bluuebunny/crossref_metadata_2025_split huggingface dataset:
Basic Limitations on the Performance of Stirling
Engines
Authors: de Boer P. C. T. 
Published: December 2006

Abstract
The performance of Stirling engines is subject to limitations resulting from power dissipation in the regenerator. The dissipation is caused by pressure gradients in the regenerator required to generate flow. Without this flow the power output would be zero. Hence the dissipation is an essential element of the operation of the engine. Using linearized theory, the pressure in the compression and expansion spaces is found as a function of the ratio of piston amplitudes and piston phase difference. The regenerator is taken to be thermally perfect. All variations are taken to be sinusoidal in time. Expressions are derived for the dimensionless power output and the thermal efficiency at a given amplitude of the compression piston. Upper bounds on the power output and the efficiency are found as function of frequency and of regenerator void volume. Special attention is given to the case of piston amplitude ratio equal to 1.
A Logarithmic Complexity Divide-and-Conquer Algorithm for Multi-flexible Articulated Body Dynamics
Authors: Mukherjee Rudranarayan M. , Anderson Kurt S. 
Published: December 2006

Abstract
This paper presents an efficient algorithm for the dynamics simulation and analysis of multi-flexible-body systems. This algorithm formulates and solves the nonlinear equations of motion for mechanical systems with interconnected flexible bodies subject to the limitations of modal superposition, and body substructuring, with arbitrarily large rotations and translations. The large rotations or translations are modelled as rigid body degrees of freedom associated with the interconnecting kinematic joint degrees of freedom. The elastic deformation of the component bodies is modelled through the use of modal coordinates and associated admissible shape functions. Apart from the approximation associated with the elastic deformations, this algorithm is exact, non-iterative, and applicable to generalized multi-flexible chain and tree topologies. In its basic form, the algorithm is both time and processor optimal in its treatment of the nb joint variables, providing O(log(nb)) turnaround time per temporal integration step, achieved with O(nb) processors. The actual cost associated with the parallel treatment of the nf flexible degrees of freedom depends on the specific parallel method chosen for dealing with the individual coefficient matrices which are associated locally with each flexible body.
On an Implementation of the Hilber-Hughes-Taylor Method in the Context of Index 3 Differential-Algebraic Equations of Multibody Dynamics (DETC2005-85096)
Authors: Negrut Dan , Rampalli Rajiv , Ottarsson Gisli , Sajdak Anthony 
Published: December 2006

Abstract
The paper presents theoretical and implementation aspects related to a numerical integrator used for the simulation of large mechanical systems with flexible bodies and contact/impact. The proposed algorithm is based on the Hilber-Hughes-Taylor (HHT) implicit method and is tailored to answer the challenges posed by the numerical solution of index 3 differential-algebraic equations that govern the time evolution of a multibody system. One of the salient attributes of the algorithm is the good conditioning of the Jacobian matrix associated with the implicit integrator. Error estimation, integration step-size control, and nonlinear system stopping criteria are discussed in detail. Simulations using the proposed algorithm of an engine model, a model with contacts, and a model with flexible bodies indicate a 2 to 3 speedup factor when compared against benchmark MSC.ADAMS runs. The proposed HHT-based algorithm has been released in the 2005 version of the MSC.ADAMS/Solver.
Dose-Dependent Immune Response toMycobacterium bovisBCG Vaccination in Neonates
Authors: Davids Virginia , Hanekom Willem , Gelderbloem Sebastian J. , Hawkridge Anthony , Hussey Gregory , Sheperd Ronel , Workman Lesley , Soler Jorge , Murray Rose Ann , Ress Stanley R. , Kaplan Gilla 
Published: December 2006

ABSTRACTIn 10-week-old infants vaccinated at birth with JapaneseMycobacterium bovisBCG, the number of dermal needle penetrations correlated positively with frequency of proliferating CD4+T cells in whole blood following BCG stimulation for 6 days but did not correlate with secreted cytokine levels after 7 h or interferon CD4+T-cell frequency after 12 h of BCG stimulation.
Development of Serological Assays for Thottapalayam Virus, an Insectivore-Borne Hantavirus
Authors: Okumura Megumi , Yoshimatsu Kumiko , Kumperasart Sanit , Nakamura Ichiro , Ogino Michiko , Taruishi Midori , Sungdee Araya , Pattamadilok Sirima , Ibrahim Ima Nurisa , Erlina Sri , Agui Takashi , Yanagihara Richard , Arikawa Jiro 
Published: December 2006

