bluuebunny/crossref_metadata_2025_split huggingface dataset:
Herpes Simplex Virus Type 1 Glycoprotein E Mediates Retrograde Spread from Epithelial Cells to Neurites
Authors: McGraw Helen M. , Friedman Harvey M. 
Published: March 2009

ABSTRACT
In animal models of infection, glycoprotein E (gE) is required for efficient herpes simplex virus type 1 (HSV-1) spread from the inoculation site to the cell bodies of innervating neurons (retrograde direction). Retrograde spread in vivo is a multistep process, in that HSV-1 first spreads between epithelial cells at the inoculation site, then infects neurites, and finally travels by retrograde axonal transport to the neuron cell body. To better understand the role of gE in retrograde spread, we used a compartmentalized neuron culture system, in which neurons were infected in the presence or absence of epithelial cells. We found that gE-deleted HSV-1 (NS-gEnull) retained retrograde axonal transport activity when added directly to neurites, in contrast to the retrograde spread defect of this virus in animals. To better mimic the in vivo milieu, we overlaid neurites with epithelial cells prior to infection. In this modified system, virus infects epithelial cells and then spreads to neurites, revealing a 100-fold retrograde spread defect for NS-gEnull. We measured the retrograde spread defect of NS-gEnull from a variety of epithelial cell lines and found that the magnitude of the spread defect from epithelial cells to neurons correlated with epithelial cell plaque size defect, indicating that gE plays a similar role in both types of spread. Therefore, gE-mediated spread between epithelial cells and neurites likely explains the retrograde spread defect of gE-deleted HSV-1 in vivo.
Andes Virus Antigens Are Shed in Urine of Patients with Acute Hantavirus Cardiopulmonary Syndrome
Authors: Godoy Paula , Marsac Delphine , Stefas Elias , Ferrer Pablo , Tischler Nicole D. , Pino Karla , Ramdohr Pablo , Vial Pablo , Valenzuela Pablo D. T. , Ferrés Marcela , Veas Francisco , López-Lastra Marcelo 
Published: March 2009

ABSTRACTHantavirus cardiopulmonary syndrome (HCPS) is a highly pathogenic emerging disease (40% case fatality rate) caused by New World hantaviruses. Hantavirus infections are transmitted to humans mainly by inhalation of virus-contaminated aerosol particles of rodent excreta and secretions. At present, there are no antiviral drugs or immunotherapeutic agents available for the treatment of hantaviral infection, and the survival rates for infected patients hinge largely on early virus recognition and hospital admission and aggressive pulmonary and hemodynamic support. In this study, we show that Andes virus (ANDV) interacts with human apolipoprotein H (ApoH) and that ApoH-coated magnetic beads or ApoH-coated enzyme-linked immunosorbent assay plates can be used to capture and concentrate the virus from complex biological mixtures, such as serum and urine, allowing it to be detected by both immunological and molecular approaches. In addition, we report that ANDV-antigens and infectious virus are shed in urine of HCPS patients.
The γ134.5 Protein of Herpes Simplex Virus 1 Is Required To Interfere with Dendritic Cell Maturation during Productive Infection
Authors: Jin Huali , Ma Yijie , Prabhakar Bellur S. , Feng Zongdi , Valyi-Nagy Tibor , Yan Zhipeng , Verpooten Dustin , Zhang Cuizhu , Cao Youjia , He Bin 
Published: March 2009

ABSTRACTThe γ134.5 protein of herpes simplex virus 1 is an essential factor for viral virulence. In infected cells, this viral protein prevents the translation arrest mediated by double-stranded RNA-dependent protein kinase R. Additionally, it associates with and inhibits TANK-binding kinase 1, an essential component of Toll-like receptor-dependent and -independent pathways that activate interferon regulatory factor 3 and cytokine expression. Here, we show that γ134.5 is required to block the maturation of conventional dendritic cells (DCs) that initiate adaptive immune responses. Unlike wild-type virus, the γ134.5 null mutant stimulates the expression of CD86, major histocompatibility complex class II (MHC-II), and cytokines such as alpha/beta interferon in immature DCs. Viral replication in DCs inversely correlates with interferon production. These phenotypes are also mirrored in a mouse ocular infection model. Further, DCs infected with the γ134.5 null mutant effectively activate naïve T cells whereas DCs infected with wild-type virus fail to do so. Type I interferon-neutralizing antibodies partially reverse virus-induced upregulation of CD86 and MHC-II, suggesting that γ134.5 acts through interferon-dependent and -independent mechanisms. These data indicate that γ134.5 is involved in the impairment of innate immunity by inhibiting both type I interferon production and DC maturation, leading to defective T-cell activation.
Hepatitis B Virus X Protein Modulates Apoptosis in Primary Rat Hepatocytes by Regulating both NF-κB and the Mitochondrial Permeability Transition Pore
Authors: Clippinger Amy J. , Gearhart Tricia L. , Bouchard Michael J. 
Published: March 2009

