bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gentrification: What It Is, Why It Is, and What Can Be Done about It
Authors: Shaw Kate 
Published: September 2008

AbstractThis article outlines the key contemporary debates on gentrification, most of which arise from variations in the process: in interpretations, assessments of displacement, the agents involved and the forms that gentrified cities take. The variations are so extensive that some scholars argue that gentrification has become too broad a concept to retain analytical coherency. Others counter that the logic of gentrification is now so generalised that the concept captures no less than the fundamental state and market‐driven ‘class remake’ of cities throughout the world. The article agrees with the latter position and proposes that gentrification should be considered part of a broader continuum of social and economic geographic change, replacing the useful but out‐dated stage model but still accommodating the myriad of variations within its underlying logics. Understanding gentrification as a complex but coherent concept highlights the importance of time and place in the viability of progressive policy responses to gentrification's inequitable effects.
Estimation of Cavitation Limits From Local Head Loss Coefficient
Authors: Sánchez Raúl , Juana Luis , Laguna Francisco V. , Rodríguez-Sinobas Leonor 
Published: September 2008

Abstract
Cavitation effects in valves and other sudden transitions in water distribution systems are studied as their better understanding and quantification is needed for design and analysis purposes and for predicting and controlling their operation. Two dimensionless coefficients are used to characterize and verify local effects under cavitating flow conditions: the coefficient of local head losses and the minimum value of the cavitation number. In principle, both coefficients must be determined experimentally, but a semianalytical relationship between them is here proposed so that if one of them is known, its value can be used to estimate the corresponding value of the other one. This relationship is experimentally contrasted by measuring head losses and flow rates. It is also shown that cavitation number values, called cavitation limits, such as the critical cavitation limit, can be related in a simple but practical way with the mentioned minimum cavitation number and with a given pressure fluctuation level. Head losses under conditions of cavitation in sharp-edged orifices and valves are predicted for changes in upstream and downstream boundary conditions. An experimental determination of the coefficient of local head losses and the minimum value of the cavitation number is not dependent on the boundary conditions even if vapor cavity extends far enough to reach a downstream pressure tap. Also, the effects of cavitation and displacement of moving parts of valves on head losses can be split. A relatively simple formulation for local head losses including cavitation influence is presented. It can be incorporated to water distribution analysis models to improve their results when cavitation occurs. Likewise, it can also be used to elaborate information about validity limits of head losses in valves and other sudden transitions and to interpret the results of head loss tests.
The Measles Virus Fusion Protein Transmembrane Region Modulates Availability of an Active Glycoprotein Complex and Fusion Efficiency
Authors: Mühlebach Michael D. , Leonard Vincent H. J. , Cattaneo Roberto 
Published: September 2008

ABSTRACT

The glycoprotein complex of paramyxoviruses mediates receptor binding and membrane fusion. In particular, the measles virus (MV) fusion (F) protein executes membrane fusion, after receptor binding by the hemagglutinin (H) protein. Structures and single amino acids influencing fusion function have been identified in the F-protein ectodomain and cytoplasmic tail, but not in its transmembrane (TM) region. Since this region influences function of the envelope proteins of other viruses, we examined its role in the MV F protein. Alanine-scanning mutagenesis revealed that an F protein with a single mutation of a central TM region leucine (L507A) was more fusogenic than the unmodified F protein while retaining similar kinetics of proteolytic processing. In contrast, substitution of residues located near the edges of the lipid bilayer reduced fusion activity. This was true not only when the mutated F proteins were coexpressed with H but also in the context of infections with recombinant viruses. Analysis of the H-F complexes with reduced fusion activities revealed that more precursor (F
0
) than activated (F
1+2
) protein coprecipitated with H. In contrast, in complexes with enhanced fusion activity, including H-F
L507A
, the F
0
/F
1+2
ratio shifted toward F
1+2
. Thus, fusion activity correlated with an active F-H protein complex, and the MV F protein TM region modulated availability of this complex.
Localization of Herpes Simplex Virus Type 1 UL37 in the Golgi Complex Requires UL36 but Not Capsid Structures
Authors: Desai Prashant , Sexton Gerry L. , Huang Eugene , Person Stanley 
Published: September 2008

