bluuebunny/crossref_metadata_2025_split huggingface dataset:
Shoot Apex Demand Determines Assimilate and Nutrients Partitioning and Nutrient‐uptake Rate in Tobacco Plants
Authors: Yang Huai‐Yu , Li Chun‐Jian , Zhang Fu‐Suo 
Published: October 2007

Abstract Our previous experiment revealed that apex‐removed plants have larger root systems but a lower K+‐uptake rates than intact tobacco plants. Since the apex is not only a center of growth and metabolism, but also an important place of auxin synthesis and export, the aims of this study were to distinguish whether the apex demand or auxin synthesized in the apex regulates assimilate and nutrients partitioning within plant, and to explain the reason for the lower K+‐uptake rate of the apex‐removed plant. In comparison with the control plant, covering the shoot apex with a black transparent plastic bag reduced net increases in dry matter and nutrients; however, the distribution of the dry matter and nutrients between shoot and roots and nutrient‐uptake rates were not changed. Removal of the shoot apex shifted the dry mass and nutrients distributions to roots, and reduced the rate of nutrient uptake. Application of 1‐naphthylacetic acid (NAA) could partly replace the role of the removed apex, stimulated assimilate and nutrient deposition into the treated tissue, and enhanced the reduced plasma membrane ATPase activity of roots to the control level. However, treatment of the apex‐removed plants with NAA could not rescue the reduced nutrient uptake rate and the shifted assimilates and nutrients partitioning caused by excision of the apex. Higher nutrient uptake rate of the intact plants could not be explained by root growth parameters, such as total root surface area and number of root tips. The results from the present study indicate that strong apex demand determined assimilates and nutrients partitioning and nutrient‐uptake rate in tobacco (Nicotiana tabacum) plants.
Genetic Diversity of
Actinobacillus pleuropneumoniae
Assessed by Amplified Fragment Length Polymorphism Analysis
Authors: Kokotovic Branko , Angen Øystein 
Published: October 2007

ABSTRACT

Amplified fragment length polymorphism (AFLP) was evaluated as a method for genotypic characterization and subtyping within the bacterial species
Actinobacillus pleuropneumoniae
. A total of 155 isolates of
A. pleuropneumoniae
, representing the serotypic variation described to occur within this species, were analyzed. In order to elucidate the species boundaries, six strains of the phylogenetically closely related species
Actinobacillus lignieresii
were also included. Furthermore, the ability of AFLP to subtype was studied using 42 isolates of serovar 2 and the performance compared to that obtained by pulsed-field gel electrophoresis (PFGE). AFLP analysis provided a clear separation of
A. lignieresii
and
A. pleuropneumoniae
and divided the isolates of
A. pleuropneumoniae
into 20 clusters. Most of the serovars of
A. pleuropneumoniae
were represented by single and quite homogeneous clusters. The exceptions were serovars 10, K2:O7, and K1:O7, which were represented by two clusters each. In the cases where the serovars were represented by more than one cluster, the existence of these clusters was supported by additional phenotypic or genotypic properties. Furthermore, AFLP typing was able to allocate serologically nontypeable isolates to appropriate genetic groups within the species. Further investigations are needed to determine whether some of the clusters revealed through AFLP analysis represent additional serovars. When evaluated as a method for subtyping within serovar 2 of
A. pleuropneumoniae
, AFLP was found to achieve a degree of separation among isolates superior to that obtained by PFGE. However, a higher degree of separation between serovar 2 isolates was obtained by a combination of the two methods.
Detection of High-Risk Papillomavirus DNA with Commercial Invader-Technology-Based Analyte-Specific Reagents following Automated Extraction of DNA from Cervical Brushings in ThinPrep Media
Authors: Schutzbank Ted E. , Jarvis Charlene , Kahmann Nicole , Lopez Katherine , Weimer Marlea , Yount Aleta 
Published: October 2007

ABSTRACT
We compared the performances of the Third Wave Technology Invader method and the Digene Hybrid Capture 2 assay to detect high-risk human papillomaviruses in 87 cervical brushing specimens submitted in Cytyc ThinPrep media. Two different methods for the extraction of DNA from squamous epithelial cells were also evaluated.
Recognition of Escape Variants in ELISPOT Does Not Always Predict CD8
+
T-Cell Recognition of Simian Immunodeficiency Virus-Infected Cells Expressing the Same Variant Sequences
Authors: Valentine Laura E. , Piaskowski Shari M. , Rakasz Eva G. , Henry Nathan L. , Wilson Nancy A. , Watkins David I. 
Published: October 2007

