bluuebunny/crossref_metadata_2025_split huggingface dataset:
Two massive stars possibly ejected from NGC 3603 via a three-body encounter
Authors: Gvaramadze V. V. , Kniazev A. Y. , Chené A.-N. , Schnurr O. 
Published: December 2012

AbstractWe report the discovery of a bow-shock-producing star in the vicinity of the young massive star cluster NGC 3603 using archival data of the Spitzer Space Telescope. Follow-up optical spectroscopy of this star with Gemini-South led to its classification as O6 V. The orientation of the bow shock and the distance to the star (based on its spectral type) suggest that the star was expelled from the cluster, while the young age of the cluster (∼2 Myr) implies that the ejection was caused by a dynamical few-body encounter in the cluster’s core. The relative position on the sky of the O6 V star and a recently discovered O2 If*/WN6 star (located on the opposite side of NGC 3603) allows us to propose that both objects were ejected from the cluster via the same dynamical event – a three-body encounter between a single (O6 V) star and a massive binary (now the O2 If*/WN6 star). If our proposal is correct, then one can ‘weigh’ the O2 If*/WN6 star using the conservation of the linear momentum. Given a mass of the O6 V star of ≈30  M⊙, we found that at the moment of ejection the mass of the O2 If*/WN6 star was ≈175  M⊙. Moreover, the observed X-ray luminosity of the O2 If*/WN6 star (typical of a single star) suggests that the components of this originally binary system have merged (e.g., because of encounter hardening).
Adenosine A1 Receptors in Mouse Pontine Reticular Formation Depress Breathing, Increase Anesthesia Recovery Time, and Decrease Acetylcholine Release
Authors: Gettys George C. , Liu Fang , Kimlin Ed , Baghdoyan Helen A. , Lydic Ralph 
Published: December 2012

Abstract

Background:
Clinical and preclinical data demonstrate the analgesic actions of adenosine. Central administration of adenosine agonists, however, suppresses arousal and breathing by poorly understood mechanisms. This study tested the two-tailed hypothesis that adenosine A1 receptors in the pontine reticular formation (PRF) of C57BL/6J mice modulate breathing, behavioral arousal, and PRF acetylcholine release.

Methods:
Three sets of experiments used 51 mice. First, breathing was measured by plethysmography after PRF microinjection of the adenosine A1 receptor agonist N6-sulfophenyl adenosine (SPA) or saline. Second, mice were anesthetized with isoflurane and the time to recovery of righting response (RoRR) was quantified after a PRF microinjection of SPA or saline. Third, acetylcholine release in the PRF was measured before and during microdialysis delivery of SPA, the adenosine A1 receptor antagonist 1, 3-dipropyl-8-cyclopentylxanthine, or SPA and 1, 3-dipropyl-8-cyclopentylxanthine.

Results:
First, SPA significantly decreased respiratory rate (−18%), tidal volume (−12%), and minute ventilation (−16%). Second, SPA concentration accounted for 76% of the variance in RoRR. Third, SPA concentration accounted for a significant amount of the variance in acetylcholine release (52%), RoRR (98%), and breathing rate (86%). 1, 3-dipropyl-8-cyclopentylxanthine alone caused a concentration-dependent increase in acetylcholine, a decrease in RoRR, and a decrease in breathing rate. Coadministration of SPA and 1, 3-dipropyl-8-cyclopentylxanthine blocked the SPA-induced decrease in acetylcholine and increase in RoRR.

