bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reducing Costs of Censuses in Norway Through Use of Administrative Registers
Authors: Longva Svein , Thomsen Ib , Severeide Paul Inge 
Published: May 2007

SummaryThe purpose and methodology of the Norwegian census has changed considerably during the last 35 years. While the census was previously the main source of socio‐demographic information, it is to day just one of several sources. After an identification number for each individual was introduced and used in various administrative registers, the dominating role of the census has changed dramatically. For some years it has been the policy of Statistics Norway to collaborate with various governmental agencies in order to use administrative registers in statistics production. This policy has been supported politically, and a new Statistics Act has been useful in these efforts. The purpose of this paper is to present the strategy and methodology used to produce statistics in general, census statistics in particular, when based on a combined use of administrative registers and directly collected data. Experiences from Norwegian censuses since 1960 will be presented.
Statistical Thinking in Empirical Enquiry
Authors: Wild C. J. , Pfannkuch M. 
Published: May 2007

SummaryThis paper discusses the thought processes involved in statistical problem solving in the broad sense from problem formulation to conclusions. It draws on the literature and in‐depth interviews with statistics students and practising statisticians aimed at uncovering their statistical reasoning processes. From these interviews, a four‐dimensional framework has been identified for statistical thinking in empirical enquiry. It includes an investigative cycle, an interrogative cycle, types of thinking and dispositions. We have begun to characterise these processes through models that can be used as a basis for thinking tools or frameworks for the enhancement of problem‐solving. Tools of this form would complement the mathematical models used in analysis and address areas of the process of statistical investigation that the mathematical models do not, particularly areas requiring the synthesis of problem‐contextual and statistical understanding. The central element of published definitions of statistical thinking is “variation”. We further discuss the role of variation in the statistical conception of real‐world problems, including the search for causes.
Unraveling the Genetic Component of Multifactorial Diseases: Dream or Reality
Authors: Clerget‐Darpoux F. 
Published: May 2007

SummaryThe etiology of many human diseases is complex and very likely involves a combination of genetic and environmental risk factors. A popular strategy to detect genetic risk factors is to perform a systematic screening of the genome searching for linkage. The power of such and approach depends very much on the unknown characteristics of the genetic factors and the main difficulty is to establish a good trade‐off between false positives and false negatives. Besides, a precise localisation of the risk factor will generally not be obtained. The set up of a candidate gene stratery is necessary to go further in genetic factor identification. It is likely that for multicfactorioal diseases the only genetic risk factors that can be detected are those with fairly strong effect. Even in that case, it is important to design strategies which increase the power of detection and provide for a better evaluation of the associated risks.
Proposals for a Minimum Programme for Statistics in Developing Countries
Authors: Azouvi Alain 
Published: May 2007

SummaryStatistical offices in developing countries are confronted with the challenge of introducing, with limited means, methods and tools ensuring the production of durable statistics satisfying regional, national and international requirements. Taking into account the evolution, over the last years, in the attitude of national authorities, funding partners and statisticians themselves regarding the building up of relevant and durable statistics, the present paper's proposal is to have, in each developing country, a Minimum Programme for Statistics (MPS) and that this programme be centred on four domains: coordination, national accounts, economic and social short term analysis, and dissemination.
ON THE DISTRIBUTION OF DENOMINATORS IN SYLVESTER EXPANSIONS
Authors: WU JUN 
Published: May 2007

For any x ∈ (0, 1], let the series [sum ]∞n=1
1/dn(x) be the Sylvester expansion of x. Galambos has shown that
the Lebesgue measure of the set[formula here]is 1 when α = e, the base of the natural logarithm. This paper provides a proof that for any α [ges ] 1, A(α)
has Hausdorff dimension 1 when α ≠ e.
SMOOTH MORPHISMS OF MODULE SCHEMES
Authors: ZWARA G. 
Published: May 2007

Let $\varphi:A\to B$ be a homomorphism of finite-dimensional algebras over an algebraically closed field and $\varphi^{(c)}:{\rm mod}_B^c\to{\rm mod}_A^c$ the induced morphism of the associated module schemes for any integer $c\geq 1$. We prove that if the induced functor ${\rm mod\,} B\to{\rm mod\,} A$ is hom-controlled then the restriction of $\varphi^{(c)}$ to any connected component of ${\rm mod}_B^c$ is a composition of a smooth morphism followed by an immersion. Some new results on the types of singularities in the orbit closures of module schemes are also proved.2000 Mathematical Subject Classification: 14B05, 14L30, 16G10.
THE MONOID OF FAMILIES OF QUIVER REPRESENTATIONS
Authors: REINEKE MARCUS 
Published: May 2007

