bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential expression of the genes involved in amino acids and nitrogen metabolisms during liver regeneration of mice
Authors: Yuan Yunsheng , Wu Xiaoying , Ou Qiuxiang , Gao Jin , Tennant Bud C. , Han Wei , Yu Yan 
Published: December 2008

Aim:  Liver regeneration is a highly coordinated response to hepatic injury or resection that is controlled by the body's overall requirement for liver function. The level of circulating amino acids in blood increases after acute liver injury and administration of amino acid mixtures induces hepatic DNA replication. These findings suggest a close connection between amino acid metabolism and hepatic proliferation. However, the underlying molecular mechanisms have not been completely elucidated. Here, we applied a cDNA micro‐array technique to analyze expression profiles of the genes associated with nitrogen and amino acid metabolism during liver regeneration in mice following treatment with CCl4.Methods:  Seventy‐nine genes were identified for their significantly altered expression patterns at different stages of liver damage and regeneration.Results:  We observed that the numbers of down‐regulated genes were remarkably higher than that of up‐regulated genes at 1.5 days following carbon tetrachloride administration when hepatic DNA replication was most active, indicating the existence of a counter balance between cell proliferation and liver metabolism functions.Conclusions:  Our results suggest that suppression of amino acids metabolism after acute liver injury results in the accumulation of amino acids in plasma that serves as a driving force for liver regeneration.
Traction in EHL Line Contacts Using Free-Volume Pressure-Viscosity Relationship With Thermal and Shear-Thinning Effects
Authors: Kumar Punit , Khonsari M. M. 
Published: December 2008

Abstract
This paper investigates the traction behavior in heavily loaded thermo-elastohydrodynamic lubrication (EHL) line contacts using the Doolittle free-volume equation, which closely represents the experimental viscosity-pressure-temperature relationship and has recently gained attention in the field of EHL, along with Tait’s equation of state for compressibility. The well-established Carreau viscosity model has been used to describe the simple shear-thinning encountered in EHL. The simulation results have been used to develop an approximate equation for traction coefficient as a function of operating conditions and material properties. This equation successfully captures the decreasing trend with increasing slide to roll ratio caused by the thermal effect. The traction-slip characteristics are expected to be influenced by the limiting shear stress and pressure dependence of lubricant thermal conductivity, which need to be incorporated in the future.
Revaccination with Marek's Disease Vaccines Induces Productive Infection and Superior Immunity
Authors: Wu Changxin , Gan Junji , Jin Qiao , Chen Chuangfu , Liang Ping , Wu Yantao , Liu Xuefen , Ma Li , Davison Fred 
Published: December 2008

ABSTRACT

The most common lymphoproliferative disease in chickens is Marek's disease (MD), which is caused by the oncogenic herpesvirus Marek's disease virus (MDV). The emergence of hypervirulent pathotypes of MDV has led to vaccine failures, which have become common and which have resulted in serious economic losses in some countries, and a revaccination strategy has been introduced in practice. The mechanism by which revaccination invokes superior immunity against MD is unknown. After field trials which showed that revaccination provided protection superior to that provided by a single vaccination were performed, experiments were conducted to explore the interaction between revaccinated chickens and MDV. The results showed that the chickens in the revaccination groups experienced two consecutive productive infections but that the chickens in the single-vaccination groups experienced one productive infection, demonstrating that revaccination of viruses caused the chickens to have productive and then latent infections. Revaccination of the virus induced in the chickens a higher and a longer temporary expansion of the CD8
+
, CD4
+
, and CD3
+
T-lymphocyte subpopulations, stronger peripheral blood lymphocyte proliferative activity; and higher levels of neutralizing antibody than single vaccination. These findings disagree with the postulate that MDV antigens persist, stimulate the immune system, and maintain a high level immunity after vaccination. The suppression of productive infection by maternal antibodies in chickens receiving the primary vaccination and a lower level of productive infection in the revaccination groups challenged with MDV were observed. The information obtained in this study suggests that the productive infection with revaccinated MDV in chickens plays a crucial role in the induction of superior immunity. This finding may be exploited for the development of a novel MD vaccine that results in the persistence of the antigen supply and that maintains a high level of immunity and may also have implications for other viral oncogenic diseases in humans and animals.
Normal Ranges of Streptococcal Antibody Titers Are Similar Whether Streptococci Are Endemic to the Setting or Not
Authors: Steer Andrew C. , Vidmar Suzanna , Ritika Roselyn , Kado Joseph , Batzloff Michael , Jenney Adam W. J. , Carlin John B. , Carapetis Jonathan R. 
Published: December 2008

