bluuebunny/crossref_metadata_2025_split huggingface dataset:
Early Antibody Responses to Experimental
Mycobacterium bovis
Infection of Cattle
Authors: Waters W. R. , Palmer M. V. , Thacker T. C. , Bannantine J. P. , Vordermeier H. M. , Hewinson R. G. , Greenwald R. , Esfandiari J. , McNair J. , Pollock J. M. , Andersen P. , Lyashchenko K. P. 
Published: June 2006

ABSTRACT

Bovine tuberculosis persists as a costly zoonotic disease in numerous countries despite extensive eradication and control efforts. Sequential serum samples obtained from
Mycobacterium bovis
-infected cattle were evaluated for seroreactivity to mycobacterial antigens. Animals received
M. bovis
by aerosol, intratonsil, intranasal, or intratracheal inoculation. Assays included the multiantigen print immunoassay for determination of antigen recognition patterns, immunoblot analysis for sensitive kinetic studies, and the VetTB STAT-PAK test, a novel, rapid test based on lateral-flow technology. Responses to MPB83 were detected for all
M. bovis
-infected animals regardless of the route or strain of
M. bovis
used for inoculation. Other less commonly recognized antigens included ESAT-6, CFP-10, and MPB70. Responses to MPB83 were detectable as early as 4 weeks after inoculation, were boosted upon injection of purified protein derivatives for skin testing, and persisted throughout the course of each of the four challenge studies. MPB83-specific immunoglobulin M (IgM) was detected prior to MPB83-specific IgG detection; however, early IgM responses rapidly waned, suggesting a benefit of tests that detect both IgM- and IgG-specific antibodies. The VetTB STAT-PAK test detected responses in sera from 60% (15/25) of the animals by 7 weeks after challenge and detected responses in 96% (24/25) of the animals by 18 weeks. These findings demonstrate the potential for new-generation antibody-based tests for the early detection of
M. bovis
infection in cattle.
Identification of a Haarlem Genotype-Specific Single Nucleotide Polymorphism in the
mgtC
Virulence Gene of
Mycobacterium tuberculosis
Authors: Alix Eric , Godreuil Sylvain , Blanc-Potard Anne-Béatrice 
Published: June 2006

ABSTRACT

MgtC is a virulence factor common to several intracellular pathogens, including
Mycobacterium tuberculosis
, that might have been acquired through horizontal gene transfer. In the present study, we investigated the polymorphism of
mgtC
in clinical isolates representative of the main epidemic groups of
M. tuberculosis
. MgtC appears to have a low polymorphism rate in
M. tuberculosis
that consists exclusively of nonsynonymous mutations. We identified a single nucleotide polymorphism (SNP) at
mgtC
codon 182 (
mgtC
182
) specifically associated with the Haarlem genotype. A simple PCR assay, called the “on/off switch assay,” using phosphorothioate-modified primers and
Pfu
polymerase allowed us to distinguish Haarlem from non-Haarlem strains based on the
mgtC
182
SNP. The amino acid change (H182R) associated with the
mgtC
182
SNP in Haarlem strains does not appear to procure a selective advantage. Our results offer a simple and rapid tool to distinguish between Haarlem and non-Haarlem strains. In addition, the on/off switch assay, which allows the detection of SNPs on chromosomal DNA and
M. tuberculosis
cultures, provides a novel approach for the screening of known SNPs in
M. tuberculosis
.
Keratitis Due to
Shigella flexneri
Authors: Muytjens Harry L. , Eggink Catharina A. , Dijkman Frederik C. A. P. , Bakkers Judith M. J. E. , Melchers Willem J. G. 
Published: June 2006

ABSTRACT

Multiresistant
Shigella flexneri
isolates were cultured from the cornea and stool of a girl. Genetic analysis showed the isolates were identical.
Shigella
spp. are rare causes of ulcerative keratitis; there have only been 14 published cases since 1943. Although prognosis after local treatment is good, shigellosis is a systemic infection, possibly leading to dehydration.
Variability of Kinetoplast DNA Gene Signatures of
Trypanosoma cruzi
II Strains from Patients with Different Clinical Forms of Chagas' Disease in Brazil
Authors: Lages-Silva Eliane , Ramírez Luis Eduardo , Pedrosa André Luiz , Crema Eduardo , da Cunha Galvão Lúcia Maria , Junho Pena Sérgio Danilo , Macedo Andrea Mara , Chiari Egler 
Published: June 2006