Conclusions:
Endogenous adenosine acting at adenosine A1 receptors in the PRF modulates breathing, behavioral arousal, and acetylcholine release. The results support the interpretation that an adenosinergic-cholinergic interaction within the PRF comprises one neurochemical mechanism underlying the wakefulness stimulus for breathing.
On the gcd of local Rankin–Selberg integrals for even orthogonal groups
Authors: Kaplan Eyal 
Published: December 2012

AbstractWe study the Rankin–Selberg integral for a pair of representations of ${\rm SO}_{2l}\times {\rm GL}_{n}$, where ${\rm SO}_{2l}$ is defined over a local non-Archimedean field and is either split or quasi-split. The integrals span a fractional ideal, and its unique generator, which contains any pole which appears in the integrals, is called the greatest common divisor (gcd) of the integrals. We describe the properties of the gcd and establish upper and lower bounds for the poles. In the tempered case we can relate it to the $L$-function of the representations defined by Shahidi. Results of this work may lead to a gcd definition for the $L$-function.
Hepatitis B Virus Surface Antigen (HBsAg)-Positive and HBsAg-Negative Hepatitis B Virus Infection among Mother-Teenager Pairs 13 Years after Neonatal Hepatitis B Virus Vaccination
Authors: Yao Qing-Qing , Dong Xiao-Lian , Wang Xue-Cai , Ge Sheng-Xiang , Hu An-Qun , Liu Hai-Yan , Wang Yueping Alex , Yuan Quan , Zheng Ying-Jie 
Published: December 2012

ABSTRACT

It is unclear whether a mother who is negative for hepatitis B virus surface antigen (HBsAg) but positive for hepatitis B virus (HBV) is at potential risk for mother-to-child transmission of HBV. This study, using a paired mother-teenager population, aimed to assess whether maternal HBsAg-negative HBV infection (
hn
HBI) is a significant source of child HBV infection (HBI). A follow-up study with blood collection has been conducted on the 93 mother-teenager pairs from the initial 135 pregnant woman-newborn pairs 13 years after neonatal HBV vaccination. Serological and viral markers of HBV have been tested, and phylogenetic analysis of HBV isolates has been done. The HBI prevalence was 1.9% (1
hn
HBI/53) for teenage children of non-HBI mothers, compared with 16.7% (1
hn
HBI/6) for those of
hn
HBI mothers and 2.9% (1 HBsAg-positive HBV infection [
hp
HBI]/34) for those of
hp
HBI mothers. Similar viral sequences have been found in one pair of whom both the mother and teenager have had
hn
HBI. In comparison with the
hp
HBI cases, those with
hn
HBI had a lower level of HBV load and a higher proportion of genotype-C strains, which were accompanied by differentiated mutations (Q129R, K141E, and Y161N) of the “a” determinant of the HBV surface gene. Our findings suggest that mother-to-teenager transmission of
hn
HBI can occur among those in the neonatal HBV vaccination program.
Investigation into Low-Level Anti-Rubella Virus IgG Results Reported by Commercial Immunoassays
Authors: Dimech Wayne , Arachchi Nilukshi , Cai Jingjing , Sahin Terri , Wilson Kim 
Published: December 2012

ABSTRACT

Since the 1980s, commercial anti-rubella virus IgG assays have been calibrated against a WHO International Standard and results have been reported in international units per milliliter (IU/ml). Laboratories testing routine patients' samples collected 100 samples that gave anti-rubella virus IgG results of 40 IU/ml or less from each of five different commercial immunoassays (CIA). The total of 500 quantitative results obtained from 100 samples from each CIA were compared with results obtained from an in-house enzyme immunoassay (IH-EIA) calibrated using the WHO standard. All 500 samples were screened using a hemagglutination inhibition assay (HAI). Any sample having an HAI titer of 1:8 or less was assigned a negative anti-rubella virus antibody status. If the HAI titer was greater than 1:8, the sample was tested in an immunoblot (IB) assay. If the IB result was negative, the sample was assigned a negative anti-rubella virus IgG status; otherwise, the sample was assigned a positive status. Concordance between the CIA qualitative results and the assigned negative status ranged from 50.0 to 93.8% and 74.5 to 97.8% for the assigned positive status. Using a receiver operating characteristic analysis with the cutoff set at 10 IU/ml, the estimated sensitivity and specificity ranged from 70.2 to 91.2% and 65.9 to 100%, respectively. There was poor correlation between the quantitative CIA results and those obtained by the IH-EIA, with the coefficient of determination (
R
2
) ranging from 0.002 to 0.413. Although CIAs have been calibrated with the same international standard for more than 2 decades, the level of standardization continues to be poor. It may be time for the scientific community to reevaluate the relevance of quantification of anti-rubella virus IgG.
High Frequency and Diversity of Species C Enteroviruses in Cameroon and Neighboring Countries
Authors: Sadeuh-Mba Serge Alain , Bessaud Maël , Massenet Denis , Joffret Marie-Line , Endegue Marie-Claire , Njouom Richard , Reynes Jean-Marc , Rousset Dominique , Delpeyroux Francis 
Published: December 2012