ABSTRACT

Thottapalayam virus (TPMV), a member of the genus
Hantavirus
in the family
Bunyaviridae
, was isolated from an insectivore,
Suncus murinus
(musk shrew), captured in southern India in 1964. While the isolation of TPMV predates the discovery of the prototype Hantaan virus, little is known about its genetics and biology. To date, preliminary evidence suggests that TPMV differs significantly, both antigenically and genetically, from all known rodent-borne hantaviruses. However, since detailed epizootiological studies have not been conducted, it is unclear if TPMV is naturally harbored by an insectivore host or if TPMV represents a “spillover” from its natural rodent reservoir host. Moreover, to what extent TPMV causes infection and/or disease in humans is not known. To address these issues, we first studied the antigenic profile of TPMV using monoclonal antibodies against Hantaan and Seoul viruses and polyclonal immune sera against Puumala virus and TPMV. Armed with this newfound information, we developed an enzyme-linked immunosorbent assay system for the diagnosis of TPMV infections in shrews and humans, using a recombinant TPMV N antigen manipulated to have an E5/G6 epitope to be captured by monoclonal antibody clone E5/G6. Using this assay, we found anti-TPMV antibodies in sera from a patient with high fever of unknown etiology in Thailand and from two shrews captured in Indonesia. Seropositivity was verified by the indirect immunofluorescence antibody test, Western blotting analysis, and focus reduction neutralization test. Collectively, our data indicate that TPMV is harbored by
Suncus murinus
as its host in nature and is capable of infecting humans.
Comparison of Cepheid's Analyte-Specific Reagents with BD Directigen for Detection of Respiratory Syncytial Virus
Authors: Goodrich Jennifer S. , Miller Melissa B. 
Published: December 2006

ABSTRACT
For detection of respiratory syncytial virus (RSV), the BD Directigen RSV rapid antigen assay was compared to Cepheid's real-time reverse transcriptase PCR RSV analyte-specific reagents. The Directigen RSV assay resulted in a 23% false-negative rate, using PCR and chart review as the gold standard, indicating that rapid RSV PCR results would be advantageous.
The C-Terminal Portion of the Hrs Protein Interacts with Tsg101 and Interferes with Human Immunodeficiency Virus Type 1 Gag Particle Production
Authors: Bouamr Fadila , Houck-Loomis Brian R. , De Los Santos Martha , Casaday Rebecca J. , Johnson Marc C. , Goff Stephen P. 
Published: December 2006

ABSTRACT
The human immunodeficiency virus type 1 (HIV-1) Gag protein recruits Tsg101 to facilitate HIV-1 particle budding and release. In uninfected cells, the Hrs protein recruits the ESCRT-I complex to the endosome, also through an interaction with Tsg101, to promote the sorting of host proteins into endosomal vesicles and multivesicular bodies. Here, we show that the overexpression of the C-terminal fragment of Hrs (residues 391 to 777) or Hrs mutants lacking either the N-terminal FYVE domain (mutant dFYVE) or the PSAP (residues 348 to 351) motif (mutant ASAA) all efficiently inhibit HIV-1 Gag particle production. Expression of the dFYVE or ASAA mutants of Hrs had no effect on the release of Moloney murine leukemia virus. Coimmunoprecipitation analysis showed that the expression of Hrs mutant dFYVE or ASAA significantly reduced or abolished the HIV-1 Gag-Tsg101 interaction. Yeast-two hybrid assays were used to identify two new and independent Tsg101 binding sites, one in the Hrs coiled-coil domain and one in the proline/glutamic acid-rich domain. Scanning electron microscopy of HeLa cells expressing HIV-1 Gag and the Hrs ASAA mutant showed viral particles arrested in “lump-like” structures that remained attached to the cell surface. Together, these data indicate that fragments of Hrs containing the C-terminal portion of the protein can potently inhibit HIV-1 particle release by efficiently sequestering Tsg101 away from the Gag polyprotein.
Inhibition of Filovirus Replication by the Zinc Finger Antiviral Protein
Authors: Müller Stefanie , Möller Peggy , Bick Matthew J. , Wurr Stephanie , Becker Stephan , Günther Stephan , Kümmerer Beate M. 
Published: December 2006

