bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assembly reconciliation
Authors: Zimin Aleksey V. , Smith Douglas R. , Sutton Granger , Yorke James A. 
Published: December 2007

Abstract
Motivation: Many genomes are sequenced by a collaboration of several centers, and then each center produces an assembly using their own assembly software. The collaborators then pick the draft assembly that they judge to be the best and the information contained in the other assemblies is usually not used.
Methods: We have developed a technique that we call assembly reconciliation that can merge draft genome assemblies. It takes one draft assembly, detects apparent errors, and, when possible, patches the problem areas using pieces from alternative draft assemblies. It also closes gaps in places where one of the alternative assemblies has spanned the gap correctly.
Results: Using the Assembly Reconciliation technique, we produced reconciled assemblies of six Drosophila species in collaboration with Agencourt Bioscience and The J. Craig Venter Institute. These assemblies are now the official (CAF1) assemblies used for analysis. We also produced a reconciled assembly of Rhesus Macaque genome, and this assembly is available from our website http://www.genome.umd.edu.
Availability: The reconciliation software is available for download from http://www.genome.umd.edu/software.htm
Contact: alekseyz@ipst.umd.edu
Thrombocytopenia in hydropic fetuses with parvovirus B19 infection: incidence, treatment and correlation with fetal B19 viral load
Authors: De Haan TR , Van Den Akker ESA , Porcelijn L , Oepkes D , Kroes ACM , Walther FJ 
Published: December 2007

Objective  To examine (1) the incidence of fetal thrombocytopenia in hydropic fetuses with congenital B19 virus infection, (2) the effect of intrauterine platelet transfusions and (3) the correlation between fetal B19 viral load and severity of thrombocytopenia.Design  Retrospective analysis of data from prospectively collected fetal blood samples.Setting  Leiden University Medical Centre, the national centre for management of intrauterine fetal disease in the Netherlands.Population  Thirty hydropic fetuses treated with intrauterine red blood cell and platelet transfusions for human B19 virus‐induced severe fetal anaemia and thrombocytopenia over a 10‐year period.Methods  Fetal blood samples (n= 30) taken before and after intrauterine transfusion were investigated. No cases were excluded, and there was no loss to follow up.Main outcome measures  Parameters recorded were gestational age, experienced fetal movements, gravidity and parity, severity of fetal hydrops, severity of fetal anaemia and thrombocytopenia and megakaryocyte and reticulocyte counts. Survival and procedure‐associated complications were documented. Quantitative B19 viral load measurements were performed on all fetal samples.Results  Forty‐six percent of all hydropic fetuses showed severe thrombocytopenia. No antenatal intracerebral haemorrhage or procedure‐associated bleeding occurred. Overall, survival was 77%. Platelet counts increased following platelet transfusion and decreased significantly following red blood cell transfusion alone. No correlation was found between fetal viral loads and platelet counts.Conclusion  Thrombocytopenia was frequently encountered in fetal B19V infection, but fetal bleeding complications were not noted. Absence of a direct relationship between fetal B19 viral load and platelet counts suggests a temporal dissociation between these findings. Dilutional thrombocytopenia is frequently seen in the fetus following red blood cell transfusion alone. The clinical significance of this phenomenon is unclear. The risk of fluid overload by fetal platelet transfusion in a severely hydropic fetus should be weighed against the low incidence of fetal bleeding complications.
β-Lactam Failure in Treatment of Two Group G
Streptococcus dysgalactiae
subsp.
equisimilis
Pharyngitis Patients
Authors: Savini Vincenzo , Catavitello Chiara , Talia Marzia , Manna Assunta , Pompetti Franca , Di Bonaventura Giovanni , Di Giuseppe Nicola , Febbo Fabio , Balbinot Andrea , Di Zacomo Silvia , Esattore Francesca , D'Antonio Domenico 
Published: December 2007

ABSTRACT

We present two cases of exudative pharyngitis due to
Streptococcus dysgalactiae
subsp.
equisimilis
, Lancefield group G. While the participation of this organism as an agent of pharyngitis is well documented, we focus on failure of beta-lactam therapy, a phenomenon that is well described for pharyngitis due to
Streptococcus pyogenes
. Therefore, these case reports add to our knowledge of pharyngitis caused by non-
S. pyogenes
streptococci.
Kaposi's Sarcoma-Associated Herpesvirus Induces Sustained Levels of Vascular Endothelial Growth Factors A and C Early during In Vitro Infection of Human Microvascular Dermal Endothelial Cells: Biological Implications
Authors: Sivakumar Ramu , Sharma-Walia Neelam , Raghu Hari , Veettil Mohanan Valiya , Sadagopan Sathish , Bottero Virginie , Varga Laszlo , Levine Rita , Chandran Bala 
Published: December 2007

