bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analysis of the Differential Host Cell Nuclear Proteome Induced by Attenuated and Virulent Hemorrhagic Arenavirus Infection
Authors: Bowick Gavin C. , Spratt Heidi M. , Hogg Alison E. , Endsley Janice J. , Wiktorowicz John E. , Kurosky Alexander , Luxon Bruce A. , Gorenstein David G. , Herzog Norbert K. 
Published: November 2008

ABSTRACTArenaviruses are important emerging pathogens and include a number of hemorrhagic fever viruses classified as NIAID category A priority pathogens and CDC potential biothreat agents. Infection of guinea pigs with the New World arenavirusPichindé virus(PICV) has been used as a biosafety level 2 model for theLassa virus. Despite continuing research, little is known about the molecular basis of pathogenesis, and this has hindered the design of novel antiviral therapeutics. Modulation of the host response is a potential strategy for the treatment of infectious diseases. We have previously investigated the global host response to attenuated and lethal arenavirus infections by using high-throughput immunoblotting and kinomics approaches. In this report, we describe the differential nuclear proteomes of a murine cell line induced by mock infection and infection with attenuated and lethal variants of PICV, investigated by using two-dimensional gel electrophoresis. Spot identification using tandem mass spectrometry revealed the involvement of a number of proteins that regulate inflammation via potential modulation of NF-κB activity and of several heterogeneous nuclear ribonuclear proteins. Pathway analysis revealed a potential role for transcription factor XBP-1, a transcription factor involved in major histocompatibility complex II (MHC-II) expression; differential DNA-binding activity was revealed by electrophoretic mobility shift assay, and differences in surface MHC-II expression were seen following PICV infection. These data are consistent with the results of several previous studies and highlight potential differences between transcriptional and translational regulation. This study provides a number of differentially expressed targets for further research and suggests that key events in pathogenesis may be established early in infection.
Overexpression of Interleukin-15 Compromises CD4-Dependent Adaptive Immune Responses against Herpes Simplex Virus 2
Authors: Gill Navkiran , Ashkar Ali A. 
Published: November 2008

ABSTRACT

Interleukin-15 (IL-15) is necessary for the development and function of NK/NKT cells and the maintenance of naive and memory CD8
+
T cells. In the absence of IL-15, protective innate immunity is not available; however, a functional adaptive immune response against vaginal herpes simplex virus 2 (HSV-2) is generated. Mice overexpressing IL-15 (IL-15tg mice) have higher numbers of NK cells, greater NK-derived gamma interferon, and more CD8
+
T cells. Here we examined the consequences of IL-15 overexpression for innate and adaptive immunity against genital HSV-2. Surprisingly, IL-15tg mice immunized against HSV-2 were not protected against genital HSV-2 challenge compared to control immunized mice. IL-15tg mice had a higher frequency of NK cells in the genital mucosa than control mice. However, immunized IL-15tg mice had significantly lower numbers of HSV-2-specific CD4
+
T cells than B6 mice. We then confirmed that CD4
+
T cells, but not CD8
+
T cells, are essential for protection against intravaginal HSV-2 challenge. Since we observed less protection in immunized IL-15tg mice, we then examined if the adaptive immune responses generated in an environment with overexpression of IL-15 could provide protection against HSV-2 in an environment with normal levels of IL-15 expression. We adoptively transferred immunized cells from IL-15tg and B6 mice into naive RAG-1
−/−
mice and found that the cells from immunized IL-15tg mice were able to provide protection in this IL-15-normal environment. Our data suggest that overexpression of IL-15 results in a reduced CD4
+
T cell-mediated adaptive immune response against genital HSV-2.
Differential Sensitivity of “Old” versus “New” APOBEC3G to Human Immunodeficiency Virus Type 1 Vif
Authors: Goila-Gaur Ritu , Khan Mohammad A. , Miyagi Eri , Strebel Klaus 
Published: November 2008

ABSTRACT

HIV-1 Vif counteracts the antiviral activity of APOBEC3G by inhibiting its encapsidation into virions. Here, we compared the relative sensitivity to Vif of APOBEC3G in stable HeLa cells containing APOBEC3G (HeLa-A3G cells) versus that of newly synthesized APOBEC3G. We observed that newly synthesized APOBEC3G was more sensitive to degradation than preexisting APOBEC3G. Nevertheless, preexisting and transiently expressed APOBEC3G were packaged with similar efficiencies into
vif
-deficient human immunodeficiency virus type 1 (HIV-1) virions, and Vif inhibited the encapsidation of both forms of APOBEC3G into HIV particles equally well. Our results suggest that HIV-1 Vif preferentially induces degradation of newly synthesized APOBEC3G but indiscriminately inhibits encapsidation of “old” and “new” APOBEC3G.
The Dynamics of the ENSO–Atlantic Hurricane Teleconnection: ENSO-Related Changes to the North African–Asian Jet Affect Atlantic Basin Tropical Cyclogenesis
Authors: Shaman Jeffrey , Esbensen Steven K. , Maloney Eric D. 
Published: November 2008