ABSTRACT
Human enteroviruses (HEVs) are endemic worldwide and among the most common viruses infecting humans. Nevertheless, there are very limited data on the circulation and genetic diversity of HEVs in developing countries and sub-Saharan Africa in particular. We investigated the circulation and genetic diversity of HEVs among 436 healthy children in a limited area of the far north region of Cameroon in 2008 and 2009. We also characterized the genetic biodiversity of 146 nonpolio enterovirus (NPEV) isolates obtained throughout the year 2008 from stool specimens of patients with acute flaccid paralysis (AFP) in Cameroon, Chad, and Gabon. We found a high rate of NPEV infections (36.9%) among healthy children in the far north region of Cameroon. Overall, 45 different HEV types were found among healthy children and AFP patients. Interestingly, this study uncovered a high rate of HEVs of species C (HEV-C) among all typed NPEVs: 63.1% (94/149) and 39.5% (49/124) in healthy children and AFP cases, respectively. Besides extensive circulation, the most prevalent HEV-C type, coxsackievirus A-13, featured a tremendous intratypic diversity. Africa-specific HEV lineages were discovered, including HEV-C lineages and the recently reported EV-A71 “genogroup E.” Virtually all pathogenic circulating vaccine-derived polioviruses (cVDPVs) that have been fully characterized were recombinants between oral poliovaccine (OPV) strains and cocirculating HEV-C strains. The extensive circulation of diverse HEV-C types and lineages in countries where OPV is massively used constitutes a major viral factor that could promote the emergence of recombinant cVDPVs in the Central African subregion.
Rapid Identification of Bacteria and Yeasts from Positive-Blood-Culture Bottles by Using a Lysis-Filtration Method and Matrix-Assisted Laser Desorption Ionization–Time of Flight Mass Spectrum Analysis with the SARAMIS Database
Authors: Fothergill Amy , Kasinathan Vyjayanti , Hyman Jay , Walsh John , Drake Tim , Wang Yun F. (Wayne) 
Published: December 2012

ABSTRACT
Rapid identification of microorganisms causing bloodstream infections directly from a positive blood culture would decrease the time to directed antimicrobial therapy and greatly improve patient care. Matrix-assisted laser desorption ionization–time of flight (MALDI-TOF) mass spectrometry (MS) is a fast and reliable method for identifying microorganisms from positive culture. This study evaluates the performance of a novel filtration-based method for processing positive-blood-culture broth for immediate identification of microorganisms by MALDI-TOF with a Vitek MS research-use-only system (VMS). BacT/Alert non-charcoal-based blood culture bottles that were flagged positive by the BacT/Alert 3D system were included. An aliquot of positive-blood-culture broth was incubated with lysis buffer for 2 to 4 min at room temperature, the resulting lysate was filtered through a membrane, and harvested microorganisms were identified by VMS. Of the 259 bottles included in the study, VMS identified the organisms in 189 (73%) cultures to the species level and 51 (19.7%) gave no identification (ID), while 6 (2.3%) gave identifications that were considered incorrect. Among 131 monomicrobic isolates from positive-blood-culture bottles with one spot having a score of 99.9%, the IDs for 131 (100%) were correct to the species level. In 202 bottles where VMS was able to generate an ID, the IDs for 189 (93.6%) were correct to the species level, whereas the IDs provided for 7 isolates (3.5%) were incorrect. In conclusion, this method does not require centrifugation and produces a clean spectrum for VMS analysis in less than 15 min. This study demonstrates the effectiveness of the new lysis-filtration method for identifying microorganisms directly from positive-blood-culture bottles in a clinical setting.
Poly(ADP-Ribose) Polymerase 1 Promotes Transcriptional Repression of Integrated Retroviruses
Authors: Bueno Murilo T. D. , Reyes Daniel , Valdes Luis , Saheba Adarsh , Urias Eduardo , Mendoza Crystal , Fregoso Oliver I. , Llano Manuel 
Published: December 2012