ABSTRACT
Kaposi's sarcoma (KS), a vascular tumor associated with human immunodeficiency virus type 1 infection, is characterized by spindle-shaped endothelial cells, inflammatory cells, cytokines, growth and angiogenic factors, and angiogenesis. KS spindle cells are believed to be of the lymphatic endothelial cell (LEC) type. Kaposi's sarcoma-associated herpesvirus (KSHV, or human herpesvirus 8) is etiologically linked to KS, and in vitro KSHV infection of primary human dermal microvascular endothelial cells (HMVEC-d) is characterized by the induction of preexisting host signal cascades, sustained expression of latency-associated genes, transient expression of a limited number of lytic genes, sustained induction of NF-κB and several cytokines, and growth and angiogenic factors. KSHV induced robust vascular endothelial growth factor A (VEGF-A) and VEGF-C gene expression as early as 30 min postinfection (p.i.) in serum-starved HMVEC-d, which was sustained throughout the observation period of 72 h p.i. Significant amounts of VEGF-A and -C were also detected in the culture supernatant of infected cells. VEGF-A and -C were also induced by UV-inactivated KSHV and envelope glycoprotein gpK8.1A, thus suggesting a role for virus entry stages in the early induction of VEGF and requirement of KSHV viral gene expression for sustained induction. Exogenous addition of VEGF-A and -C increased KSHV DNA entry into target cells and moderately increased latent ORF73 and lytic ORF50 promoter activation and gene expression. KSHV infection also induced the expression of lymphatic markers Prox-1 and podoplanin as early as 8 h p.i., and a paracrine effect was seen in the neighboring uninfected cells. Similar observations were also made in the pure blood endothelial cell (BEC)-TIME cells, thus suggesting that commitment to the LEC phenotype is induced early during KSHV infection of blood endothelial cells. Treatment with VEGF-C alone also induced Prox-1 expression in the BEC-TIME cells. Collectively, these studies show that the in vitro microenvironments of KSHV-infected endothelial cells are enriched, with VEGF-A and -C molecules playing key roles in KSHV biology, such as increased infection and gene expression, as well as in angiogenesis and lymphangiogenesis, thus recapitulating the microenvironment of early KS lesions.
Latent Membrane Protein 2B Regulates Susceptibility to Induction of Lytic Epstein-Barr Virus Infection
Authors: Rechsteiner Markus P. , Berger Christoph , Zauner Ludwig , Sigrist Jürg A. , Weber Matthias , Longnecker Richard , Bernasconi Michele , Nadal David 
Published: December 2007

ABSTRACT
The B-lymphotropic Epstein-Barr virus (EBV) encodes two isoforms of latent membrane protein 2 (LMP2), LMP2A and LMP2B, which are expressed during latency in B cells. The function of LMP2B is largely unknown, whereas LMP2A blocks B-cell receptor (BCR) signaling transduction and induction of lytic EBV infection, thereby promoting B-cell survival. Transfection experiments on LMP2B in EBV-negative B cells and the silencing of LMP2B in EBV-harboring Burkitt's lymphoma-derived Akata cells suggest that LMP2B interferes with the function of LMP2A, but the role of LMP2B in the presence of functional EBV has not been established. Here, LMP2B, LMP2A, or both were overexpressed in EBV-harboring Akata cells to study the function of LMP2B. The overexpression of LMP2B increased the magnitude of EBV switching from its latent to its lytic form upon BCR cross-linking, as indicated by a more-enhanced upregulation and expression of EBV lytic genes and significantly increased production of transforming EBV compared to Akata vector control cells or LMP2A-overexpressing cells. Moreover, LMP2B lowered the degree of BCR cross-linking required to induce lytic EBV infection. Finally, LMP2B colocalized with LMP2A as demonstrated by immunoprecipitation and immunofluorescence and restored calcium mobilization upon BCR cross-linking, a signaling process inhibited by LMP2A. Thus, our findings suggest that LMP2B negatively regulates the function of LMP2A in preventing the switch from latent to lytic EBV replication.
Replication of Beta- and Gammaretroviruses Is Restricted in I/LnJ Mice via the Same Genetic Mechanism
Authors: Case Laure K. , Petell Lydia , Yurkovetskiy Leonid , Purdy Alexandra , Savage Katherine J. , Golovkina Tatyana V. 
Published: December 2007

