bluuebunny/crossref_metadata_2025_split huggingface dataset:
Resource competition and adaptive radiation in a microbial microcosm
Authors: Craig MacLean R. , Dickson Alison , Bell Graham 
Published: December 2004

AbstractTheory predicts that competition for shared resources in a monomorphic population generates divergent selection for adaptation to alternative resources. Experimental tests of this hypothesis are scarce. We selected populations of the bacteriumPseudomonas fluorescensin spatially homogeneous microcosms containing a complex mixture of resources. Initially, all populations consisted of two isogenic clones. The outcome of selection was the evolution of a diverse community of genotypes within each population. Sympatric genotypes exhibited differentiation in metabolic traits related to resource acquisition and frequency‐dependent trade‐offs in competitive ability, as we would expect if different genotypes consumed different resources. These results are consistent with the hypothesis of adaptive radiation driven by resource competition. Reconciling the results of this study with those of earlier experiments provides a new interpretation of the ecological causes of adaptive radiation in microbial microcosms.
Effects of mycorrhizal symbiosis on tallgrass prairie plant–herbivore interactions
Authors: Kula Abigail A. R. , Hartnett David C. , Wilson Gail W. T. 
Published: December 2004

AbstractComplex relationships occur among plants, mycorrhizal fungi, and herbivores. By altering plant nutrient status, mycorrhizas may alter herbivory or plant tolerance to herbivory via compensatory regrowth. We examined these interactions by assessing grasshopper preference and plant growth and fungal colonization responses to herbivory under mycorrhizal and non‐mycorrhizal conditions within tallgrass prairie microcosms. Mycorrhizal symbiosis increased plant regrowth following defoliation, and some strongly mycotrophic plant species showed overcompensation in response to herbivory when they were mycorrhizal. Although grasshoppers spent more time on mycorrhizal plants, herbivory intensity did not differ between mycorrhizal and non‐mycorrhizal plants. Aboveground herbivory by grasshoppers significantly increased mycorrhizal fungal colonization of plant roots. Thus mycorrhizas may greatly benefit plants subjected to herbivory by stimulating compensatory growth, and herbivores, in turn, may increase the development of the symbiosis. Our results also indicate strong interspecific differences among tallgrass prairie plant species in their responses to the interaction of aboveground herbivores and mycorrhizal symbionts.
Mechanisms of disease‐induced extinction
Authors: De Castro Francisco , Bolker Benjamin 
Published: December 2004

AbstractParasites are important determinants of ecological dynamics. Despite the widespread perception that parasites (in the broad sense, including microbial pathogens) threaten species with extinction, the simplest deterministic models of parasite dynamics (i.e. of specialist parasites with density‐dependent transmission) predict that parasites will always go extinct before their hosts. We review the primary theoretical mechanisms that allow disease‐induced extinction and compare them with the empirical literature on parasitic threats to populations to assess the importance of different mechanisms in threatening natural populations. Small pre‐epidemic population size and the presence of reservoirs are the most commonly cited factors for disease‐induced extinction in empirical studies.
The Quality of Social Security Benefit Data in the British Family Resources Survey: Implications for Investigating Income Support Take-Up by Pensioners
Authors: Hancock Ruth , Barker Geraldine 
Published: December 2004

SummaryFamily Resources Survey (FRS) data for April 1997 to March 2000 are used to estimate the take-up of income support (IS) by a subset of pensioners. We scrutinize the quality of FRS data for this purpose and describe a process of identifying and correcting inconsistencies in the data. Comparisons are made, before and after corrections to the data, of take-up estimates, logistic regression take-up models and predictions of take-up responses to changes in IS rates. Overall, the corrections do not have large effects on estimated take-up rates but suggest that non-take-up is marginally less serious than the uncorrected data imply. Logistic regressions using corrected and uncorrected data were in broad agreement on the factors influencing take-up. There were some differences in the scale of these influences, with implications for predictions of take-up responses to changes in the generosity of IS. Desirable improvements in the FRS are identified.
Exploring Road Mortality Ratios in Europe: NationalVersusRegional Realities
Authors: Lassarre Sylvain , Thomas Isabelle 
Published: December 2004