ABSTRACT
The herpes simplex virus type 1 (HSV-1) UL37 gene encodes a 120-kDa polypeptide which resides in the tegument structure of the virion and is important for morphogenesis. The goal of this study was to use green fluorescent protein (GFP) to follow the fate of UL37 within cells during the normal course of virus replication. GFP was inserted in frame at the C terminus of UL37 to generate a fluorescent-protein-tagged UL37 polypeptide. A virus designated K37eGFP, which replicated normally on Vero cells, was isolated and was shown to express the fusion polypeptide. When cells infected with this virus were examined by confocal microscopy, the fluorescence was observed to be predominantly cytoplasmic. As the infection progressed, fluorescence began to accumulate in a juxtanuclear structure. Mannosidase II and giantin were observed to colocalize with UL37eGFP at these structures, as judged by immunofluorescence assays. Therefore, UL37 traffics to the Golgi complex during infection. A VP26mRFP marker (red fluorescent protein fused to VP26) was recombined into K37eGFP, and when cells infected with this “dual-color” virus were examined, colocalization of the red (capsid) and green (UL37) fluorescence in the Golgi structure was observed. Null mutations in VP5 (ΔVP5), which abolished capsid assembly, and in UL36 (Δ36) were recombined into the K37eGFP virus genome. In cells infected with K37eGFP/ΔVP5, localization of UL37eGFP to the Golgi complex was similar to that for the parental virus (K37eGFP), indicating that trafficking of UL37eGFP to the Golgi complex did not require capsid structures. Confocal analysis of cells infected with K37eGFP/Δ36 showed that, in the absence of UL36, accumulation of UL37eGFP at the Golgi complex was not evident. This indicates an interaction between these two proteins that is important for localization of UL37 in the Golgi complex and thus possibly for cytoplasmic envelopment of the capsid. This is the first demonstration of a functional role for UL36:UL37 interaction in HSV-1-infected cells.
Role of Cellular Glycosaminoglycans and Charged Regions of Viral G Protein in Human Metapneumovirus Infection
Authors: Thammawat Sutthiwan , Sadlon Tania A. , Hallsworth Peter G. , Gordon David L. 
Published: September 2008

ABSTRACT

Human metapneumovirus (hMPV) is an important cause of lower respiratory tract disease, particularly in infants and young children. hMPV has two major glycoproteins, G and F, which are responsible for virus attachment and membrane fusion, respectively. We investigated the role of cellular glycosaminoglycans (GAGs) and G protein in hMPV infection. The pretreatment of hMPV with soluble heparin markedly inhibited the infection of HEp-2 cells. Recombinant G protein, comprising the extracellular domain of G, bound to heparin-agarose columns and also to HEp-2 cells. hMPV infection and G protein binding to HEp-2 cells was inhibited by other soluble GAGs, including chondroitin sulfates, by the enzymatic removal of cell surface GAGs with GAG lyases or by the pretreatment of cells with basic fibroblast growth factor. The role of cellular GAGs was confirmed by the binding of G protein to wild-type CHO cells but not to GAG-deficient CHO-pgsA745 cells. An analysis of the G protein sequence revealed two adjacent clusters of positively charged amino acids (
149
EKKKTRA
155
and
159
QRRGKGKE
166
). Truncated G fragments were expressed, and only the fragment containing these putative heparin binding domains retained heparin binding. The alanine mutagenesis of charged residues in either of these regions resulted in the loss of binding to heparin and to HEp-2 cells, suggesting that both sites are likely to be required for hMPV attachment. These results, taken together with the inhibition of hMPV infection by soluble G protein, indicate an important role for G protein and cellular GAGs in hMPV infection.
Engineered Expression of the TLR5 Ligand Flagellin Enhances Paramyxovirus Activation of Human Dendritic Cell Function
Authors: Arimilli Subhashini , Johnson John B. , Clark Kimberly M. , Graff Aaron H. , Alexander-Miller Martha A. , Mizel Steven B. , Parks Griffith D. 
Published: September 2008