Abstract
The nature of the teleconnection linking ENSO variability with Atlantic basin tropical storm formation is investigated. Solutions of the linearized barotropic vorticity equation forced with August–October El Niño event divergence produce upper-tropospheric vorticity anomalies over the Sahel and at the mouth of the North African–Asian (NAA) jet over the tropical Atlantic. These responses are similar in magnitude and orientation to observed ENSO vorticity variability for this region.
Further investigation reveals that the vorticity anomalies over the subtropical Atlantic develop primarily in response to very low wavenumber, westward-propagating stationary Rossby waves excited by El Niño–related convective activity over the equatorial Pacific Ocean. However, the dynamics of this teleconnection change as the Atlantic basin hurricane season progresses. In August and September the response is dominated by the westward-propagating stationary Rossby waves that alter vorticity within the NAA jet and to its south. The upper-tropospheric nondivergent zonal wind anomalies produced by these vorticity anomalies are similar in pattern to observed zonal wind and vertical zonal wind shear anomalies, which suppress Atlantic basin tropical cyclogenesis.
By October, eastward-propagating signals also develop over the tropical Atlantic Ocean in response to El Niño conditions. Over the main development region of Atlantic basin tropical cyclogenesis, these eastward-propagating Rossby waves appear to destructively interfere with the vorticity changes produced by the westward-propagating Rossby waves within the NAA jet. In addition, the NAA jet has shifted south by October. Consequently, the resultant upper-tropospheric nondivergent zonal wind perturbations for October are weak and suggest that ENSO should have little effect on rates of Atlantic basin tropical cyclogenesis during October. Statistical analyses of monthly ENSO-related changes in Atlantic basin tropical storm formation support this hypothesis.
Relationship between the Tibetan Snow in Spring and the East Asian Summer Monsoon in 2003: A Global and Regional Modeling Study
Authors: Seol Kyung-Hee , Hong Song-You 
Published: November 2008

AbstractIn 2003, a climate extreme accompanying a wet and cool summer over East Asia was recorded over the East Asian countries including central China, Korea, and Japan. A possible relation of this record-breaking summer in East Asia to above-normal snowfall over the Tibetan Plateau in spring has been investigated using the National Centers for Environmental Prediction (NCEP) global and regional models. The changes in the simulated East Asian summer monsoon circulations in response to snow anomalies over Tibet are highlighted.The results from both global and regional model experiments suggest that above-normal snowfall over the Tibetan Plateau in May induces a weakening of the Tibetan high, which leads to the formation of favorable upper-level circulations accompanying cyclonic circulation anomalies covering the East Asian region in summer. These circulation anomalies in response to the snow anomalies over the plateau are more robust and closer to what was observed in the regional than in the global model results. The sensitivity experiments also show that the precipitation and lower-level circulation anomalies in summer, caused by the snow anomalies in spring, influence the above-normal precipitation in the lower reaches of the Yangtze River basin, as revealed in previous observational studies. However, the experiments do not fully explain the observed signals in Korea and Japan since the spring snow anomaly over Tibet plays a role in weakening the western Pacific subtropical high in the simulated summer, whereas in reality the intensity of the high was stronger than normal in 2003.
Mcl-1 expression predicts progression-free survival in chronic lymphocytic leukemia patients treated with pentostatin, cyclophosphamide, and rituximab
Authors: Awan Farrukh T. , Kay Neil E. , Davis Melanie E. , Wu Wenting , Geyer Susan M. , Leung Nelson , Jelinek Diane F. , Tschumper Renee C. , Secreto Charla R. , Lin Thomas S. , Grever Michael R. , Shanafelt Tait D. , Zent Clive S. , Call Timothy G. , Heerema Nyla A. , Lozanski Gerard , Byrd John C. , Lucas David M. 
Published: November 2008