ABSTRACT

The clinical course of Chagas' disease varies widely among different patients and geographic regions. For reasons that are not completely understood but involve host and parasite factors, some patients never develop the disease while others present cardiac and/or gastrointestinal symptoms. Many studies have been conducted in order to correlate the genetic variability of the parasites with the clinical forms of the disease, but no conclusive data have been obtained. Our research aims at characterizing the genetic profiles of
Trypanosoma cruzi
isolates recently obtained from 70 chagasic patients who either showed pathological lesions with symptoms of various intensities or were asymptomatic. All patients came from an area where Chagas' disease is endemic in southeast Brazil where vectorial transmission has been controlled and different clinical forms of the disease can be found. The molecular characterization of parasites evaluated the polymorphisms of the 3′ region of the 24Sα rRNA gene and the variability of kinetoplast DNA (kDNA) minicircles of
T. cruzi
populations by low-stringency single specific primer PCR. Data presented here provide a strong correlation between
T. cruzi
II and human infection in this region. However, a high degree of variability was observed within
T. cruzi
II, as demonstrated by intense kDNA polymorphism among all clinical forms and also within each of them, irrespective of the intensity of pathological processes.
Microsatellite Analysis of Three Phylogenetic Species of
Paracoccidioides brasiliensis
Authors: Matute Daniel R. , Sepulveda Victoria E. , Quesada Lina M. , Goldman Gustavo H. , Taylor John W. , Restrepo Angela , McEwen Juan G. 
Published: June 2006

ABSTRACT

Paracoccidioides brasiliensis
is the etiological agent of paracoccidioidomycosis, an important human systemic mycosis in Latin America. Recently, the existence of three different phylogenetic species (S1, PS2, and PS3) of
P. brasiliensis
was demonstrated. Despite being genetically isolated, all three species were capable of inducing disease in both humans and animals, although lower virulence has been found with the PS2 species. The available molecular methods developed to characterize and type strains have not been useful for assigning isolates to the described species, creating the need for molecular markers capable of distinguishing genetically isolated groups. Here, we describe a PCR and sequencing-based microsatellite marker system that is stable, easy to assay, adaptable to large series of isolates, and discriminatory enough to be used as a typing system in identifying the three proposed species of
P. brasiliensis
. In addition, this system provides an unambiguous tool for strain discrimination between two (S1 and PS2) of the three phylogenetic species.
Multilocus Sequence Typing Scheme for
Enterococcus faecalis
Reveals Hospital-Adapted Genetic Complexes in a Background of High Rates of Recombination
Authors: Ruiz-Garbajosa Patricia , Bonten Marc J. M. , Robinson D. Ashley , Top Janetta , Nallapareddy Sreedhar R. , Torres Carmen , Coque Teresa M. , Cantón Rafael , Baquero Fernando , Murray Barbara E. , del Campo Rosa , Willems Rob J. L. 
Published: June 2006

ABSTRACT

A multilocus sequence typing (MLST) scheme based on seven housekeeping genes was used to investigate the epidemiology and population structure of
Enterococcus faecalis
. MLST of 110 isolates from different sources and geographic locations revealed 55 different sequence types that grouped into four major clonal complexes (CC2, CC9, CC10, and CC21) by use of eBURST. Two of these clonal complexes, CC2 and CC9, are particularly fit in the hospital environment, as CC2 includes the previously described BVE clonal complex identified by an alternative MLST scheme and CC9 includes exclusively isolates from hospitalized patients. Identical alleles were found in genetically diverse isolates with no linkage disequilibrium, while the different MLST loci gave incongruent phylogenetic trees. This demonstrates that recombination is an important mechanism driving genetic variation in
E. faecalis
and suggests an epidemic population structure for
E. faecalis
. Our novel MLST scheme provides an excellent tool for investigating local and short-term epidemiology as well as global epidemiology, population structure, and genetic evolution of
E. faecalis
.
Evaluation of the BD Phoenix Automated Microbiology System for Identification and Antimicrobial Susceptibility Testing of Staphylococci and Enterococci
Authors: Carroll Karen C. , Borek Anita P. , Burger Chad , Glanz Brian , Bhally Hasan , Henciak Susan , Flayhart Diane C. 
Published: June 2006

