bluuebunny/crossref_metadata_2025_split huggingface dataset:
Forward node-selecting queries over trees
Authors: Olteanu Dan 
Published: April 2007

Node-selecting queries over trees lie at the core of several important XML languages for the web, such as the node-selection language XPath, the query language XQuery, and the transformation language XSLT. The main syntactic constructs of such queries are the backward predicates, for example, ancestor and preceding, and the forward predicates, for example, descendant and following. Forward predicates are included in the depth-first, left-to-right preorder relation associated with the input tree, whereas backward predicates are included in the inverse of this preorder relation.
This work is devoted to an expressiveness study of node-selecting queries with proven theoretical and practical applicability, especially in the field of query evaluation against XML streams. The main question it answers positively is whether, for each input query with forward and backward predicates, there exists an equivalent forward-only output query. This question is then positively answered for input and output queries of varying structural complexity, using LOGLIN and PSPACE reductions.
Various existing applications based on the results of this work are reported, including query optimization and streamed evaluation.
Erratum: "Assisting E-Government Users with Animated Talking Faces" by P. Foglia, F. Giuntoli, C. A. Prete, and M. Zanda
Authors: Staff interactions 
Published: April 2007

The references were inadvertently removed from an article entitled "Assisting E-Government Users with Animated Talking Faces" in the January-February 2007 issue of
<interactions>
. We apologize for this oversight. The information is available below.

1. Cullen, R., O'Connor D., Veritt A. An Evaluation of Local Government Web sites in New Zealand. In The World of EGovernment (ed. Curtin G.C., Sommer M.H., Sommer V.), Haworth, 2003.
2. Foglia P., Prete C.A., Zanda M. Modelling Public Administration Portals. In Encyclopaedia of Portal Technology and Application (ed. Tatnall A.), Idea Group (in press).
3. Haxby J.V., Gobbini M.I., Furey M.L., Ishai A., Schouten, J.L., Pietrini P. Distributed and overlapping representations of faces and objects in ventral temporal cortex. Science, Sept. 28; 293(5539):2405-7, 2001.
4. Nielsen J. Talking-Head video is boring online, AlertBox, Dec. 5, 2005.
5. Qiu L., Benbasat I. An Investigation into the effects of text-to-speech voice and 3D avatars on the perception of presence and flow of live help in electronic commerce. ACM Transactions on Computer Human Interaction (TOCHI), 12(4); 2005.
6. Reis F. E-Government: Internet based interaction with the European businesses and citizens; Statistics in Focus; Eurostat, 2005.
7. Stewart O., Huerta J.M. Transition relevance place: a proposal for adaptive user interface in natural language dialog management systems. ACM SIGCHI Conference Work in progress, 2006.
Dynamic load balancing without packet reordering
Authors: Kandula Srikanth , Katabi Dina , Sinha Shantanu , Berger Arthur 
Published: April 2007

Dynamic load balancing is a popular recent technique that protects ISP networks from sudden congestion caused by load spikes or link failures. Dynamic load balancing protocols, however, require schemes for splitting traffic across multiple paths at a fine granularity. Current splitting schemes present a tussle between slicing granularity and packet reordering. Splitting traffic at the granularity of packets quickly and accurately assigns the desired traffic share to each path, but can reorder packets within a TCP flow, confusing TCP congestion control. Splitting traffic at the granularity of a flow avoids packet reordering but may overshoot the desired shares by up to 60% in dynamic environments, resulting in low end-to-end network goodput
Contrary to popular belief, we show that one can systematically split a single flow across multiple paths without causing packet reordering. We propose FLARE, a new traffic splitting algorithm that operates on bursts of packets, carefully chosen to avoid reordering. Using a combination of analysis and trace-driven simulations, we show that FLARE attains accuracy and responsiveness comparable to packet switching without reordering packets. FLARE is simple and can be implemented with a few KB of router state
Effect of Human Skin-Derived Stem Cells on Vessel Architecture, Tumor Growth, and Tumor Invasion in Brain Tumor Animal Models
Authors: Pisati Federica , Belicchi Marzia , Acerbi Francesco , Marchesi Chiara , Giussani Carlo , Gavina Manuela , Javerzat Sophie , Hagedorn Martin , Carrabba Giorgio , Lucini Valeria , Gaini Sergio Maria , Bresolin Nereo , Bello Lorenzo , Bikfalvi Andreas , Torrente Yvan 
Published: April 2007

