bluuebunny/crossref_metadata_2025_split huggingface dataset:
Recovery of
Herbaspirillum
Species from Persons with Cystic Fibrosis
Authors: Spilker Theodore , Uluer Ahmet Z. , Marty Francisco M. , Yeh Wendy W. , Levison Julie H. , Vandamme Peter , LiPuma John J. 
Published: June 2008

ABSTRACT

Herbaspirillum
species are not known to be human pathogens. We report on the identification of
Herbaspirillum
from cultures from 28 persons with cystic fibrosis (CF). Most isolates were initially identified as members of the
Burkholderia cepacia
complex. Although the role that these species play in lung disease in persons with CF is not known, their differentiation from other species is important and has serious implications for clinical care and patient well-being.
Salmonella
Serovar Identification Using PCR-Based Detection of Gene Presence and Absence
Authors: Arrach Nabil , Porwollik Steffen , Cheng Pui , Cho Ann , Long Fred , Choi Sang-Ho , McClelland Michael 
Published: June 2008

ABSTRACT

There are more than 2,500 known
Salmonella
serovars, and some of these can be further subclassified into groups of strains that differ profoundly in their gene content. We refer to these groups of strains as “genovars.” A compilation of comparative genomic hybridization data on 291
Salmonella
isolates, including 250
S. enterica
subspecies I strains from 32 serovars (52 genovars), was used to select a panel of 384 genes whose presence and absence among serovars and genovars was of potential taxonomic value. A subset of 146 genes was used for real-time PCR to successfully identify 12 serovars (16 genovars) in 24
S. enterica
strains. A further subset of 64 genes was used to identify 8 serovars (9 genovars) in 12 multiplex PCR mixes on 11
S. enterica
strains. These gene panels distinguish all tested
S. enterica
subspecies I serovars and their known genovars, almost all by two or more informative markers. Thus, a typing methodology based on these predictive genes would generally alert users if there is an error, an unexpected polymorphism, or a potential new genovar.
Molecular Phylogenetic Diversity, Multilocus Haplotype Nomenclature, and In Vitro Antifungal Resistance within theFusarium solaniSpecies Complex
Authors: O'Donnell Kerry , Sutton Deanna A. , Fothergill Annette , McCarthy Dora , Rinaldi Michael G. , Brandt Mary E. , Zhang Ning , Geiser David M. 
Published: June 2008

ABSTRACTMembers of the species-richFusarium solanispecies complex (FSSC) are responsible for approximately two-thirds all fusarioses of humans and other animals. In addition, many economically important phytopathogenic species are nested within this complex. Due to their increasing clinical relevance and because most of the human pathogenic and plant pathogenic FSSC lack Latin binomials, we have extended the multilocus haplotype nomenclatural system introduced in a previous study (D. C. Chang, G. B. Grant, K. O'Donnell, K. A. Wannemuehler, J. Noble-Wang, C. Y. Rao, L. M. Jacobson, C. S. Crowell, R. S. Sneed, F. M. T. Lewis, J. K. Schaffzin, M. A. Kainer, C. A. Genese, E. C. Alfonso, D. B. Jones, A. Srinivasan, S. K. Fridkin, and B. J. Park, JAMA 296:953-963, 2006) to all 34 species within the medically important FSSC clade 3 to facilitate global epidemiological studies. The typing scheme is based on polymorphisms in portions of the following three genes: the internal transcribed spacer region and domains D1 plus D2 of the nuclear large-subunit rRNA, the translation elongation factor 1 alpha gene (EF-1α), and the second largest subunit of RNA polymerase II gene (RPB2). Of the 251 isolates subjected to multilocus DNA sequence typing, 191 sequence types were differentiated, and these were distributed among three strongly supported clades designated 1, 2, and 3. All of the mycosis-associated isolates were restricted to FSSC clade 3, as previously reported (N. Zhang, K. O'Donnell, D. A. Sutton, F. A Nalim, R. C. Summerbell, A. A. Padhye, and D. M. Geiser, J. Clin. Microbiol. 44:2186-2190, 2006), and these represent at least 20 phylogenetically distinct species. Analyses of the combined DNA sequence data by use of two separate phylogenetic methods yielded the most robust hypothesis of evolutionary relationships and genetic diversity within the FSSC to date. The in vitro activities of 10 antifungals tested against 19 isolates representing 18 species that span the breadth of the FSSC phylogeny show that members of this complex are broadly resistant to these drugs.
Identification of a Second CtBP Binding Site in Adenovirus Type 5 E1A Conserved Region 3
Authors: Bruton Rachel K. , Pelka Peter , Mapp Katie L. , Fonseca Gregory J. , Torchia Joseph , Turnell Andrew S. , Mymryk Joe S. , Grand Roger J. A. 
Published: June 2008