Abstract
Myeloid cell leukemia-1 (Mcl-1) is an antiapoptotic member of the Bcl-2 protein family. Increased Mcl-1 expression is associated with failure to achieve remission after treatment with fludarabine and chlorambucil in patients with chronic lymphocytic leukemia (CLL). However, the influence of Mcl-1 expression has not been examined in CLL trials using chemoimmunotherapy. We investigated Mcl-1 protein expression prospectively as part of a phase 2 study evaluating the efficacy of pentostatin, cyclophosphamide, and rituximab in patients with untreated CLL. No significant difference by Mcl-1 expression was noted in pretreatment or response parameters. However, in patients with higher Mcl-1 expression, both minimal residual disease-negative status and progression-free survival was found to be significantly reduced (57% vs 19%, P = .01; 50.8 vs 18.7 months; P = .02; respectively). Mcl-1 expression may therefore be useful in predicting poor response to chemoimmunotherapy. These findings further support pursuing treatment strategies targeting this important antiapoptotic protein. (Because the trials described were conducted before the requirement to register them was implemented, they are not registered in a clinical trial database.)
Salmonellainduces death of CD8α+ dendritic cells but not CD11cintCD11b+ inflammatory cells in vivo via MyD88 and TNFR1
Authors: Sundquist Malin , Wick Mary Jo 
Published: November 2008

AbstractDendritic cells (DCs), whose lifespan influences their ability to stimulate the immune system, are potent APCs that are critical for initiating immunity. Here, we show that oral infection with Salmonella enterica serovar Typhimurium induces death of DCs in the gut-draining lymph nodes. Although CD8α+ DCs were sensitive to Salmonella-induced death, CD8α– DCs and in particular recruited CD11cintCD11b+ inflammatory cells, were resistant. Infecting mice deficient for MyD88 revealed that Salmonella-induced death of CD8α+ DCs was dependent on this adaptor for TLR signaling. In addition, CD8α+ DCs in infected, TNFR1-deficient mice were resistant to Salmonella-induced death. These data, combined with the strict MyD88-dependent production of TNF in Salmonella-infected mice, suggest that MyD88-dependent TNF mediates DC death. As recruited CD11cintCD11b+ cells were resistant to Salmonella-induced death, they could compensate for the infection-induced loss of DCs if they function as APCs. However, in contrast to DCs, CD11cintCD11b+ cells could not present the model antigen OVA expressed in Salmonella to OVA-specific CD4 T cells. These results show that Salmonella induces DC death after oral infection via MyD88 and TNFR1, which could have a negative impact on the initiation of antibacterial immunity.
Quantification and characterization of cricket bowling technique for the development of the parameters required for a novel training system for cricket
Authors: Justham L , West A , Cork A 
Published: November 2008

Cricket bowling has traditionally been referenced using ball release speed, and existing classifications consider the four major bowling types as fast, fast—medium, medium, and spin. A research project based at Loughborough University has recognized the need for an extended bowling classification that not only considers the ball speed, but also its initial flight characteristics, including any spin imparted at release. The purpose of this paper has been the development of an extended bowling classification, which has been used in the development of a requirements specification for an advanced ball delivery system for cricket, to ensure the accurate recreation of technically correct bowling deliveries. Data collected during training and match play have been used to define bowling quantitatively. The initial ball flight characteristics of 30 elite-level bowlers have been filmed in training using a Photron FASTCAM ultima APX high-speed video camera. These videos have been used to determine the speed, the rate of spin, and the initial flight trajectory of the ball at release. Additionally, Hawk-Eye ball-tracking software has been used to investigate the full flight characteristics of seven elite bowlers during a five Test match series.
The Origin of Cis Effect in 1,2-Dihaloethenes: The Quantitative Comparison of Electron Delocalizations and Steric Exchange Repulsions
Authors: Yamamoto Takashi , Kaneno Daisuke , Tomoda Shuji 
Published: November 2008

