bluuebunny/crossref_metadata_2025_split huggingface dataset:
Peroxiredoxin 1 Is Required for Efficient Transcription and Replication of Measles Virus
Authors: Watanabe Akira , Yoneda Misako , Ikeda Fusako , Sugai Akihiro , Sato Hiroki , Kai Chieko 
Published: December 2010

ABSTRACTMeasles is a highly contagious human disease caused by the measles virus (MeV). In this study, by proteomic analysis, we identified peroxiredoxin 1 (Prdx1) as a host factor that binds to the C-terminal region of the nucleoprotein (N; NTAIL) of MeV. GlutathioneS-transferase (GST) pulldown experiments showed that the Prdx1-binding site overlapped with the MeV phosphoprotein (P)-binding site on NTAILand that Prdx1 competed for the binding to NTAILwith the P protein, which is a component of RNA-dependent RNA polymerase (RdRp). Furthermore, RNA interference for Prdx1 resulted in a significant reduction in MeV growth in HEK293-SLAM cells. A minigenome assay indicated that Prdx1 suppression affected the viral RNA transcription and/or replication step. Relative quantification of viral RNA by real-time PCR (RT-PCR) showed that Prdx1 suppression not only reduced viral RNA transcription and replication but also enhanced polar attenuation in viral mRNA transcription. Surface plasmon resonance analysis showed that the binding affinity of Prdx1 to MeV-N was 40-fold lower than that of MeV-P to MeV-N, which suggested that Prdx1 might be involved in the early stage of MeV infection, when the expression level of Prdx1 was much higher than that of MeV-P. Since Prdx1 was expressed abundantly and constitutively in various cells, the results in this study indicate that Prdx1 is one of the inherent host factors implicated in MeV RNA synthesis.
Characterization of a
Xenopus tropicalis
Endogenous Retrovirus with Developmental and Stress-Dependent Expression
Authors: Sinzelle L. , Carradec Q. , Paillard E. , Bronchain O. J. , Pollet N. 
Published: December 2010

ABSTRACT

We report on the identification and characterization of XTERV1, a full-length endogenous retrovirus (ERV) within the genome of the western clawed frog (
Xenopus tropicalis
). XTERV1 contains all the basic genetic elements common to ERVs, including the classical 5′-long terminal repeat (LTR)-
gag
-
pol
-
env
-3′-LTR architecture, as well as conserved functional motifs inherent to each retroviral protein. Using phylogenetic analysis, we show that XTERV1 is related to the
Epsilonretrovirus
genus. The
X. tropicalis
genome harbors a single full-length copy with intact
gag
and
pol
open reading frames that localizes to the centromeric region of chromosome 5. About 10 full-length defective copies of XTERV1 are found interspersed in the genome, and 2 of them could be assigned to chromosomes 1 and 3. We find that XTERV1 genes are zygotically transcribed in a regulated spatiotemporal manner during frog development, including metamorphosis. Moreover, XTERV1 transcription is upregulated under certain cellular stress conditions, including cytotoxic and metabolic stresses. Interestingly, XTERV1 Env is found to be homologous to FR47, a protein upregulated following cold exposure in the freeze-tolerant wood frog (
Rana sylvatica
). In addition, we find that
R. sylvatica
FR47 mRNA originated from a retroviral element. We discuss the potential role(s) of ERVs in physiological processes in vertebrates.
Targeting Hepatitis B Virus-Infected Cells with a T-Cell Receptor-Like Antibody
Authors: Sastry Konduru S. R. , Too Chien Tei , Kaur Kaval , Gehring Adam J. , Low Lionel , Javiad Alia , Pollicino Teresa , Li Li , Kennedy Patrick T. F. , Lopatin Uri , Macary Paul A. , Bertoletti Antonio 
Published: December 2010

ABSTRACTVirus-specific CD8 T cells are activated when their T-cell receptors (TCRs) recognize the specific viral peptide/major histocompatibility complex (MHC) class I (pMHC) complexes present on the surface of infected cells. Antibodies able to recognize the specific pMHC can mimic TCR specificity and both represent a valuable biological tool to visualize pMHC complexes on infected cells and serve as a delivery system for highly targeted therapies. To evaluate these possibilities, we created a monoclonal antibody able to specifically recognize a hepatitis B virus (HBV) envelope epitope (Env at positions 183 to 91 [Env183-91]) presented by the HLA-A201 molecule, and we tested its ability to recognize HBV-infected hepatocytes and to deliver a cargo to a specific target. We demonstrate that this antibody detects and visualizes the processed product of HBV proteins produced in naturally HBV-infected cells, is not inhibited by soluble HBV proteins present in patient sera, and mediates the intracellular delivery of a fluorescent molecule to target cells. Additionally, compared to CD8 T cells specific for the same HBV epitope, the TCR-like antibody has both a superior sensitivity and a specificity focused on distinct amino acids within the epitope. These data demonstrate that a T-cell receptor-like antibody can be used to determine the quantitative relationship between HBV replication and specific antigen presentation to CD8 T cells and serves as a novel therapeutic delivery platform for personalized health care for HBV-infected patients.
Newcastle Disease Virus Expressing a Dendritic Cell-Targeted HIV Gag Protein Induces a Potent Gag-Specific Immune Response in Mice
Authors: Maamary Jad , Array Frida , Gao Qinshan , García-Sastre Adolfo , Steinman Ralph M. , Palese Peter , Nchinda Godwin 
Published: December 2010

