bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of Methods for Identification and Determination of the Taxonomic Status of Strains Belonging to the Streptococcus porcinus-Streptococcus pseudoporcinus Complex Isolated from Animal, Human, and Dairy Sources
Authors: Shewmaker Patricia Lynn , Steigerwalt Arnold G. , Whitney Anne M. , Morey Roger E. , Graziano James C. , Facklam Richard R. , Musser Kimberlee A. , Merquior Vânia L. C. , Teixeira Lucia M. 
Published: August 2012

ABSTRACT

Ninety-seven animal, human, and dairy
Streptococcus porcinus
or
Streptococcus pseudoporcinus
isolates in the CDC
Streptococcus
strain collection were evaluated on the basis of DNA-DNA reassociation, 16S rRNA and
rpoB
gene sequencing, conventional biochemical and Rapid ID 32 Strep identification methods, and antimicrobial susceptibility testing to determine their taxonomic status, characteristics for species differentiation, antimicrobial susceptibility, and relevance of clinical source. Nineteen of the 97 isolates (1 human, 18 swine) were identified as
S. porcinus
. The remaining 72 human isolates and 6 dairy isolates were identified as
S. pseudoporcinus.
The use of 16S rRNA or
rpoB
gene sequencing was required to differentiate
S. porcinus
from
S. pseudoporcinus
. The human and dairy
S. pseudoporcinus
isolates were biochemically distinct from each other as well as distinct by 16S rRNA and
rpoB
gene sequencing. Therefore, we propose the subspecies denominations
S. pseudoporcinus
subsp
. hominis
subsp. nov. for the human isolates and
S. pseudoporcinus
subsp.
lactis
subsp. nov. for the dairy isolates. Most strains were susceptible to the antimicrobials tested, with the exception of tetracycline. Two strains of each species were also resistant to clindamycin and erythromycin and carried the
erm
(A) (
S. pseudoporcinus
) or the
erm
(B) (
S. porcinus
) gene.
S. porcinus
was identified from a single human isolate recovered from a wound in an abattoir worker.
S. pseudoporcinus
was primarily isolated from the genitourinary tract of women but was also associated with blood, placental, and wound infections. Isolates reacting with group B antiserum and demonstrating wide beta-hemolysis should be suspected of being
S. pseudoporcinus
and not
S. agalactiae
.
Rapid Determination of Lymphogranuloma Venereum Serovars of Chlamydia trachomatis by Quantitative High-Resolution Melt Analysis (HRMA)
Authors: Twin Jimmy , Stevens Matthew P. , Garland Suzanne M. , Zaia Angelo M. , Tabrizi Sepehr N. 
Published: August 2012

ABSTRACT

A quantitative high-resolution melt analysis assay was developed to differentiate lymphogranuloma venereum-causing serovars of
Chlamydia trachomatis
(L1 to L3) from other
C. trachomatis
serovars (D to K). The detection limit of this assay is approximately 10 copies per reaction, comparable to the limits of other quantitative-PCR-based methods.
Comparative Evaluation of Tigecycline Susceptibility Testing Methods for Expanded-Spectrum Cephalosporin- and Carbapenem-Resistant Gram-Negative Pathogens
Authors: Zarkotou Olympia , Pournaras Spyros , Altouvas George , Pitiriga Vassiliki , Tziraki Maria , Mamali Vassiliki , Themeli-Digalaki Katerina , Tsakris Athanassios 
Published: August 2012

