonio David A. , Dunkinson Christy , Bovenkamp Diane E. , Van Eyk Jennifer E. 
Published: September 2005

AbstractThe protein constituents of serum can range from grams to picograms per liter, making it technically difficult to achieve in‐depth proteomic analysis. Removal of highly abundant proteins, such as albumin, coupled to powerful protein separation methods is required for increased sample load, thus facilitating detection and identification of low‐abundant proteins. We report here a chemical‐based extraction method for the effective and specific removal of albumin from serum.
Identification of novel lysosomal matrix proteins by proteome analysis
Authors: Kollmann Katrin , Mutenda Kudzai E. , Balleininger Martina , Eckermann Ellen , von Figura Kurt , Schmidt Bernhard , Lübke Torben 
Published: September 2005

AbstractThe lysosomal matrix is estimated to contain about 50 different proteins. Most of the matrix proteins are acid hydrolases that depend on mannose 6‐phosphate receptors (MPR) for targeting to lysosomes. Here, we describe a comprehensive proteome analysis of MPR‐binding proteins from mouse. Mouse embryonic fibroblasts defective in both MPR (MPR 46‐/– and MPR 300‐/–) are known to secrete the lysosomal matrix proteins. Secretions of these cells were affinity purified using an affinity matrix derivatized with MPR46 and MPR300. In the protein fraction bound to the affinity matrix and eluted with mannose 6‐phosphate, 34 known lysosomal matrix proteins, 4 candidate proteins of the lysosomal matrix and 4 non‐lysosomal contaminants were identified by mass spectrometry after separation by two‐dimensional gel electrophoresis or by multidimensional protein identification technology. For 3 of the candidate proteins, mammalian ependymin‐related protein‐2 (MERP‐2), retinoid‐inducible serine carboxypeptidase (RISC) and the hypothetical 66.3‐kDa protein we could verify that C‐terminally tagged forms bound in an M6P‐dependent manner to an MPR‐affinity matrix and were internalized via MPR‐mediated endocytosis. Hence these 3 proteins are likely to represent hitherto unrecognized lysosomal matrix proteins.
Accelerated iterative strategy for the divergent synthesis of dendritic macromolecules using a combination of living radical polymerization and an irreversible terminator multifunctional initiator
Authors: Percec Virgil , Grigoras Cristian , Bera Tushar K. , Barboiu Bogdan , Bissel Philippe 
Published: September 2005

AbstractOur laboratory has reported the elaboration of an iterative strategy for the synthesis of dendritic macromolecules from conventional monomers. This synthetic method involves a combination of self‐regulated metal‐catalyzed living radical polymerization initiated from arenesulfonyl chlorides and an irreversible terminator multifunctional initiator (TERMINI). The previous TERMINI, (1,1‐dimethylethyl)[[1‐[3,5‐bis(S‐phenyl‐4‐N,N′ diethylthiocarbamate)phenyl]ethenyl]oxy]dimethylsilane, was prepared in nine reaction steps. The replacement of the previous TERMINI with one that requires only three steps for its synthesis, diethylthiocarbamic acid S‐{3‐[1‐(tert‐butyl‐dimethyl‐silanyloxy)‐vinyl]‐5‐diethylcarbamoylsulfanyl‐phenyl} ester, and the use of the more reactive Cu2S/2,2′‐bipyridine rather than the Cu2O/2,2′‐bipyridine self‐regulated catalyst have generated an accelerated method for the synthesis of dendritic macromolecules. This method provides rational design strategies for the synthesis of dendritic macromolecules with different compaction by the use of a single monomer. © 2005 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 43: 4894–4906, 2005
Miscible blend dynamics and the length scale of local compositions
Authors: García Sakai Victoria , Maranas Janna K. , Chowdhuri Zema , Peral Inmaculada , Copley John R. D. 
Published: September 2005

AbstractWe consider the influence of a local, or effective, composition on dynamics in the miscible polymer blend PEO/PMMA. Quasielastic neutron scattering in combination with deuterium labeling is employed to determine characteristic relaxation times of the PEO component over spatial scales from 3 to 10 Å. Information about the distribution of relaxation times is obtained indirectly from the stretching parameters in a stretched exponential fit. We examine the behavior of these parameters with spatial scale and temperature, finding that their variation supports a distribution of PEO mobility in the blend which is far wider than pure PEO and narrows with decreasing temperature for small spatial scales. This is linked to the concept of local compositions defined over varying spatial scales, and indicates that the concept of a local composition, linked to PEO dynamics, is important in this system. © 2005 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 43: 2914–2923, 2005
Plastic deformation of MoSi2 single crystals along 〈110〉
Authors: Dietzsch Christian , Bartsch Martin , Messerschmidt Ulrich 
Published: September 2005

AbstractMoSi2 single crystals were deformed along the soft 〈110〉 compression axis between room temperature and 1050 °C. The strain rate sensitivity of the flow stress was determined by stress relaxation tests. The temperature dependence of the flow stress shows three temperature ranges, a low and a high‐temperature range with a normal decrease of the flow stress with increasing temperature and an intermediate range with an anomalous flow stress increase. In the latter range, the strain rate sensitivity decreases (inversely) with increasing strain rate. The dislocation structures of the deformed samples were imaged in diffraction contrast in a high‐voltage electron microscope. In contrast to the low and high‐temperature ranges, the dislocations are straight and oriented along 〈111〉 directions in the anomaly range. The results are interpreted by a large athermal stress component, the action of the Peierls mechanism in the low temperature range, a new dissociation model of the dislocations requiring conservative climb in the dislocation core in the anomaly range, and recovery‐controlled deformation in the high‐temperature range. (© 2005 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)