ABSTRACT

Human immunodeficiency virus (HIV)'s tremendous sequence variability is a major obstacle for the development of cytotoxic-T-lymphocyte-based vaccines, especially since much of this variability is selected for by CD8
+
T cells. We investigated to what extent reactivity to escape variant peptides in standard enzyme-linked immunospot (ELISPOT) assays predicts the recognition of cells infected with corresponding escape variant viruses. Most of the variant peptides tested were recognized in standard ELISPOT and intracellular cytokine stain (ICS) assays. Functional avidity of epitope-specific T cells for some of the variants was, however, markedly reduced. These mutations which reduced avidity also abrogated recognition by epitope-specific CD8
+
T cells in a viral suppression assay. Our results indicate that “cross-reactive” CD8
+
T-cell responses identified in ELISPOT and ICS assays using a single high concentration of variant peptide often fail to predict the recognition of cells infected with variant viruses.
Adaptation of the Human Immunodeficiency Virus Type 1 Envelope Glycoproteins to New World Monkey Receptors
Authors: Pacheco Beatriz , Basmaciogullari Stephane , LaBonte Jason A. , Xiang Shi-Hua , Sodroski Joseph 
Published: October 2007

ABSTRACT
Human immunodeficiency virus type 1 (HIV-1) infection encounters an early block in the cells of New World monkeys because the CD4 receptor does not efficiently support HIV-1 entry. We adapted HIV-1(NL4-3) and HIV-1(KB9), two HIV-1 variants with different envelope glycoproteins, to replicate efficiently in cells expressing the CD4 and CXCR4 proteins of the common marmoset, a New World monkey. The HIV-1(NL4-3) adaptation involves three gp120 changes that result in a specific increase in affinity for the marmoset CD4 glycoprotein. The already high affinity of the HIV-1(KB9) envelope glycoproteins for marmoset CD4 did not significantly change as a result of the adaptation. Instead, changes in the gp120 variable loops and gp41 ectodomain resulted in improved replication in cells expressing the marmoset receptors. HIV-1(KB9) became relatively sensitive to neutralization by soluble CD4 and antibodies as a result of the adaptation. These results demonstrate the distinct mechanistic pathways by which the HIV-1 envelope glycoproteins can adapt to less-than-optimal CD4 molecules and provide HIV-1 variants that can overcome some of the early blocks in New World monkey cells.
Human Immunodeficiency Virus Type 1 Vpu Protein Interacts with CD74 and Modulates Major Histocompatibility Complex Class II Presentation
Authors: Hussain Amjad , Wesley Clement , Khalid Mohammad , Chaudhry Ashutosh , Jameel Shahid 
Published: October 2007

ABSTRACT
The human immunodeficiency virus type 1 (HIV-1) Vpu accessory protein is a transmembrane protein that down regulates CD4 expression and promotes the release of new virions. We screened a human leukocyte-specific yeast two-hybrid expression library to discover novel Vpu-interacting cellular proteins. The major histocompatibility complex class II (MHC II) invariant chain, also called Ii or CD74, was found to be one such protein. We show direct binding of Vpu and CD74 by using a yeast two-hybrid assay and coimmunoprecipitation from HIV-1-infected cells. The cytoplasmic region of Vpu was found to interact with the 30-amino-acid cytoplasmic tail of CD74. Human monocytic U937 cells infected with wild-type or Vpu-defective HIV-1 and transfected cells showed that Vpu down modulated the surface expression of mature MHC II molecules. The reduction in cell surface mature MHC II molecules correlated with decreased antigen presentation to T cells in culture. Thus, the Vpu protein also contributes to viral persistence by attenuating immune responses during HIV infection. This report further exemplifies the rich diversity and redundancy shown by HIV in immune evasion.
Expression of the E3L Gene of Vaccinia Virus in Transgenic Mice Decreases Host Resistance to Vaccinia Virus and
Leishmania major
Infections
Authors: Domingo-Gil Elena , Pérez-Jiménez Eva , Ventoso Iván , Nájera José L. , Esteban Mariano 
Published: October 2007