ABSTRACT

We evaluated the Vitek2, Etest, and MIC Test Strip (MTS) methods of tigecycline susceptibility testing with 241 expanded-spectrum cephalosporin-resistant and/or carbapenem-resistant
Enterobacteriaceae
and
Acinetobacter baumannii
clinical isolates by using dry-form broth microdilution (BMD) as the reference method. The MIC
50/90
s were as follows: BMD, 1/4 μg/ml; Vitek2, 4/≥8 μg/ml; Etest, 2/4 μg/ml; MTS, 0.5/2 μg/ml. Vitek2 produced 9.1/21.2% major errors, Etest produced 0.4/0.8% major errors, and MTS produced no major errors but 0.4/3.3% very major errors (FDA/EUCAST breakpoints). Vitek2 tigecycline results require confirmation by BMD or Etest for multidrug-resistant pathogens.
Genetic Heterogeneity and Recombination in Human Type 2 Astroviruses
Authors: De Grazia S. , Medici M. C. , Pinto P. , Moschidou P. , Tummolo F. , Calderaro A. , Bonura F. , Banyai K. , Giammanco G. M. , Martella V. 
Published: August 2012

ABSTRACT
Novel lineages of human astrovirus (HAstV) types 2, 2c, and 2d have been identified. Upon sequencing of the 3′ end of the genome, the type 2c and 2d HAstVs were found to be open reading frame 1b (ORF1b)-ORF2 recombinant, with ORF1b being derived from type 3 and type 1 HAstVs, respectively. An ORF2 interlineage recombinant strain, 2c/2b, was also identified.
Antibody-Independent Thrombocytopenia in Lactate Dehydrogenase-Elevating Virus-Infected Mice
Authors: Su Dan , Musaji Andrei , Legrain Sarah , Detalle Laurent , van der Kaa Jos , Verbeek J. Sjef , Ryffel Bernhard , Coutelier Jean-Paul 
Published: August 2012

ABSTRACT
Previously we demonstrated that antibody-mediated thrombocytopenia is strongly enhanced by lactate dehydrogenase-elevating virus (LDV) infection. Here we report that mice infected with LDV develop a moderate thrombocytopenia, even in the absence of immunoglobulins or Fc receptors. A similar decrease of platelet counts was observed after mouse hepatitis virus infection. LDV-induced type I interferon-independent thrombocytopenia was partly suppressed by treatment with clodronate-containing liposomes. Therefore, we conclude that the thrombocytopenia results from increased phagocytosis of nonopsonized platelets by macrophages.
p33-Independent Activation of a Truncated p92 RNA-Dependent RNA Polymerase of Tomato Bushy Stunt Virus in Yeast Cell-Free Extract
Authors: Pogany Judit , Nagy Peter D. 
Published: August 2012

ABSTRACT

Plus-stranded RNA viruses replicate in membrane-bound structures containing the viral replicase complex (VRC). A key component of the VRC is the virally encoded RNA-dependent RNA polymerase (RdRp), which should be activated and incorporated into the VRC after its translation. To study the activation of the RdRp of
Tomato bushy stunt virus
(TBSV), a small tombusvirus of plants, we used N-terminal truncated recombinant RdRp, which supported RNA synthesis in a cell-free yeast extract-based assay. The truncated RdRp required a
cis
-acting RNA replication element and soluble host factors, while unlike the full-length TBSV RdRp, the truncated RdRp did not need the viral p33 replication cofactor or cellular membranes for RNA synthesis. Interestingly, the truncated RdRp used 3′-terminal extension for initiation and terminated prematurely at an internal
cis
-acting element. However, the truncated RdRp could perform
de novo
initiation on a TBSV plus-strand RNA template in the presence of the p33 replication cofactor, cellular membranes, and soluble host proteins. Altogether, the data obtained with the truncated RdRp indicate that this RdRp still requires activation, but with the participation of fewer components than with the full-length RdRp, making it suitable for future studies on dissection of the RdRp activation mechanism.
Maintenance of the Flip Sequence Orientation of the Ears in the Parvoviral Left-End Hairpin Is a Nonessential Consequence of the Critical Asymmetry in the Hairpin Stem
Authors: Li Lei , Cotmore Susan F. , Tattersall Peter 
Published: August 2012