ABSTRACT

C-terminal binding protein (CtBP) binds to adenovirus early region 1A (AdE1A) through a highly conserved PXDLS motif close to the C terminus. We now have demonstrated that CtBP1 also interacts directly with the transcriptional activation domain (conserved region 3 [CR3]) of adenovirus type 5 E1A (Ad5E1A) and requires the integrity of the entire CR3 region for optimal binding. The interaction appears to be at least partially mediated through a sequence (
161
RRNTGDP
167
) very similar to a recently characterized novel CtBP binding motif in ZNF217 as well as other regions of CR3. Using reporter assays, we further demonstrated that CtBP1 represses Ad5E1A CR3-dependent transcriptional activation. Ad5E1A also appears to be recruited to the E-cadherin promoter through its interaction with CtBP. Significantly, Ad5E1A, CtBP1, and ZNF217 form a stable complex which requires CR3 and the PLDLS motif. It has been shown that Ad513SE1A, containing the CR3 region, is able to overcome the transcriptional repressor activity of a ZNF217 polypeptide fragment in a GAL4 reporter assay through recruitment of CtBP1. These results suggest a hitherto-unsuspected complexity in the association of Ad5E1A with CtBP, with the interaction resulting in transcriptional activation by recruitment of CR3-bound factors to CtBP1-containing complexes.
Epstein-Barr Virus Latent Membrane Protein 1 Represses DNA Repair through the PI3K/Akt/FOXO3a Pathway in Human Epithelial Cells
Authors: Chen Yi-Ren , Liu Ming-Tsan , Chang Yu-Ting , Wu Chung-Chun , Hu Chi-Yuan , Chen Jen-Yang 
Published: June 2008

ABSTRACT
Latent membrane protein 1 (LMP1), an Epstein-Barr virus (EBV) oncoprotein, mimics a constitutively activated tumor necrosis factor receptor and activates various signaling pathways, including phosphatidylinositol 3-kinase (PI3K)/Akt. LMP1 is essential for EBV-mediated B-cell transformation and is sufficient to transform several cell lines. Cellular transformation has been associated strongly with genomic instability, while DNA repair plays an important role in maintaining genomic stability. Previously, we have shown that LMP1 represses DNA repair by the C-terminal activating region 1 (CTAR1) in human epithelial cells. In the present study, we demonstrate that the PI3K/Akt pathway is required for LMP1-mediated repression of DNA repair. Through the LMP1/PI3K/Akt pathway, FOXO3a, which can induce DNA repair, is inactivated because of phosphorylation and relocalization. Expression of a constitutively active FOXO3a mutant can rescue LMP1-mediated repression of DNA repair. Furthermore, LMP1 can decrease the expression of DNA damage-binding protein 1 (DDB1), which functions in nucleotide excision repair, through the PI3K/Akt/FOXO3a pathway. LMP1-mediated repression of DNA repair is restored by DDB1, although only partially. These results suggest that LMP1 triggers the PI3K/Akt pathway to inactivate FOXO3a and decrease DDB1, which can lead to repression of DNA repair and may contribute to genomic instability in human epithelial cells.
Autologous Neutralizing Humoral Immunity and Evolution of the Viral Envelope in the Course of Subtype B Human Immunodeficiency Virus Type 1 Infection
Authors: Bunnik Evelien M. , Pisas Linaida , van Nuenen Ad C. , Schuitemaker Hanneke 
Published: June 2008

