bluuebunny/crossref_metadata_2025_split huggingface dataset:
Development of compound microsatellite markers in red‐tide‐causing dinoflagellate Akashiwo sanguinea (Dinophyceae)
Authors: CHO S‐Y. , NAGAI S. , NISHITANI G. , HAN M‐S. 
Published: January 2009

AbstractWe isolated 13 polymorphic microsatellites from the red‐tide causing dinoflagellate Akashiwo sanguinea. These loci were highly variable, with between 2 and 10 alleles per locus, and estimated gene diversity ranging from 0.08 to 0.82. These loci have the potential to reveal genetic structure and estimate gene flow among A. sanguinea populations.
New microsatellite loci for the endangered scalloped hammerhead shark, Sphyrna lewini
Authors: NANCE HOLLY A. , DALY‐ENGEL TOBY S. , MARKO PETER B. 
Published: January 2009

AbstractWe isolated 15 microsatellite markers for the scalloped hammerhead shark, Sphyrna lewini. Loci were tested on 80 specimens of S. lewini from four Eastern Pacific samples. The number of alleles per locus ranged from 6 to 31 (mean = 14). Observed and expected levels of heterozygosity per locus ranged from 0.39 to 0.91 (mean = 0.70) and from 0.54 to 0.90 (mean = 0.76), respectively. No pairs of loci were in gametic disequilibrium after Bonferroni correction of α. One locus showed significantly lower heterozygosity than expected under Hardy–Weinberg proportions in two populations, possibly caused by null alleles.
Repair of large segmental bone defects using bone marrow stromal cells with demineralized bone matrix
Authors: Xu Jian‐zhong , Qin Hui , Wang Xu‐quan , Zhou Qiang , Luo Fei , Hou Tian‐yong , He Qing‐yi 
Published: January 2009

Objective:  The aim of the present study was to evaluate the effect of tissue‐engineered constructs on repair of large segmental bone defects in goats.Methods:  Allogenic demineralized bone matrix (aDBM) was seeded with autologous marrow stromal cells (aMSC) for seven days to construct DBM–MSC grafts prior to implantation. 24 goats were randomly divided into three groups (eight in each). In each group, 3 cm diaphyseal femoral defects were created unilaterally, and subsequently filled with the DBM‐MSC grafts, DBM alone and an untreated control, respectively. Radiological analysis and biomechanical evaluation were performed at 12 and 24 weeks after operation.Results:  Obvious increases in radiological scoring and biomechanical strength were found in the DBM‐MSC group when compared to the DBM group. X‐ray examination showed excellent bone healing in the DBM‐MSC group, whereas only partial bone repair was seen in the DBM group, and no healing in untreated controls. Histologically, a tendency to bone regeneration and remodeling was far more obvious for the DBM‐MSC group than the DBM only and untreated controls.Conclusion:  Our results strongly suggest that transplantation of bone MSC within a DBM could have advantages for the bone repair of large segmental defects.
The clinical features of, and microendoscopic decompression for, extraforaminal entrapment of the L5 spinal nerve
Authors: Zhou Yue , Zheng Wen‐jie , Wang Jian , Chu Tong‐wei , Li Chang‐qing , Zhang Zheng‐feng , Wang Wei‐dong 
Published: January 2009

Objective:  To evaluate the clinical results of, and surgical techniques for, microendoscopic (METRx) decompression of extraforaminal entrapment of the L5 spinal nerve at the lumbosacral tunnel.Methods:  Five patients with extraforaminal entrapment of the L5 spinal nerve in the lumbosacral tunnel were treated in our department, including three men and two women. The average age was 65.6 years. All patients suffered severe leg pain and neurological deficits compatible with L5 radiculopathy. Minimally invasive decompression of the L5 spinal nerve was performed under METRx intertransverse decompression.Results:  With an average follow‐up of 17.8 months, clinical results were assessed based on Nakai criteria and Visual Analogue scale (VAS). All patients experienced immediate pain relief postoperatively. Clinical outcomes were excellent in three patients and good in two. The average intraoperative blood loss was 59 ml, with an average operative time of 103 min. Average post‐operative stay in bed was 7 days, and average cost was $1860.Conclusion:  Extraforaminal entrapment of the L5 spinal nerve in the lumbosacral tunnel can cause L5 radiculopathy. METRx partial resection of the L5 transverse processes, sacral ala and osteophytes of L5‐S1 vertebral bodies to relieve extraforaminal entrapment of the L5 spinal nerve is a very effective and minimally invasive surgical option.
A DNA Vaccine Encoding the Enterohemorragic
Escherichia coli
Shiga-Like Toxin 2 A
2
and B Subunits Confers Protective Immunity to Shiga Toxin Challenge in the Murine Model
Authors: Bentancor Leticia V. , Bilen Marcos , Brando Romina J. Fernández , Ramos María Victoria , Ferreira Luis C. S. , Ghiringhelli Pablo D. , Palermo Marina S. 
Published: January 2009