ABSTRACT

We evaluated the Phoenix automated microbiology system (BD Diagnostic Systems, Sparks, MD) for the identification (ID) and antimicrobial susceptibility testing (AST) of challenge and clinical staphylococci and enterococci recovered from patients in a tertiary-care medical center. In total, 424 isolates were tested: 90 enterococci; 232
Staphylococcus aureus
isolates, including 14 vancomycin-intermediate
S. aureus
isolates; and 102 staphylococci other than
S. aureus
(non-
S. aureus
). The Phoenix panels were inoculated according to the manufacturer's instructions. The reference methods for ID comparisons were conventional biochemicals and cell wall fatty acid analysis with the Sherlock microbial identification system (v 3.1; MIDI, Inc. Newark, DE). Agar dilution was the reference AST method. The overall rates of agreement for identification to the genus and the species levels were 99.7% and 99.3%, respectively. All
S. aureus
isolates and enterococci were correctly identified by the Phoenix panels. For the non-
S. aureus
staphylococci, there was 98.0% agreement for the ID of 16 different species. The AST results were stratified by organism group. For
S. aureus
, the categorical agreement (CA) and essential agreement (EA) were 98.2% and 98.8%, respectively. Three of three very major errors (VMEs; 1.7%) were with oxacillin. For non-
S. aureus
staphylococci, the CA, EA, VME, major errors, and minor error rates were 95.7%, 96.8%, 0.7%, 1.7%, and 2.9%, respectively. The two VMEs were with oxacillin. For the enterococci, there was 100% CA and 99.3% EA. All 36 vancomycin-resistant enterococci were detected by the Phoenix system. The Phoenix system compares favorably to traditional methods for the ID and AST of staphylococci and enterococci.
TheEscherichia coliProteome: Past, Present, and Future Prospects
Authors: Han Mee-Jung , Lee Sang Yup 
Published: June 2006

SUMMARYProteomics has emerged as an indispensable methodology for large-scale protein analysis in functional genomics. TheEscherichia coliproteome has been extensively studied and is well defined in terms of biochemical, biological, and biotechnological data. Even before the entireE. coliproteome was fully elucidated, the largest available data set had been integrated to decipher regulatory circuits and metabolic pathways, providing valuable insights into global cellular physiology and the development of metabolic and cellular engineering strategies. With the recent advent of advanced proteomic technologies, theE. coliproteome has been used for the validation of new technologies and methodologies such as sample prefractionation, protein enrichment, two-dimensional gel electrophoresis, protein detection, mass spectrometry (MS), combinatorial assays withn-dimensional chromatographies and MS, and image analysis software. These important technologies will not only provide a great amount of additional information on theE. coliproteome but also synergistically contribute to other proteomic studies. Here, we review the past development and current status ofE. coliproteome research in terms of its biological, biotechnological, and methodological significance and suggest future prospects.
Human Immunodeficiency Virus Type 1 Nef: Adapting to Intracellular Trafficking Pathways
Authors: Roeth Jeremiah F. , Collins Kathleen L. 
Published: June 2006

SUMMARYThe Nef protein of primate lentiviruses is a unique protein that has evolved in several ways to manipulate the biology of an infected cell to support viral replication, immune evasion, pathogenesis, and viral spread. Nef is a small (25- to 34-kDa), myristoylated protein that binds to a collection of cellular factors and acts as an adaptor to generate novel protein interactions to accomplish specific functions. Of the many biological activities attributed to Nef, the reduction of surface levels of the viral receptor (CD4) and antigen-presenting molecules (major histocompatibility complex class I) has been intensely examined; recent evidence demonstrates that Nef utilizes multiple, distinct pathways to affect these proteins. To accomplish this, Nef promotes the formation of multiprotein complexes, recruiting host adaptor proteins to commandeer intracellular vesicular trafficking routes. The altered trafficking of several other host molecules has also been reported, and an emerging theory suggests that Nef generates pleiotrophic effects in the secretory and endocytic pathways that reprogram intracellular protein trafficking and may ultimately provide an efficient platform for viral assembly. This review critically discusses some of the major findings regarding the impact of human immunodeficiency virus type 1 Nef on host protein transport and addresses some emerging directions in this area of human immunodeficiency virus biology.
The Climate Sensitivity of the Community Climate System Model Version 3 (CCSM3)
Authors: Kiehl Jeffrey T. , Shields Christine A. , Hack James J. , Collins William D. 
Published: June 2006