ABSTRACTThe hepatitis B virus (HBV) X protein (HBx) is a multifunctional protein that regulates numerous cellular signal transduction pathways, including those that modulate apoptosis. However, different HBx-dependent effects on apoptosis have been reported; these differences are likely the consequence of the exact conditions and cell types used in a study. Many of the previously reported studies that analyzed HBx regulation of apoptosis were conducted in immortalized or transformed cells, and the alterations that have transformed or immortalized these cells likely impact apoptotic pathways. We examined the effects of HBx on apoptotic pathways in cultured primary rat hepatocytes, a biologically relevant system that mimics normal hepatocytes in the liver. We analyzed the effects of HBx on apoptosis both when HBx was expressed in the absence of other HBV proteins and in the context of HBV replication. HBx stimulation of NF-κB inhibited the activation of apoptotic pathways in cultured primary rat hepatocytes. However, when HBx-induced activation of NF-κB was blocked, HBx stimulated apoptosis; blocking the activity of the mitochondrial permeability transition pore inhibited HBx activation of apoptosis. These results suggest that HBx can be either proapoptotic or antiapoptotic in hepatocytes, depending on the status of NF-κB, and confirm previous studies that link some HBx activities to modulation of the mitochondrial permeability transition pore. Overall, our studies define apoptotic pathways that are regulated by HBx in cultured primary hepatocytes and provide potential mechanisms for the development of HBV-associated liver cancer.
Hell Disarmed? The Function of Hell in Reformation Spirituality
Authors: Rasmussen Tarald 
Published: March 2009

In Late Medieval Christianity, the concept of hell was closely connected to the sacrament of penance. Hell could be avoided through the right use of penance. And the cleansing sufferings in purgatory could to a certain extent replace the eternal sufferings in hell. The Protestant Reformation rejected purgatory, and returned to a traditional dualistic view of the relationship between heaven and hell. At the same time, hell seems to lose some of its religious importance in early Protestant spirituality. This change is illustrated through a comparison of two central texts belonging more or less to the same genre: on the one hand the famous Late Medieval illustrated
Ars moriendi
and on the other Luther's
Sermon von der Bereitung zum Sterben
from 1519.
The Longue Durée of the French Bourgeoisie
Authors: Heller Henry 
Published: March 2009

AbstractBeginning with Engels, Marxist historiography viewed the absolute monarchy in France as mediating between the nobility and the emergent capitalist bourgeoisie. More recent Marxist accounts stress that the absolute monarchy reflected the interests of the nobility. Revisionist Marxist historians have taken this perspective to an extreme arguing that, at the height of the Bourbon monarchy in the seventeenth century, a capitalist bourgeoisie did not exist. This paper argues that, in taking such a view, these historians have ignored the ongoing dialectical opposition between the forces of rent and profit in the early-modern period. As a result, they have severed the connection between the ancien régime and the Revolution of 1789. Despite being thrown on the defensive by the advance of rent and the crystallisation of the absolutist state, a capitalist bourgeoisie that emerged in sixteenth-century France survived and persevered during the seventeenth century. It resumed the initiative in the succeeding period of the Enlightenment.
Contradiction and Abstraction: A Reply to Finelli
Authors: Arthur Christopher 
Published: March 2009

AbstractFollowing the publication of my book The New Dialectic and Marx's 'Capital', and the symposium on it in Historical Materialism 13.2, a critique by Roberto Finelli recently appeared: 'Abstraction versus Contradiction: Observations on Chris Arthur's The New Dialectic and Marx's “Capital”' in Historical Materialism 15.2. Finelli argues that my systematic dialectic is not taken sufficiently far, in that I retain presuppositions not posited by the capitalist totality. Here, I argue against Finelli's closed totality of wholly abstract forms, not least because it affords no realistic exit strategy. I reaffirm that the logic of contradiction is required to conceptualise the capital relation.
Die radikale Linke als Massenbewegung. Kommunisten in Harburg-Wilhelmsburg 1918–1933
Authors: Bois Marcel 
Published: March 2009

