bluuebunny/crossref_metadata_2025_split huggingface dataset:
Specific Serodiagnosis of Canine Visceral Leishmaniasis Using
Leishmania
Species Ribosomal Protein Extracts
Authors: Coelho Eduardo A. F. , Ramírez Laura , Costa Mariana A. F. , Coelho Vinicio T. S. , Martins Vivian T. , Chávez-Fumagalli Miguel A. , Oliveira Dulcilene M. , Tavares Carlos A. P. , Bonay Pedro , Nieto Carlos Gómez , Abánades Daniel R. , Alonso Carlos , Soto Manuel 
Published: October 2009

ABSTRACT

In the present work, we have analyzed the antigenicity of
Leishmania
species ribosomal proteins (LRPs). To accomplish this,
Leishmania infantum
ribosomes were biochemically purified from promastigote cytosolic extracts, and their reactivities were analyzed by using the sera from dogs naturally infected with
L. infantum
. Since antibodies reacting against different ribosomal proteins were observed in all the serum samples obtained from dogs with symptomatic visceral leishmaniasis tested, we have analyzed the potential usefulness of the LRP extracts in the development of an enzyme-linked immunosorbent assay (ELISA) for the serodiagnosis of canine visceral leishmaniasis (CVL) in an area of Brazil where visceral leishmaniasis is endemic due to infection by
Leishmania chagasi
. A comparative ELISA with crude soluble
Leishmania chagasi
antigen (SLA) and
L. infantum
LRPs was performed. LRP- and SLA-based ELISAs gave similar sensitivities for the diagnosis of symptomatic CVL, but the LRP extract provided a very high sensitivity for the detection of oligosymptomatic and asymptomatic dogs. In addition, an LRP-based ELISA showed a higher specificity when the sera from dogs harboring other infections were included in the analysis. The LRP antigen displayed no cross-reactivity with sera from dogs that had any of the other diseases tested, notably, Chagas' disease. Our findings suggest that LRPs are a potential tool for the diagnosis of CVL and will be particularly useful for the diagnosis of asymptomatic CVL.
Spurious Amplification of a
Plasmodium vivax
Small-Subunit RNA Gene by Use of Primers Currently Used To Detect
P. knowlesi
Authors: Imwong Mallika , Tanomsing Naowarat , Pukrittayakamee Sasithon , Day Nicholas P. J. , White Nicholas J. , Snounou Georges 
Published: October 2009

ABSTRACT

The PCR primers commonly used to detect
Plasmodium knowlesi
infections in humans were found to cross-react stochastically with
P. vivax
genomic DNA. A nested primer set that targets one of the
P. knowlesi
small-subunit rRNA genes was validated for specificity and for sensitivity of detection of <10 parasite genomes.
Postoperative Mediastinitis Due to
Finegoldia magna
with Negative Blood Cultures
Authors: Kernéis Solen , Matta Matta , Hoï Annie Buu , Podglajen Isabelle , Gutmann Laurent , Novara Ana , Latremouille Christian , Mainardi Jean-Luc 
Published: October 2009

ABSTRACT

We report a case of
Finegoldia magna
(formerly known as
Peptostreptococcus magnus
) mediastinitis following coronary artery bypass in a 50-year-old patient. Even if staphylococci remain the main causative organism of postoperative mediastinitis, the responsibility of anaerobic bacteria must be considered in cases of fever and sternal drainage with negative blood cultures.
Practical Disk Diffusion Test for Detecting Group B Streptococcus with Reduced Penicillin Susceptibility
Authors: Kimura Kouji , Wachino Jun-ichi , Kurokawa Hiroshi , Suzuki Satowa , Yamane Kunikazu , Shibata Naohiro , Arakawa Yoshichika 
Published: October 2009

ABSTRACT
Although group B streptococcus (GBS) has been considered to be uniformly susceptible to β-lactams, the presence of GBS with reduced penicillin susceptibility (PRGBS) was recently confirmed genetically. We developed a feasible and reliable method for screening PRGBS in clinical microbiology laboratories using a combination of ceftibuten, oxacillin, and ceftizoxime disks.
Detection of Novel Sequences Related to African Swine Fever Virus in Human Serum and Sewage
Authors: Loh Joy , Zhao Guoyan , Presti Rachel M. , Holtz Lori R. , Finkbeiner Stacy R. , Droit Lindsay , Villasana Zoilmar , Todd Collin , Pipas James M. , Calgua Byron , Girones Rosina , Wang David , Virgin Herbert W. 
Published: October 2009