ABSTRACTMost human immunodeficiency virus type 1 (HIV-1)-infected individuals develop an HIV-specific neutralizing antibody (NAb) response that selects for escape variants of the virus. Here, we studied autologous NAb responses in five typical CCR5-using progressors in relation to viral NAb escape and molecular changes in the viral envelope (Env) in the period from seroconversion until after AIDS diagnosis. In sera from three patients, high-titer neutralizing activity was observed against the earliest autologous virus variants, followed by declining humoral immune responses against subsequent viral escape variants. Autologous neutralizing activity was undetectable in sera from two patients. Patients with high-titer neutralizing activity in serum showed the strongest positive selection pressure on Env early in infection. In the initial phase of infection, gp160 length and the number of potential N-linked glycosylation sites (PNGS) increased in viruses from all patients. Over the course of infection, positive selection pressure declined as the NAb response subsided, coinciding with reversions of changes in gp160 length and the number of PNGS. A number of identical amino acid changes were observed over the course of infection in the viral quasispecies of different patients. Our results indicate that although neutralizing autologous humoral immunity may have a limited effect on the disease course, it is an important selection pressure in virus evolution early in infection, while declining HIV-specific humoral immunity in later stages may coincide with reversion of NAb-driven changes in Env.
A Single N-Linked Glycosylation Site in the Japanese Encephalitis Virus prM Protein Is Critical for Cell Type-Specific prM Protein Biogenesis, Virus Particle Release, and Pathogenicity in Mice
Authors: Kim Jeong-Min , Yun Sang-Im , Song Byung-Hak , Hahn Youn-Soo , Lee Chan-Hee , Oh Hyun-Woo , Lee Young-Min 
Published: June 2008

ABSTRACT

The prM protein of Japanese encephalitis virus (JEV) contains a single potential N-linked glycosylation site, N
15
-X
16
-T
17
, which is highly conserved among JEV strains and closely related flaviviruses. To investigate the role of this site in JEV replication and pathogenesis, we manipulated the RNA genome by using infectious JEV cDNA to generate three prM mutants (N15A, T17A, and N15A/T17A) with alanine substiting for N
15
and/or T
17
and one mutant with silent point mutations introduced into the nucleotide sequences corresponding to all three residues in the glycosylation site. An analysis of these mutants in the presence or absence of endoglycosidases confirmed the addition of oligosaccharides to this potential glycosylation site. The loss of prM N glycosylation, without significantly altering the intracellular levels of viral RNA and proteins, led to an ≈20-fold reduction in the production of extracellular virions, which had protein compositions and infectivities nearly identical to those of wild-type virions; this reduction occurred at the stage of virus release, rather than assembly. This release defect was correlated with small-plaque morphology and an N-glycosylation-dependent delay in viral growth. A more conservative mutation, N15Q, had the same effect as N15A. One of the four prM mutants, N15A/T17A, showed an additional defect in virus growth in mosquito C6/36 cells but not human neuroblastoma SH-SY5Y or hamster BHK-21 cells. This cell type dependence was attributed to abnormal N-glycosylation-independent biogenesis of prM. In mice, the elimination of prM N glycosylation resulted in a drastic decrease in virulence after peripheral inoculation. Overall, our findings indicate that this highly conserved N-glycosylation motif in prM is crucial for multiple stages of JEV biology: prM biogenesis, virus release, and pathogenesis.
Effects of Lamin A/C, Lamin B1, and Viral U
S
3 Kinase Activity on Viral Infectivity, Virion Egress, and the Targeting of Herpes Simplex Virus U
L
34-Encoded Protein to the Inner Nuclear Membrane
Authors: Mou Fan , Wills Elizabeth G. , Park Richard , Baines Joel D. 
Published: June 2008

ABSTRACT

Previous results indicated that the U
L
34 protein (pU
L
34) of herpes simplex virus 1 (HSV-1) is targeted to the nuclear membrane and is essential for nuclear egress of nucleocapsids. The normal localization of pU
L
34 and virions requires the U
S
3-encoded kinase that phosphorylates U
L
34 and lamin A/C. Moreover, pU
L
34 was shown to interact with lamin A in vitro. In the present study, glutathione
S
-transferase/pU
L
34 was shown to specifically pull down lamin A and lamin B1 from cellular lysates. To determine the role of these interactions on viral infectivity and pU
L
34 targeting to the inner nuclear membrane (INM), the localization of pU
L
34 was determined in LmnA
−/−
and LmnB1
−/−
mouse embryonic fibroblasts (MEFs) by indirect immunofluorescence and immunogold electron microscopy in the presence or absence of U
S
3 kinase activity. While pU
L
34 INM targeting was not affected by the absence of lamin B1 in MEFs infected with wild-type HSV as viewed by indirect immunofluorescence, it localized in densely staining scalloped-shaped distortions of the nuclear membrane in lamin B1 knockout cells infected with a U
S
3 kinase-dead virus. Lamin B1 knockout cells were relatively less permissive for viral replication than wild-type MEFs, with viral titers decreased at least 10-fold. The absence of lamin A (i) caused clustering of pU
L
34 in the nuclear rim of cells infected with wild-type virus, (ii) produced extensions of the INM bearing pU
L
34 protein in cells infected with a U
S
3 kinase-dead mutant, (iii) precluded accumulation of virions in the perinuclear space of cells infected with this mutant, and (iv) partially restored replication of this virus. The latter observation suggests that lamin A normally impedes viral infectivity and that U
S
3 kinase activity partially alleviates this impediment. On the other hand, lamin B1 is necessary for optimal viral replication, probably through its well-documented effects on many cellular pathways. Finally, neither lamin A nor B1 was absolutely required for targeting pU
L
34 to the INM, suggesting that this targeting is mediated by redundant functions or can be mediated by other proteins.
How Bacteria Consume Their Own Exoskeletons (Turnover and Recycling of Cell Wall Peptidoglycan)
Authors: Park James T. , Uehara Tsuyoshi 
Published: June 2008