ABSTRACT

Production of verocytotoxin or Shiga-like toxin (Stx), particularly Stx2, is the basis of hemolytic uremic syndrome, a frequently lethal outcome for subjects infected with Stx2-producing enterohemorrhagic
Escherichia coli
(EHEC) strains. The toxin is formed by a single A subunit, which promotes protein synthesis inhibition in eukaryotic cells, and five B subunits, which bind to globotriaosylceramide at the surface of host cells. Host enzymes cleave the A subunit into the A
1
peptide, endowed with N-glycosidase activity to the 28S rRNA, and the A
2
peptide, which confers stability to the B pentamer. We report the construction of a DNA vaccine (pStx2ΔAB) that expresses a nontoxic Stx2 mutated form consisting of the last 32 amino acids of the A
2
sequence and the complete B subunit as two nonfused polypeptides. Immunization trials carried out with the DNA vaccine in BALB/c mice, alone or in combination with another DNA vaccine encoding granulocyte-macrophage colony-stimulating factor, resulted in systemic Stx-specific antibody responses targeting both A and B subunits of the native Stx2. Moreover, anti-Stx2 antibodies raised in mice immunized with pStx2ΔAB showed toxin neutralization activity in vitro and, more importantly, conferred partial protection to Stx2 challenge in vivo. The present vector represents the second DNA vaccine so far reported to induce protective immunity to Stx2 and may contribute, either alone or in combination with other procedures, to the development of prophylactic or therapeutic interventions aiming to ameliorate EHEC infection-associated sequelae.
The Region Approximately between Amino Acids 81 and 137 of Proteinase K-Resistant PrP
Sc
Is Critical for the Infectivity of the Chandler Prion Strain
Authors: Shindoh Ryo , Kim Chan-Lan , Song Chang-Hyun , Hasebe Rie , Horiuchi Motohiro 
Published: January 2009

ABSTRACT

Although the major component of the prion is believed to be the oligomer of PrP
Sc
, little information is available concerning regions on the PrP
Sc
molecule that affect prion infectivity. During the analysis of PrP
Sc
molecules from various prion strains, we found that PrP
Sc
of the Chandler strain showed a unique property in the conformational-stability assay, and this property appeared to be useful for studying the relationship between regions of the PrP
Sc
molecule and prion infectivity. Thus, we analyzed PrP
Sc
of the Chandler strain in detail and analyzed the infectivities of the N-terminally denatured and truncated forms of proteinase K-resistant PrP. The N-terminal region of PrP
Sc
of the Chandler strain showed region-dependent resistance to guanidine hydrochloride (GdnHCl) treatment. The region approximately between amino acids (aa) 81 and 137 began to be denatured by treatment with 1.5 M GdnHCl. Within this stretch, the region comprising approximately aa 81 to 90 was denatured almost completely by 2 M GdnHCl. Furthermore, the region approximately between aa 90 and 137 was denatured completely by 3 M GdnHCl. However, the C-terminal region thereafter was extremely resistant to the GdnHCl treatment. This property was not observed in PrP
Sc
molecules of other prion strains. Denaturation of the region between aa 81 and 137 by 3 M GdnHCl significantly prolonged the incubation periods in mice compared to that for the untreated control. More strikingly, the denaturation and removal of this region nearly abolished the infectivity. This finding suggests that the conformation of the region between aa 81 and 137 of the Chandler strain PrP
Sc
molecule is directly associated with prion infectivity.
Induction of a Striking Systemic Cytokine Cascade prior to Peak Viremia in Acute Human Immunodeficiency Virus Type 1 Infection, in Contrast to More Modest and Delayed Responses in Acute Hepatitis B and C Virus Infections
Authors: Stacey Andrea R. , Norris Philip J. , Qin Li , Haygreen Elizabeth A. , Taylor Elizabeth , Heitman John , Lebedeva Mila , DeCamp Allan , Li Dongfeng , Grove Douglas , Self Steven G. , Borrow Persephone 
Published: January 2009