Abstract
Glioblastomas represent an important cause of cancer-related mortality with poor survival. Despite many advances, the mean survival time has not significantly improved in the last decades. New experimental approaches have shown tumor regression after the grafting of neural stem cells and human mesenchymal stem cells into experimental intracranial gliomas of adult rodents. However, the cell source seems to be an important limitation for autologous transplantation in glioblastoma. In the present study, we evaluated the tumor targeting and antitumor activity of human skin-derived stem cells (hSDSCs) in human brain tumor models. The hSDSCs exhibit tumor targeting characteristics in vivo when injected into the controlateral hemisphere or into the tail vein of mice. When implanted directly into glioblastomas, hSDSCs distributed themselves extensively throughout the tumor mass, reduced tumor vessel density, and decreased angiogenic sprouts. In addition, transplanted hSDSCs differentiate into pericyte cell and release high amounts of human transforming growth factor-β1 with low expression of vascular endothelial growth factor, which may contribute to the decreased tumor cell invasion and number of tumor vessels. In long-term experiments, the hSDSCs were also able to significantly inhibit tumor growth and to prolong animal survival. Similar behavior was seen when hSDSCs were implanted into two different tumor models, the chicken embryo experimental glioma model and the transgenic Tyrp1-Tag mice. Taken together, these data validate the use of hSDSCs for targeting human brain tumors. They may represent therapeutically effective cells for the treatment of intracranial tumors after autologous transplantation. [Cancer Res 2007;67(7):3054–63]
RaLP, a New Member of the Src Homology and Collagen Family, Regulates Cell Migration and Tumor Growth of Metastatic Melanomas
Authors: Fagiani Ernesta , Giardina Giuseppina , Luzi Lucilla , Cesaroni Matteo , Quarto Micaela , Capra Maria , Germano Giovanni , Bono Maria , Capillo Manuela , Pelicci PierGiuseppe , Lanfrancone Luisa 
Published: April 2007

Abstract
The Src homology and collagen (Src) family of adaptor proteins comprises six Shc-like proteins encoded by three loci in mammals (Shc, Rai, and Sli). Shc-like proteins are tyrosine kinase substrates, which regulate diverse signaling pathways and cellular functions, including Ras and proliferation (p52/p46Shc), phosphatidylinositol 3-kinase and survival (p54Rai), and mitochondrial permeability transition and apoptosis (p66Shc). Here, we report the identification, cloning, and sequence characterization of a new member of the Shc family that we termed RaLP. RaLP encodes a 69-kDa protein characterized by the CH2-PTB-CH1-SH2 modularity, typical of the Shc protein family, and expressed, among adult tissues, only in melanomas. Analysis of RaLP expression during the melanoma progression revealed low expression in normal melanocytes and benign nevi, whereas high levels of RaLP protein were found at the transition from radial growth phase to vertical growth phase and metastatic melanomas, when tumor cells acquire migratory competence and invasive potential. Notably, silencing of RaLP expression in metastatic melanomas by RNA interference reduced tumorigenesis in vivo. Analysis of RaLP in melanoma signal transduction pathways revealed that (a) when ectopically expressed in RaLP-negative melanocytes and nonmetastatic melanoma cells, it functions as a substrate of activated insulin-like growth factor-1 and epidermal growth factor receptors and increases Ras/mitogen-activated protein kinase (MAPK) signaling and cell migration, whereas (b) its silencing in RaLP-positive melanoma cells abrogates cell migration in vitro, without affecting MAPK signaling, suggesting that RaLP activates both Ras-dependent and Ras-independent migratory pathways in melanomas. These findings indicate that RaLP is a specific marker of metastatic melanomas, a critical determinant in the acquisition of the migratory phenotype by melanoma cells, and a potential target for novel anti-melanoma therapeutic strategies. [Cancer Res 2007;67(7):3064–73]
Construction and Validation of Improved Triple Fusion Reporter Gene Vectors for Molecular Imaging of Living Subjects
Authors: Ray Pritha , Tsien Roger , Gambhir Sanjiv Sam 
Published: April 2007