ABSTRACTMice of the I/LnJ inbred strain are unique in their ability to mount a robust and sustained humoral immune response capable of neutralizing infection with a betaretrovirus, mouse mammary tumor virus (MMTV). Virus-neutralizing antibodies (Abs) coat MMTV virions secreted by infected cells, preventing virus spread and hence the formation of mammary tumors. To investigate whether I/LnJ mice resist infection with other retroviruses besides MMTV, the animals were infected with murine leukemia virus (MuLV), a gammaretrovirus. MuLV-infected I/LnJ mice produced virus-neutralizing Abs that block virus transmission and virally induced disease. Generation of virus-neutralizing Abs required gamma interferon but was independent of interleukin-12. This unique mechanism of retrovirus resistance is governed by a single recessive gene,virusinfectivitycontroller1(vic1), mapped to chromosome 17. In addition to controlling the antivirus humoral immune response,vic1is also required for an antiviral cytotoxic response. Both types of responses were maintained in mice of the susceptible genetic background but congenic for the I/LnJvic1locus. Although thevic1-mediated resistance to MuLV resembles the mechanism of retroviral recovery controlled by theresistance toFriendvirus3(rfv3) gene, therfv3gene has been mapped to chromosome 15 and confers resistance to MuLV but not to MMTV. Thus, we have identified a unique virus resistance mechanism that controls immunity against two distinct retroviruses.
An Integrative Bioinformatic Approach for Studying Escape Mutations in Human Immunodeficiency Virus Type 1gagin the Pumwani Sex Worker Cohort
Authors: Peters Harold O. , Mendoza Mark G. , Capina Rupert E. , Luo Ma , Mao Xiaojuan , Gubbins Michael , Nagelkerke Nico J. D. , MacArthur Ian , Sheardown Brent B. , Kimani Joshua , Wachihi Charles , Thavaneswaran Subo , Plummer Francis A. 
Published: December 2007

ABSTRACTHuman immunodeficiency virus type 1 (HIV-1) is able to evade the host cytotoxic T-lymphocyte (CTL) response through a variety of escape avenues. Epitopes that are presented to CTLs are first processed in the presenting cell in several steps, including proteasomal cleavage, transport to the endoplasmic reticulum, binding by the HLA molecule, and finally presentation to the T-cell receptor. An understanding of the potential of the virus to escape CTL responses can aid in designing an effective vaccine. To investigate such a potential, we analyzed HIV-1gagfrom 468 HIV-1-positive Kenyan women by using several bioinformatic approaches that allowed the identification of positively selected amino acids in the HIV-1gagregion and study of the effects that these mutations could have on the various stages of antigen processing. Correlations between positively selected residues and mean CD4 counts also allowed study of the effect of mutation on HIV disease progression. A number of mutations that could create or destroy proteasomal cleavage sites or reduce binding affinity of the transport antigen processing protein, effectively hindering epitope presentation, were identified. Many mutations correlated with the presence of specific HLA alleles and with lower or higher CD4 counts. For instance, the mutation V190I in subtype A1-infected individuals is associated with HLA-B*5802 (P= 4.73 × 10−4), a rapid-progression allele according to other studies, and also to a decreased mean CD4 count (P= 0.019). Thus, V190I is a possible HLA escape mutant. This method classifies many positively selected mutations across the entiregagregion according to their potential for immune escape and their effect on disease progression.
Evolution of the Chaperone/Usher Assembly Pathway: Fimbrial Classification Goes Greek
Authors: Nuccio Sean-Paul , Bäumler Andreas J. 
Published: December 2007

SUMMARYMany Proteobacteria use the chaperone/usher pathway to assemble proteinaceous filaments on the bacterial surface. These filaments can curl into fimbrial or nonfimbrial surface structures (e.g., a capsule or spore coat). This article reviews the phylogeny of operons belonging to the chaperone/usher assembly class to explore the utility of establishing a scheme for subdividing them into clades of phylogenetically related gene clusters. Based on usher amino acid sequence comparisons, our analysis shows that the chaperone/usher assembly class is subdivided into six major phylogenetic clades, which we have termed α-, β-, γ-, κ-, π-, and σ-fimbriae. Members of each clade share related operon structures and encode fimbrial subunits with similar protein domains. The proposed classification system offers a simple and convenient method for assigning newly discovered chaperone/usher systems to one of the six major phylogenetic groups.
Transient permeability and reseal hardening in fault zones: evidence from dilation breccia textures
Authors: Woodcock N. H. , Dickson J. A. D. , Tarasewicz J. P. T. 
Published: December 2007