ABSTRACT

The E3L gene of vaccinia virus (VACV) encodes the E3 protein that in cultured cells inhibits the activation of interferon (IFN)-induced proteins, double-stranded RNA-dependent protein kinase (PKR), 2′-5′-oligoadenylate synthetase/RNase L (2-5A system) and adenosine deaminase (ADAR-1), thus helping the virus to evade host responses. Here, we have characterized the in vivo E3 functions in a murine inducible cell culture system (E3L-TetOFF) and in transgenic mice (TgE3L). Inducible E3 expression in cultured cells conferred on cells resistance to the antiviral action of IFN against different viruses, while expression of the E3L gene in TgE3L mice triggered enhanced sensitivity of the animals to pathogens. Virus infection monitored in TgE3L mice by different inoculation routes (intraperitoneal and tail scarification) showed that transgenic mice became more susceptible to VACV infection than control mice. TgE3L mice were also more susceptible to
Leishmania major
infection, leading to an increase in parasitemia compared to control mice. The enhanced sensitivity of TgE3L mice to VACV and
L
.
major
infections occurred together with alterations in the host immune system, as revealed by decreased T-cell responses to viral antigens in the spleen and lymph nodes and by differences in the levels of specific innate cell populations. These results demonstrate that expression of the E3L gene in transgenic mice partly reverses the resistance of the host to viral and parasitic infections and that these effects are associated with immune alterations.
Suppression of Acute Anti-Friend Virus CD8+T-Cell Responses by Coinfection with Lactate Dehydrogenase-Elevating Virus
Authors: Robertson Shelly J. , Ammann Christoph G. , Messer Ronald J. , Carmody Aaron B. , Myers Lara , Dittmer Ulf , Nair Savita , Gerlach Nicole , Evans Leonard H. , Cafruny William A. , Hasenkrug Kim J. 
Published: October 2007

ABSTRACTFriend virus (FV) and lactate dehydrogenase-elevating virus (LDV) are endemic mouse viruses that can cause long-term chronic infections in mice. We found that numerous mouse-passaged FV isolates also contained LDV and that coinfection with LDV delayed FV-specific CD8+T-cell responses during acute infection. While LDV did not alter the type of acute pathology induced by FV, which was severe splenomegaly caused by erythroproliferation, the immunosuppression mediated by LDV increased both the severity and the duration of FV infection. Compared to mice infected with FV alone, those coinfected with both FV and LDV had delayed CD8+T-cell responses, as measured by FV-specific tetramers. This delayed response accounted for the prolonged and exacerbated acute phase of FV infection. Suppression of FV-specific CD8+T-cell responses occurred not only in mice infected concomitantly with LDV but also in mice chronically infected with LDV 8 weeks prior to infection with FV. The LDV-induced suppression was not mediated by T regulatory cells, and no inhibition of the CD4+T-cell or antibody responses was observed. Considering that most human adults are carriers of chronically infectious viruses at the time of new virus insults and that coinfections with viruses such as human immunodeficiency virus and hepatitis C virus are currently epidemic, it is of great interest to determine how infection with one virus may impact host responses to a second infection. Coinfection of mice with LDV and FV provides a well-defined, natural host model for such studies.
Identification and Classification of Endogenous Retroviruses in Cattle
Authors: Xiao Rui , Park Kwangha , Lee Hoontaek , Kim Jinhoi , Park Chankyu 
Published: October 2007

ABSTRACT

The aim of this study was to identify the endogenous retrovirus (ERV) sequences in a bovine genome. We subjected bovine genomic DNA to PCR with degenerate or ovine ERV (OERV) family-specific primers that aimed to amplify the retroviral
pro/pol
region. Sequence analysis of 113 clones obtained by PCR revealed that 69 were of retroviral origin. On the basis of the OERV classification system, these clones from degenerate PCR could be divided into the β3, γ4, and γ9 families. PCR with OERV family-specific primers revealed an additional ERV that was classified into the bovine endogenous retrovirus (BERV) γ7 family. In conclusion, here we report the results of a genome scale study of the BERV. Our study shows that the ERV family expansion in cattle may be somewhat limited, while more diverse family members of ERVs have been reported from other artiodactyls, such as pigs and sheep.
Different Abilities of Escape Mutant-Specific Cytotoxic T Cells To Suppress Replication of Escape Mutant and Wild-Type Human Immunodeficiency Virus Type 1 in New Hosts
Authors: Fujiwara Mamoru , Tanuma Junko , Koizumi Hirokazu , Kawashima Yuka , Honda Kazutaka , Mastuoka-Aizawa Saori , Dohki Sachi , Oka Shinichi , Takiguchi Masafumi 
Published: October 2007