ABSTRACT

The family
Asfarviridae
contains only a single virus species, African swine fever virus (ASFV). ASFV is a viral agent with significant economic impact due to its devastating effects on populations of domesticated pigs during outbreaks but has not been reported to infect humans. We report here the discovery of novel viral sequences in human serum and sewage which are clearly related to the asfarvirus family but highly divergent from ASFV. Detection of these sequences suggests that greater genetic diversity may exist among asfarviruses than previously thought and raises the possibility that human infection by asfarviruses may occur.
Heparan Sulfate Proteoglycans Are Required for Cellular Binding of the Hepatitis E Virus ORF2 Capsid Protein and for Viral Infection
Authors: Kalia Manjula , Chandra Vivek , Rahman Sheikh Abdul , Sehgal Deepak , Jameel Shahid 
Published: October 2009

ABSTRACT
The hepatitis E virus (HEV), a nonenveloped RNA virus, is the causative agent of hepatitis E. The mode by which HEV attaches to and enters into target cells for productive infection remains unidentified. Open reading frame 2 (ORF2) of HEV encodes its major capsid protein, pORF2, which is likely to have the determinants for virus attachment and entry. Using an ∼56-kDa recombinant pORF2 that can self-assemble as virus-like particles, we demonstrated that cell surface heparan sulfate proteoglycans (HSPGs), specifically syndecans, play a crucial role in the binding of pORF2 to Huh-7 liver cells. Removal of cell surface heparan sulfate by enzymatic (heparinase) or chemical (sodium chlorate) treatment of cells or competition with heparin, heparan sulfate, and their oversulfated derivatives caused a marked reduction in pORF2 binding to the cells. Syndecan-1 is the most abundant proteoglycan present on these cells and, hence, plays a key role in pORF2 binding. Specificity is likely to be dictated by well-defined sulfation patterns on syndecans. We show that pORF2 binds syndecans predominantly via 6-O sulfation, indicating that binding is not entirely due to random electrostatic interactions. Using an in vitro infection system, we also showed a marked reduction in HEV infection of heparinase-treated cells. Our results indicate that, analogous to some enveloped viruses, a nonenveloped virus like HEV may have also evolved to use HSPGs as cellular attachment receptors.
Rift Valley Fever Virus L Protein Forms a Biologically Active Oligomer
Authors: Zamoto-Niikura Aya , Terasaki Kaori , Ikegami Tetsuro , Peters C. J. , Makino Shinji 
Published: October 2009

ABSTRACT

Rift Valley fever virus
(RVFV) (genus
Phlebovirus
, family
Bunyaviridae
) causes mosquito-borne epidemic diseases in humans and livestock. The virus carries three RNA segments, L, M, and S, of negative or ambisense polarity. L protein, an RNA-dependent RNA polymerase, encoded in the L segment, and N protein, encoded in the S segment, exert viral RNA replication and transcription. Coexpression of N, hemagglutinin (HA)-tagged L, and viral minigenome resulted in minigenome replication and transcription, a finding that demonstrated HA-tagged L was biologically active. Likewise L tagged with green fluorescent protein (GFP) was biologically competent. Coimmunoprecipitation analysis using extracts from cells coexpressing HA-tagged L and GFP-tagged L showed the formation of an L oligomer. Bimolecular fluorescence complementation analysis and coimmunoprecipitation studies demonstrated the formation of an intermolecular L-L interaction through its N-terminal and C-terminal regions and also suggested an intramolecular association between the N-terminal and C-terminal regions of L protein. A biologically inactive L mutant, in which the conserved signature SDD motif was replaced by the amino acid residues GNN, exhibited a dominant negative phenotype when coexpressed with wild-type L in the minigenome assay system. Expression of this mutant L also inhibited viral gene expression in virus-infected cells. These data provided compelling evidence for the importance of oligomerization of RVFV L protein for its polymerase activity.
Identification of Hepatitis C Virus NS5A Inhibitors
Authors: Lemm Julie A. , O'Boyle Donald , Liu Mengping , Nower Peter T. , Colonno Richard , Deshpande Milind S. , Snyder Lawrence B. , Martin Scott W. , St. Laurent Denis R. , Serrano-Wu Michael H. , Romine Jeffrey L. , Meanwell Nicholas A. , Gao Min 
Published: October 2009