AbstractIn the mid-1990s, Klaus-Michael Mallmann published his study on 'Communists in the Weimar Republic'. His newly established social-historical approach on the Communist Party of Germany (KPD) has since been taken up by other historians. One of them is Christian Gotthardt, who recently published a book with the promising title 'The Radical Left as a Mass Movement'. Here he focuses on the regional history of the KPD in the city of Harburg-Wilhelmsburg. The great strength of his book is the detailed description of the local Communists' day-to-day work. However, when turning his attention to the turning points of KPD history, the problems associated with adopting Mallman's social-historical approach become obvious. For example this leads them both to reject the theory of 'Stalinisation'. The article shows that Gotthardt, as well as Mallmann, had come to questionable conclusions on the development of the KPD of the Weimar Republic by focusing on events outside of their context in time and space.
Meniscal Repair in the Elite Athlete
Authors: Logan Martin , Watts Mark , Owen James , Myers Peter 
Published: March 2009

Background The preservation of meniscal tissue is important to protect joint surfaces. Purpose We have an aggressive approach to meniscal repair, including repairing tears other than those classically suited to repair. Here we present the medium- to long-term outcome of meniscal repair (inside-out) in elite athletes. Study Design Case series; Level of evidence, 4. Methods Forty-two elite athletes underwent 45 meniscal repairs. All repairs were performed using an arthroscopically assisted inside-out technique. Eighty-three percent of these athletes had ACL reconstruction at the same time. Patients returned a completed questionnaire (including Lysholm and International Knee Documentation Committee [IKDC] scores). Mean follow-up was 8.5 years. Failure was defined by patients developing symptoms of joint line pain and/or locking or swelling requiring repeat arthroscopy and partial meniscectomy. Results The average Lysholm and subjective IKDC scores were 89.6 and 85.4, respectively. Eighty-one percent of patients returned to their main sport and most to a similar level at a mean time of 10.4 months after repair, reflecting the high level of ACL reconstruction in this group. We identified 11 definite failures, 10 medial and 1 lateral meniscus, that required excision; this represents a 24% failure rate. We identified 1 further patient who had possible failed repairs, giving a worst-case failure rate of 26.7% at a mean of 42 months after surgery. However, 7 of these failures were associated with a further injury. Therefore, the atraumatic failure rate was 11%. Age and size and location of the tears were not associated with a higher failure rate. Medial meniscal repairs were significantly more likely to fail than lateral meniscal repairs, with a failure rate of 36.4% and 5.6%, respectively ( P < .05). Conclusion Meniscal repair and healing are possible, and most elite athletes can return to their preinjury level of activity.
Proshchenkoite-(Y) from Russia — a new mineral species in the vicanite group: descriptive data and crystal structure
Authors: Raade G. , Grice J. D. , Erambert M. , Kristiansson P. , Witzke T. 
Published: March 2009

AbstractA REE-bearing fluorosilicate from the Tommot REE-Nb deposit in Yakutia, Russia, described without a name in 1966, is characterized here as a new species, proshchenkoite-(Y), of the vicanite group of borosilicates. Wavelength-dispersive electron probe analyses gave the following empirical formula: Y3.70REE7.54Ca1.55Na1.16Mn0.77Th0.10Pb0.01)Σ14.83(Fe2+0.83Mn0.15Ti0.02)Σ1.00Ca1.00(P0.70Si0.26As0.04)Σ1.00Si0.26B3.20(O34.55F13.45)Σ48. Boron was analysed with a nuclear microprobe method based on the nuclear reaction 11B(p,α)2α. The simplified formula is (Y,REE,Ca,Mn)15(Fe2+,Mn)Ca(P,Si)Si6B3O34F14. The mineral is trigonal, R3m, with a = 10.7527(7) Å, c = 27.4002(18) Å, V = 2743.6(6) Å 3, Z = 3. The crystal structure was refined to Rl = 0.042 for 1819 observed reflections. Proshchenkoite-(Y) is isostructural with okanoganite-(Y), vicanite-(Ce) and hundholmenite-(Y), and the differences in site occupancies are discussed. The strongest six reflections of the X-ray powder-diffraction pattern [dobs in Å, (I), (hkl)] are: 4.441, (36), (202); 3.144, (77), (214); 3.028, (45). (009); 2.968, (100), (027); 1.782, (32), (330); and 1.713, (32), (1.2.14). The mineral is optically uniaxial (—) with ω 1.734(2) and 8 1.728(2). The Mohs hardness is about 5; density measured on material subject to incipient metamictization is 4.72 g/cm3, as compared to Dcalc = 4.955 g/cm3.The result of electron microprobe analyses of alleged okanoganite-(Y) from the type locality in Okanogan County, Washington, USA, is also presented. We find here also that P > Si at one of the sites, whereas the analytical data of Boiocchi et al. (2004) indicate Si > P. Consequently, the mineral we have analysed is the P analogue of okanoganite-(Y), another new species.
The Fe-Mn phosphate aplite ‘Silbergrube’ near Waidhaus, Germany: epithermal phosphate mineralization in the Hagendorf-Pleystein pegmatite province
Authors: Dill H. G. , Weber B. , Gerdes A. , Melcher F. 
Published: March 2009