ABSTRACT

Viral vaccine vectors have emerged as an attractive strategy for the development of a human immunodeficiency virus (HIV) vaccine. Recombinant Newcastle disease virus (rNDV) stands out as a vaccine vector since it has a proven safety profile in humans, it is a potent inducer of both alpha interferon (IFN-α) and IFN-β) production, and it is a potent inducer of dendritic cell (DC) maturation. Our group has previously generated an rNDV vector expressing a codon-optimized HIV Gag protein and demonstrated its ability to induce a Gag-specific CD8
+
T cell response in mice. In this report we demonstrate that the Gag-specific immune response can be further enhanced by the targeting of the rNDV-encoded HIV Gag antigen to DCs. Targeting of the HIV Gag antigen was achieved by the addition of a single-chain Fv (scFv) antibody specific for the DC-restricted antigen uptake receptor DEC205 such that the DEC205 scFv-Gag molecule was encoded for expression as a fusion protein. The vaccination of mice with rNDV coding for the DC-targeted Gag antigen induced an enhanced Gag-specific CD8
+
T cell response and enhanced numbers of CD4
+
T cells and CD8
+
T cells in the spleen relative to vaccination with rNDV coding for a nontargeted Gag antigen. Importantly, mice vaccinated with the DEC205-targeted vaccine were better protected from challenge with a recombinant vaccinia virus expressing the HIV Gag protein. Here we demonstrate that the targeting of the HIV Gag antigen to DCs via the DEC205 receptor enhances the ability of an rNDV vector to induce a potent antigen-specific immune response.
Double-Stranded RNA Adenosine Deaminase ADAR-1-Induced Hypermutated Genomes among Inactivated Seasonal Influenza and Live Attenuated Measles Virus Vaccines
Authors: Suspène Rodolphe , Petit Vincent , Puyraimond-Zemmour David , Aynaud Marie-Ming , Henry Michel , Guétard Denise , Rusniok Christophe , Wain-Hobson Simon , Vartanian Jean-Pierre 
Published: December 2010

ABSTRACT
We sought to examine ADAR-1 editing of measles and influenza virus genomes derived from inactivated seasonal influenza and live attenuated measles virus vaccines grown on chicken cells as the culture substrate. Using highly sensitive 3DI-PCR (R. Suspène et al., Nucleic Acids Res. 36:e72, 2008), it was possible to show that ADAR-1 could hyperdeaminate adenosine residues in both measles virus and influenza virus A genomes. Detailed analysis of the dinucleotide editing context showed preferences for 5′ArA and 5′UrA, which is typical of editing in mammalian cells. The hyperedited mutant frequency, including genomes and antigenomes, was a log greater for influenza virus compared to measles virus, suggesting a greater sensitivity to restriction by ADAR-1.
Production of Hepatitis C Virus Lacking the Envelope-Encoding Genes for Single-Cycle Infection by Providing Homologous Envelope Proteins or Vesicular Stomatitis Virus Glycoproteins in
trans
Authors: Li Rui , Qin Yan , He Ying , Tao Wanyin , Zhang Nan , Tsai Cheguo , Zhou Paul , Zhong Jin 
Published: December 2010