Abstract
The “cis effect” is a phenomenon in which the cis isomer is more stable than the corresponding trans isomer or almost the same stability in some molecules with double bonds. In order to clarify the predominant factor of this cis effect in the 1,2-dihaloethenes (XHC=CHX; 1: X=F, 2: Cl, and 3: Br), the energetic amount of electron delocalizations and steric exchange repulsions were theoretically estimated using the natural bond orbital (NBO) theory at MP2/6-311++G(3df,3pd) level. Two delocalization mechanisms, periplanar hyperconjugations (synperiplanar and antiperiplanar effects) and halogen lone pair delocalizations into the C=C bond antibonding orbitals (LP effect), were found as the cis stabilizing forces, in which the total amount of LP effect was greater than those of periplanar effects, the dominant factor of the cis effect. Moreover, the origin of the cis preference of the LP effect was clearly elucidated with the application of orbital phase theory, i.e., the cyclic orbital interaction was continuous only in the cis isomers of 1–3. The total steric exchange repulsion between two isomers were all trans stabilizing and their energetic gains were 1.26, 16.48, and 23.22 kJ mol−1 for 1, 2, and 3, respectively. These steric forces obviously counteract against cis preferable delocalization mechanisms, especially in compounds with larger halogen atoms, but their amounts are apparently less than those of electron delocalizations (29.82, 40.00, and 34.46 kJ mol−1 for 1, 2, and 3, respectively). Therefore, electron delocalization, not exchange repulsion, has the largest responsibility for the relative energies of 1,2-dihaloethene systems. The importance of this work is the quantitative elucidation of the dominance of delocalization mechanisms over steric effects on the electronic and energetic view of a simple molecular structure.
Preparation and Characterization of an α-Wells–Dawson-Type [V2Mo18O62]6− Complex
Authors: Himeno Sadayuki , Kawasaki Keishi , Hashimoto Masato 
Published: November 2008

Abstract
An orange-yellow vanadomolybdate complex was prepared by heating a 100 mM MoVI–20 mM VV–0.45 M HCl–20% (v/v) CH3CN system at 70 °C for 24 h, being isolated as the tetrapropylammonium (Pr4N+) salt. The Pr4N+ salt crystallized in the orthorhombic space group P21212; the lattice constants were a=18.417(4), b=20.869(5), c=15.280(3) Å, V=5873(2) Å3, and Z=2. The crystallographic study revealed that the structure consists of an α-Wells–Dawson-type [V2Mo18O62]6− anion, in which vanadates serve as the central tetrahedra. The α-[V2Mo18O62]6− complex underwent a two-step one-electron reduction in CH3CN, and the presence of acid caused the one-electron waves to be converted into three two-electron waves. The formation conditions were elucidated by 51V NMR measurements.
3′ Poly(dA)-Tailed Thrombin DNA Aptamer to Increase DNase-Resistance and Clotting Inhibitory Activity
Authors: Uehara Shuichiro , Shimada Naohiko , Takeda Yoichi , Koyama Yoshikazu , Takei Yoshifumi , Ando Hironori , Satoh Susumu , Uno Atsushi , Sakurai Kazuo 
Published: November 2008

Abstract
Aptamers are an attractive candidate for a molecular-targeted drug since they can show ability to precisely recognize proteins with a large affinity similar to antibodies. A drawback of aptamers is that they can be easily degraded under biological conditions by DNase (or RNase). In this study, we attached poly(dA) tail to the 3′ end of thrombin DNA aptamer and found that its survival time in human plasma was prolonged by about threefold compared to the original aptamers (i.e., without the tail). We found that the attachment of a poly(dA) tail at the 3′ end caused an increase of the clotting inhibitory activity. A preliminary in vivo assay using BALB/c mice confirmed a considerably elongated clotting time for the tailed aptamer. When the poly(dA) tail was attached to three other DNA aptamers, DNase resistance was increased, indicating that the present finding can be universally applied to increase stability of DNA aptamers.
Impact of detergents on the activity of acetylcholinesterase and on the effectiveness of its inhibitors
Authors: Zimmermann Martina , Westwell Martin S. , Greenfield Susan A. 
Published: November 2008

Abstract
Acetylcholinesterase (AChE) plays a central role in the development of Alzheimer's disease: AChE inhibition for preventing the characteristic dwindling of acetylcholine levels constitutes the current standard treatment for the disorder. Amongst the diverse risk factors contributing to the degenerative process, high cholesterol causes a reduction in the effectiveness of the otherwise therapeutic inhibitors of AChE. Our biochemical study on the activity of AChE elucidates the effect of amphiphilic molecules on the activity and kinetics of AChE, and sheds light onto the nature of the impact of these amphiphilic molecules on enzyme-inhibitor interactions. Using kinetic studies we discovered that detergents alter the enzymatic activity of AChE through an uncompetitive mechanism. Additional experiments using AChE inhibitors (amphiphilic procaine hydrochloride, hydrophobic tetrabutylammonium bromide) in the absence or presence of detergent further illustrate the detergent-enzyme-solvent interactions. The results contribute to the understanding of the importance of hydrophobic-lipophilic interactions for the correct function of AChE and its inhibitors. We present a model system for the study of lipid-related alterations in the activity of isolated AChE in the central nervous system. This model may also be used to assess and predict the effectiveness of AChE inhibitors, which are traditionally used for the treatment of cognitive impairment, under pathological (high-cholesterol) conditions.
The ADP-ribosylating thermozyme from Sulfolobus solfataricus is a DING protein
Authors: Di Maro Antimo , De Maio Anna , Castellano Sabrina , Parente Augusto , Farina Benedetta , Faraone-Mennella Maria Rosaria 
Published: November 2008