A monoid structure on families of representations of a quiver is introduced by taking extensions of representations in families, that is, subvarieties of the varieties of representations. The study of this monoid leads to interesting interactions between representation theory, algebraic geometry and quantum group theory. For example, it produces a wealth of interesting examples of families of quiver representations, which can be analysed by representation-theoretic and geometric methods. Conversely, results from representation theory, in particular A. Schofield's work on general properties of quiver representations, allow us to relate the monoid to certain degenerate forms of quantized enveloping algebras.2000 Mathematical Subject Classification: 16G20, 14L30, 17B37.
CCR5Δ32 Protein Expression and Stability Are Critical for Resistance to Human Immunodeficiency Virus Type 1 In Vivo
Authors: Agrawal Lokesh , Jin Qingwen , Altenburg Jeff , Meyer L. , Tubiana R. , Theodorou Ioannis , Alkhatib Ghalib 
Published: May 2007

ABSTRACTHuman immunodeficiency virus type 1 (HIV-1) infection of individuals carrying the two alleles of the CCR5Δ32 mutation (CCR5−/−) has rarely been reported, but how the virus overcomes theCCR5Δ32protective effect in these cases has not been delineated. We have investigated this in 6 infected (HIV+) and 25 HIV−CCR5−/−individuals. CD4+T lymphocytes isolated from HIV−CCR5−/−peripheral blood mononuclear cells (PBMCs) showed lower levels of CXCR4 expression that correlated with lower X4 Env-mediated fusion. Endogenous CCR5Δ32 protein was detected in all HIV−CCR5−/−PBMC samples (n= 25) but not in four of six unrelated HIV+CCR5−/−PBMC samples. Low levels were detected in another two HIV+CCR5−/−PBMC samples. The expression of adenovirus 5 (Ad5)-encoded CCR5Δ32 protein restored the protective effect in PBMCs from three HIV+CCR5−/−individuals but failed to restore the protective effect in PBMCs isolated from another three HIV+CCR5−/−individuals. In the latter samples, pulse-chase analyses demonstrated the disappearance of endogenous Ad5-encoded CCR5Δ32 protein and the accumulation of Ad5-encoded CCR5 during the chase periods. PBMCs isolated from CCR5−/−individuals showed resistance to primary X4 but were readily infected by a lab-adapted X4 strain. Low levels of Ad5-encoded CCR5Δ32 protein conferred resistance to primary X4 but not to lab-adapted X4 virus. These data provide strong support for the hypothesis that the CCR5Δ32 protein actively confers resistance to HIV-1 in vivo and suggest that the loss or reduction of CCR5Δ32 protein expression may account for HIV-1 infection of CCR5−/−individuals. The results also suggest that other cellular or virally induced factors may be involved in the stability of CCR5Δ32 protein.
The Neutralizing Activity of Anti-Hepatitis C Virus Antibodies Is Modulated by Specific Glycans on the E2 Envelope Protein
Authors: Helle François , Goffard Anne , Morel Virginie , Duverlie Gilles , McKeating Jane , Keck Zhen-Yong , Foung Steven , Penin François , Dubuisson Jean , Voisset Cécile 
Published: May 2007

ABSTRACT
Hepatitis C virus (HCV) envelope glycoproteins are highly glycosylated, with up to 5 and 11 N-linked glycans on E1 and E2, respectively. Most of the glycosylation sites on HCV envelope glycoproteins are conserved, and some of the glycans associated with these proteins have been shown to play an essential role in protein folding and HCV entry. Such a high level of glycosylation suggests that these glycans can limit the immunogenicity of HCV envelope proteins and restrict the binding of some antibodies to their epitopes. Here, we investigated whether these glycans can modulate the neutralizing activity of anti-HCV antibodies. HCV pseudoparticles (HCVpp) bearing wild-type glycoproteins or mutants at individual glycosylation sites were evaluated for their sensitivity to neutralization by antibodies from the sera of infected patients and anti-E2 monoclonal antibodies. While we did not find any evidence that N-linked glycans of E1 contribute to the masking of neutralizing epitopes, our data demonstrate that at least three glycans on E2 (denoted E2N1, E2N6, and E2N11) reduce the sensitivity of HCVpp to antibody neutralization. Importantly, these three glycans also reduced the access of CD81 to its E2 binding site, as shown by using a soluble form of the extracellular loop of CD81 in inhibition of entry. These data suggest that glycans E2N1, E2N6, and E2N11 are close to the binding site of CD81 and modulate both CD81 and neutralizing antibody binding to E2. In conclusion, this work indicates that HCV glycans contribute to the evasion of HCV from the humoral immune response.
Inhibition of Interferon Regulatory Factor 7 (IRF7)-Mediated Interferon Signal Transduction by the Kaposi's Sarcoma-Associated Herpesvirus Viral IRF Homolog vIRF3
Authors: Joo Chul Hyun , Shin Young C. , Gack Michaela , Wu Liguo , Levy David , Jung Jae U. 
Published: May 2007