ABSTRACT

Hepatitis C virus (HCV) infection is a major worldwide health problem. The envelope glycoproteins are the major components of viral particles. Here we developed a
trans
-complementation system that allows the production of infectious HCV particles in whose genome the regions encoding envelope proteins are deleted (HCVΔE). The lack of envelope proteins could be efficiently complemented by the expression of homologous envelope proteins in
trans
. HCVΔE production could be enhanced significantly by previously described adaptive mutations in NS3 and NS5A. Moreover, HCVΔE could be propagated and passaged in packaging cells stably expressing HCV envelope proteins, resulting in only single-round infection in wild-type cells. Interestingly, we found that vesicular stomatitis virus (VSV) glycoproteins could efficiently rescue the production of HCV lacking endogenous envelope proteins, which no longer required apolipoprotein E for virus production. VSV glycoprotein-mediated viral entry could allow for the bypass of the natural HCV entry process and the delivery of HCV replicon RNA into HCV receptor-deficient cells. Our development provides a new tool for the production of single-cycle infectious HCV particles, which should be useful for studying individual steps of the HCV life cycle and may also provide a new strategy for HCV vaccine development.
Spread of Herpes Simplex Virus to the Spinal Cord Is Independent of Spread to Dorsal Root Ganglia
Authors: Ohashi Masahiro , Bertke Andrea S. , Patel Amita , Krause Philip R. 
Published: December 2010

ABSTRACT
Levels of herpes simplex virus 1 (HSV-1) and HSV-2 DNA in dorsal root ganglia (DRG) and spinal cord (SC) were quantified after inoculation of guinea pig genitals and footpads. In genital infection, viral DNA reached SC and DRG simultaneously (at 2 to 3 days after inoculation) but was more abundant in SC than in DRG. After inoculation of footpads, which lack parasympathetic innervation, the viruses spread more efficiently to DRG than to SC. These results show important differences between genital and footpad infections, including independence of spread to DRG and SC, and imply that autonomic neurons may play an important role in the pathogenesis of viral latency after genital inoculation.
Inverse relationship between percentage body weight change and finishing time in 643 forty-two-kilometre marathon runners
Authors: Zouhal Hassane , Groussard Carole , Minter Guenolé , Vincent Sophie , Cretual Armel , Gratas-Delamarche Arlette , Delamarche Paul , Noakes Timothy David 
Published: December 2010

ObjectiveThe purpose of this study was to determine the relationship between athletic performance and the change in body weight (BW) during a 42 km marathon in a large cohort of runners.MethodsThe study took place during the 2009 Mont Saint-Michel Marathon (France). 643 marathon finishers (560 males and 83 females) were studied. The change in BW during the race was calculated from measurements of each runner's BW immediately before and after the race.ResultsBW loss was 2.3±2.2% (mean±SEM) (p<0.01). BW loss was −3.1±1.9% for runners finishing the marathon in less than 3 h; −2.5±2.1% for runners finishing between 3 and 4 h; and −1.8±2.4% for runners who required more than 4 h to complete the marathon. The degree of BW loss was linearly related to 42 km race finishing time (p<0.0000001). Neither age nor gender influenced BW loss during the race.ConclusionsBW loss during the marathon was inversely related to race finishing time in 643 marathon runners and was >3% in runners completing the race in less than 3 h. These data are not compatible with laboratory-derived data suggesting that BW loss greater than 2% during exercise impairs athletic performance. They match an extensive body of evidence showing that the most successful athletes in marathon and ultra-marathon running and triathlon events are frequently those who lose substantially more than 3–4% BW during competition.
Ishikawa Iterative Process for a Pair of Single-valued and Multivalued Nonexpansive Mappings in Banach Spaces
Authors: Sokhuma K , Kaewkhao A 
Published: December 2010

AbstractLet "Equation missing" be a nonempty compact convex subset of a uniformly convex Banach space "Equation missing", and let "Equation missing" and "Equation missing" be a single-valued nonexpansive mapping and a multivalued nonexpansive mapping, respectively. Assume in addition that "Equation missing" and "Equation missing" for all "Equation missing". We prove that the sequence of the modified Ishikawa iteration method generated from an arbitrary "Equation missing" by "Equation missing", "Equation missing", where "Equation missing" and "Equation missing", "Equation missing" are sequences of positive numbers satisfying "Equation missing", "Equation missing", converges strongly to a common fixed point of "Equation missing" and "Equation missing"; that is, there exists "Equation missing" such that "Equation missing".
RalA Function in Dermal Fibroblasts Is Required for the Progression of Squamous Cell Carcinoma of the Skin
Authors: Sowalsky Adam G. , Alt-Holland Addy , Shamis Yulia , Garlick Jonathan A. , Feig Larry A. 
Published: December 2010