ABSTRACT

Characterization of the immune responses induced in the initial stages of human immunodeficiency virus type 1 (HIV-1) infection is of critical importance for an understanding of early viral pathogenesis and prophylactic vaccine design. Here, we used sequential plasma samples collected during the eclipse and exponential viral expansion phases from subjects acquiring HIV-1 (or, for comparison, hepatitis B virus [HBV]or hepatitis C virus [HCV]) to determine the nature and kinetics of the earliest systemic elevations in cytokine and chemokine levels in each infection. Plasma viremia was quantitated over time, and levels of 30 cytokines and chemokines were measured using Luminex-based multiplex assays and enzyme-linked immunosorbent assays. The increase in plasma viremia in acute HIV-1 infection was found to be associated with elevations in plasma levels of multiple cytokines and chemokines, including rapid and transient elevations in alpha interferon (IFN-α) and interleukin-15 (IL-15) levels; a large increase in inducible protein 10 (IP-10) levels; rapid and more-sustained increases in tumor necrosis factor alpha and monocyte chemotactic protein 1 levels; more slowly initiated elevations in levels of additional proinflammatory factors including IL-6, IL-8, IL-18, and IFN-γ; and a late-peaking increase in levels of the immunoregulatory cytokine IL-10. Notably, there was comparatively little perturbation in plasma cytokine levels during the same phase of HBV infection and a delayed response of more intermediate magnitude in acute HCV infection, indicating that the rapid activation of a striking systemic cytokine cascade is not a prerequisite for viral clearance (which occurs in a majority of HBV-infected individuals). The intense early cytokine storm in acute HIV-1 infection may have immunopathological consequences, promoting immune activation, viral replication, and CD4
+
T-cell loss.
Identification of TRIM23 as a Cofactor Involved in the Regulation of NF-κB by Human Cytomegalovirus
Authors: Poole Emma , Groves Ian , Macdonald Andrew , Pang Yin , Alcami Antonio , Sinclair John 
Published: January 2009

ABSTRACT
Human cytomegalovirus (HCMV) regulates NF-κB during infection by a variety of mechanisms. For example, the HCMV gene product, UL144, is known to activate NF-κB in a tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6)-dependent manner, causing the upregulation of the chemokine CCL22 (MDC). Viral UL144 is expressed from the UL/b′ region of the HCMV genome at early times postinfection and is a TNFR1-like homologue. Despite this homology to the TNFR1 receptor superfamily, UL144 does not bind to members of the TNF ligand superfamily. We show here that the upregulation of NF-κB by UL144 is dependent upon cellular tripartite motif 23 (TRIM23) protein. We propose a mechanism by which UL144 activates NF-κB through a direct interaction with the cellular protein TRIM23 in a complex containing TRAF6. In contrast, TRIM23 is not involved in conventional double-stranded RNA signaling via NF-κB. Therefore, we present a novel role for TRIM23 that is specific to UL144-mediated activation of NF-κB during the course of virus infection.
Organ-Specific Attenuation of Murine Hepatitis Virus Strain A59 by Replacement of Catalytic Residues in the Putative Viral Cyclic Phosphodiesterase ns2
Authors: Roth-Cross Jessica K. , Stokes Helen , Chang Guohui , Chua Ming Ming , Thiel Volker , Weiss Susan R. , Gorbalenya Alexander E. , Siddell Stuart G. 
Published: January 2009

ABSTRACTTheMurine hepatitis virus(MHV) strain A59 ns2 protein is a 30-kDa nonstructural protein that is expressed from a subgenomic mRNA in the cytoplasm of virus-infected cells. Its homologs are also encoded in other closely related group 2a coronaviruses and more distantly related toroviruses. Together, these proteins comprise a subset of a large superfamily of 2H phosphoesterase proteins that are distinguished by a pair of conserved His-x-Thr/Ser motifs encompassing catalytically important residues. We have used a vaccinia virus-based reverse genetic system to produce recombinant viruses encoding ns2 proteins with single-amino-acid substitutions in, or adjacent to, these conserved motifs, namely, inf-ns2 H46A, inf-ns2 S48A, inf-ns2-S120A, and inf-ns2-H126R. All of the mutant viruses replicate in mouse 17 clone 1 fibroblast cells and mouse embryonic cells to the same extent as the parental wild-type recombinant virus, inf-MHV-A59. However, compared to inf-MHV-A59, the inf-ns2 H46A and inf-ns2-H126R mutants are highly attenuated for replication in mouse liver following intrahepatic inoculation. Interestingly, none of the mutant viruses were attenuated for replication in mouse brain following intracranial inoculation. These results show that the ns2 protein of MHV-A59 has an important role in virus pathogenicity and that a substitution of the histidine residues of the MHV-A59 ns2 His-x-Thr/Ser motifs is critical for virus virulence in the liver but not in the brain. This novel phenotype suggests a strategy to investigate the function of the MHV-A59 ns2 protein involving the search for organ-specific proteins or RNAs that react differentially to wild-type and mutant ns2 proteins.
Transcriptional Coactivators Are Not Required for Herpes Simplex Virus Type 1 Immediate-Early Gene Expression In Vitro
Authors: Kutluay Sebla B. , DeVos Sarah L. , Klomp Jennifer E. , Triezenberg Steven J. 
Published: January 2009