ABSTRACT

Parvoviral terminal hairpins are essential for viral DNA amplification but are also implicated in multiple additional steps in the viral life cycle. The palindromes at the two ends of the minute virus of mice (MVM) genome are dissimilar and are processed by different resolution mechanisms that selectively direct encapsidation of predominantly negative-sense progeny genomes and conserve a single Flip sequence orientation at the 3′ (left) end of such progeny. The sequence and predicted structure of these 3′ hairpins are highly conserved within the genus
Parvovirus
, exemplified by the 121-nucleotide left-end sequence of MVM, which folds into a Y-shaped hairpin containing small internal palindromes that form the “ears” of the Y. To explore the potential role(s) of this hairpin in the viral life cycle, we constructed infectious clones with the ear sequences either inverted, to give the antiparallel Flop orientation, or with multiple transversions, conserving their base composition but changing their sequence. These were compared with a “bubble” mutant, designed to activate the normally silent origin in the inboard arm of the hairpin, thus potentially rendering symmetric the otherwise asymmetric junction resolution mechanism that drives maintenance of Flip. This mutant exhibited a major defect in viral duplex and single-strand DNA replication, characterized by the accumulation of covalently closed turnaround forms of the left end, and was rapidly supplanted by revertants that restored asymmetry. In contrast, both sequence and orientation changes in the hairpin ears were tolerated, suggesting that maintaining the Flip orientation of these structures is a consequence of, but not the reason for, asymmetric left-end processing.
A Novel Assay for Antibody-Dependent Cell-Mediated Cytotoxicity against HIV-1- or SIV-Infected Cells Reveals Incomplete Overlap with Antibodies Measured by Neutralization and Binding Assays
Authors: Alpert Michael D. , Heyer Lisa N. , Williams David E. J. , Harvey Jackson D. , Greenough Thomas , Allhorn Maria , Evans David T. 
Published: August 2012

ABSTRACTThe resistance of human immunodeficiency virus type 1 (HIV-1) to antibody-mediated immunity often prevents the detection of antibodies that neutralize primary isolates of HIV-1. However, conventional assays for antibody functions other than neutralization are suboptimal. Current methods for measuring the killing of virus-infected cells by antibody-dependent cell-mediated cytotoxicity (ADCC) are limited by the number of natural killer (NK) cells obtainable from individual donors, donor-to-donor variation, and the use of nonphysiological targets. We therefore developed an ADCC assay based on NK cell lines that express human or macaque CD16 and a CD4+T-cell line that expresses luciferase from a Tat-inducible promoter upon HIV-1 or simian immunodeficiency virus (SIV) infection. NK cells and virus-infected targets are mixed in the presence of serial plasma dilutions, and ADCC is measured as the dose-dependent loss of luciferase activity. Using this approach, ADCC titers were measured in plasma samples from HIV-infected human donors and SIV-infected macaques. For the same plasma samples paired with the same test viruses, this assay was approximately 2 orders of magnitude more sensitive than optimized assays for neutralizing antibodies—frequently allowing the measurement of ADCC in the absence of detectable neutralization. Although ADCC correlated with other measures of Env-specific antibodies, neutralizing and gp120 binding titers did not consistently predict ADCC activity. Hence, this assay affords a sensitive method for measuring antibodies capable of directing ADCC against HIV- or SIV-infected cells expressing native conformations of the viral envelope glycoprotein and reveals incomplete overlap of the antibodies that direct ADCC and those measured in neutralization and binding assays.
Evidence thatIn VitroSusceptibility of CD3+T Lymphocytes to Equine Arteritis Virus Infection Reflects Genetic Predisposition of Naturally Infected Stallions To Become Carriers of the Virus
Authors: Go Yun Young , Bailey Ernest , Timoney Peter J. , Shuck Kathleen M. , Balasuriya Udeni B. R. 
Published: August 2012