Abstract
A large body of evidence has shown that stromal cells play a significant role in determining the fate of neighboring tumor cells through the secretion of various cytokines. How cytokine secretion by stromal cells is regulated in this context is poorly understood. In this study, we used a bioengineered human tissue model of skin squamous cell carcinoma progression to reveal that RalA function in dermal fibroblasts is required for tumor progression of neighboring neoplastic keratinocytes. This conclusion is based on the observations that suppression of RalA expression in dermal fibroblasts blocked tumorigenic keratinocytes from invading into the dermal compartment of engineered tissues and suppressed more advanced tumor progression after these tissues were transplanted onto the dorsum of mice. RalA executes this tumor-promoting function of dermal fibroblasts, at least in part, by mediating hepatocyte growth factor (HGF) secretion through its effector proteins, the Sec5 and Exo84 subunits of the exocyst complex. These findings reveal a new level of HGF regulation and highlight the RalA signaling cascade in dermal fibroblasts as a potential anticancer target. Cancer Res; 71(3); 758–67. ©2010 AACR.
Comprehensive Mapping of p53 Pathway Alterations Reveals an Apparent Role for Both SNP309 and MDM2 Amplification in Sarcomagenesis
Authors: Ito Moriko , Barys Louise , O'Reilly Terence , Young Sophie , Gorbatcheva Bella , Monahan John , Zumstein-Mecker Sabine , Choong Peter F. , Dickinson Ian , Crowe Philip , Hemmings Christine , Desai Jayesh , Thomas David M. , Lisztwan Joanna 
Published: December 2010

Abstract
Purpose: Reactivation of p53 tumor suppressor activity in diseases such as soft-tissue sarcoma is considered an attractive means of targeted therapy. By systematically assessing alterations affecting the p53 pathway, we aimed to (a) classify sarcoma subtypes, (b) define a potential role in malignancy, and (c) identify potential patient biomarkers in this heterogeneous disease.
Experimental Design: We have mapped mutational events in a panel of 192 benign or malignant bone and soft-tissue sarcomas. Analyses included TP53 and CDKN2A mutational and SNP status, MDM2 and MDM4 amplification and MDM2 SNP309 status.
Results: We found an inverse relationship between MDM2 amplification and TP53 mutations, with a predominantly wild-type CDKN2A background. A high rate of point mutations in TP53 was observed uniquely in leiomyosarcoma, osteosarcoma, and MFH. Both MDM2 and MDM4 were also amplified in a subtype-specific manner, which was frequently seen as a coamplification event. We have also analyzed the risk allele frequencies for MDM2 SNP309, and show that the G allele was strongly associated with both liposarcomas and MDM2 amplification.
Conclusions: Our data emphasize the critical role of p53 inactivation in sarcomagenesis, whereby different pathway alterations may be related to the heterogeneity of the disease. Moreover, we observed a strong association of malignancy with TP53 mutation, or MDM2 amplification and the presence of a G allele in SNP309, especially in lipoma versus liposarcoma. We propose, therefore, that MDM2 markers along with TP53 sequencing should be considered as patient biomarkers in clinical trials of sarcomas using MDM2 antagonists. Clin Cancer Res; 17(3); 416–26. ©2010 AACR.
Androgen Deprivation Boosts Prostatic Infiltration of Cytotoxic and Regulatory T Lymphocytes and Has No Effect on Disease-Free Survival in Prostate Cancer Patients
Authors: Sorrentino Carlo , Musiani Piero , Pompa Paolo , Cipollone Giuseppe , Di Carlo Emma 
Published: December 2010

Abstract
Purpose: The value of neoadjuvant hormone therapy (NHT) prior to radical prostatectomy as a means of restraining prostate cancer (PCa) and strengthening its immunotherapy is still uncertain. This article asks whether it subverts immunoregulatory pathways governing tumor microenvironments, and has an impact on patient outcome.
Experimental Design: We microdissected epithelium and stroma from cancerous and normal prostate specimens from 126 prostatectomized patients, of whom 76 had received NHT, to detect cytokine/chemokine gene expression levels by real-time reverse transcriptase PCR. Confocal microscopy was used to identify cytokine/chemokine cell sources, and immunostainings to characterize lymphocyte subsets whose prognostic effects were assessed by Kaplan–Meier analyses.
Results: NHT boosted the expression of IL-7 in the stroma and that of IFNγ-inducible protein-10/CXCL10 in the glandular epithelium of normal prostate tissue, and restored the CD8+ lymphocyte depletion occurring in PCa, whereas it significantly increased the CD4+ lymphocyte infiltrate. Lymphocytes, mostly with CD8+ phenotype, expressed the T-cell intracellular antigen-1, granzyme-B, and perforin, typical of cytotoxic-effector T cells. NHT also induced thymus and activation-regulated chemokine/CCL17 production by monocytes/macrophages in the prostate and draining lymph nodes, and increased the number of their Forkhead box P3 (Foxp3)+CD25+CD127− T regulatory (Treg) cells. The χ2 test disclosed the lack of association (P = 0.27) between NHT and the high intratumoral CD8+/Treg ratio indicative of a good prognosis.
Conclusions: Androgen withdrawal regulates cytokine/chemokine gene expression in normal prostate and lymphoid tissues, and this probably favors both CD8+ and Treg infiltrates, leaves their intratumoral balance unchanged, and thus has no impact on disease-free survival. Clin Cancer Res; 17(6); 1571–81. ©2010 AACR.
Effect of different extraction methods on fiber quality of nettle (Urtica dioica L.)
Authors: Bacci Laura , Di Lonardo Sara , Albanese Lorenzo , Mastromei Giorgio , Perito Brunella 
Published: December 2010