SummaryThe paper analyses the geographical pattern(s) of road mortality in western Europe for three standard levels of data aggregation. A new adjusted road mortality ratio is proposed. Unlike most mortality ratios, the standardization uses population density rather than age and sex. The hypothesis to be tested is that changes in the level of spatial aggregation of the data produce significant differences in the values of some basic descriptive statistics, and hence in operational conclusions. The paper shows that population density works as a proxy for structural factors that may be difficult to change by policies and that working with 264 regions confirms the north–south divergences in terms of road safety in Europe but also stresses the local or regional differences due to political, geographical, economic, environmental and statistical disparities. Safe countries include unsafe regions, and there are safe regions in unsafe countries. Decision makers should be aware of this when comparing countries.
Why McNemar's Procedure Needs to be Included in the Business Statistics Curriculum
Authors: Berenson Mark L. , Koppel Nicole B. 
Published: December 2004

ABSTRACTIn business research situations it is often of interest to examine the differences in the responses in repeated measurements of the same subjects or from among matched or paired subjects. A simple and useful procedure for comparing differences between proportions in two related samples was devised by McNemar (1947) nearly 60 years ago. Although the technique has enjoyed widespread usage in both behavioral and medical research, it has unfortunately not received proper attention in marketing, advertising, consumer research, public relations, operations management, or organizational behavior endeavors—disciplines wherein it is particularly desirable to evaluate the significance of changes in attitudes, opinions, or beliefs regarding some campaign or strategy. Perhaps the major reason for this obscurity is simply a general lack of awareness as to its value and practical power. The McNemar test is generally not currently being taught to business statistics students. It is the purpose of this article to demonstrate the usefulness and applicability of the McNemar procedure to these aforementioned disciplines so that it may be more appropriately employed as an important confirmatory data analysis tool within the basic business statistics curriculum.
The levels of plasma and salivary antioxidants in the patient with recurrent aphthous stomatitis
Authors: Karincaoglu Yelda , Batcioglu Kadir , Erdem Tamer , Esrefoglu Muammer , Genc Metin 
Published: December 2004

Background:  Despite plenty of research, the cause of recurrent aphthous stomatitis (RAS) remains obscure. It has been proposed that, the aetiological factors such as local trauma, smoking, vitamin deficiencies and viral infections lead to aphthae formation via final common pathway based on increased oxidative stress. The aim of this investigation was to evaluate the antioxidant enzyme superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx) alterations in plasma and saliva, and in addition uric acid (UA) in saliva, in patients with RAS and healthy controls.Methods:  Thirty‐two patients with RAS and 30 healthy controls were included into the study. The SOD, CAT, GSHPx and UA levels were measured in plasma and saliva in study and control groups.Results:  In the RAS group, although the mean SOD (P < 0.001) and CAT (P < 0.05) levels of plasma were lower, GSHPx (P < 0.001) levels were higher than control group. The salivary concentrations of the SOD (P < 0.001), CAT (P < 0.05) and GSHPx (P < 0.001) in RAS group were entirely opposite to plasma concentrations. UA were not significant between RAS group and controls.Conclusion:  Since we found salivary SOD and CAT levels were high whereas plasma levels were low, it has been thought that, salivary defence mechanisms via antioxidant agents may be stimulated against to the ulcerous lesion. We consider that the organism might mobilize the antioxidant potential to the sites where they were needed. At this point, decrease of SOD and CAT levels in the plasma may be related to this shift. It is also thought that GSHPx secretion in the saliva may also be increased but the increase in its turnover may be responsible for the diminished activity.
Methylation of Tat by PRMT6 Regulates Human Immunodeficiency Virus Type 1 Gene Expression
Authors: Boulanger Marie-Chloé , Liang Chen , Russell Rodney S. , Lin Rongtuan , Bedford Mark T. , Wainberg Mark A. , Richard Stéphane 
Published: December 2004