SUMMARYThe phenomenon of peptidoglycan recycling is reviewed. Gram-negative bacteria such asEscherichia colibreak down and reuse over 60% of the peptidoglycan of their side wall each generation. Recycling of newly made peptidoglycan during septum synthesis occurs at an even faster rate. Nine enzymes, one permease, and one periplasmic binding protein inE. colithat appear to have as their sole function the recovery of degradation products from peptidoglycan, thereby making them available for the cell to resynthesize more peptidoglycan or to use as an energy source, have been identified. It is shown that all of the amino acids and amino sugars of peptidoglycan are recycled. The discovery and properties of the individual proteins and the pathways involved are presented. In addition, the possible role of various peptidoglycan degradation products in the induction of β-lactamase is discussed.
Hourly variation in fine particle exposure is associated with transiently increased risk of ST segment depression
Authors: Lanki T , Hoek G , Timonen K L , Peters A , Tiittanen P , Vanninen E , Pekkanen J 
Published: June 2008

Objectives:To evaluate whether hourly changes in fine particle (PM2.5, diameter<2.5 µm) exposure or outdoor particle concentrations are associated with rapid ischaemic responses.Methods:41 non-smoking elderly people with coronary heart disease were followed up with biweekly clinic visits in Helsinki, Finland. The occurrence of ST segment depressions >0.1 mV was recorded during submaximal exercise tests. Hourly variations in personal PM2.5exposure and outdoor levels of PM2.5and ultrafine particles (<0.1 µm) were recorded for 24 h before a clinic visit. Associations between particulate air pollution and ST segment depressions were evaluated using logistic regression.Results:Both personal and outdoor PM2.5concentrations, but not outdoor ultrafine particle counts, were associated with ST segment depressions. The odds ratio (per 10 µg/m3) for personal PM2.5concentration during the hour preceding a clinic visit was 3.26 (95% CI 1.07 to 9.99) and for 4 h average outdoor PM2.5it was 2.47 (95% CI 1.05 to 5.85).Conclusions:Even very short-term elevations in fine particle exposure might increase the risk of myocardial ischaemia. The precise mechanism is still unknown but could involve changes in autonomic nervous control of the heart.
Excess of mesotheliomas after exposure to chrysotile in Balangero, Italy
Authors: Mirabelli D , Calisti R , Barone-Adesi F , Fornero E , Merletti F , Magnani C 
Published: June 2008

Background:Chrysotile from the mine in Balangero, Italy is considered to be free of tremolite. In a cohort study of miners and millers only two pleural cancers were reported, a finding considered to indicate that chrysotile has a low potency for inducing mesothelioma. However, follow-up ended in 1987 and white-collar workers and the employees of subcontractors were not studied.Methods:To complete the case ascertainment, the study searched the Registry of Malignant Mesotheliomas of Piedmont for records of cases of pleural mesothelioma among the following: mine employees; employees of subcontractors or of other firms transporting or refining Balangero asbestos, asbestos ore or mine tailings; individuals exposed to air pollution from the mine or living with mine employees; and individuals exposed to mine tailings from Balangero.Results:The study identified four new cases of pleural mesothelioma among blue-collar workers in the mine, in addition to the two reported in the cohort study. Thus, six mesotheliomas occurred, compared to the 1.5 expected (p<0.01). The study also identified three mesothelioma cases among white-collar employees at the mine, five in workers in the mine hired by subcontracting firms, and three among workers processing Balangero chrysotile outside the mine. Finally, 10 additional cases due to non-occupational exposure or exposure to re-used mine tailings were identified.Conclusions:The cluster of 14 mesothelioma cases among workers who were active in the mine and 13 among other people exposed to Balangero chrysotile provides further evidence that tremolite-free chrysotile is carcinogenic.
Isolation and characterization of ZH14 with antiviral activity againstTobacco mosaic virus
Authors: Zhou Wen-Wen , Zhang Li-Xiang , Zhang Bin , Wang Fei , Liang Zhi-Hong , Niu Tian-Gui 
Published: June 2008