Chemical extraction, water retting, microbiological and enzymatic methods were applied on entire nettle stalks and/or unretted decorticated fiber of a selected fiber nettle clone. Morphological and mechanical properties and chemical composition were then determined on fiber samples. The first interesting result concerned the good degree of separation between fibers and shives obtained by mechanical scutching applied on stalks stored for 1 year, probably resulting from natural retting processes occurring during the storage. Microbiological retting (anaerobic plus aerobic bacteria) of entire stalks and/or unretted decorticated fiber produced fibers with a higher quality than water retting. Both enzymes used (Viscozyme ® L and Pectinex® Ultra SP-L), improved fiber quality if EDTA was added. The enzyme vat retting gave good results on both water-retted fibers and unretted decorticated fibers, while the spray enzyme treated fibers usually displayed thicker diameter, lower cellulose content and, for Viscozyme ® L, lower strength values, without differences between the two storage methods used after enzyme application.
Noxa mediates p18INK4c cell-cycle control of homeostasis in B cells and plasma cell precursors
Authors: Bretz Jamieson , Garcia Josefina , Huang Xiangao , Kang Lin , Zhang Yang , Toellner Kai-Michael , Chen-Kiang Selina 
Published: December 2010

Abstract
Inhibition of Cdk4/Cdk6 by p18INK4c (p18) is pivotal for generation of noncycling immunoglobulin (Ig)-secreting plasma cells (PCs). In the absence of p18, CD138+ plasmacytoid cells continue to cycle and turnover rapidly, suggesting that p18 controls PC homeostasis. We now show that p18 selectively acts in a rare population of rapidly cycling CD138hi/B220hi intermediate PCs (iPCs). While retaining certain B-cell signatures, iPCs are poised to differentiate to end-stage PCs although the majority undergo apoptosis. p18 is dispensable for the development of the PC transcriptional circuitry, and Blimp-1 and Bcl-6 are expressed fully and mutually exclusively in individual iPCs. However, a minor proportion of iPCs express both, and they are preferentially protected by p18 or Bcl-xL overexpression, consistent with expansion of the iPC pool by Bcl-xL overexpression, or loss of proapoptotic Bim or Noxa. Expression of Noxa is induced during B-cell activation, peaks in iPCs, and selectively repressed by p18. It is required to promote apoptosis of cycling B cells, especially in the absence of p18. These findings define the first physiologic function for Noxa and suggest that by repressing Noxa, induction of G1 arrest by p18 bypasses a homeostatic cell-cycle checkpoint in iPCs for PC differentiation.
Barriers and facilitators of disclosures of domestic violence by
mental health service users: qualitative study
Authors: Rose Diana , Trevillion Kylee , Woodall Anna , Morgan Craig , Feder Gene , Howard Louise 
Published: December 2010

BackgroundMental health service users are at high risk of domestic violence but
this is often not detected by mental health services.AimsTo explore the facilitators and barriers to disclosure of domestic
violence from a service user and professional perspective.MethodA qualitative study in a socioeconomically deprived south London borough,
UK, with 18 mental health service users and 20 mental health
professionals. Purposive sampling of community mental health service
users and mental healthcare professionals was used to recruit
participants for individual interviews. Thematic analysis was used to
determine dominant and subthemes. These were transformed into conceptual
maps with accompanying illustrative quotations.ResultsService users described barriers to disclosure of domestic violence to
professionals including: fear of the consequences, including fear of
Social Services involvement and consequent child protection proceedings,
fear that disclosure would not be believed, and fear that disclosure
would lead to further violence; the hidden nature of the violence;
actions of the perpetrator; and feelings of shame. The main themes for
professionals concerned role boundaries, competency and confidence.
Service users and professionals reported that the medical diagnostic and
treatment model with its emphasis on symptoms could act as a barrier to
enquiry and disclosure. Both groups reported that enquiry and disclosure
were facilitated by a supportive and trusting relationship between the
individual and professional.ConclusionsMental health services are not currently conducive to the disclosure of
domestic violence. Training of professionals in how to address domestic
violence to increase their confidence and expertise is recommended.