ABSTRACT
Upon viral infection, the major defense mounted by the host immune system is activation of the interferon (IFN)-mediated antiviral pathway that is mediated by IFN regulatory factors (IRFs). In order to complete their life cycle, viruses must modulate the host IFN-mediated immune response. Kaposi's sarcoma-associated herpesvirus (KSHV), a human tumor-inducing herpesvirus, has developed a unique mechanism for antagonizing cellular IFN-mediated antiviral activity by incorporating viral homologs of the cellular IRFs, called vIRFs. Here, we report a novel immune evasion mechanism of KSHV vIRF3 to block cellular IRF7-mediated innate immunity in response to viral infection. KSHV vIRF3 specifically interacts with either the DNA binding domain or the central IRF association domain of IRF7, and this interaction leads to the inhibition of IRF7 DNA binding activity and, therefore, suppression of alpha interferon (IFN-α) production and IFN-mediated immunity. Remarkably, the central 40 amino acids of vIRF3, containing the double α helix motifs, are sufficient not only for binding to IRF7, but also for inhibiting IRF7 DNA binding activity. Consequently, the expression of the double α helix motif-containing peptide effectively suppresses IRF7-mediated IFN-α production. This demonstrates a remarkably efficient means of viral avoidance of host antiviral activity.
Matrix Fibronectin Binds Gammaretrovirus and Assists in Entry: New Light on Viral Infections
Authors: Beer Christiane , Pedersen Lene 
Published: May 2007

ABSTRACT
A major entry route for the gammaretrovirus amphotropic murine leukemia virus (A-MLV) into NIH 3T3 fibroblasts is via caveola-dependent endocytosis. However, during the infection time, few viral particles can be observed intracellularly. Analyzing the dynamics of the A-MLV infection process by using total internal reflection fluorescence microscopy, we show that the majority of viruses are extracellular and bound to the fibronectin matrix. Moreover, the amounts of bound virus and of fibronectin correlated. Using confocal microscopy, nanoparticles targeted to fibronectin by a III1C-fibronectin fragment or anti-fibronectin antibody were detected intracellularly in NIH 3T3 cells; unconjugated nanoparticles neither bound to cells nor were detectable intracellularly. Furthermore, A-MLV colocalized intracellularly with the fibronectin-targeted nanoparticles, suggesting that they were taken up by the same cellular pathway. Both A-MLV entry and fibronectin turnover depend on caveolar endocytosis, and we found that inhibiting viral binding to the extracellular NIH 3T3 fibronectin-matrix dramatically reduced A-MLV infection, indeed, showing an active role of fibronectin in infection. We suggest that binding to the cellular fibronectin matrix provides a new mechanism by which viruses can enter cells.
Guinea Pig-Adapted Foot-and-Mouth Disease Virus with Altered Receptor Recognition Can Productively Infect a Natural Host
Authors: Núñez José I. , Molina Nicolas , Baranowski Eric , Domingo Esteban , Clark Stuart , Burman Alison , Berryman Stephen , Jackson Terry , Sobrino Francisco 
Published: May 2007

ABSTRACTWe report that adaptation to infect the guinea pig did not modify the capacity of foot-and-mouth disease virus (FMDV) to kill suckling mice and to cause an acute and transmissible disease in the pig, an important natural host for this pathogen. Adaptive amino acid replacements (I248→T in 2C, Q44→R in 3A, and L147→P in VP1), selected upon serial passages of a type C FMDV isolated from swine (biological clone C-S8c1) in the guinea pig, were maintained after virus multiplication in swine and suckling mice. However, the adaptive replacement L147→P, next to the integrin-binding RGD motif at the GH loop in VP1, abolished growth of the virus in different established cell lines and modified its antigenicity. In contrast, primary bovine thyroid cell cultures could be productively infected by viruses with replacement L147→P, and this infection was inhibited by antibodies to αvβ6 and by an FMDV-derived RGD-containing peptide, suggesting that integrin αvβ6 may be used as a receptor for these mutants in the animal (porcine, guinea pig, and suckling mice) host. Substitution T248→N in 2C was not detectable in C-S8c1 but was present in a low proportion of the guinea pig-adapted virus. This substitution became rapidly dominant in the viral population after the reintroduction of the guinea pig-adapted virus into pigs. These observations illustrate how the appearance of minority variant viruses in an unnatural host can result in the dominance of these viruses on reinfection of the original host species.
Protein Kinase PKR Plays a Stimulus- and Virus-Dependent Role in Apoptotic Death and Virus Multiplication in Human Cells
Authors: Zhang Ping , Samuel Charles E. 
Published: May 2007