Abstract
It is well established that earthquake faulting can create permeability along a fault zone in high competence rocks - by mismatch of the fault walls and by secondary fracture in a surrounding damage zone - and that this permeability is created repeatedly during successive earthquake cycles. Less well proven is that such permeability is transient, being episodically reduced by precipitation of cements in the fracture porosity. The textures of carbonate dilation breccias, formed at around 1.7 km depth on the Dent Fault zone (NW England), lend support to this economically important concept of transient fracture permeability. The key observation is that many breccias reflect only a single episode of brecciation and reseal. A generally applicable explanation of such single-phase breccias is that they were resealed in the interval between major earthquakes, that this reseal made the breccia stronger that the intact rock, and that subsequent brecciation in the same rock volume was inhibited. This reseal-hardening model implies that transient permeability in fault zones may last no longer than the recurrence times of large earthquakes, and that the permeability conduits will change position in the damage zone with time, unless focused at a major fault jog or termination.
Pre-development fracture modelling in the Clair field, west of Shetland
Authors: Barr David , Savory Kay E. , Fowler Sue R. , Arman Kate , McGarrity John P. 
Published: December 2007

Abstract
The Clair oilfield is a large fractured sandstone reservoir lying 75 km west of Shetland on the UK continental shelf. Fracture analysis and modelling was carried out in preparation for the phase 1 development, which started production early in 2005. Fracture clusters and discrete fluid inflows observed in wells are associated with faults and other localized deformation features tens or hundreds of metres apart. The reservoir has moderate to good matrix permeability, but well flow rates and profiles are fracture-dominated. Full-field geological models were built using conventional object modelling approaches for matrix and discrete fracture networks for fractures, and upscaled to populate a reservoir simulation grid. Dual-porosity, dual-permeability dynamic modelling (full-field and well-test) was undertaken to understand the fracture and matrix flow contributions and their interaction. Fracture models were conditioned to wells and to seismic data, including coherency and multi-azimuthal velocity information from a four-component, ocean bottom cable three-dimensional seismic survey. At this early stage in field development, there is insufficient calibration to select a single fracture model. Instead, well and depletion plans have been tested against multiple fracture models chosen to encompass a wide range of plausible outcomes.
Vicarious liability for the carrier by river?
Authors: Wijffels Alain 
Published: December 2007

AbstractA case-study of a litigation during the years 1566–1574 between merchants from Oudenaarde and the Corporation of Free Shippers in Ghent shows that the corporation's liability for damage caused by one of its members was controversial. Although art. 20 of the ordinance of 14 February 1541 appeared to phrase the corporation's vicarious or subsidiary liability in general terms, the corporation's counsel, assisted by consultancies from a.o. E. Leoninus and J. Wamesius, successfully argued that in the light of the ordinance's rationale, which limited the free shippers' privileges in the aftermath of Charles V's punishment of Ghent in 1540, the corporation's liability had correspondingly to be construed restrictively, viz. only with regard to cargo shipped in Ghent under its control.
The role of horizontal transfer in the evolution of a highly variable lipopolysaccharide biosynthesis locus in xanthomonads that infect rice, citrus and crucifers
Authors: Patil Prabhu B , Bogdanove Adam J , Sonti Ramesh V 
Published: December 2007

Abstract

Background
Lipopolysaccharide (LPS) is a pathogen associated molecular pattern (PAMP) of animal and plant pathogenic bacteria. Variation at the interstrain level is common in LPS biosynthetic gene clusters of animal pathogenic bacteria. This variation has been proposed to play a role in evading the host immune system. Even though LPS is a modulator of plant defense responses, reports of interstrain variation in LPS gene clusters of plant pathogenic bacteria are rare.