ABSTRACTWe investigated the correlation betweenin vitrosusceptibility of CD3+T lymphocytes to equine arteritis virus (EAV) infection and establishment of persistent infection among 14 stallions following natural infections. The data showed that carrier stallions with a CD3+T lymphocyte susceptibility phenotype toin vitroEAV infection may be at higher risk of becoming carriers than those that lack this phenotype (P= 0.0002).
Visualization of the Two-Step Fusion Process of the Retrovirus Avian Sarcoma/Leukosis Virus by Cryo-Electron Tomography
Authors: Cardone Giovanni , Brecher Matthew , Fontana Juan , Winkler Dennis C. , Butan Carmen , White Judith M. , Steven Alasdair C. 
Published: August 2012

ABSTRACT
Retrovirus infection starts with the binding of envelope glycoproteins to host cell receptors. Subsequently, conformational changes in the glycoproteins trigger fusion of the viral and cellular membranes. Some retroviruses, such as avian sarcoma/leukosis virus (ASLV), employ a two-step mechanism in which receptor binding precedes low-pH activation and fusion. We used cryo-electron tomography to study virion/receptor/liposome complexes that simulate the interactions of ASLV virions with cells. Binding the soluble receptor at neutral pH resulted in virions capable of binding liposomes tightly enough to alter their curvature. At virion-liposome interfaces, the glycoproteins are ∼3-fold more concentrated than elsewhere in the viral envelope, indicating specific recruitment to these sites. Subtomogram averaging showed that the oblate globular domain in the prehairpin intermediate (presumably the receptor-binding domain) is connected to both the target and the viral membrane by 2.5-nm-long stalks and is partially disordered, compared with its native conformation. Upon lowering the pH, fusion took place. Fusion is a stochastic process that, once initiated, must be rapid, as only final (postfusion) products were observed. These fusion products showed glycoprotein spikes on their surface, with their interiors occupied by patches of dense material but without capsids, implying their disassembly. In addition, some of the products presented a density layer underlying and resolved from the viral membrane, which may represent detachment of the matrix protein to facilitate the fusion process.
Human CRM1 Augments Production of Infectious Human and Feline Immunodeficiency Viruses from Murine Cells
Authors: Elinav Hila , Wu Yuanfei , Coskun Ayse , Hryckiewicz Katarzyna , Kemler Iris , Hu Yani , Rogers Hilary , Hao Bing , Ben Mamoun Choukri , Poeschla Eric , Sutton Richard 
Published: August 2012

ABSTRACT
Productive replication of human immunodeficiency virus type 1 (HIV-1) occurs efficiently only in humans. The posttranscriptional stages of the HIV-1 life cycle proceed poorly in mouse cells, with a resulting defect in viral assembly and release. Previous work has shown that the presence of human chromosome 2 increases HIV-1 production in mouse cells. Recent studies have shown that human chromosome region maintenance 1 (hCRM1) stimulates Gag release from rodent cells. Here we report that expressions of hCRM1 in murine cells resulted in marked increases in the production of infectious HIV-1 and feline immunodeficiency virus (FIV). HIV-1 production was also increased by hSRp40, and a combination of hCRM1 and hSRp40 resulted in a more-than-additive effect on HIV-1 release. In contrast, the overexpression of mouse CRM1 (mCRM1) minimally affected HIV-1 and FIV production and did not antagonize hCRM1. In the presence of hCRM1 there were large increases in the amounts of released capsid, which paralleled the increases in the infectious titers. Consistent with this finding, the ratios of unspliced to spliced HIV-1 mRNAs in mouse cells expressing hCRM1 and SRp40 became similar to those of human cells. Furthermore, imaging of intron-containing FIV RNA showed that hCRM1 increased RNA export to the cytoplasm.By testing chimeras between mCRM1 and hCRM1 and comparing those sequences to feline CRM1, we mapped the functional domain to HEAT (Huntingtin, elongation factor 3, protein phosphatase 2A, and the yeast kinase TOR1) repeats 4A to 9A and a triple point mutant in repeat 9A, which showed a loss of function. Structural analysis suggested that this region of hCRM1 may serve as a binding site for viral or cellular factors to facilitate lentiviral RNA nuclear export.
INTRA-LEFT VENTRICULAR FLOW DISTRIBUTIONS IN DIASTOLIC AND SYSTOLIC PHASES, BASED ON ECHO VELOCITY FLOW MAPPING OF NORMAL SUBJECTS AND HEART FAILURE PATIENTS, TO CHARACTERIZE LEFT VENTRICULAR PERFORMANCE OUTCOMES OF HEART FAILURE
Authors: LE THU-THAO , TAN RU-SAN , HUANG FEIQIONG , ZHONG LIANG , IDAPALAPATI SRIDHAR , GHISTA DHANJOO 
Published: August 2012