ABSTRACTThe paramyxovirus simian virus 5 (SV5) is a poor activator of human dendritic cell (DC) maturation pathways in vitro, and infected DC do not upregulate cell surface costimulatory proteins or secretion of immunomodulatory cytokines. We evaluated the hypothesis that activation of SV5-infected DC would be enhanced by engineering SV5 to express a Toll-like-receptor (TLR) ligand. To test this hypothesis, a novel virus was engineered such that the gene encoding an intracellular form of the TLR5 ligand flagellin was expressed from the genome of wild-type (WT) SV5 (SV5-flagellin). Cells infected in vitro with the flagellin-expressing virus released low levels of biologically active flagellin, which was capable of stimulating TLR5 signaling. Infection of human peripheral blood mononuclear cell-derived immature DC with SV5-flagellin resulted in enhanced levels of interleukin-6 (IL-6) and IL-12 compared to infection with DC with the parental virus, WT SV5. In contrast to cytokine induction, the flagellin-expressing virus did not appreciably increase DC surface expression of the costimulatory molecule CD80 or CD86 above the level seen with WT SV5 alone. In mixed-culture assays, DC infected with the flagellin-expressing virus were more effective at activating gamma interferon secretion from both CD8+and CD4+allogeneic T cells than DC infected with WT SV5. Our results with SV5-directed intracellular expression of flagellin may be applicable to other vectors or pathogenic viruses where overcoming impairment of DC activation could contribute to the development of safer and more effective vaccines.
Molecular Basis of the Interaction between Complement Receptor Type 2 (CR2/CD21) and Epstein-Barr Virus Glycoprotein gp350
Authors: Young Kendra A. , Herbert Andrew P. , Barlow Paul N. , Holers V. Michael , Hannan Jonathan P. 
Published: September 2008

ABSTRACTThe binding of the Epstein-Barr virus glycoprotein gp350 by complement receptor type 2 (CR2) is critical for viral attachment to B lymphocytes. We set out to test hypotheses regarding the molecular nature of this interaction by developing an enzyme-linked immunosorbent assay (ELISA) for the efficient analysis of the gp350-CR2 interaction by utilizing wild-type and mutant forms of recombinant gp350 and also of the CR2 N-terminal domains SCR1 and SCR2 (designated CR2 SCR1-2). To delineate the CR2-binding site on gp350, we generated 17 gp350 single-site substitutions targeting an area of gp350 that has been broadly implicated in the binding of both CR2 and the major inhibitory anti-gp350 monoclonal antibody (MAb) 72A1. These site-directed mutations identified a novel negatively charged CR2-binding surface described by residues Glu-21, Asp-22, Glu-155, Asp-208, Glu-210, and Asp-296. We also identified gp350 amino acid residues involved in non-charge-dependent interactions with CR2, including Tyr-151, Ile-160, and Trp-162. These data were supported by experiments in which phycoerythrin-conjugated wild-type and mutant forms of gp350 were incubated with CR2-expressing K562 cells and binding was assessed by flow cytometry. The ELISA was further utilized to identify several positively charged residues (Arg-13, Arg-28, Arg-36, Lys-41, Lys-57, Lys-67, Arg-83, and Arg-89) within SCR1-2 of CR2 that are involved in the binding interaction with gp350. These experiments allowed a comparison of those CR2 residues that are important for binding gp350 to those that define the epitope for an effective inhibitory anti-CR2 MAb, 171 (Asn-11, Arg-13, Ser-32, Thr-34, Arg-36, and Tyr-64). The mutagenesis data were used to calculate a model of the CR2-gp350 complex using the soft-docking program HADDOCK.
Numerical simulation of the dynamics of fluid oscillations in a gravitationally unstable, compositionally stratified fissure
Authors: Longo Antonella , Barbato David , Papale Paolo , Saccorotti Gilberto , Barsanti Michele 
Published: September 2008

Abstract

We have simulated the dynamics of convection, mixing and ascent of two basaltic magmas differing in their volatile and crystal content, giving rise to a gravitationally unstable configuration along a dyke or fissure. Numerical simulations are performed by a recently developed code which describes the transient 2D dynamics of multicomponent fluids from the incompressible to the compressible regime, and the initial and boundary conditions are inspired to the paroxysmal eruption which occurred at Stromboli in 2003 (

D'Auria
et al.
2006

). Multicomponent (H
2
O+CO
2
) saturation is accounted for by modelling the non-ideal equilibrium between the gas phase and the melt. The numerical results show the formation of a rising bulge of light magma, and the sink of discrete batches of dense magma towards deep fissure regions. Such dynamics are associated with a complex evolution of the pressure field, which shows variations occurring over a wide spectrum of frequencies. A first order analysis of the propagation of such pressure disturbances through the country rocks shows that the pre-eruptive fissure dynamics are able to produce mm-size, mainly radial deformation of the volcano, and a detectable seismic signal with spectral peaks at periods of about 50 s.
Trends in activity at Pu'u 'O'o during 2001–2003: insights from the continuous thermal record
Authors: Marchetti Emanuele , Harris Andrew J. L. 
Published: September 2008