ABSTRACTThere is much evidence that in human immunodeficiency virus type 1 (HIV-1)-infected individuals, strong cytotoxic T lymphocyte (CTL)-mediated immune pressure results in the selection of HIV-1 mutants that have escaped from wild-type-specific CTLs. If escape mutant-specific CTLs are not elicited in new hosts sharing donor HLA molecules, the transmission of these mutants results in the accumulation of escape mutants in the population. However, whether escape mutant-specific CTLs are definitively not elicited in new hosts sharing donor HLA molecules still remains unclear. A previous study showed that a Y-to-F substitution at the second position (2F) of the Nef138-10 epitope is significantly detected in HLA-A*2402+hemophilic donors. Presently, we confirmed that this 2F mutant was an escape mutant by demonstrating strong and weak abilities of Nef138-10-specific CTL clones to suppress replication of the wild-type and 2F mutant viruses, respectively. We demonstrated the existence of the 2F-specific CTLs in three new hosts who had been primarily infected with the 2F mutant. The 2F-specific CTL clones suppressed the replication of both wild-type and mutant viruses. However, the abilities of these clones to suppress replication of the 2F virus were much weaker than those of wild-type-specific and the 2F-specific ones to suppress replication of the wild-type virus. These findings indicate that the 2F mutant is conserved in HIV-1-infected donors having HLA-A*2402, because the 2F-specific CTLs failed to completely suppress the 2F mutant replication and effectively prevented viral reversion in new hosts carrying HLA-A*2402.
Identification of Human Cytomegalovirus UL84 Virus- and Cell-Encoded Binding Partners by Using Proteomics Analysis
Authors: Gao Yang , Colletti Kelly , Pari Gregory S. 
Published: October 2007

ABSTRACT

Human cytomegalovirus (HCMV) UL84 is a phosphoprotein that shuttles from the nucleus to the cytoplasm and is required for
ori
Lyt-dependent DNA replication and viral growth. UL84 was previously shown to interact with IE2 (IE86) in infected cells, and this interaction down-regulates IE2-mediated transcriptional activation in transient assays. UL84 and IE2 were also shown to cooperatively activate a promoter within HCMV
ori
Lyt. UL84 alone can interact with an RNA stem-loop within
ori
Lyt and is bound to this structure within the virion. In an effort to investigate the binding partners for UL84 in infected cells, we pulled down UL84 from protein lysates prepared from HCMV-infected human fibroblasts by using a UL84-specific antibody and resolved the immunoprecipitated protein complexes by two-dimensional gel electrophoresis. We subsequently identified individual proteins by matrix-assisted laser desorption ionization-tandem time of flight analysis. This analysis revealed that UL84 interacts with viral proteins UL44, pp65, and IE2. In addition, a number of cell-encoded proteins were identified, including ubiquitin-conjugating enzyme E2, casein kinase II (CKII), and the multifunctional protein p32. We also confirmed the interaction between UL84 and IE2 as well as the interaction of UL84 with importin α. UL44, pp65, and CKII interactions were confirmed to occur in infected and cotransfected cells by coimmunoprecipitation assays followed by Western blotting. Ubiquitination of UL84 occurred in the presence and absence of the proteasome activity inhibitor MG132 in infected cells. The identification of UL84 binding partners is a significant step toward the understanding of the function of this significant replication protein.
Reovirus Apoptosis and Virulence Are Regulated by Host Cell Membrane Penetration Efficiency
Authors: Danthi Pranav , Kobayashi Takeshi , Holm Geoffrey H. , Hansberger Mark W. , Abel Ty W. , Dermody Terence S. 
Published: October 2007