ABSTRACT
Virion protein 16 (VP16) of herpes simplex virus type 1 (HSV-1) is a potent transcriptional activator of viral immediate-early (IE) genes. The VP16 activation domain can recruit various transcriptional coactivators to target gene promoters. However, the role of transcriptional coactivators in HSV-1 IE gene expression during lytic infection had not been fully defined. We showed previously that transcriptional coactivators such as the p300 and CBP histone acetyltransferases and the BRM and Brg-1 chromatin remodeling complexes are recruited to viral IE gene promoters in a manner dependent mostly on the presence of the activation domain of VP16. In this study, we tested the hypothesis that these transcriptional coactivators are required for viral IE gene expression during infection of cultured cells. The disrupted expression of the histone acetyltransferases p300, CBP, PCAF, and GCN5 or the BRM and Brg-1 chromatin remodeling complexes did not diminish IE gene expression. Furthermore, IE gene expression was not impaired in cell lines that lack functional p300, or BRM and Brg-1. We also tested whether these coactivators are required for the VP16-dependent induction of IE gene expression from transcriptionally inactive viral genomes associated with high levels of histones in cultured cells. We found that the disruption of coactivators also did not affect IE gene expression in this context. Thus, we conclude that the transcriptional coactivators that can be recruited by VP16 do not contribute significantly to IE gene expression during lytic infection or the induction of IE gene expression from nucleosomal templates in vitro.
The Infected Cell Protein 0 Encoded by Bovine Herpesvirus 1 (bICP0) Associates with Interferon Regulatory Factor 7 and Consequently Inhibits Beta Interferon Promoter Activity
Authors: Saira Kazima , Zhou You , Jones Clinton 
Published: January 2009

ABSTRACT

The bICP0 protein encoded by bovine herpesvirus 1 stimulates productive infection and viral gene expression but inhibits interferon (IFN)-dependent transcription. bICP0 inhibits beta IFN (IFN-β) promoter activity and induces degradation of IFN regulatory factor 3 (IRF3). Although bICP0 inhibits the
trans
-activation activity of IRF7, IRF7 protein levels are not reduced. In this study, we demonstrate that bICP0 is associated with IRF7. Furthermore, bICP0 inhibits the ability of IRF7 to
trans
-activate the IFN-β promoter in the absence of IRF3 expression. The interaction between bICP0 and IRF7 correlates with reduced
trans
-activation of the IFN-β promoter by IRF7.
Functional Replacement of a Domain in the Rubella Virus P150 Replicase Protein by the Virus Capsid Protein
Authors: Tzeng Wen-Pin , Frey Teryl K. 
Published: January 2009

ABSTRACT
The rubella virus (RUBV) capsid (C) protein rescues mutants with a lethal deletion between two in-frame NotI sites in the P150 replicase gene, a deletion encompassing nucleotides 1685 to 2192 of the RUBV genome and amino acids (aa) 548 to 717 of P150 (which has a total length of 1,301 aa). The complete domain rescuable by the C protein was mapped to aa 497 to 803 of P150. Introduction of aa 1 to 277 of the C protein (lacking the C-terminal E2 signal sequence) between the NotI sites in the P150 gene in a replicon construct yielded a viable construct that synthesized viral RNA with wild-type kinetics, indicating that C and this region of P150 share a common function. Further genetic analysis revealed that an arginine-rich motif between aa 60 and 68 of the C protein was necessary for the rescue of ΔNotI deletion mutants and substituted for an arginine-rich motif between aa 731 and 735 of the P150 protein when the C protein was introduced into P150. Possible common functions shared by these arginine-rich motifs include RNA binding and interaction with cell proteins.
Adenovirus Serotype 5 L4-22K and L4-33K Proteins Have Distinct Functions in Regulating Late Gene Expression
Authors: Morris Susan J. , Leppard Keith N. 
Published: January 2009