ABSTRACT
The human immunodeficiency virus (HIV) transactivator protein, Tat, stimulates transcription from the viral long terminal repeats via an arginine-rich transactivating domain. Since arginines are often known to be methylated, we investigated whether HIV type 1 (HIV-1) Tat was a substrate for known protein arginine methyltransferases (PRMTs). Here we identify Tat as a substrate for the arginine methyltransferase, PRMT6. Tat is specifically associated with and methylated by PRMT6 within cells. Overexpression of wild-type PRMT6, but not a methylase-inactive PRMT6 mutant, decreased Tat transactivation of an HIV-1 long terminal repeat luciferase reporter plasmid in a dose-dependent manner. Knocking down PRMT6 consistently increased HIV-1 production in HEK293T cells and also led to increased viral infectiousness as shown in multinuclear activation of a galactosidase indicator assays. Our study demonstrates that arginine methylation of Tat negatively regulates its transactivation activity and that PRMT6 acts as a restriction factor for HIV replication.
The Unique Stacked Rings in the Nucleocapsid of the White Spot Syndrome Virus Virion Are Formed by the Major Structural Protein VP664, the Largest Viral Structural Protein Ever Found
Authors: Leu Jiann-Horng , Tsai Jyh-Ming , Wang Han-Ching , Wang Andrew H.-J. , Wang Chung-Hsiung , Kou Guang-Hsiung , Lo Chu-Fang 
Published: December 2004

ABSTRACT

One unique feature of the shrimp white spot syndrome virus (WSSV) genome is the presence of a giant open reading frame (ORF) of 18,234 nucleotides that encodes a long polypeptide of 6,077 amino acids with a hitherto unknown function. In the present study, by applying proteomic methodology to analyze the sodium dodecyl sulfate-polyacrylamide gel electrophoresis profile of purified WSSV virions by liquid chromatography-mass spectrometry (LC-MS/MS), we found that this giant polypeptide, designated VP664, is one of the viral structural proteins. The existence of the corresponding 18-kb transcript was confirmed by sequencing analysis of reverse transcription-PCR products, which also showed that
vp664
was intron-less. A time course analysis showed that this transcript was actively transcribed at the late stage, suggesting that this gene product should contribute primarily to the assembly and morphogenesis of the virion. Several polyclonal antisera against this giant protein were prepared, and one of them was successfully used for immunoelectron microscopy analysis to localize the protein in the virion. Immunoelectron microscopy with a gold-labeled secondary antibody showed that the gold particles were regularly distributed around the periphery of the nucleocapsid with a periodicity that matched the characteristic stacked ring subunits that appear as striations. From this and other evidence, we argue that this giant ORF in fact encodes the major WSSV nucleocapsid protein.
Silencing the Morphogenesis of Rotavirus
Authors: López Tomas , Camacho Minerva , Zayas Margarita , Nájera Rebeca , Sánchez Rosana , Arias Carlos F. , López Susana 
Published: December 2004

ABSTRACT
The morphogenesis of rotaviruses follows a unique pathway in which immature double-layered particles (DLPs) assembled in the cytoplasm bud across the membrane of the endoplasmic reticulum (ER), acquiring during this process a transient lipid membrane which is modified with the ER resident viral glycoproteins NSP4 and VP7; these enveloped particles also contain VP4. As the particles move towards the interior of the ER cisternae, the transient lipid membrane and the nonstructural protein NSP4 are lost, while the virus surface proteins VP4 and VP7 rearrange to form the outermost virus protein layer, yielding mature infectious triple-layered particles (TLPs). In this work, we have characterized the role of NSP4 and VP7 in rotavirus morphogenesis by silencing the expression of both glycoproteins through RNA interference. Silencing the expression of either NSP4 or VP7 reduced the yield of viral progeny by 75 to 80%, although the underlying mechanism of this reduction was different in each case. Blocking the synthesis of NSP4 affected the intracellular accumulation and the cellular distribution of several viral proteins, and little or no virus particles (neither DLPs nor TLPs) were assembled. VP7 silencing, in contrast, did not affect the expression or distribution of other viral proteins, but in its absence, enveloped particles accumulated within the lumen of the ER, and no mature infectious virus was produced. Altogether, these results indicate that during a viral infection, NSP4 serves as a receptor for DLPs on the ER membrane and drives the budding of these particles into the ER lumen, while VP7 is required for removing the lipid envelope during the final step of virus morphogenesis.
Mouse Cytomegalovirus Early M112/113 Proteins Control the Repressive Effect of IE3 on the Major Immediate-Early Promoter
Authors: Tang Qiyi , Li Luge , Maul Gerd G. 
Published: December 2004