ABSTRACT
The
zinc finger antiviral protein (ZAP) was recently shown to inhibit
Moloney murine leukemia virus and Sindbis virus replication. We tested
whether ZAP also acts against Ebola virus (EBOV) and Marburg virus
(MARV). Antiviral effects were observed after infection of cells
expressing the N-terminal part of ZAP fused to the product of the
zeocin resistance gene (NZAP-Zeo) as well as after infection of cells
inducibly expressing full-length ZAP. EBOV was inhibited by up to 4 log
units, whereas MARV was inhibited between 1 to 2 log units. The
activity of ZAP was dependent on the integrity of the second and fourth
zinc finger motif, as tested with cell lines expressing NZAP-Zeo
mutants. Heterologous expression of EBOV- and MARV-specific sequences
fused to a reporter gene suggest that ZAP specifically targets L gene
sequences. The activity of NZAP-Zeo in this assay was also dependent on
the integrity of the second and fourth zinc finger motif. Time-course
experiments with infectious EBOV showed that ZAP reduces the level of L
mRNA before the level of genomic or antigenomic RNA is affected.
Transient expression of ZAP decreased the activity of an EBOV replicon
system by up to 95%. This inhibitory effect could be partially
compensated for by overexpression of L protein. In conclusion, the data
demonstrate that ZAP exhibits antiviral activity against filoviruses,
presumably by decreasing the level of viral
mRNA.
Mouse Hepatitis Coronavirus A59 Nucleocapsid Protein Is a Type I Interferon Antagonist
Authors: Ye Ye , Hauns Kevin , Langland Jeffrey O. , Jacobs Bertram L. , Hogue Brenda G. 
Published: December 2006

ABSTRACT
The recent emergence of several new coronaviruses, including the etiological cause of severe acute respiratory syndrome, has significantly increased the importance of understanding virus-host cell interactions of this virus family. We used mouse hepatitis virus (MHV) A59 as a model to gain insight into how coronaviruses affect the type I alpha/beta interferon (IFN) system. We demonstrate that MHV is resistant to type I IFN. Protein kinase R (PKR) and the alpha subunit of eukaryotic translation initiation factor are not phosphorylated in infected cells. The RNase L activity associated with 2′,5′-oligoadenylate synthetase is not activated or is blocked, since cellular RNA is not degraded. These results are consistent with lack of protein translation shutoff early following infection. We used a well-established recombinant vaccinia virus (VV)-based expression system that lacks the viral IFN antagonist E3L to screen viral genes for their ability to rescue the IFN sensitivity of the mutant. The nucleocapsid (N) gene rescued VVΔE3L from IFN sensitivity. N gene expression prevents cellular RNA degradation and partially rescues the dramatic translation shutoff characteristic of the VVΔE3L virus. However, it does not prevent PKR phosphorylation. The results indicate that the MHV N protein is a type I IFN antagonist that likely plays a role in circumventing the innate immune response.
In Vitro Treatment of Human Monocytes/Macrophages with Myristoylated Recombinant Nef of Human Immunodeficiency Virus Type 1 Leads to the Activation of Mitogen-Activated Protein Kinases, IκB Kinases, and Interferon Regulatory Factor 3 and to the Release of Beta Interferon
Authors: Mangino Giorgio , Percario Zulema A. , Fiorucci Gianna , Vaccari Gabriele , Manrique Santiago , Romeo Giovanna , Federico Maurizio , Geyer Matthias , Affabris Elisabetta 
Published: December 2006

ABSTRACTThe viral protein Nef is a virulence factor that plays multiple roles during the early and late phases of human immunodeficiency virus (HIV) replication. Nef regulates the cell surface expression of critical proteins (including down-regulation of CD4 and major histocompatibility complex class I), T-cell receptor signaling, and apoptosis, inducing proapoptotic effects in uninfected bystander cells and antiapoptotic effects in infected cells. It has been proposed that Nef intersects the CD40 ligand signaling pathway in macrophages, leading to modification in the pattern of secreted factors that appear able to recruit and activate T lymphocytes, rendering them susceptible to HIV infection. There is also increasing evidence that in vitro cell treatment with Nef induces signaling effects. Exogenous Nef treatment is able to induce apoptosis in uninfected T cells, maturation in dendritic cells, and suppression of CD40-dependent immunoglobulin class switching in B cells. Previously, we reported that Nef treatment of primary human monocyte-derived macrophages (MDMs) induces a cycloheximide-independent activation of NF-κB and the synthesis and secretion of a set of chemokines/cytokines that activate STAT1 and STAT3. Here, we show that Nef treatment is capable of hijacking cellular signaling pathways, inducing a very rapid regulatory response in MDMs that is characterized by the rapid and transient phosphorylation of the α and β subunits of the IκB kinase complex and of JNK, ERK1/2, and p38 mitogen-activated protein kinase family members. In addition, we have observed the activation of interferon regulatory factor 3, leading to the synthesis of beta interferon mRNA and protein, which in turn induces STAT2 phosphorylation. All of these effects require Nef myristoylation.
Dendritic Cell-Mediated
trans
-Enhancement of Human Immunodeficiency Virus Type 1 Infectivity Is Independent of DC-SIGN
Authors: Boggiano Cesar , Manel Nicolas , Littman Dan R. 
Published: December 2006