ABSTRACT

Poly(ADP-ribose) polymerase 1 (PARP-1) is a cellular enzyme with a fundamental role in DNA repair and the regulation of chromatin structure, processes involved in the cellular response to retroviral DNA integration. However, the function of PARP-1 in retroviral DNA integration is controversial, probably due to the functional redundancy of the PARP family in mammalian cells. We evaluated the function of PARP-1 in retroviral infection using the chicken B lymphoblastoid cell line DT40. These cells lack significant PARP-1 functional redundancy and efficiently support the postentry early events of the mammalian-retrovirus replication cycle. We observed that DT40 PARP-1
−/−
cells were 9- and 6-fold more susceptible to infection by human immunodeficiency virus type 1 (HIV-1)- and murine leukemia virus (MLV)-derived viral vectors, respectively, than cells expressing PARP-1. Production of avian Rous-associated virus type 1 was also impaired by PARP-1. However, the susceptibilities of these cell lines to infection by the nonretrovirus vesicular stomatitis virus were indistinguishable. Real-time PCR analysis of the HIV-1 life cycle demonstrated that PARP-1 did not impair reverse transcription, nuclear import of the preintegration complex, or viral DNA integration, suggesting that PARP-1 regulates a postintegration step. In support of this hypothesis, pharmacological inhibition of the epigenetic mechanism of transcriptional silencing increased retroviral expression in PARP-1-expressing cells, suppressing the differences observed. Further analysis of the implicated molecular mechanism indicated that PARP-1-mediated retroviral silencing requires the C-terminal region, but not the enzymatic activity, of the protein. In sum, our data indicate a novel role of PARP-1 in the transcriptional repression of integrated retroviruses.
Recruitment and Retention of B Cells in the Central Nervous System in Response to Alphavirus Encephalomyelitis
Authors: Metcalf Talibah U. , Baxter Victoria K. , Nilaratanakul Voraphoj , Griffin Diane E. 
Published: December 2012

ABSTRACTSindbis virus (SINV) infection of neurons results in nonfatal viral encephalomyelitis and provides a model system for understanding recovery from virus infection of the central nervous system (CNS). Infection is followed by clearance of infectious virus, a gradual decrease in viral RNA, and then long-term maintenance of low levels of viral RNA. Antibody to the E2 glycoprotein is important for virus clearance, and B cells enter the CNS along with CD4+and CD8+T cells during the early clearance phase. Antibody-secreting cells (ASCs) are present in the CNS and become enriched for SINV-specific ASCs. We have evaluated the factors within the CNS that facilitate continued local antibody production after infection. Expression of CXCL9, CXCL10, CCL1, CCL2, and CCL5 chemokine mRNAs increased early, and infiltrating B cells expressed CXCR3, CXCR5, and CCR7. The mRNAs for IL-10 and IL-21, cytokines important for B cell proliferation and differentiation, rose rapidly and remained elevated long after clearance of infectious virus. Active proliferation of B cells, as indicated by Ki-67 expression, continued for months. Bromodeoxyuridine (BrdU) labeling of proliferating cells showed that ASCs produced in the draining cervical lymph nodes during the early germinal center response were preferentially retained in the CNS. Sustained increase in B-cell-activating factor (BAFF) mRNA in the CNS and BAFF receptor expression by B cells coincided with the long-term maintenance of SINV-specific ASCs in the brain. We conclude that multiple changes in the brain microenvironment facilitate B-cell entry and support proliferation and differentiation and long-term survival of antiviral ASCs during recovery from alphaviral encephalomyelitis.
Evidence for a Different Susceptibility of Primate Lentiviruses to Type I Interferons
Authors: Cordeil Stéphanie , Nguyen Xuan-Nhi , Berger Gregory , Durand Stéphanie , Ainouze Michelle , Cimarelli Andrea 
Published: December 2012