ABSTRACT
The mouse cytomegalovirus major immediate-early (IE) transcript is differentially spliced to produce two IE proteins: IE1, which functions partly to maintain its own promoter, the major IE promoter (MIEP), free from repression, and IE3, which functions partly as a repressor of MIEP. Paradoxically, the site where transcription of the viral genome occurs is also the site where the greatest amounts of IE3 accumulate. This raises the question of how the repression capabilities of IE3 are controlled so soon after infection. We detected IE3, an activator of early proteins, contemporaneously with gene products of the early M112/113 locus. Both IE3 and the early M112/113 gene products colocalize and coimmunoprecipitate. Protein interaction most likely occurs between IE3 and the 87-kDa splice form of M112/113, because only the 87-kDa component coimmunoprecipitated with IE3. The complex also includes PML. Transiently expressed M112/113 can form large domains alone, even in the absence of full viral genomes or PML. Coexpression of M112/113 products and IE3 results in segregation of IE3 into newly formed M112/113-based domains. Importantly, coexpression eliminates the IE3-based repressive effect on MIEP, as determined by MIEP-driven reporter assays. The consequence of segregating IE3 into the M112/113-containing prereplication domains appears to make IE3 unavailable for binding and repressing MIEP during the earliest stages of infection. These findings establish a new feedback mechanism between IE and early proteins, a new mechanism of promoter control via segregation of the repressor, and a new function for proteins from the M112/113 locus.
The Infectivity and Lytic Activity of Minute Virus of Mice Wild-Type and Derived Vector Particles Are Strikingly Different
Authors: Lang Susanne I. , Boelz Stephanie , Stroh-Dege Alexandra Y. , Rommelaere Jean , Dinsart Christiane , Cornelis Jan J. 
Published: December 2004

ABSTRACTGene therapy vectors have been developed from autonomous rodent parvoviruses that carry a therapeutic gene or a marker gene in place of the genes encoding the capsid proteins. These vectors are currently evaluated in preclinical experiments. The infectivity of the vector particles deriving from the fibroblastic strain of minute virus of mice (MVMp) (produced by transfection in human cells) was found to be far less (approximately 50-fold-less) infectious than that of wild-type virus particles routinely produced by infection of A9 mouse fibroblasts. Similarly, wild-type MVMp produced by transfection also had a low infectivity in mouse cells, indicating that the method and producer cells influence the infectivity of the virus produced. Interestingly, producer cells made as many full vector particles as wild-type particles, arguing against deficient packaging being responsible for the low infectivity of viruses recovered from transfected cells. The hurdle to infection with full particles produced through transfection was found to take place at an early step following entry and limiting viral DNA replication and gene expression. Infections with transfection or infection-derived virus stocks normalized for their replication ability yielded similar monomer and dimer DNA amplification and gene expression levels. Surprisingly, at equivalent replication units, the capacity of parvovirus vectors to kill tumor cells was lower than that of the parental wild-type virus produced under the same transfection conditions, suggesting that beside the viral nonstructural proteins, the capsid proteins, assembled capsids, or the corresponding coding region contribute to the lytic activity of these viruses.
Herpes Simplex Virus Type 1 gK Is Required for gB-Mediated Virus-Induced Cell Fusion, While neither gB and gK nor gB and UL20p Function Redundantly in Virion De-Envelopment
Authors: Melancon Jeffrey M. , Luna Rafael E. , Foster Timothy P. , Kousoulas Konstantin G. 
Published: December 2004