ABSTRACT

Dendritic cells (DCs) enhance human immunodeficiency virus type 1 (HIV-1) infection of CD4
+
T lymphocytes in
trans
. The C-type lectin DC-SIGN, expressed on DCs, binds to the HIV-1 envelope glycoprotein gp120 and confers upon some cell lines the capacity to enhance
trans
-infection. Using a short hairpin RNA approach, we demonstrate that DC-SIGN is not required for efficient
trans
-enhancement by DCs. In addition, the DC-SIGN ligand mannan and an anti-DC-SIGN antibody did not inhibit DC-mediated enhancement. HIV-1 particles were internalized and were protected from protease treatment following binding to DCs, but not from binding to DC-SIGN-expressing Raji cells. Thus, DC-SIGN is not required for DC-mediated
trans
-enhancement of HIV infectivity.
Tissue-Specific Regulation of CD8+T-Lymphocyte Immunodominance in Respiratory Syncytial Virus Infection
Authors: Lee Sujin , Miller Scott A. , Wright David W. , Rock Michael T. , Crowe James E. 
Published: December 2006

ABSTRACTCytotoxic T lymphocytes (CTLs) are critical for control of respiratory syncytial virus (RSV) infection in humans and mice. To investigate cellular immune responses to infection, it is important to identify major histocompatibility complex (MHC) class I-restricted CTL epitopes. In this study, we identified a new RSV-specific, H-2Kd-restricted subdominant epitope in the M2 protein, M2127-135(amino acids 127 to 135). This finding allowed us to study the frequency of T lymphocytes responding to two H-2Kd-presented epitopes in the same protein following RSV infection by enzyme-linked immunospot (ELISPOT) and intracellular cytokine assays for both lymphoid and nonlymphoid tissues. For the subdominant epitope, we identified an optimal nine-amino-acid peptide, VYNTVISYI, which contained an H-2Kdconsensus sequence with Y at position 2 and I at position 9. In addition, an MHC class I stabilization assay using TAP-2-deficient RMA-S cells transfected with Kdor Ldindicated that the epitope was presented by Kd. The ratios of T lymphocytes during the peak CTL response to RSV infection that were specific for M282-90(dominant) to T lymphocytes specific for M2127-135(subdominant) were approximately 3:1 in the spleen and 10:1 in the lung. These ratios were observed consistently in primary or secondary infection by the ELISPOT assay and in secondary infection by MHC/peptide tetramer staining. The number of antigen-specific T lymphocytes dropped in the 6 weeks after infection; however, the proportions of T lymphocytes specific for the immunodominant and subdominant epitopes were maintained to a remarkable degree in a tissue-specific manner. These studies will facilitate investigation of the regulation of immunodominance of RSV-specific CTL epitopes.
Human Immunodeficiency Virus Type 1 Pathobiology Studied in Humanized BALB/c-Rag2
−/−
γ
c
−/−
Mice
Authors: Gorantla Santhi , Sneller Hannah , Walters Lisa , Sharp John G. , Pirruccello Samuel J. , West John T. , Wood Charles , Dewhurst Stephen , Gendelman Howard E. , Poluektova Larisa 
Published: December 2006

ABSTRACT

The specificity of human immunodeficiency virus type 1 (HIV-1) for human cells precludes virus infection in most mammalian species and limits the utility of small animal models for studies of disease pathogenesis, therapy, and vaccine development. One way to overcome this limitation is by human cell xenotransplantation in immune-deficient mice. However, this has proved inadequate, as engraftment of human immune cells is limited (both functionally and quantitatively) following transplantation of mature human lymphocytes or fetal thymus/liver. To this end, a human immune system was generated from umbilical cord blood-derived CD34
+
hematopoietic stem cells in BALB/c-Rag2
−/−
γ
c
−/−
mice. Intrapartum busulfan administration followed by irradiation of newborn pups resulted in uniform engraftment characterized by human T-cell development in thymus, B-cell maturation in bone marrow, lymph node development, immunoglobulin M (IgM)/IgG production, and humoral immune responses following ActHIB vaccination. Infection of reconstituted mice by CCR5-coreceptor utilizing HIV-1
ADA
and subtype C 1157 viral strains elicited productive viral replication and lymphadenopathy in a dose-dependent fashion. We conclude that humanized BALB/c-Rag2
−/−
γ
c
−/−
mice represent a unique and valuable resource for HIV-1 pathobiology studies.
Liver-Infiltrating Lymphocytes in Chronic Human Hepatitis C Virus Infection Display an Exhausted Phenotype with High Levels of PD-1 and Low Levels of CD127 Expression
Authors: Radziewicz Henry , Ibegbu Chris C. , Fernandez Marina L. , Workowski Kimberly A. , Obideen Kamil , Wehbi Mohammad , Hanson Holly L. , Steinberg James P. , Masopust David , Wherry E. John , Altman John D. , Rouse Barry T. , Freeman Gordon J. , Ahmed Rafi , Grakoui Arash 
Published: December 2006