A large number of bacteria were isolated from plant samples and screened for antiviral activity against the Tobacco mosaic virus (TMV). The bacterium ZH14, which was isolated from Chinese Anxi oolong tea, secreted the antiviral substances, having 94.2% virus inhibition when the bacterial culture filtrate and TMV extract were mixed at a ratio of 1:1. The ZH14 strain is a gram-positive, spore-forming rod and has the ability to degrade ribonucleic acid. Based on its effectiveness on virus inhibition, ZH14 was selected for characterization and was identified as a strain of the Bacillus cereus group based on phenotypic tests and comparative analysis of its 16S rDNA sequence. At the same time, we determined the antiviral product of ZH14 as an extracellular protein with high molecular mass, having an optimum temperature of 15–60 °C and an optimum pH of 6–10. Hence, the ZH14 strain and its culture filtrate have potential application in controlling plant diseases caused by TMV.
In vitro evaluation of the effect of nicotine, cotinine, and caffeine on oral microorganisms
Authors: Cogo Karina , Montan Michelle Franz , Bergamaschi Cristiane de Cássia , D. Andrade Eduardo , Rosalen Pedro Luiz , Groppo Francisco Carlos 
Published: June 2008

The aim of this in vitro study was to evaluate the effects of nicotine, cotinine, and caffeine on the viability of some oral bacterial species. It also evaluated the ability of these bacteria to metabolize those substances. Single-species biofilms of Streptococcus gordonii , Porphyromonas gingivalis , or Fusobacterium nucleatum and dual-species biofilms of S. gordonii – F. nucleatum and F. nucleatum – P. gingivalis were grown on hydroxyapatite discs. Seven species were studied as planktonic cells, including Streptococcus oralis , Streptococcus mitis , Propionibacterium acnes , Actinomyces naeslundii , and the species mentioned above. The viability of planktonic cells and biofilms was analyzed by susceptibility tests and time-kill assays, respectively, against different concentrations of nicotine, cotinine, and caffeine. High-performance liquid chromatography was performed to quantify nicotine, cotinine, and caffeine concentrations in the culture media after the assays. Susceptibility tests and viability assays showed that nicotine, cotinine, and caffeine cannot reduce or stimulate bacterial growth. High-performance liquid chromatography results showed that nicotine, cotinine, and caffeine concentrations were not altered after bacteria exposure. These findings indicate that nicotine, cotinine, and caffeine, in the concentrations used, cannot affect significantly the growth of these oral bacterial strains. Moreover, these species do not seem to metabolize these substances.
COMPARATIVE ANALYSIS OF DISEASE-ASSOCIATED MUTATIONS IN THE CODING REGIONS OF ALTERNATIVELY AND CONSTITUTIVELY SPLICED HUMAN GENES
Authors: HUANG QIANLI , LI YONG , LI-LING JESSE , HUANG HUIFANG , CHEN XUEPING , MA FEI 
Published: June 2008

To better understand the evolutionary and molecular mechanisms of alternative splicing causing human diseases, we have systematically compared the pattern, the distribution and the density of disease-associated mutations as well as the influence of codon usage bias on the single mutation between alternatively and constitutively spliced genes through analysis of the large datasets from human disease genes. The results indicated that:1. The most common pattern of single mutation in alternatively and constitutively spliced genes are, respectively, C/T (25.17%), (22.81%) and G/A (21.54%), (22.73%), suggesting that the two types of disease genes are prone to C → T and G → A mutations.2. There is an overall preponderance for transitions over transversions in alternatively (62.88% versus 37.12%) and constitutively (64.41% versus 35.59%) spliced disease genes.3. For the second base of codons, there exist significant differences in transitions and transversions between the two types of genes.4. Our data indicated that the single mutation tends to occur preferentially when the upstream neighboring-nucleotide is C or G in human disease genes.5. Codon usage bias and synonymous codon usage have great influence on the single mutation in both alternatively and constitutively spliced genes. The GC content and gene length also have very evident influence on such mutations.Our results seem to imply that disease-associated mutations within the coding regions of alternatively spliced human disease genes have different mechanisms from constitutively spliced genes. Such findings may facilitate understanding the molecular mechanism of alternative splicing causing human diseases, and the development of gene therapies for such diseases.