ABSTRACT
Multiple amino acid changes within herpes simplex virus type 1 (HSV-1) gB and gK cause extensive virus-induced cell fusion and the formation of multinucleated cells (syncytia). Early reports established that syncytial mutations in gK could not cause cell-to-cell fusion in the absence of gB. To investigate the interdependence of gB, gK, and UL20p in virus-induced cell fusion and virion de-envelopment from perinuclear spaces as well as to compare the ultrastructural phenotypes of the different mutant viruses in a syngeneic HSV-1 (F) genetic background, gB-null, gK-null, UL20-null, gB/gK double-null, and gB/UL20 double-null viruses were constructed with the HSV-1 (F) bacterial artificial chromosome pYEBac102. The gK/gB double-null virus YEbacΔgBΔgK was used to isolate the recombinant viruses gBsyn3ΔgK and gBamb1511ΔgK, which lack the gK gene and carry the gBsyn3 or gBamb1511 syncytial mutation, respectively. Both viruses formed small nonsyncytial plaques on noncomplementing Vero cells and large syncytial plaques on gK-complementing cells, indicating that gK expression was necessary for gBsyn3- and gBamb1511-induced cell fusion. Lack of virus-induced cell fusion was not due to defects in virion egress, since recombinant viruses specifying the gBsyn3 or gKsyn20 mutation in the UL19/UL20 double-null genetic background caused extensive cell fusion on UL20-complementing cells. As expected, the gB-null virus failed to produce infectious virus, but enveloped virion particles egressed efficiently out of infected cells. The gK-null and UL20-null viruses exhibited cytoplasmic defects in virion morphogenesis like those of the corresponding HSV-1 (KOS) mutant viruses. Similarly, the gB/gK double-null and gB/UL20 double-null viruses accumulated capsids in the cytoplasm, indicating that gB, gK, and UL20p do not function redundantly in membrane fusion during virion de-envelopment at the outer nuclear lamellae.
Mutations in the RNase H Primer Grip Domain of Murine Leukemia Virus Reverse Transcriptase Decrease Efficiency and Accuracy of Plus-Strand DNA Transfer
Authors: Mbisa Jean L. , Nikolenko Galina N. , Pathak Vinay K. 
Published: December 2004

ABSTRACT

The RNase H primer grip of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) contacts the DNA primer strand and positions the template strand near the RNase H active site, influencing RNase H cleavage efficiency and specificity. Sequence alignments show that 6 of the 11 residues that constitute the RNase H primer grip have functional equivalents in murine leukemia virus (MLV) RT. We previously showed that a Y586F substitution in the MLV RNase H primer grip resulted in a 17-fold increase in substitutions within 18 nucleotides of adenine-thymine tracts, which are associated with a bent DNA conformation. To further determine the effects of the MLV RNase H primer grip on replication fidelity and viral replication, we performed additional mutational analysis. Using either β-galactosidase (
lacZ
) or green fluorescent protein (
GFP
) reporter genes, we found that S557A, A558V, and Q559L substitutions resulted in statistically significant increases in viral mutation rates, ranging from 2.1- to 3.8-fold. DNA sequencing analysis of nonfluorescent
GFP
clones indicated that the mutations in RNase H primer grip significantly increased the frequency of deletions between the primer-binding site (PBS) and sequences downstream of the PBS. In addition, quantitative real-time PCR analysis of reverse transcription products revealed that the mutant RTs were substantially inefficient in plus-strand DNA transfer relative to the wild-type control. These results indicate that the MLV RNase H primer grip is an important determinant of in vivo fidelity of DNA synthesis and suggest that the mutant RT was unable to copy through the DNA-RNA junction of the minus-strand DNA and the tRNA because of its bent conformation resulting in error-prone plus-strand DNA transfer.
Expression of Cellular Oncogene Bcl-xL Prevents Coronavirus-Induced Cell Death and Converts Acute Infection to Persistent Infection in Progenitor Rat Oligodendrocytes
Authors: Liu Yin , Zhang Xuming 
Published: December 2004

ABSTRACTMurine coronavirus mouse hepatitis virus (MHV) causes persistent infection of the central nervous system (CNS) in rodents, which has been associated with demyelination. However, the precise mechanism of MHV persistence in the CNS remains elusive. Here we show that the progenitor oligodendrocytes (central glial 4 [CG-4] cells) derived from newborn rat brain were permissive to MHV infection, which resulted in cell death, although viral replication was restricted. Interestingly, treatment with fetal bovine serum or exogenous expression of cellular oncogene Bcl-xL prevented CG-4 cells from MHV-induced cell death. Significantly, overexpression of Bcl-xL alone was sufficient to convert acute to persistent, nonproductive infection in CG-4 cells. This finding indicates that intracellular factors rather than viral components play a critical role in establishing viral persistence in CNS cells. Although viral genomic RNAs continuously persisted in Bcl-xL-expressing CG-4 cells over 10 passages, infectious virus could no longer be isolated beyond 2 passages of the cell. Such a phenomenon resembles the persistent MHV infection in animal CNS. Thus, the establishment of a persistent, nonproductive infection in CG-4 cells may provide a useful in vitro model for studying viral persistence in animal CNS. The data also suggest that direct virus-host cell interaction is one of the underlying mechanisms that regulate viral persistence in CNS cells.