Abstract
The partial amino acid sequence of the sulfolobal thermoprotein biochemically characterized as poly(ADP-ribose)polymerase-like enzyme overlaps those of DING proteins. This group of proteins, widely occurring in animals, plants and eubacteria, shows a characteristic and highly conserved N-terminus, DINGGGATL. The sequence of the N-terminal region and of the analyzed tryptic peptides of the sulfolobal thermozyme shows a high similarity with most of the DING proteins from databases. This is the first example of a DING protein from a sulfolobal source.
Heavy metals induce phosphorylation of the Bcl-2 protein by Jun N-terminal kinase
Authors: Ondroušková Eva , Slováčková Jana , Pelková Vendula , Procházková Jiřina , Souček Karel , Beneš Petr , Šmarda Jan 
Published: November 2008

Abstract
The Bcl-2 protein is one of the key components of biochemical pathways controlling programmed cell death. The function of this protein can be regulated by posttranslational modifications. Phosphorylation of Bcl-2 has been considered to be significantly associated with cell cycle arrest in the G2/M phase of the cell cycle, and with cell death caused by defects of microtubule dynamics. This study shows that phosphorylation of Bcl-2 can be induced by heavy metals due to activation of the Jun N-terminal kinase pathway that is not linked to the G2/M cell cycle arrest. Furthermore, we demonstrate that hyperphosphorylated Bcl-2 protein is a more potent inhibitor of zinc-induced cell death than its hypophosphorylated mutant form. These data suggest that regulation of Bcl-2 protein function by phosphorylation is an important part of cell responses to stress.
Applicability of superfolder YFP bimolecular fluorescence complementation in vitro
Authors: Ottmann Corinna , Weyand Michael , Wolf Alexander , Kuhlmann Jürgen , Ottmann Christian 
Published: November 2008

Abstract
Bimolecular fluorescence complementation (BiFC) using yellow fluorescent protein (YFP) is a widely employed method to study protein-protein interactions in cells. As yet, this technique has not been used in vitro. To evaluate a possible application of BiFC in vitro, we constructed a ‘superfolder split YFP’ system where 15 mutations enhance expression of the fusion proteins in Escherichia coli and enable a native purification due to improved solubility. Here, we present the crystal structure of ‘superfolder YFP’, providing the structural basis for the enhanced folding and stability characteristics. Complementation between the two non-fluorescent YFP fragments fused to HRas and Raf1RBD or to 14-3-3 and PMA2-CT52 resulted in the constitution of the functional fluorophore. The in vivo BiFC with these protein interaction pairs was demonstrated in eukaryotic cell lines as well. Here, we present for the first time BiFC in vitro studies with natively purified superfolder YFP fusion proteins and show the potential and drawbacks of this method for analyzing protein-protein interactions.
Mannose 6-phosphate receptor-dependent endocytosis of lysosomal enzymes is increased in sulfatide-storing kidney cells
Authors: Klein Diana , Yaghootfam Afshin , Matzner Ullrich , Koch Bettina , Braulke Thomas , Gieselmann Volkmar 
Published: November 2008

Abstract
Metachromatic leukodystrophy is a lysosomal disorder caused by the deficiency of arylsulfatase A (ASA). This leads to the storage of the sphingolipid 3-O-sulfogalactosylceramide (sulfatide) in various cell types, such as renal tubular cells. Examination of mannose 6-phosphate receptor (MPR300)-dependent endocytosis revealed that uptake of lysosomal enzymes is more than two-fold increased in sulfatide-storing kidney cells. Expression of MPR300 and its internalization rate is increased in these cells, whereas the recycling rate is decreased. Similar alterations can be found for the transferrin receptor, indicating that sulfatide storage leads to a general alteration of the endocytotic pathway. These data allow calculating that the endosomal pool from which receptors can recycle is 1.4- to 2-fold increased in lipid-storing cells. Immunocytochemistry demonstrates that the MPR300 in lipid-storing cells does not co-localize with accumulated sulfatide, suggesting that the kinetics of internalization and recycling appear to be altered indirectly.