ABSTRACTGroup A streptococcal (GAS) serology is used for the diagnosis of post-streptococcal diseases, such as acute rheumatic fever, and occasionally for the diagnosis of streptococcal pharyngitis. Experts recommend that the upper limits of normal for streptococcal serology be determined for individual populations because of differences in the epidemiology of GAS between populations. Therefore, we performed a study to determine the values of the upper limit of normal for anti-streptolysin O (ASO) and anti-DNase B (ADB) titers in Fiji. Participants with a history of GAS disease, including pharyngitis or impetigo, were excluded. A total of 424 serum samples from people of all ages (with a sample enriched for school-aged children) were tested for their ASO and ADB titers. Reference values, including titers that were 80% of the upper limit of normal, were obtained by regression analysis by use of a curve-fitting method instead of the traditional nonparametric approach. Normal values for both the ASO titer and the ADB titer rose sharply during early childhood and then declined gradually with age. The estimated titers that were 80% of the upper limit or normal at age 10 years were 276 IU/ml for ASO and 499 IU/ml for ADB. Data from our study are similar to those found in countries with temperate climates, suggesting that a uniform upper limit of normal for streptococcal serology may be able to be applied globally.
Case of Indolent Endocarditis Due to
Pseudomonas stutzeri
with Genetic Evidence of Relapse after 4 Years
Authors: Grimaldi David , Podglajen Isabelle , Aubert Agnès , Buu-Hoï Annie , Diebold Benoit , Mainardi Jean-Luc 
Published: December 2008

ABSTRACT

Pseudomonas stutzeri
, a gram-negative bacterium, is a common inhabitant of soil and water. We report an unusual case of a relapse of infective endocarditis due to
P. stutzeri
4 years after the initial episode. The identity of the strains was proven by genomic analysis.
Evaluation of an Immunochromatographic Assay Kit for Rapid Identification of
Mycobacterium tuberculosis
Complex in Clinical Isolates
Authors: Park Mi Young , Kim Young Jin , Hwang Sang Hyun , Kim Hyoung Hoi , Lee Eun Yup , Jeong Seok Hoon , Chang Chulhun L. 
Published: December 2008

ABSTRACT

We evaluated a new immunochromatographic assay (ICA) using mouse monoclonal anti-MPT64 antibody for rapid discrimination between
Mycobacterium tuberculosis
and nontuberculous mycobacteria in clinical isolates. A study with mycobacteria and other organisms showed excellent sensitivity (≅99%) and specificity (100%) and an appropriate detection limit (10
5
CFU/ml) when tested with
M. tuberculosis
H37Rv. This ICA can simplify the identification of
M. tuberculosis
in clinical laboratories.
Phylogeny and Identification of
Pantoea
Species and Typing of
Pantoea agglomerans
Strains by Multilocus Gene Sequencing
Authors: Delétoile Alexis , Decré Dominique , Courant Stéphanie , Passet Virginie , Audo Jennifer , Grimont Patrick , Arlet Guillaume , Brisse Sylvain 
Published: December 2008