ABSTRACT
Using a cell-based replicon screen, we identified a class of compounds with a thiazolidinone core structure as inhibitors of hepatitis C virus (HCV) replication. The concentration of one such compound, BMS-824, that resulted in a 50% inhibition of HCV replicon replication was ∼5 nM, with a therapeutic index of >10,000. The compound showed good specificity for HCV, as it was not active against several other RNA and DNA viruses. Replicon cells resistant to BMS-824 were isolated, and mutations were identified. A combination of amino acid substitutions of leucine to valine at residue 31 (L31V) and glutamine to leucine at residue 54 (Q54L) in NS5A conferred resistance to this chemotype, as did a single substitution of tyrosine to histidine at amino acid 93 (Y93H) in NS5A. To further explore the region(s) of NS5A involved in inhibitor sensitivity, genotype-specific NS5A inhibitors were used to evaluate a series of genotype 1a/1b hybrid replicons. Our results showed that, consistent with resistance mapping, the inhibitor sensitivity domain also mapped to the N terminus of NS5A, but it could be distinguished from the key resistance sites. In addition, we demonstrated that NS5A inhibitors, as well as an active-site inhibitor that specifically binds NS3 protease, could block the hyperphosphorylation of NS5A, which is believed to play an essential role in the viral life cycle. Clinical proof of concept has recently been achieved with derivatives of these NS5A inhibitors, indicating that small molecules targeting a nontraditional viral protein like NS5A, without any known enzymatic activity, can also have profound antiviral effects on HCV-infected subjects.
Effects of Major Capsid Proteins, Capsid Assembly, and DNA Cleavage/Packaging on the pU
L
17/pU
L
25 Complex of Herpes Simplex Virus 1
Authors: Scholtes Luella , Baines Joel D. 
Published: October 2009

ABSTRACT

The U
L
17 and U
L
25 proteins (pU
L
17 and pU
L
25, respectively) of herpes simplex virus 1 are located at the external surface of capsids and are essential for DNA packaging and DNA retention in the capsid, respectively. The current studies were undertaken to determine whether DNA packaging or capsid assembly affected the pU
L
17/pU
L
25 interaction. We found that pU
L
17 and pU
L
25 coimmunoprecipitated from cells infected with wild-type virus, whereas the major capsid protein VP5 (encoded by the U
L
19 gene) did not coimmunoprecipitate with these proteins under stringent conditions. In addition, pU
L
17 (i) coimmunoprecipitated with pU
L
25 in the absence of other viral proteins, (ii) coimmunoprecipitated with pU
L
25 from lysates of infected cells in the presence or absence of VP5, (iii) did not coimmunoprecipitate efficiently with pU
L
25 in the absence of the triplex protein VP23 (encoded by the U
L
18 gene), (iv) required pU
L
25 for proper solubilization and localization within the viral replication compartment, (v) was essential for the sole nuclear localization of pU
L
25, and (vi) required capsid proteins VP5 and VP23 for nuclear localization and normal levels of immunoreactivity in an indirect immunofluorescence assay. Proper localization of pU
L
25 in infected cell nuclei required pU
L
17, pU
L
32, and the major capsid proteins VP5 and VP23, but not the DNA packaging protein pU
L
15. The data suggest that VP23 or triplexes augment the pU
L
17/pU
L
25 interaction and that VP23 and VP5 induce conformational changes in pU
L
17 and pU
L
25, exposing epitopes that are otherwise partially masked in infected cells. These conformational changes can occur in the absence of DNA packaging. The data indicate that the pU
L
17/pU
L
25 complex requires multiple viral proteins and functions for proper localization and biochemical behavior in the infected cell.
Conversion of VPg into VPgpUpU
OH
before and during Poliovirus Negative-Strand RNA Synthesis
Authors: Steil Benjamin P. , Barton David J. 
Published: October 2009