AbstractThe Silbergrube Aplite (SA) in the Hagendorf-Pleystein Pegmatite District, near Waidhaus, Germany, is a mildly peraluminous NW-SE directed leucogranite dyke. It occurs in association with quartz dykes and aplitic metamorphic mobilizates in the NE Bavarian crystalline basement. The SA differs from other aplitic mobilizates in the region in having a less well developed strain-related mineral orientation and in containing only minor amounts of garnet and tourmaline. The aplitic metamorphic mobilizates and the SA are chemically and mmeralogically almost identical and yield the same age of formation of ∼302 Ma (stage I). The age of formation of the Hagendorf pegmatites seemingly post-dates the emplacement of the SA. The SA was emplaced at the boundary between fine-grained biotite granites and metamorphic country rocks within a zone of structural weakness, favouring the formation of disseminated late magmatic to hydrothermal mineralization of Li-bearing Fe-Mn phosphates (stages II and III). Brittle deformation along this zone was conducive to the faultbound Fe-Mn-Ca phosphates. Mineral telescoping is evident from the presence of Fe2+, Fe3+ and Mn2+ phosphates in fissures and vugs in a texturally highly variable host-rock environment (stage IV). This intimate intergrowth of phosphate minerals reflects contrasting physical and chemical conditions prevailing in a near-surface/ shallow epithermal S-deficient phosphate system (stage IV), similar to what is known from Cu-Au epithermal systems. The most recent mineral assemblages that formed under predominantly oxidizing conditions are correlated with the subtropical weathering during the Neogene which resulted in the formation of a peneplain truncating the SA and its country rocks (stage V). The SA is the root zone of the felsic aplitic-pegmatitic mobilizates in this region and is overprinted by an epithermal phosphate system.
Induction of type I IFN is required for overcoming tumor-specific T-cell tolerance after stem cell transplantation
Authors: Horkheimer Ian , Quigley Michael , Zhu Jiangao , Huang Xiaopei , Chao Nelson J. , Yang Yiping 
Published: March 2009

AbstractTumor-specific T-cell tolerance represents one major mechanism of tumor-induced immune evasion. Myeloablative chemotherapy with stem cell transplantation may offer the best chance of achieving a state of minimal residual disease and, thus, minimize tumor-induced immune evasion. However, studies have shown that tumor-specific T-cell tolerance persists after transplantation. Here, we showed that CD4+CD25+ regulatory T (TReg) cells play a critical role in tumor-specific CD8+ T-cell tolerance after transplantation. Removal of TReg cells from the donor lymphocyte graft did not overcome this tolerance because of rapid conversion of donor CD4+CD25− T cells into CD4+CD25+Foxp3+ TReg cells in recipients after transplantation, and depletion of TReg cells in recipients was necessary for the reversal of tumor-specific tolerance. These results suggest that strategies capable of overcoming T-cell tolerance in recipients are required to promote antitumor immunity after transplantation. Toward this goal, we showed that dendritic cell (DC) vaccines coadministered with the TLR9 ligand, CpG could effectively overcome tumor-specific tolerance, leading to significant prolongation of tumor-free survival after transplantation. We further showed that CpG-induced type I interferon was critical for the reversal of tumor-specific tolerance in vivo. Collectively, these results may suggest effective immunotherapeutic strategies for treating cancer after stem cell transplantation.
HIV-1 transactivator protein induction of suppressor of cytokine signaling-2 contributes to dysregulation of IFNγ signaling
Authors: Cheng Sherman M. , Li James C. B. , Lin San San , Lee Davy C. W. , Liu Li , Chen Zhiwei , Lau Allan S. Y. 
Published: March 2009