ABSTRACTThe protein kinase regulated by double-stranded RNA (dsRNA), PKR, is implicated in a range of biologic processes, including apoptotic death and interferon antiviral responses, based in part on studies with mouse cells genetically deficient inPkr. To test the role of the PKR protein in human cells, an RNA interference silencing strategy was used to generate stable HeLa cell lines with less than 2% of the PKR protein (PKR deficient) compared to either parental or control knockdown HeLa lines. Phosphorylation of the α subunit of eukaryotic initiation factor 2 on serine 51 was not detectably increased in response to dsRNA in PKR-deficient HeLa cells but was elevated severalfold in PKR-sufficient cells. PKR-deficient cells displayed reduced dsRNA-induced apoptosis compared to PKR-sufficient cell lines, whereas tumor necrosis factor alpha (TNF-α)-induced apoptosis was comparable between the HeLa lines. NF-κB was activated to a comparable extent in PKR-deficient and PKR-sufficient HeLa cells upon treatment with either dsRNA or TNF-α. The antiviral response against vesicular stomatitis virus was reduced in interferon-treated PKR-deficient compared to PKR-sufficient HeLa cells. However, the growth of two human viruses, adenovirus and reovirus, was unaffected by the PKR knockdown. Surprisingly, the yield of mutant adenovirus that fails to encode VAI RNA was not enhanced in PKR-deficient cells, indicating the importance of host factors in addition to PKR in conferring the VAI RNA phenotype.
Identification of Nonessential Regions of the nsp2 Replicase Protein of Porcine Reproductive and Respiratory Syndrome Virus Strain VR-2332 for Replication in Cell Culture
Authors: Han Jun , Liu Gongping , Wang Yue , Faaberg Kay S. 
Published: May 2007

ABSTRACT
The nonstructural protein 2 (nsp2) of porcine reproductive and respiratory syndrome virus (PRRSV) is a multidomain protein and has been shown to undergo remarkable genetic variation, primarily in its middle region, while exhibiting high conservation in the N-terminal putative protease domain and the C-terminal predicted transmembrane region. A reverse genetics system of PRRSV North American prototype VR-2332 was developed to explore the importance of different regions of nsp2 for viral replication. A series of mutants with in-frame deletions in the nsp2 coding region were engineered, and infectious viruses were subsequently recovered from transfected cells and further characterized. The results demonstrated that the cysteine protease domain (PL2), the PL2 downstream flanking sequence (amino acids [aa] 181 to 323), and the putative transmembrane domain were critical for replication. In contrast, the segment of nsp2 preceding the PL2 domain (aa 13 to 35) was dispensable for viral replication, and the nsp2 middle hypervariable region (aa 324 to 813) tolerated 100-aa or 200-aa deletions but could not be removed as a whole; the largest deletion was about 400 aa (nsp2Δ324-726). Characterization of the mutants demonstrated that those with small deletions possessed growth kinetics and RNA expression profiles similar to those of the parental virus, while the nsp2Δ324-726 mutant displayed decreased cytolytic activity on MARC-145 cells and did not develop visible plaques. Finally, the utilization of the genetic flexibility of nsp2 to express foreign genes was examined by inserting the gene encoding green fluorescent protein (GFP) in frame into one nsp2 deletion mutant construct. The recombinant virus was viable but impaired and unstable and gradually gained parental growth kinetics by the loss of most of the GFP gene.
Human Parainfluenza Viruses hPIV1 and hPIV3 Bind Oligosaccharides with α2-3-Linked Sialic Acids That Are Distinct from Those Bound by H5 Avian Influenza Virus Hemagglutinin
Authors: Amonsen Mary , Smith David F. , Cummings Richard D. , Air Gillian M. 
Published: May 2007