ABSTRACT

There are two protein primers involved in picornavirus RNA replication, VPg, the viral protein of the genome, and VPgpUpU
OH
. A
cis
-acting replication element (CRE) within the open reading frame of poliovirus (PV) RNA allows the viral RNA-dependent RNA polymerase 3D
Pol
to catalyze the conversion of VPg into VPgpUpU
OH
. In this study, we used preinitiation RNA replication complexes (PIRCs) to determine when CRE-dependent VPg uridylylation occurs relative to the sequential synthesis of negative- and positive-strand RNA. Guanidine HCl (2 mM), a reversible inhibitor of PV 2C
ATPase
, prevented CRE-dependent VPgpUpU
OH
synthesis and the initiation of negative-strand RNA synthesis. VPgpUpU
OH
and nascent negative-strand RNA molecules were synthesized coincident in time following the removal of guanidine, consistent with PV RNA functioning simultaneously as a template for CRE-dependent VPgpUpU
OH
synthesis and negative-strand RNA synthesis. The amounts of [
32
P]UMP incorporated into VPgpUpU
OH
and negative-strand RNA products indicated that 100 to 400 VPgpUpU
OH
molecules were made coincident in time with each negative-strand RNA. 3′-dCTP inhibited the elongation of nascent negative-strand RNAs without affecting CRE-dependent VPg uridylylation. A 3′ nontranslated region mutation which inhibited negative-strand RNA synthesis did not inhibit CRE-dependent VPg uridylylation. Together, the data implicate 2C
ATPase
in the mechanisms whereby PV RNA functions as a template for reiterative CRE-dependent VPg uridylylation before and during negative-strand RNA synthesis.
Visualizing what lies inside
Authors: Correa Carlos D. 
Published: October 2009

Medical imaging has given radiologists an ability that photography was not able to provide: it lets them see inside the human body. With the advent of 3D visualization systems, these images can be put together into crisp and impressive renderings of the human body from a variety of perspectives that were only dreamt of before, revolutionizing clinical practice.
Light transport models soon emerged to allow light interactions that, although not realistic in the physical sense, proved to be more effective for understanding the complex relationships among the anatomical structures. For instance, bone could be made semi-transparent to provide visibility of brain tissue. Skin could be removed altogether from an image to show only muscle or internal organs. However, soon it became evident that simply rendering these images in their raw form was no longer effective and the clear visualization of internal structures remains elusive.
The depiction of internal parts in the context of the enclosing space is a difficult problem that has occupied the mind of artists, illustrators and visualization practitioners. Despite the advances made in computer graphics for simulating the light transport in semi-transparent media, the problem of visualizing internal objects is no longer a rendering problem, but that of classification. Medical imaging technology obtains representations of anatomical structures via indirect ways, such as the response of tissue to X-rays or the alignment of electrons in a magnetic field. Therefore, the absence of semantic information prevents visualization practitioners from clearly marking up the regions that must be visualized. Without access to those regions, exploration becomes tedious and time-consuming. The predominant approach has been the use of transfer functions, or opacity mappings, which assign transparency properties to different intervals in the data. This method, however, does not guarantee that internal structures are visible. Other strategies must be used. In this article, I describe some visualization techniques that have emerged to obtain clear views of internal features in 3D volume data.
Speculative N-Way barriers (abstract only)
Authors: Ziarek Lukasz , Jagannathan Suresh , Fluet Matthew , Acar Umut A. 
Published: October 2009

Speculative execution is an important technique that has historically been used to extract concurrency from sequential programs. While techniques to support speculation work well when computations perform relatively simple actions (e.g., reads and writes to known locations), understanding speculation for multi-threaded programs in which threads may communicate and synchronize through multiple shared references is significantly more challenging, and is the focus of this paper.
We use as our reference point a simple higher-order concurrent language extended with an n-way barrier and a fork/join execution model. Our technique permits the expression guarded by the barrier to speculatively proceed before the barrier has been satisfied (i.e., before all threads that synchronize on that barrier have done so) and to have participating threads that would normally block on the barrier to speculatively proceed as well. Our solution formulates safety properties under which speculation is correct in a fork/join model, and per-synchronization basis.
Controlling chaos
Authors: Herhut Stephan , Scholz Sven-Bodo , Grelck Clemens 
Published: October 2009