Heart failure (HF), one of the most common diseases in the world, causes left ventricular dysfunction (LV) and high mortality. HF patients are stratified into two groups based on their LV ejection fraction (EF) — HF with normal EF (HFNEF) and with reduced EF (HFREF). EF is a commonly used measure of LV contractile performance. Despite preserved EF, a complex mixture of systolic and diastolic dysfunction and variable degrees of LV remodelling underlying HFNEF poses challenges to diagnose and provide pharmacological treatment for HFNEF. In recent years, the velocity flow mapping (VFM) technique has been developed to generate flow velocity vector fields by post-processing color Doppler echocardiographic (echo) images. We aim to obtain the intra-LV blood flow patterns for patients with HFNEF, HFREF, and normal subjects, in order to characterize the LV performance outcomes of normal subjects and HF patients.Two subjects from each group of HFNEF, HFREF, and normal underwent echo scans. Velocity vector distributions throughout the cardiac cycle were then analysed using the VFM technique. In each subject, the outflow rate during systole, inflow rate during diastole, as well as wall stress-based pressure-normalized contractility index, dσ*/dtmax, were computed and compared among the groups.This study demonstrated the use of VFM to visualize LV blood flow patterns in HF patients and normal subjects. Different patterns of flow distributions were observed in these subjects. In HFREF patients, dσ*/dtmax, the peak outflow rate and peak inflow rate during early filling were markedly reduced. In HFNEF patients, peak outflow rates were increased compared to those of normal subjects.
Superior Efficacy of a Combined Epigenetic Therapy against Human Mantle Cell Lymphoma Cells
Authors: Fiskus Warren , Rao Rekha , Balusu Ramesh , Ganguly Siddhartha , Tao Jianguo , Sotomayor Eduardo , Mudunuru Uma , Smith Jacqueline E. , Hembruff Stacey L. , Atadja Peter , Marquez Victor E. , Bhalla Kapil 
Published: August 2012

Abstract
Purpose: A deregulated epigenome contributes to the transformed phenotype of mantle cell lymphoma (MCL). This involves activity of the polycomb repressive complex (PRC) 2, containing three core proteins, EZH2, SUZ12, and EED, in which the SET domain of EZH2 mediates the histone methyltransferase activity. We determined the effects of 3-deazaneplanocin A (DZNep), an S-adenosylhomocysteine hydrolase inhibitor, and/or pan-histone deacetylase inhibitor panobinostat (PS) on cultured and primary MCL cells.
Experimental Design: Following treatment with DZNep and/or PS, apoptosis and the levels and activity of EZH2 and PRC2 proteins in cultured and primary MCL cells were determined.
Results: Treatment with DZNep depleted EZH2, SUZ12, and 3MeK27H3 in the cultured human MCL cells. DZNep also increased expression of p21, p27, and FBXO32, whereas it depleted Cyclin D1 and Cyclin E1 levels in MCL cells. In addition, DZNep treatment induced cell-cycle arrest and apoptosis in cultured and primary MCL cells. Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. Combined treatment with DZNep and PS synergistically induced apoptosis of cultured and primary MCL cells while relatively sparing normal CD34 + cells. Cotreatment with DZNep and PS also caused significantly greater inhibition of tumor growth of JeKo-1 xenografts in NOD/SCID mice.
Conclusions: These preclinical in vitro and in vivo findings show that cotreatment with DZNep and PS is an active combined epigenetic therapy worthy of further in vivo testing against MCL. Clin Cancer Res; 18(22); 6227–38. ©2012 AACR.
Intraoperative Near-Infrared Imaging of Surgical Wounds after Tumor Resections Can Detect Residual Disease
Authors: Madajewski Brian , Judy Brendan F. , Mouchli Anas , Kapoor Veena , Holt David , Wang May D. , Nie Shuming , Singhal Sunil 
Published: August 2012