ABSTRACT

Pantoea agglomerans
and other
Pantoea
species cause infections in humans and are also pathogenic to plants, but the diversity of
Pantoea
strains and their possible association with hosts and disease remain poorly known, and identification of
Pantoea
species is difficult. We characterized 36
Pantoea
strains, including 28 strains of diverse origins initially identified as
P. agglomerans
, by multilocus gene sequencing based on six protein-coding genes, by biochemical tests, and by antimicrobial susceptibility testing. Phylogenetic analysis and comparison with other species of
Enterobacteriaceae
revealed that the genus
Pantoea
is highly diverse. Most strains initially identified as
P. agglomerans
by use of API 20E strips belonged to a compact sequence cluster together with the type strain, but other strains belonged to diverse phylogenetic branches corresponding to other species of
Pantoea
or
Enterobacteriaceae
and to probable novel species. Biochemical characteristics such as fosfomycin resistance and utilization of
d
-tartrate could differentiate
P. agglomerans
from other
Pantoea
species. All 20 strains of
P. agglomerans
could be distinguished by multilocus sequence typing, revealing the very high discrimination power of this method for strain typing and population structure in this species, which is subdivided into two phylogenetic groups. PCR detection of the
repA
gene, associated with pathogenicity in plants, was positive in all clinical strains of
P. agglomerans
, suggesting that clinical and plant-associated strains do not form distinct populations. We provide a multilocus gene sequencing method that is a powerful tool for
Pantoea
species delineation and identification and for strain tracking.
Epstein-Barr Virus BGLF4 Kinase Suppresses the Interferon Regulatory Factor 3 Signaling Pathway
Authors: Wang Jiin-Tarng , Doong Shin-Lian , Teng Shu-Chun , Lee Chung-Pei , Tsai Ching-Hwa , Chen Mei-Ru 
Published: December 2008

ABSTRACTThe BGLF4 protein kinase of Epstein-Barr virus (EBV) is a member of the conserved family of herpesvirus protein kinases which, to some extent, have a function similar to that of the cellular cyclin-dependent kinase in regulating multiple cellular and viral substrates. In a yeast two-hybrid screening assay, a splicing variant of interferon (IFN) regulatory factor 3 (IRF3) was found to interact with the BGLF4 protein. This interaction was defined further by coimmunoprecipitation in transfected cells and glutathioneS-transferase (GST) pull-down in vitro. Using reporter assays, we show that BGLF4 effectively suppresses the activities of the poly(I:C)-stimulated IFN-β promoter and IRF3-responsive element. Moreover, BGLF4 represses the poly(I:C)-stimulated expression of endogenous IFN-β mRNA and the phosphorylation of STAT1 at Tyr701. In searching for a possible mechanism, BGLF4 was shown not to affect the dimerization, nuclear translocation, or CBP recruitment of IRF3 upon poly(I:C) treatment. Notably, BGLF4 reduces the amount of active IRF3 recruited to the IRF3-responsive element containing the IFN-β promoter region in a chromatin immunoprecipitation assay. BGLF4 phosphorylates GST-IRF3 in vitro, but Ser339-Pro340 phosphorylation-dependent, Pin1-mediated downregulation is not responsible for the repression. Most importantly, we found that three proline-dependent phosphorylation sites at Ser123, Ser173, and Thr180, which cluster in a region between the DNA binding and IRF association domains of IRF3, contribute additively to the BGLF4-mediated repression of IRF3(5D) transactivation activity. IRF3 signaling is activated in reactivated EBV-positive NA cells, and the knockdown of BGLF4 further stimulates IRF3-responsive reporter activity. The data presented here thus suggest a novel mechanism by which herpesviral protein kinases suppress host innate immune responses and facilitate virus replication.
Differential Sensitivity of Differentiated Epithelial Cells to Respiratory Viruses Reveals Different Viral Strategies of Host Infection
Authors: Goris Katherina , Uhlenbruck Sabine , Schwegmann-Wessels Christel , Köhl Wiebke , Niedorf Frank , Stern Michael , Hewicker-Trautwein Marion , Bals Robert , Taylor Geraldine , Braun Armin , Bicker Gerd , Kietzmann Manfred , Herrler Georg 
Published: December 2008

ABSTRACT
To address the initiation of virus infection in the respiratory tract, we established two culture systems for differentiated bovine airway epithelial cells (BAEC). Filter-grown BAEC differentiated under air-liquid interface (ALI) conditions to generate a pseudo-stratified mucociliary epithelium. Alternatively, precision-cut lung slices (PCLS) from the bovine airways were generated that retained the original composition and distribution of differentiated epithelial cells. With both systems, epithelial cells were readily infected by bovine parainfluenza virus 3 (BPIV3). Ciliated cells were the most prominent cell type affected by BPIV3. Surprisingly, differentiated BAEC were resistant to infection by bovine respiratory syncytial virus (BRSV), when the virus was applied at the same multiplicity of infection that was sufficient for infection by BPIV3. In the case of PCLS, infection by BRSV was observed in cells located in lower cell layers but not in epithelial cells facing the lumen of the airways. The identity of the infected cells could not be determined because of a lack of specific antibodies. Increasing the virus titer 30-fold resulted in infection of the ALI cultures of BAEC, whereas in PCLS the ciliated epithelium was still refractory to infection by BRSV. These results indicate that differentiated BAEC are readily infected by BPIV3 but rather resistant to infection by BRSV. Disease caused by BRSV may require that calves encounter environmental stimuli that render BAEC susceptible to infection.
The C Proteins of Human Parainfluenza Virus Type 1 (HPIV1) Control the Transcription of a Broad Array of Cellular Genes That Would Otherwise Respond to HPIV1 Infection
Authors: Boonyaratanakornkit Jim B. , Bartlett Emmalene J. , Amaro-Carambot Emerito , Collins Peter L. , Murphy Brian R. , Schmidt Alexander C. 
Published: December 2008