Results
In this study we report the complete sequence of a variant 19.9 kb LPS locus present in the BXO8 strain of Xanthomonas oryzae pv. oryzae (Xoo), the bacterial blight pathogen of rice. This region is completely different in size, number and organization of genes from the LPS locus present in most other strains of Xoo from India and Asia. Surprisingly, except for one ORF, all the other ORFs at the BXO8 LPS locus are orthologous to the genes present at this locus in a sequenced strain of X. axonopodis pv. citri (Xac; a pathogen of citrus plants). One end of the BXO8 LPS gene cluster, comprised of ten genes, is also present in the related rice pathogen, X. oryzae pv. oryzicola (Xoc). In Xoc, the remainder of the LPS gene cluster, consisting of seven genes, is novel and unrelated to LPS gene clusters of any of the sequenced xanthomonads. We also report substantial interstrain variation suggestive of very recent horizontal gene transfer (HGT) at the LPS biosynthetic locus of Xanthomonas campestris pv. campestris (Xcc), the black rot pathogen of crucifers.

Conclusion
Our analyses indicate that HGT has altered the LPS locus during the evolution of Xanthomonas oryzae pathovars and suggest that the ancestor of all Xanthomonas oryzae pathovars had an Xac type of LPS gene cluster. Our finding of interstrain variation in two major xanthomonad pathogens infecting different hosts suggests that the LPS locus in plant pathogenic bacteria, as in animal pathogens, is under intense diversifying selection.
Recent discoveries in the pathways to cobalamin (coenzyme B12) achieved through chemistry and biology
Authors: Scott A. Ian , Roessner Charles A. 
Published: December 2007

Abstract
The genetic engineering of Escherichia coli for the over-expression of enzymes of the aerobic and anaerobic pathways to cobalamin has resulted in the in vivo and in vitro biosynthesis of new intermediates and other products that were isolated and characterized using a combination of bioorganic chemistry and high-resolution NMR. Analyses of these products were used to deduct the functions of the enzymes that catalyze their synthesis. CobZ, another enzyme for the synthesis of precorrin-3B of the aerobic pathway, has recently been described, as has been BluB, the enzyme responsible for the oxygen-dependent biosynthesis of dimethylbenzimidazole. In the anaerobic pathway, functions have recently been experimentally confirmed for or assigned to the CbiMNOQ cobalt transport complex, CbiA (a,c side chain amidation), CbiD (C-1 methylation), CbiF (C-11 methylation), CbiG (lactone opening, deacylation), CbiP (b,d,e,g side chain amidation), and CbiT (C-15 methylation, C-12 side chain decarboxylation). The dephosphorylation of adenosylcobalamin-phosphate, catalyzed by CobC, has been proposed as the final step in the biosynthesis of adenosylcobalamin.
Analysis of extended human leukocyte antigen haplotype association with Addison's disease in three populations
Authors: Gombos Z , Hermann R , Kiviniemi M , Nejentsev S , Reimand K , Fadeyev V , Peterson P , Uibo R , Ilonen J 
Published: December 2007

ObjectiveAddison's disease is an organ-specific autoimmune disorder with a polygenic background. The aim of the study was to identify non-class II human leukocyte antigen (HLA) susceptibility genes for Addison's disease.Design and methodsAddison's disease patients from three European populations were analysed for selected HLA–DR–DQ alleles and for 11 microsatellite markers covering ∼4 Mb over the HLA region. Subjects were 69 patients with Addison's disease from Estonia (24), Finland (14) and Russia (31). Consecutively recruited healthy newborns from the same geographical regions were used as controls (269 Estonian, 1000 Finnish and 413 Russian). Association measures for HLA–DRB1, DQB1, DQA1 and 11 microsatellites between D6S273 and D6S2223 were taken. A low-resolution full-house typing was used for HLA class II genes, while microsatellite markers were studied using fluorescence-based DNA fragment sizing technology.ResultsWe confirmed that the HLA–DR3–DQ2 and the DQB1*0302–DRB1*0404 haplotypes confer disease susceptibility. In Russian patients, we also found an increase of DRB1*0403 allele, combined with DQB1*0305 allele in three out of six cases (P<0.0001). Analysis of 11 microsatellite markers including STR MICA confirmed the strong linkage in DR3–DQ2 haplotypes but DRB1*0404–DQB1*0302 haplotypes were diverse. MICA5.1 allele was found in 22 out of 24 Estonian patients, but results from Finnish and Russian patients did not support its independent role in disease susceptibility.ConclusionHLA–DRB1*0403 was identified as a novel susceptibility allele for Addison's disease. Additionally, we found no evidence of a non-class II HLA disease susceptibility locus; however, the HLA–DR3–DQ2 haplotype appeared more conserved in patient groups with high DR–DQ2 frequencies.