ABSTRACTWe investigated the binding of human parainfluenza virus types 1 and 3 (hPIV1 and hPIV3, respectively) to the glycan array of the Consortium for Functional Glycomics and binding and their release from erythrocytes under conditions where neuraminidase is inactive or active. hPIV1 and hPIV3 bind modifications of Neu5Acα2-3Galβ1-4GlcNAc, including the sialyl-Lewisxmotif and structures containing 6-sulfogalactose. hPIV1 and hPIV3 thus bind typical N-linked glycans, in contrast to avian influenza virus H5 hemagglutinin (J. Stevens, O. Blixt, T. M. Tumpey, J. K. Taubenberger, J. C. Paulson, and I. A. Wilson, Science 312:404-410, 2006), which binds less-common motifs. While the receptor is not the sole determinant of tropism, hPIV or H5 influenza virus infection of specific cells that express receptors may contribute to their different pathologies.
Cytomegalovirus Destruction of Focal Adhesions Revealed in a High-Throughput Western Blot Analysis of Cellular Protein Expression
Authors: Stanton R. J. , McSharry B. P. , Rickards C. R. , Wang E. C. Y. , Tomasec P. , Wilkinson G. W. G. 
Published: May 2007

ABSTRACTHuman cytomegalovirus (HCMV) systematically manages the expression of cellular functions, rather than exerting the global shutoff of host cell protein synthesis commonly observed with other herpesviruses during the lytic cycle. While microarray technology has provided remarkable insights into viral control of the cellular transcriptome, HCMV is known to encode multiple mechanisms for posttranscriptional and posttranslation regulation of cellular gene expression. High-throughput Western blotting (BD Biosciences Powerblot technology) with 1,009 characterized antibodies was therefore used to analyze and compare the effects of infection with attenuated high-passage strain AD169 and virulent low-passage strain Toledo at 72 hpi across gels run in triplicate for each sample. Six hundred ninety-four proteins gave a positive signal in the screen, of which 68 from strain AD169 and 71 from strain Toledo were defined as being either positively or negatively regulated by infection with the highest level of confidence (BD parameters). In follow-up analyses, a subset of proteins was selected on the basis of the magnitude of the observed effect or their potential to contribute to defense against immune recognition. In analyses performed at 24, 72, and 144 hpi, connexin 43 was efficiently downregulated during HCMV infection, implying a breakdown of intercellular communication. Mitosis-associated protein Eg-5 was found to be differentially upregulated in the AD169 and Toledo strains of HCMV. Focal adhesions link the actin cytoskeleton to the extracellular matrix and have key roles in initiating signaling pathways and substrate adhesion and regulating cell migration. HCMV suppressed expression of the focal-adhesion-associated proteins Hic-5, paxillin, and α-actinin. Focal adhesions were clearly disrupted in HCMV-infected fibroblasts, with their associated intracellular and extracellular proteins being dispersed. Powerblot shows potential for rapid screening of the cellular proteome during HCMV infection.
Human Immunodeficiency Virus Type 1 Vif Inhibits Packaging and Antiviral Activity of a Degradation-Resistant APOBEC3G Variant
Authors: Opi Sandrine , Kao Sandra , Goila-Gaur Ritu , Khan Mohammad A. , Miyagi Eri , Takeuchi Hiroaki , Strebel Klaus 
Published: May 2007

ABSTRACT
Human immunodeficiency virus type 1 (HIV-1) Vif counteracts the antiviral activity of the human cytidine deaminase APOBEC3G (APO3G) by inhibiting its incorporation into virions. This has been attributed to the Vif-induced degradation of APO3G by cytoplasmic proteasomes. We recently demonstrated that although APO3G has a natural tendency to form RNA-dependent homo-multimers, multimerization was not essential for encapsidation into HIV-1 virions or antiviral activity. We now demonstrate that a multimerization-defective APO3G variant (APO3G C97A) is able to assemble into RNase-sensitive high-molecular-mass (HMM) complexes, suggesting that homo-multimerization of APO3G and assembly into HMM complexes are unrelated RNA-dependent processes. Interestingly, APO3G C97A was highly resistant to Vif-induced degradation even though the two proteins were found to interact in coimmunoprecipitation experiments and exhibited partial colocalization in transfected HeLa cells. Surprisingly, encapsidation and antiviral activity of APO3G C97A were both inhibited by Vif despite resistance to degradation. These results demonstrate that targeting of APO3G to proteasome degradation and interference with viral encapsidation are distinct functional properties of Vif.