ABSTRACTType I interferons induce a complex transcriptional program that leads to a generalized antiviral response against a large panel of viruses, including human immunodeficiency virus type 1 (HIV-1). However, despite the fact that interferons negatively regulate HIV-1ex vivo, a chronic interferon state is linked to the progression of AIDS and to robust viral replication, rather than protection,in vivo. To explain this apparent contradiction, we hypothesized that HIV-1 may have evolved a partial resistance to interferon, and to test this hypothesis, we analyzed the effects of alpha interferon (IFN-α) on the infectivity of HIV-1, human immunodeficiency virus type 2 (HIV-2), and rhesus monkey simian immunodeficiency virus (SIVmac). The results we obtained indicate that HIV-1 is more resistant to an IFN-α-induced response than are HIV-2 and SIVmac. Our data indicate that the accumulation of viral DNA is more compromised following the infection of IFN-α-treated cells with HIV-2 and SIVmac than with HIV-1. This defect correlates with a faster destabilization of HIV-2 viral nucleoprotein complexes (VNCs), suggesting a link between VNC destabilization and impaired viral DNA (vDNA) accumulation. The differential susceptibilities to IFN-α of the primate lentiviruses tested here do not map to the capsid protein (CA), excludingde factoa role for human tripartite motif protein isoform 5 alpha (Trim5α) in this restriction; this also suggests that an additional restriction mechanism differentially affects primate lentivirus infection. The different behaviors of HIV-1 and HIV-2 with respect to IFN-α responses may account at least in part for the differences in pathogenesis observed between these two virus types.
Mutant Fusion Proteins with Enhanced Fusion Activity Promote Measles Virus Spread in Human Neuronal Cells and Brains of Suckling Hamsters
Authors: Watanabe Shumpei , Shirogane Yuta , Suzuki Satoshi O. , Ikegame Satoshi , Koga Ritsuko , Yanagi Yusuke 
Published: December 2012

ABSTRACT
Subacute sclerosing panencephalitis (SSPE) is a fatal degenerative disease caused by persistent measles virus (MV) infection in the central nervous system (CNS). From the genetic study of MV isolates obtained from SSPE patients, it is thought that defects of the matrix (M) protein play a crucial role in MV pathogenicity in the CNS. In this study, we report several notable mutations in the extracellular domain of the MV fusion (F) protein, including those found in multiple SSPE strains. The F proteins with these mutations induced syncytium formation in cells lacking SLAM and nectin 4 (receptors used by wild-type MV), including human neuronal cell lines, when expressed together with the attachment protein hemagglutinin. Moreover, recombinant viruses with these mutations exhibited neurovirulence in suckling hamsters, unlike the parental wild-type MV, and the mortality correlated with their fusion activity. In contrast, the recombinant MV lacking the M protein did not induce syncytia in cells lacking SLAM and nectin 4, although it formed larger syncytia in cells with either of the receptors. Since human neuronal cells are mainly SLAM and nectin 4 negative, fusion-enhancing mutations in the extracellular domain of the F protein may greatly contribute to MV spread via cell-to-cell fusion in the CNS, regardless of defects of the M protein.
Early Adaptive Immune Responses in the Respiratory Tract of Foot-and-Mouth Disease Virus-Infected Cattle
Authors: Pega J. , Bucafusco D. , Di Giacomo S. , Schammas J. M. , Malacari D. , Capozzo A. V. , Arzt J. , Pérez-Beascoechea C. , Maradei E. , Rodríguez L. L. , Borca M. V. , Pérez-Filgueira M. 
Published: December 2012