ABSTRACTApoptosis plays an important role in the pathogenesis of reovirus encephalitis and myocarditis in infected animals. Differences in apoptosis efficiency displayed by reovirus strains are linked to the viral μ1-encoding M2 gene segment. Studies using pharmacologic inhibitors of reovirus replication demonstrate that apoptosis induction by reovirus requires viral disassembly in cellular endosomes but not RNA synthesis. Since the μ1 protein functions to pierce endosomal membranes during this temporal window, these findings point to an important role for μ1 in activating signaling pathways that lead to apoptosis. To understand mechanisms used by μ1 to induce apoptosis, a panel of μ1 mutant viruses generated by reverse genetics was analyzed for the capacities to penetrate host cell membranes, activate proapoptotic signaling pathways, evoke cell death, and produce encephalitis in newborn mice. We found that single amino acid changes within the δ region of μ1 reduce the efficiency of membrane penetration. These mutations also diminish the capacities of reovirus to activate proapoptotic transcription factors NF-κB and IRF-3 and elicit apoptosis. Additionally, we observed that following intracranial inoculation, an apoptosis-deficient μ1 mutant is less virulent in newborn mice in comparison to the wild-type virus. These results indicate a critical function for the membrane penetration activity of μ1 in evoking prodeath signaling pathways that regulate reovirus pathogenesis.
Lateralization of the Posterior Parietal Cortex for Internal Monitoring of Self- versus Externally Generated Movements
Authors: Ogawa Kenji , Inui Toshio 
Published: October 2007

Abstract
Internal monitoring or state estimation of movements is essential for human motor control to compensate for inherent delays and noise in sensorimotor loops. Two types of internal estimation of movements exist: self-generated movements, and externally generated movements. We used functional magnetic resonance imaging to investigate differences in brain activity for internal monitoring of self- versus externally generated movements during visual occlusion. Participants tracked a sinusoidally moving target with a mouse cursor. On some trials, vision of either target (externally generated) or cursor (self-generated) movement was transiently occluded, during which subjects continued tracking by estimating current position of either the invisible target or cursor on screen. Analysis revealed that both occlusion conditions were associated with increased activity in the presupplementary motor area and decreased activity in the right lateral occipital cortex compared to a control condition with no occlusion. Moreover, the right and left posterior parietal cortex (PPC) showed greater activation during occlusion of target and cursor movements, respectively. This study suggests lateralization of the PPC for internal monitoring of internally versus externally generated movements, fully consistent with previously reported clinical findings.
Challenges in Mesoscale Prediction of a Nocturnal Stratocumulus-Topped Marine Boundary Layer and Implications for Operational Forecasting
Authors: Vellore Ramesh , Koračin Darko , Wetzel Melanie , Chai Steven , Wang Qing 
Published: October 2007

Abstract
A numerical study using the fifth-generation Pennsylvania State University–National Center for Atmospheric Research Mesoscale Model (MM5) was performed to assess the impact of initial and boundary conditions, the parameterization of turbulence transfer and its coupling with cloud-driven radiation, and cloud microphysical processes on the accuracy of mesoscale predictions and forecasts of the cloud-capped marine boundary layer. Aircraft, buoy, and satellite data and the large eddy simulation (LES) results during the Dynamics and Chemistry of Marine Stratocumulus field experiment (DYCOMS II) in July 2001 were used in the assessment. Three of the tested input fields (Eta, NCEP, and ECMWF) show deficiencies, mainly in the thermodynamic structure of the lowest 1500 m of the marine atmosphere. On a positive note, the simulated marine-layer depth showed good agreement with aircraft observations using the Eta fields, while using the NCEP and ECMWF datasets underestimated the marine-layer depth by about 20%–30%. The predicted turbulence kinetic energy (inversion strength) was about 50% of that obtained from the LES results (aircraft observed). As a consequence of moisture overprediction, the predicted liquid water path was twice the observed by 1–2 g kg−1. The sensitivity tests have shown that the selections of turbulence and cloud microphysical schemes significantly influence the turbulence estimates and cloud parameters. Two of the tested turbulence schemes (Eta PBL and Burk–Thompson) did not exhibit the coupling with radiation. The significant differences in the simulated turbulence estimates appear to be a consequence of the use of water-conserving potential temperature variables. The microphysical parameterization, which uses the number concentration of cloud drops in the autoconversion process, simulates a realistic evolution of precipitable hydrometeors in the cloudy marine layer on the positive side, but on the other hand enhances the decoupling in the turbulence structure. This study can provide guidance to operational forecasters concerning accuracy issues of the commonly used large-scale analyses for model initialization, and optimal selection of model parameterizations in order to simulate and forecast the cloudy atmospheric boundary layer over the ocean.