Abstract
Purpose: Surgical resection remains the most effective therapy for solid tumors worldwide. The most important prognostic indicator for cure following cancer surgery is a complete resection with no residual disease. However, intraoperative detection of retained cancer cells after surgery is challenging, and residual disease continues to be the most common cause of local failure. We hypothesized that visual enhancement of tumors using near-infrared imaging could potentially identify tumor deposits in the wound after resection.
Experimental Design: A small animal model of surgery and retained disease was developed. Residual tumor deposits in the wound were targeted using an U.S. Food and Drug Administration–approved imaging agent, indocyanine green, by the enhanced permeability and retention effect. A novel handheld spectrometer was used to optically visualize retained disease after surgery.
Results: We found residual disease using near-infrared imaging during surgery that was not visible to the naked eye or micro-CT. Furthermore, examination of tumor nodules was remarkably precise in delineating margins from normal surrounding tissues. This approach was most successful for tumors with increased neovasculature.
Conclusions: The results suggest that near-infrared examination of the surgical wound after curative resection can potentially enable the surgeon to locate residual disease. The data in this study is the basis of an ongoing Phase I/II clinical trial in patients who undergo resection for lung and breast cancer. Clin Cancer Res; 18(20); 5741–51. ©2012 AACR.
IDO Expression in Brain Tumors Increases the Recruitment of Regulatory T Cells and Negatively Impacts Survival
Authors: Wainwright Derek A. , Balyasnikova Irina V. , Chang Alan L. , Ahmed Atique U. , Moon Kyung-Sub , Auffinger Brenda , Tobias Alex L. , Han Yu , Lesniak Maciej S. 
Published: August 2012

AbstractPurpose: Glioblastoma multiforme (GBM) is an aggressive adult brain tumor with a poor prognosis. One hallmark of GBM is the accumulation of immunosuppressive and tumor-promoting CD4+FoxP3+GITR+ regulatory T cells (Tregs). Here, we investigated the role of indoleamine 2,3 dioxygenase (IDO) in brain tumors and the impact on Treg recruitment.Experimental Design: To determine the clinical relevance of IDO expression in brain tumors, we first correlated patient survival to the level of IDO expression from resected glioma specimens. We also used novel orthotopic and transgenic models of glioma to study how IDO affects Tregs. The impact of tumor-derived and peripheral IDO expression on Treg recruitment, GITR expression, and long-term survival was determined.Results: Downregulated IDO expression in glioma predicted a significantly better prognosis in patients. Coincidently, both IDO-competent and deficient mice showed a survival advantage bearing IDO-deficient brain tumors, when compared with IDO-competent brain tumors. Moreover, IDO deficiency was associated with a significant decrease in brain-resident Tregs, both in orthotopic and transgenic mouse glioma models. IDO deficiency was also associated with lower GITR expression levels on Tregs. Interestingly, the long-term survival advantage conferred by IDO deficiency was lost in T-cell–deficient mice.Conclusions: These clinical and preclinical data confirm that IDO expression increases the recruitment of immunosuppressive Tregs that lead to tumor outgrowth. In contrast, IDO deficiency decreases Treg recruitment and enhances T-cell–mediated tumor rejection. Thus, the data suggest a critical role for IDO-mediated immunosuppression in glioma and support the continued investigation of IDO–Treg interactions in the context of brain tumors. Clin Cancer Res; 18(22); 6110–21. ©2012 AACR.