ABSTRACT
Foot-and-mouth disease (FMD) is a highly contagious viral disease which affects both domestic and wild biungulate species. This acute disease, caused by the FMD virus (FMDV), usually includes an active replication phase in the respiratory tract for up to 72 h postinfection, followed by hematogenous dissemination and vesicular lesions at oral and foot epithelia. The role of the early local adaptive immunity of the host in the outcome of the infection is not well understood. Here we report the kinetics of appearance of FMDV-specific antibody-secreting cells (ASC) in lymphoid organs along the respiratory tract and the spleen in cattle infected by aerosol exposure. While no responses were observed for up to 3 days postinfection (dpi), all animals developed FMDV-ASC in all the lymphoid organs studied at 4 dpi. Tracheobronchial lymph nodes were the most reactive organs at this time, and IgM was the predominant isotype, followed by IgG1. Numbers of FMDV-ASC were further augmented at 5 and 6 dpi, with an increasing prevalence in upper respiratory organs. Systemic antibody responses were slightly delayed compared with the local reaction. Also, IgM was the dominant isotype in serum at 5 dpi, coinciding with a sharp decrease of viral RNA detection in peripheral blood. These results indicate that following aerogenous administration, cattle develop a rapid and vigorous genuine local antibody response throughout the respiratory tract. Time course and isotype profiles indicate the presence of an efficient T cell-independent antibody response which drives the IgM-mediated virus clearance in cattle infected by FMDV aerosol exposure.
The PA-Gene-Mediated Lethal Dissemination and Excessive Innate Immune Response Contribute to the High Virulence of H5N1 Avian Influenza Virus in Mice
Authors: Hu Jiao , Hu Zenglei , Song Qingqing , Gu Min , Liu Xiaowen , Wang Xiaoquan , Hu Shunlin , Chen Chaoyang , Liu Huimou , Liu Wenbo , Chen Sujuan , Peng Daxin , Liu Xiufan 
Published: December 2012

ABSTRACT
Highly pathogenic H5N1 influenza A virus remains a substantial threat to public health. To understand the molecular basis and host mechanism for the high virulence of H5N1 viruses in mammals, we compared two H5N1 isolates which have similar genetic backgrounds but greatly differ in their virulence in mice. A/Chicken/Jiangsu/k0402/2010 (CK10) is highly pathogenic, whereas A/Goose/Jiangsu/k0403/2010 (GS10) is nonpathogenic. We first showed that CK10 elicited a more potent innate immune response than did GS10 in mouse lungs by increasing the number and expression levels of activated genes. We then generated a series of reassortants between the two viruses and evaluated their virulence in mice. Inclusion of the CK10 PA gene in the GS10 background resulted in a dramatic increase in virulence. Conversely, expression of the GS10 PA gene in the CK10 background significantly attenuated the virulence. These results demonstrated that the PA gene mainly determines the pathogenicity discrepancy between CK10 and GS10 in mice. We further determined that arginine (R) at position 353 of the PA gene contributes to the high virulence of CK10 in mice. The reciprocal substitution at position 353 in PA or the exchange of the entire PA gene largely caused the transfer of viral phenotypes, including virus replication, polymerase activity, and manipulation of the innate response, between CK10 and GS10. We therefore defined a novel molecular marker associated with the high virulence of H5N1 influenza viruses, providing further insights into the pathogenesis of H5N1 viruses in mammals.