Abstract
A permanent thermal monitoring system deployed on the north rim of Pu'u 'O'o crater (Kilauea, Hawaii) provided an 811-day-long data-set spanning March 2001–December 2003. These data allowed us to characterize three emission styles from vents on the crater floor: lava flows, sustained degassing and gas-piston events. Lava flows were recorded as sudden increases in temperature followed by smooth and relatively long-lasting decreases as the lava cooled. Sustained degassing was associated with persistently high levels of thermal signal and was the most common signal type. Finally, gas-piston events were all preceded by marked reductions in temperature (due to diminished degassing) and were marked by abrupt increases (due to the arrival of a gas jet) followed by 50–300 second waning phases. Lava flow occurrence, maximum temperature recorded during degassing, gas-piston thermal amplitude, occurrence and waveform all showed coupled, systematic changes through time. This implies modification of a common source process, and may be a result of a slight change in the magma level beneath the crater so as to modify the conduit geometry/primary degassing pathways, and hence gas collection and release processes, as well as slug ascent dynamics.
From Strombolian explosions to fire fountains at Etna Volcano (Italy): what do we learn from acoustic measurements?
Authors: Vergniolle S. , Ripepe M. 
Published: September 2008

Abstract
The 2001 eruption of Etna volcano, prior to the flank eruption, was marked by 16 episodes separated from one another by few days of quiescence. Insights into fire fountain formation are provided by a close comparison of the sound produced by an episode solely involving a series of Strombolian explosions (4 July) and one also showing a transition to a fire fountain (12 July). The best fit between measured and synthetic waveforms gives the temporal evolution of the bubble length, 8–100 m, and overpressure, 0.2 MPa. Both episodes result from the coalescence of a foam layer trapped at the top of the reservoir. At the transition towards a fire fountain, the number of explosions and the bubble length increase simultaneously, suggesting that the foam destabilization is more efficient when a fire fountain is produced. Acoustic records give access to the gas volume trapped within the foam, called ‘active’ degassing, while the height of fire fountains also includes the gas from passive degassing. The small bubbles from passive degassing are carried to the surface via the wake of the slugs, coming from the depth of the reservoir. The proportion between active and total gas volume represents 38–48%.
EphA4 promotes cell proliferation and migration through a novel EphA4-FGFR1 signaling pathway in the human glioma U251 cell line
Authors: Fukai Junya , Yokote Hideyuki , Yamanaka Ryuya , Arao Tokuzo , Nishio Kazuto , Itakura Toru 
Published: September 2008

Abstract
The Eph receptor tyrosine kinases and their ephrin ligands form a unique cell-cell contact-mediated bidirectional signaling mechanism for regulating cell localization and organization. High expression of Eph receptors in a wide variety of human tumors indicates some roles in tumor progression, which makes these proteins potential targets for anticancer therapy. For this purpose, we did gene expression profiling for 47 surgical specimens of brain tumors including 32 high-grade glioma using a microarray technique. The analysis, focused on the receptor tyrosine kinases, showed that EphA4 mRNA in the tumors was 4-fold higher than in normal brain tissue. To investigate the biological significance of EphA4 overexpression in these tumors, we analyzed EphA4-induced phenotypic changes and the signaling mechanisms using human glioma U251 cells. EphA4 promoted fibroblast growth factor 2-mediated cell proliferation and migration accompanied with enhancement of fibroblast growth factor 2-triggered mitogen-activated protein kinase and Akt phosphorylation. In addition, active forms of Rac1 and Cdc42 increased in the EphA4-overexpressing cells. Furthermore, we found that EphA4 formed a heteroreceptor complex with fibroblast growth factor receptor 1 (FGFR1) in the cells and that the EphA4-FGFR1 complex potentiated FGFR-mediated downstream signaling. Thus, our results indicate that EphA4 plays an important role in malignant phenotypes of glioblastoma by enhancing cell proliferation and migration through accelerating a canonical FGFR signaling pathway. [Mol Cancer Ther 2008;7(9):2768–78]
Interleukin-8 signaling attenuates TRAIL- and chemotherapy-induced apoptosis through transcriptional regulation of c-FLIP in prostate cancer cells
Authors: Wilson Catherine , Wilson Timothy , Johnston Patrick G. , Longley Daniel B. , Waugh David J.J. 
Published: September 2008