ABSTRACT

The majority of people infected with hepatitis C virus (HCV) fail to generate or maintain a T-cell response effective for viral clearance. Evidence from murine chronic viral infections shows that expression of the coinhibitory molecule PD-1 predicts CD8
+
antiviral T-cell exhaustion and may contribute to inadequate pathogen control. To investigate whether human CD8
+
T cells express PD-1 and demonstrate a dysfunctional phenotype during chronic HCV infection, peripheral and intrahepatic HCV-specific CD8
+
T cells were examined. We found that in chronic HCV infection, peripheral HCV-specific T cells express high levels of PD-1 and that blockade of the PD-1/PD-L1 interaction led to an enhanced proliferative capacity. Importantly, intrahepatic HCV-specific T cells, in contrast to those in the periphery, express not only high levels of PD-1 but also decreased interleukin-7 receptor alpha (CD127), an exhausted phenotype that was HCV antigen specific and compartmentalized to the liver, the site of viral replication.
Declining Growth Rate of West Nile Virus in North America
Authors: Snapinn Katherine W. , Holmes Edward C. , Young David S. , Bernard Kristen A. , Kramer Laura D. , Ebel Gregory D. 
Published: December 2006

ABSTRACT
To determine the demographic history of West Nile virus (WNV) in North America, we employed a coalescent method to envelope coding region data sets for the NY99 and WN02 genotypes. Although the observed genetic diversities in both genotypes were of approximately the same age, the mean rate of epidemiological growth of the WN02 population was approximately three times that of the NY99 population, a finding compatible with the recent dominance of the former genotype. However, there has also been a marked decrease in the recent growth rate of WN02, suggesting that WNV has reached its peak prevalence in North America.
Spatiotemporal Analysis of Purkinje Cell Degeneration Relative to Parasagittal Expression Domains in a Model of Neonatal Viral Infection
Authors: Williams Brent L. , Yaddanapudi Kavitha , Hornig Mady , Lipkin W. Ian 
Published: December 2006

ABSTRACTInfection of newborn Lewis rats with Borna disease virus (neonatal Borna disease [NBD]) results in cerebellar damage without the cellular inflammation associated with infections in later life. Purkinje cell (PC) damage has been reported for several models of early-life viral infection, including NBD; however, the time course and distribution of PC pathology have not been investigated rigorously. This study examined the spatiotemporal relationship between PC death and zonal organization in NBD cerebella. Real-time PCR at postnatal day 28 (PND28) revealed decreased cerebellar levels of mRNAs encoding the glycolytic enzymes aldolase C (AldoC, also known as zebrin II) and phosphofructokinase C and the excitatory amino acid transporter 4 (EAAT4). Zebrin II and EAAT4 immunofluorescence analysis in PND21, PND28, PND42, and PND84 NBD rat cerebella revealed a complex pattern of PC degeneration. Early cell loss (PND28) was characterized by preferential apoptotic loss of zebrin II/EAAT4-negative PC subsets in the anterior vermis. Consistent with early preferential loss of zebrin II/EAAT4-negative PCs in the vermis, the densities of microglia and the Bergmann glial expression of metallothionein I/II and the hyaluronan receptor CD44 were higher in zebrin II/EAAT4-negative zones. In contrast, early loss in lateral cerebellar lobules did not reflect a similar discrimination between PC phenotypes. Patterns of vermal PC loss became more heterogeneous at PND42, with the loss of both zebrin II/EAAT4-negative and zebrin II/EAAT4-positive neurons. At PND84, zebrin II/EAAT4 patterning was abolished in the anterior cerebellum, with preferential PC survival in lobule X. Our investigation reveals regional discrimination between patterns of PC subset loss, defined by zebrin II/EAAT4 expression domains, following neonatal viral infection. These findings suggest a differential vulnerability of PC subsets during the early stages of virus-induced neurodegeneration.