Abstract
The climate sensitivity of the Community Climate System Model (CCSM) is described in terms of the equilibrium change in surface temperature due to a doubling of carbon dioxide in a slab ocean version of the Community Atmosphere Model (CAM) and the transient climate response, which is the surface temperature change at the point of doubling of carbon dioxide in a 1% yr−1 CO2 simulation with the fully coupled CCSM. For a fixed atmospheric horizontal resolution across model versions, we show that the equilibrium sensitivity has monotonically increased across CSM1.4, CCSM2, to CCSM3 from 2.01° to 2.27° to 2.47°C, respectively. The transient climate response for these versions is 1.44° to 1.09° to 1.48°C, respectively.
Using climate feedback analysis, it is shown that both clear-sky and cloudy-sky processes have contributed to the changes in transient climate response. The dependence of these sensitivities on horizontal resolution is also explored. The equilibrium sensitivity of the high-resolution (T85) version of CCSM3 is 2.71°C, while the equilibrium response for the low-resolution model (T31) is 2.32°C. It is shown that the shortwave cloud response of the high-resolution version of the CCSM3 is anomalous compared to the low- and moderate-resolution versions.
In vivo tumor growth is inhibited by cytosolic iron deprivation caused by the expression of mitochondrial ferritin
Authors: Nie Guangjun , Chen Guohua , Sheftel Alex D. , Pantopoulos Kostas , Ponka Prem 
Published: June 2006

AbstractMitochondrial ferritin (MtFt) is a mitochondrial iron-storage protein whose function and regulation is largely unknown. Our previous results have shown that MtFt overexpression markedly affects intracellular iron homeostasis in mammalian cells. Using tumor xenografts, we examined the effects of MtFt overexpression on tumor iron metabolism and growth. The expression of MtFt dramatically reduced implanted tumor growth in nude mice. Mitochondrial iron deposition in MtFt-expressing tumors was directly observed by transmission electron microscopy. A cytosolic iron starvation phenotype in MtFt-expressing tumors was revealed by increased RNA-binding activity of iron regulatory proteins, and concomitantly both an increase in transferrin receptor levels and a decrease in cytosolic ferritin. MtFt overexpression also led to decreases in total cellular heme content and heme oxygenase-1 levels. In addition, elevated MtFt in tumors was also associated with a decrease in total aconitase activity and lower frataxin protein level. In conclusion, our study shows that high MtFt levels can significantly affect tumor iron homeostasis by shunting iron into mitochondria; iron scarcity resulted in partially deficient heme and iron-sulfur cluster synthesis. It is likely that deprivation of iron in the cytosol is the cause for the significant inhibition of xenograft tumor growth.
Maturation stage–specific regulation of megakaryopoiesis by pointed-domain Ets proteins
Authors: Pang Liyan , Xue Hai-Hui , Szalai Gabor , Wang Xun , Wang Yuhuan , Watson Dennis K. , Leonard Warren J. , Blobel Gerd A. , Poncz Mortimer 
Published: June 2006

AbstractNumerous megakaryocyte-specific genes contain signature Ets-binding sites in their regulatory regions. Fli-1 (friend leukemia integration 1), an Ets transcription factor, is required for the normal maturation of megakaryocytes and controls the expression of multiple megakaryocyte-specific genes. However, in Fli-1–/– mice, early megakaryopoiesis persists, and the expression of the early megakaryocyte-specific genes, αIIb and cMpl, is maintained, consistent with functional compensation by a related Ets factor(s). Here we identify the Ets protein GABPα (GA-binding protein α) as a regulator of early megakaryocyte-specific genes. Notably, GABPα preferentially occupies Ets elements of early megakaryocyte-specific genes in vitro and in vivo, whereas Fli-1 binds both early and late megakaryocyte-specific genes. Moreover, the ratio of GABPα/Fli-1 expression declines throughout megakaryocyte maturation. Consistent with this expression pattern, primary fetal liver–derived megakaryocytes from Fli-1–deficient murine embryos exhibit reduced expression of genes associated with late stages of maturation (glycoprotein [GP] Ibα, GPIX, and platelet factor 4 [PF4]), whereas GABPα-deficient megakaryocytes were mostly impaired in the expression of early megakaryocyte-specific genes (αIIb and cMpl). Finally, mechanistic experiments revealed that GABPα, like Fli-1, can impart transcriptional synergy between the hematopoietic transcription factor GATA-1 and its cofactor FOG-1 (friend of GATA-1). In concert, these data reveal disparate, but overlapping, functions of Ets transcription factors at distinct stages of megakaryocyte maturation.
CD32B, the human inhibitory Fc-γ receptor IIB, as a target for monoclonal antibody therapy of B-cell lymphoma
Authors: Rankin Christopher T. , Veri Maria-Concetta , Gorlatov Sergey , Tuaillon Nadine , Burke Steve , Huang Ling , Inzunza H. David , Li Hua , Thomas Shannon , Johnson Syd , Stavenhagen Jeffrey , Koenig Scott , Bonvini Ezio 
Published: June 2006