AbstractHIV infection remains a worldwide threat. HIV-1 transactivator protein Tat is one of the retroviral proteins identified as a key immunomodulator in AIDS pathogenesis. Although the primary function of Tat is to regulate HIV-1 replication in the infected cell, it also dysregulates cytokine production resulting in perturbation of the host immune response and enhancement of the retrovirus survival. Because interferon-γ (IFNγ) is a pleiotropic cytokine with potent antiviral and immunoregulatory effects, we investigated whether Tat interferes with the IFNγ signal transduction in primary monocytes. We demonstrated that Tat impaired the IFNγ-receptor signaling pathway at the level of STAT1 activation, possibly via Tat-dependent induction of suppressor of cytokine signaling-2 (SOCS-2) activity. We delineated the inhibitory role of SOCS-2 in IFNγ signaling pathway by overexpression of exogenous SOCS-2 in HEK293 cell. The results showed that SOCS-2 suppressed the IFNγ-activated STAT1 phosphorylation and consequent IFNγ-regulated transcription of specific genes. To confirm the role of SOCS2 in the Tat-induced process, we demonstrated that SOCS-2 siRNA in human blood monocytes abrogated the Tat-dependent inhibition of IFNγ signaling. Our data suggested a possible mechanism implicating the role of SOCS-2 in mediating HIV-1–induced immune evasion and dysregulation of IFNγ signaling in primary human monocytes.
Novel autoantigens immunogenic in COPD patients
Authors: Leidinger Petra , Keller Andreas , Heisel Sabrina , Ludwig Nicole , Rheinheimer Stefanie , Klein Veronika , Andres Claudia , Hamacher Jürg , Huwer Hanno , Stephan Bernhard , Stehle Ingo , Lenhof Hans-Peter , Meese Eckart 
Published: March 2009

Abstract

Background
Chronic obstructive pulmonary disease (COPD) is a respiratory inflammatory condition with autoimmune features including IgG autoantibodies. In this study we analyze the complexity of the autoantibody response and reveal the nature of the antigens that are recognized by autoantibodies in COPD patients.

Methods
An array of 1827 gridded immunogenic peptide clones was established and screened with 17 sera of COPD patients and 60 healthy controls. Protein arrays were evaluated both by visual inspection and a recently developed computer aided image analysis technique. By this computer aided image analysis technique we computed the intensity values for each peptide clone and each serum and calculated the area under the receiver operator characteristics curve (AUC) for each clone and the separation COPD sera versus control sera.

Results
By visual evaluation we detected 381 peptide clones that reacted with autoantibodies of COPD patients including 17 clones that reacted with more than 60% of the COPD sera and seven clones that reacted with more than 90% of the COPD sera. The comparison of COPD sera and controls by the automated image analysis system identified 212 peptide clones with informative AUC values. By in silico sequence analysis we found an enrichment of sequence motives previously associated with immunogenicity.

Conclusion
The identification of a rather complex humoral immune response in COPD patients supports the idea of COPD as a disease with strong autoimmune features. The identification of novel immunogenic antigens is a first step towards a better understanding of the autoimmune component of COPD.
Dissecting the bacterial type VI secretion system by a genome wide in silico analysis: what can be learned from available microbial genomic resources?
Authors: Boyer Frédéric , Fichant Gwennaële , Berthod Jérémie , Vandenbrouck Yves , Attree Ina 
Published: March 2009

Abstract

Background
The availability of hundreds of bacterial genomes allowed a comparative genomic study of the Type VI Secretion System (T6SS), recently discovered as being involved in pathogenesis. By combining comparative and phylogenetic approaches using more than 500 prokaryotic genomes, we characterized the global T6SS genetic structure in terms of conservation, evolution and genomic organization.

Results
This genome wide analysis allowed the identification of a set of 13 proteins constituting the T6SS protein core and a set of conserved accessory proteins. 176 T6SS loci (encompassing 92 different bacteria) were identified and their comparison revealed that T6SS-encoded genes have a specific conserved genetic organization. Phylogenetic reconstruction based on the core genes showed that lateral transfer of the T6SS is probably its major way of dissemination among pathogenic and non-pathogenic bacteria. Furthermore, the sequence analysis of the VgrG proteins, proposed to be exported in a T6SS-dependent way, confirmed that some C-terminal regions possess domains showing similarities with adhesins or proteins with enzymatic functions.

Conclusion
The core of T6SS is composed of 13 proteins, conserved in both pathogenic and non-pathogenic bacteria. Subclasses of T6SS differ in regulatory and accessory protein content suggesting that T6SS has evolved to adapt to various microenvironments and specialized functions. Based on these results, new functional hypotheses concerning the assembly and function of T6SS proteins are proposed.