ABSTRACT

Adenoviruses express up to 20 distinct mRNAs from five major late transcription unit (MLTU) regions, L1 to L5, by differential splicing and polyadenylation of the primary transcript. MLTU expression is regulated at transcriptional and posttranscriptional levels. The L4-33K protein acts as a splicing factor to upregulate several MLTU splice acceptor sites as the late phase progresses. The L4 region also expresses a 22K protein whose sequence is related to the sequence of L4-33K. L4-22K is shown here also to have an important role in regulating the pattern of MLTU gene expression. An adenovirus genome containing a stop codon in the L4-22K open reading frame expressed low levels of both structural and nonstructural late proteins compared to the wild-type (wt) adenovirus genome; a decrease in intermediate proteins, IVa2 and IX, was also observed. However, early protein synthesis and replication were unaffected by the absence of L4-22K. Intermediate and late protein expression was restored to wt levels by L4-22K expressed in
trans
but not by L4-33K. Increased MLTU promoter activity, resulting from stabilization of the transcriptional activator IVa2 by L4-22K, made a small contribution to this restoration of late gene expression. However, the principal effect of L4-22K was on the processing of MLTU RNA into specific cytoplasmic mRNA. L4-22K selectively increased expression of penton mRNA and protein, whereas splicing to create penton mRNA is known not to be increased by L4-33K. These results indicate that L4-22K plays a key role in the early-late switch in MLTU expression, additional to and distinct from the role of L4-33K.
Postnatal developmental renal physiology: a study of historic significance
Authors: Baum Michel 
Published: January 2009

This essay looks at the historic significance of an APS classic paper ( http://www.the-aps.org/publications/classics/ ) that is freely available online: Falk G. Maturation of renal function in infant rats. Am J Physiol 181: 157–170, 1955 ( http://ajplegacy.physiology.org/cgi/reprint/181/1/157 ).
WTO Accessions: The Story So Far
Authors: Milthorp Peter 
Published: January 2009

AbstractDrawing on his thirteen years of experience as a Counsellor in the Accessions Division of the WTO Secretariat, Peter Milthorp describes accession as consisting of 'government-to-government negotiation, conducted at two mutually interactive levels'. The multilateral negotiations among the acceding country and the collective WTO membership correspond to Putnam's Level I; while the bilateral negotiations between the acceding country and individual members to agree on market access commitments require domestic bargaining and coalition building, and provide evidence of Putnam's Level II schema. Milthorp argues that the most arduous negotiations fall upon the government of the acceding country (that is, Level II), as it must develop a focused yet flexible negotiating mandate, implement economic reforms that may cause short-term hardship to some previously protected sectors, and ensure that negotiations progress steadily — all in order to retain political support for ratification. For accession negotiations to reach the end-game, negotiators must thus engage in both international and domestic diplomacy to create a balanced package that is acceptable to both WTO members as well as domestic stakeholders.
Non-Market Economies' Accessions to the WTO: Evolution of the Approach and Implications for the Organization
Authors: Huang Chieh 
Published: January 2009

AbstractThe General Agreement on Tariffs and Trade (GATT) and its successor, the Word Trade Organization (WTO), have been the main forum of international trade since the end of the Second World War. The regime is unquestionably based on free-market rules and principles. Yet in the last two decades, formerly planned economies — including Eastern European countries, former Soviet countries and China — have attempted to join the GATT/WTO. To encourage their transition under the influence of free-market principles, and to be a truly global trade organization, the GATT/WTO has accepted applicants with a reforming planned economy. This article studies the evolution of the GATT/WTO's approaches to integrate non-market economies and shows that the approach to integrate non-market economies during the WTO era is significantly different than during the GATT. While special mechanisms were provided in GATT accession protocols to bridge different market structures, WTO accessions require non-market economies to convert their own market structures. This article holds that this intolerance of different market structures in the WTO reflects the collapse of embedded liberalism and the rise of coercive trade diplomacy. Multilateral trade diplomacy has therefore become a means of imposing a domestic restructuring of economic structures rather than providing a negotiation forum for trade liberalization.