ABSTRACT

Human parainfluenza virus type 1 (HPIV1) is an important respiratory pathogen in children and the most common cause of viral croup. We performed a microarray-based analysis of gene expression kinetics to examine how wild-type (wt) HPIV1 infection altered gene expression in human respiratory epithelial cells and what role beta interferon played in this response. We similarly evaluated HPIV1-P(C−), a highly attenuated and apoptosis-inducing virus that does not express any of the four C proteins, and HPIV1-C
F170S
, a less attenuated mutant that contains a single point mutation in C and, like wt HPIV1, does not efficiently induce apoptosis, to examine the role of the C proteins in controlling host gene expression. We also used these data to investigate whether the phenotypic differences between the two C mutants could be explained at the transcriptional level. Mutation or deletion of the C proteins of HPIV1 permitted the activation of over 2,000 cellular genes that otherwise would be repressed by HPIV1 infection. Thus, the C proteins profoundly suppress the response of human respiratory cells to HPIV1 infection. Cellular pathways targeted by the HPIV1 C proteins were identified and their transcriptional control was analyzed using bioinformatics. Transcription factor binding sites for IRF and NF-κB were overrepresented in some of the C protein-targeted pathways, but other pathways were dominated by less-known factors, such as forkhead transcription factor FOXD1. Surprisingly, the host responses to the P(C−) and C
F170S
mutants were very similar, and only subtle differences in the expression kinetics of caspase 3 and TRAIL receptor 2 were observed. Thus, changes in host cell transcription did not reflect the striking phenotypic differences observed between these two viruses.
Influenza A Virus Polymerase Is an Integral Component of the CPSF30-NS1A Protein Complex in Infected Cells
Authors: Kuo Rei-Lin , Krug Robert M. 
Published: December 2008

ABSTRACT
The NS1A protein of influenza A virus binds the cellular CPSF30 protein, thereby inhibiting the 3′-end processing of all cellular pre-mRNAs, including beta interferon pre-mRNA. X-ray crystallography identified the CPSF30-binding pocket on the influenza virus A/Udorn/72 (Ud) NS1A protein and the critical role of two hydrophobic NS1A amino acids outside the pocket, F103 and M106, in stabilizing the CPSF30-NS1A complex. Although the NS1A protein of the 1997 H5N1 influenza A/Hong Kong/483/97 (HK97) virus contains L (not F) at position 103 and I (not M) at position 106, it binds CPSF30 in vivo to a significant extent because cognate (HK97) internal proteins stabilize the CPSF30-NS1A complex in infected cells. Here we show that the cognate HK97 polymerase complex, containing the viral polymerase proteins (PB1, PB2, and PA) and the nucleocapsid protein (NP), is responsible for this stabilization. The noncognate Ud polymerase complex cannot carry out this stabilization, but it can stabilize CPSF30 binding to a mutated (F103L M106I) cognate Ud NS1A protein. These results suggested that the viral polymerase complex is an integral component of the CPSF30-NS1A protein complex in infected cells even when the cognate NS1A protein contains F103 and M106, and we show that this is indeed the case. Finally, we show that cognate PA protein and NP, but not cognate PB1 and PB2 proteins, are required for stabilizing the CPSF30-NS1A complex, indicating that the NS1A protein interacts primarily with its cognate PA protein and NP in a complex that includes the cellular CPSF30 protein.
Tight Junction Proteins Claudin-1 and Occludin Control Hepatitis C Virus Entry and Are Downregulated during Infection To Prevent Superinfection
Authors: Liu Shufeng , Yang Wei , Shen Le , Turner Jerrold R. , Coyne Carolyn B. , Wang Tianyi 
Published: December 2008