AbstractChemotherapy-induced interleukin-8 (IL-8) signaling reduces the sensitivity of prostate cancer cells to undergo apoptosis. In this study, we investigated how endogenous and drug-induced IL-8 signaling altered the extrinsic apoptosis pathway by determining the sensitivity of LNCaP and PC3 cells to administration of the death receptor agonist tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). TRAIL induced concentration-dependent decreases in LNCaP and PC3 cell viability, coincident with increased levels of apoptosis and the potentiation of IL-8 secretion. Administration of recombinant human IL-8 was shown to increase the mRNA transcript levels and expression of c-FLIPL and c-FLIPS, two isoforms of the endogenous caspase-8 inhibitor. Pretreatment with the CXCR2 antagonist AZ10397767 significantly attenuated IL-8–induced c-FLIP mRNA up-regulation whereas inhibition of androgen receptor– and/or nuclear factor-κB–mediated transcription attenuated IL-8–induced c-FLIP expression in LNCaP and PC3 cells, respectively. Inhibition of c-FLIP expression was shown to induce spontaneous apoptosis in both cell lines and to sensitize these prostate cancer cells to treatment with TRAIL, oxaliplatin, and docetaxel. Coadministration of AZ10397767 also increased the sensitivity of PC3 cells to the apoptosis-inducing effects of recombinant TRAIL, most likely due to the ability of this antagonist to block TRAIL- and IL-8–induced up-regulation of c-FLIP in these cells. We conclude that endogenous and TRAIL-induced IL-8 signaling can modulate the extrinsic apoptosis pathway in prostate cancer cells through direct transcriptional regulation of c-FLIP. Therefore, targeted inhibition of IL-8 signaling or c-FLIP expression in prostate cancer may be an attractive therapeutic strategy to sensitize this stage of disease to chemotherapy. [Mol Cancer Ther 2008;7(9):2649–61]
Soluble EP2 neutralizes prostaglandin E2–induced cell signaling and inhibits osteolytic tumor growth
Authors: Takahashi Tetsuyuki , Uehara Hisanori , Bando Yoshimi , Izumi Keisuke 
Published: September 2008

AbstractProstaglandin E2 (PGE2) plays a key role in osteolytic bone metastasis as well as roles in inflammation, cell growth, and tumor development. PGE2 exerts its effects by binding and activating E-prostanoid receptor (EP). In this study, we propose a new approach for blocking EP-mediated cell signaling using a soluble chimeric EP2 fragment. Mammalian expression vectors encoding several human EP2 cDNAs were introduced into 293 cells and the culture medium was tested for their function as a decoy receptor for PGE2. PGE2 binding assays revealed that culture medium containing the second extracellular region of EP2 (FuEP2/Ex2) had binding activity. FuEP2/Ex2 neutralized PGE2-induced cyclic AMP production, cyclic AMP–responsive element binding protein phosphorylation, and subsequent induction of cyclooxygenase-2, interleukin (IL)-1β, and IL-6 mRNAs. In human osteoblasts, this culture medium neutralized the induction of receptor activator of nuclear factor-κB ligand mRNA. A stable transfectant expressing FuEP2/Ex2 was established from human prostate cancer PC-3 cells (PC3-FuEP2/Ex2). PC3-FuEP2/Ex2 cells grew at similar rates to vector control cells under normal culture conditions, although PGE2-induced growth stimulation was suppressed. Intraosseous injection of PC3-FuEP2/Ex2 cells into the tibia of athymic nude mice revealed that the degrees of tumor growth and osteolysis were decreased compared with control cell-injected mice, with decreased osteoclasts and increased apoptotic cells. Furthermore, the cyclooxygenase-2, IL-1β, and IL-6 mRNA levels were reduced in the tumor lesions. These data suggest that FuEP2/Ex2 is useful for treating osteolytic bone metastasis and cancers that depend on EP signaling for their growth and development. [Mol Cancer Ther 2008;7(9):2807–16]