With the rising variety of hardware designs for multi-core systems, the effectiveness in exploiting implicit concurrency of programs plays a more vital role for programming such systems than ever before. We believe that a combination of a dataparallel approach with a declarative programming-style is up to that task: Data-parallel approaches are known to enable compilers to make efficient use of multi-processors without requiring low-level program annotations. Combining the dataparallel approach with a declarative programming-style guarantees semantic equivalence between sequential and concurrent executions of data parallel operations. Furthermore, the side-effect free setting and explicit model of dependencies enables compilers to maximise the size of the data-parallel program sections.
However, the strength of the rigidity of the declarative approach also constitutes its weakness: Being bound to observe all data dependencies categorically rules out the use of side-effecting operations within data-parallel sections. Not only does this limit the size of these regions in certain situations, but it may also hamper an effective workload distribution. Considering side effects such as plotting individual pixels of an image or output for debugging purposes, there are situations where a non-deterministic order of side-effects would not be considered harmful at all.
We propose a mechanism for enabling such non-determinism on the execution of side-effecting operations within data-parallel sections without sacrificing the side-effect free setting in general. Outside of the data-parallel sections we ensure singlethreading of side-effecting operations using uniqueness typing. Within data-parallel operations however we allow the sideeffecting operations of different threads to occur in any order, as long as effects of different threads are not interleaved. Furthermore, we still model the dependencies arising from the manipulated states within the data parallel sections. This measure preserves the explicitness of all data dependencies and therefore it preserves the transformational potential of any restructuring compiler.
Comparing the performance of concurrent linked-list implementations in Haskell
Authors: Sulzmann Martin , Lam Edmund S.L. , Marlow Simon 
Published: October 2009

Haskell has a rich set of synchronization primitives for implementing shared-state concurrency abstractions, ranging from the very high level (Software Transactional Memory) to the very low level (mutable variables with atomic read-modify-write).
In this paper we perform a systematic comparison of these different concurrent programming models by using them to implement the same abstraction: a concurrent linked-list. Our results are somewhat surprising: there is a full two orders of magnitude difference in performance between the slowest and the fastest implementation. Our analysis of the performance results gives new insights into the relative performance of the programming models and their implementation.
Finally, we suggest the addition of a single primitive which in our experiments improves the performance of one of the STM-based implementations by more than a factor of 7.
Some Convergence Theorems of a Sequence in Complete Metric Spaces and Its Applications
Authors: Ahmed MA , Zeyada FM 
Published: October 2009

AbstractThe concept of weakly quasi-nonexpansive mappings with respect to a sequence is introduced. This concept generalizes the concept of quasi-nonexpansive mappings with respect to a sequence due to Ahmed and Zeyada (2002). Mainly, some convergence theorems are established and their applications to certain iterations are given.
Changes in CpG Islands Promoter Methylation Patterns during Ductal Breast Carcinoma Progression
Authors: Hoque Mohammad Obaidul , Prencipe Maria , Poeta Maria Luana , Barbano Raffaela , Valori Vanna Maria , Copetti Massimiliano , Gallo Antonietta Pia , Brait Mariana , Maiello Evaristo , Apicella Adolfo , Rossiello Raffaele , Zito Francesco , Stefania Tommasi , Paradiso Angelo , Carella Massimo , Dallapiccola Bruno , Murgo Roberto , Carosi Illuminato , Bisceglia Michele , Fazio Vito Michele , Sidransky David , Parrella Paola 
Published: October 2009

Abstract
Aberrant promoter methylation of several known or putative tumor suppressor genes occurs frequently during carcinogenesis, and this epigenetic change has been considered as a potential molecular marker for cancer. We examined the methylation status of nine genes (APC, CDH1, CTNNB1, TIMP3, ESR1, GSTP1, MGMT, THBS1, and TMS1), by quantitative methylation specific PCR. Synchronous preinvasive lesions (atypical ductal hyperplasia and/or ductal carcinoma in situ) and invasive ductal breast carcinoma from 52 patients, together with pure lesions from 24 patients and 12 normal tissues paired to tumor and 20 normal breast distant from tumor were analyzed. Aberrant promoter methylation was detected in both preinvasive and invasive lesions for genes APC, CDH1, CTNNB1, TIMP3, ESR1, and GSTP1. However, hierarchical mixed model and Generalized Estimating Equations model analyses showed that only APC, CDH1, and CTNNB1 promoter regions showed a higher frequency and methylation levels in pathologic samples when compared with normal breast. Whereas APC and CTNNB1 did not show differences in methylation levels or frequencies, CDH1 showed higher methylation levels in invasive tumors as compared with preinvasive lesions (P &lt; 0.04, Mann-Whitney test with permutation correction). The analysis of APC, CDH1, and CTNNB1 methylation status was able to distinguish between normal and pathologic samples with a sensitivity of 67% (95% confidence interval, 60-71%) and a specificity of 75% (95% confidence interval, 69-81%). Our data point to the direct involvement of APC, CDH1, and CTNNB1 promoter methylation in the early stages of breast cancer progression and suggest that they may represent a useful tool for the detection of tumor cells in clinical specimens. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2694–700)