ABSTRACTA tight junction (TJ) protein, claudin-1 (CLDN1), was identified recently as a key factor for hepatitis C virus (HCV) entry. Here, we show that another TJ protein, occludin, is also required for HCV entry. Mutational study of CLDN1 revealed that its tight junctional distribution plays an important role in mediating viral entry. Together, these data support the model in which HCV enters liver cells from the TJ. Interestingly, HCV infection of Huh-7 hepatoma cells downregulated the expression of CLDN1 and occludin, preventing superinfection. The altered TJ protein expression may contribute to the morphological and functional changes observed in HCV-infected hepatocytes.
Multiple Nucleic Acid Binding Sites and Intrinsic Disorder of Severe Acute Respiratory Syndrome Coronavirus Nucleocapsid Protein: Implications for Ribonucleocapsid Protein Packaging
Authors: Chang Chung-Ke , Hsu Yen-Lan , Chang Yuan-Hsiang , Chao Fa-An , Wu Ming-Chya , Huang Yu-Shan , Hu Chin-Kun , Huang Tai-Huang 
Published: December 2008

ABSTRACT

The nucleocapsid protein (N) of the severe acute respiratory syndrome coronavirus (SARS-CoV) packages the viral genomic RNA and is crucial for viability. However, the RNA-binding mechanism is poorly understood. We have shown previously that the N protein contains two structural domains—the N-terminal domain (NTD; residues 45 to 181) and the C-terminal dimerization domain (CTD; residues 248 to 365)—flanked by long stretches of disordered regions accounting for almost half of the entire sequence. Small-angle X-ray scattering data show that the protein is in an extended conformation and that the two structural domains of the SARS-CoV N protein are far apart. Both the NTD and the CTD have been shown to bind RNA. Here we show that all disordered regions are also capable of binding to RNA. Constructs containing multiple RNA-binding regions showed Hill coefficients greater than 1, suggesting that the N protein binds to RNA cooperatively. The effect can be explained by the “coupled-allostery” model, devised to explain the allosteric effect in a multidomain regulatory system. Although the N proteins of different coronaviruses share very low sequence homology, the physicochemical features described above may be conserved across different groups of
Coronaviridae
. The current results underscore the important roles of multisite nucleic acid binding and intrinsic disorder in N protein function and RNP packaging.
A Conserved Domain in the Leader Proteinase of Foot-and-Mouth Disease Virus Is Required for Proper Subcellular Localization and Function
Authors: de los Santos Teresa , Diaz-San Segundo Fayna , Zhu James , Koster Marla , Dias Camila C. A. , Grubman Marvin J. 
Published: December 2008

ABSTRACT

The leader proteinase (L
pro
) of foot-and-mouth disease virus (FMDV) is involved in antagonizing the innate immune response by blocking the expression of interferon (IFN) and by reducing the immediate-early induction of IFN-β mRNA and IFN-stimulated genes. In addition to its role in shutting off cap-dependent host mRNA translation, L
pro
is associated with the degradation of the p65/RelA subunit of nuclear factor κB (NF-κB). Bioinformatics analysis suggests that L
pro
contains a SAP (for SAF-A/B, Acinus, and PIAS) domain, a protein structure associated in some cases with the nuclear retention of molecules involved in transcriptional control. We have introduced a single or a double mutation in conserved amino acid residues contained within this domain of L
pro
. Although three stable mutant viruses were obtained, only the double mutant displayed an attenuated phenotype in cell culture. Indirect immunofluorescence analysis showed that L
pro
subcellular distribution is altered in cells infected with the double mutant virus. Interestingly, nuclear p65/RelA staining disappeared from wild-type (WT) FMDV-infected cells but not from double mutant virus-infected cells. Consistent with these results, NF-κB-dependent transcription was not inhibited in cells infected with double mutant virus in contrast to cells infected with WT virus. However, degradation of the translation initiation factor eIF-4G was very similar for both the WT and the double mutant viruses. Since L
pro
catalytic activity was demonstrated to be a requirement for p65/RelA degradation, our results indicate that mutation of the SAP domain reveals a novel separation-of-function activity for FMDV L
pro
.