AbstractHuman CD32B (FcγRIIB), the low-affinity inhibitory receptor for IgG, is the predominant Fc receptor (FcR) present on B cells. Immunohistochemical and expression studies have identified CD32B expression in a variety of B-cell malignancies, suggesting that CD32B is a potential immunotherapeutic target for B-cell malignancies. A high-affinity monoclonal antibody (mAb 2B6), from a novel panel of anti–human CD32B–specific mAbs, was chimerized (ch2B6) and humanized (hu2B6-3.5). Both ch2B6 and hu2B6-3.5 were capable of directing cytotoxicity by peripheral blood mononuclear cells and monocyte-derived macrophages against B-lymphoma lines in vitro. In a human B-cell lymphoma mouse xenograft model, administration of ch2B6 or hu2B6-3.5 reduced tumor growth rate and improved tumor-free survival. Both the in vitro and in vivo activities of 2B6 required an intact Fc, suggesting an FcR-mediated mechanism of action. These data support the hypothesis that CD32B is a viable target for mAb treatment of B-cell lymphoproliferative disorders.
High throughput profile-profile based fold recognition for the entire human proteome
Authors: McGuffin Liam J , Smith Richard T , Bryson Kevin , Sørensen Søren-Aksel , Jones David T 
Published: June 2006

Abstract

Background
In order to maintain the most comprehensive structural annotation databases we must carry out regular updates for each proteome using the latest profile-profile fold recognition methods. The ability to carry out these updates on demand is necessary to keep pace with the regular updates of sequence and structure databases. Providing the highest quality structural models requires the most intensive profile-profile fold recognition methods running with the very latest available sequence databases and fold libraries. However, running these methods on such a regular basis for every sequenced proteome requires large amounts of processing power.
In this paper we describe and benchmark the JYDE (Job Yield Distribution Environment) system, which is a meta-scheduler designed to work above cluster schedulers, such as Sun Grid Engine (SGE) or Condor. We demonstrate the ability of JYDE to distribute the load of genomic-scale fold recognition across multiple independent Grid domains. We use the most recent profile-profile version of our mGenTHREADER software in order to annotate the latest version of the Human proteome against the latest sequence and structure databases in as short a time as possible.

Results
We show that our JYDE system is able to scale to large numbers of intensive fold recognition jobs running across several independent computer clusters. Using our JYDE system we have been able to annotate 99.9% of the protein sequences within the Human proteome in less than 24 hours, by harnessing over 500 CPUs from 3 independent Grid domains.

Conclusion
This study clearly demonstrates the feasibility of carrying out on demand high quality structural annotations for the proteomes of major eukaryotic organisms. Specifically, we have shown that it is now possible to provide complete regular updates of profile-profile based fold recognition models for entire eukaryotic proteomes, through the use of Grid middleware such as JYDE.
An evaluation of indices for quantifying tuberculosis transmission using genotypes of pathogen isolates
Authors: Tanaka Mark M , Phong Renault , Francis Andrew R 
Published: June 2006

Abstract

Background
Infectious diseases are often studied by characterising the population structure of the pathogen using genetic markers. An unresolved problem is the effective quantification of the extent of transmission using genetic variation data from such pathogen isolates.

Methods
It is important that transmission indices reflect the growth of the infectious population as well as account for the mutation rate of the marker and the effects of sampling. That is, while responding to this growth rate, indices should be unresponsive to the sample size and the mutation rate. We use simulation methods taking into account both the mutation and sampling processes to evaluate indices designed to quantify transmission of tuberculosis.

Results
Previously proposed indices generally perform inadequately according to the above criteria, with the partial exception of the recently proposed Transmission-Mutation Index.

Conclusion
Any transmission index needs to take into account mutation of the marker and the effects of sampling. Simple indices are unlikely to capture the full complexity of the underlying processes.