Abstract
Multimodality imaging using several reporter genes and imaging technologies has become an increasingly important tool in determining the location(s), magnitude, and time variation of reporter gene expression in small animals. We have reported construction and validation of several triple fusion genes composed of a bioluminescent, a fluorescent, and a positron emission tomography (PET) reporter gene in cell culture and in living subjects. However, the bioluminescent and fluorescent components of fusion reporter proteins encoded by these vectors possess lesser activities when compared with the bioluminescent and fluorescent components of the nonfusions. In this study, we first created a mutant (mtfl) of a thermostable firefly luciferase (tfl) bearing the peroxisome localization signal to have greater cytoplasmic localization and improved access for its substrate, d-luciferin. Comparison between the three luciferases [mtfl, tfl, and firefly luciferase (fl)] both in cell culture and in living mice revealed that mtfl possessed 6- to 10-fold (in vitro) and 2-fold (in vivo) higher activity than fl. The improved version of the triple fusion vector carrying mtfl as the bioluminescent reporter component showed significantly (P &lt; 0.05) higher bioluminescence than the previous triple fusion vectors. Of the three different red fluorescent reporter genes (jred, hcred, and mrfp1, isolated from jellyfish chromophore, coral Heteractis crispa, and coral Discosoma, respectively) evaluated, mrfp1 was able to preserve highest expression as a component of the triple fusion reporter gene for in vivo fluorescence imaging. A truncated version of wild-type herpes simplex virus 1 (HSV1) thymidine kinase gene (wttk) retained a higher expression level than the truncated mutant HSV1-sr39 TK (ttk) as the third reporter component of this improved triple fusion vector. Multimodality imaging of tumor-bearing mice using bioluminescence and microPET showed higher luciferase activity [(2.7 ± 0.1 versus 1.9 ± 0.1) × (106 p/s/cm2/sr)] but similar level of fluorine-18–labeled 2′-fluoro-2′-deoxyarabinofuranosyl-5-ethyluracil (18F-FEAU) uptake (1.37 ± 0.15 versus 1.37 ± 0.2) percentage injected dose per gram] by mtfl-mrfp1-wttk–expressing tumors compared with the fl-mrfp1-wttk–expressing tumors. Both tumors showed 4- to 5-fold higher accumulation (P &lt; 0.05) of 18F-FEAU than fluorine-18–labeled 9-(4-fluoro-3-hydroxymethylbutyl)guanine. This improved triple fusion reporter vector will enable high sensitivity detection of lower numbers of cells from living animals using the combined bioluminescence, fluorescence, and microPET imaging techniques. [Cancer Res 2007;67(7):3085–93]
Androgen Deprivation Increases p300 Expression in Prostate Cancer Cells
Authors: Heemers Hannelore V. , Sebo Thomas J. , Debes Jose D. , Regan Kevin M. , Raclaw Kristin A. , Murphy Linda M. , Hobisch Alfred , Culig Zoran , Tindall Donald J. 
Published: April 2007

Abstract
Standard therapy for nonorgan confined prostate cancer aims to block the production or action of androgens. Although initially successful, antiandrogen therapy eventually fails and androgen depletion independent (ADI) disease emerges. Remarkably, ADI prostate cancers still rely on a functional androgen receptor (AR). Aberrant expression of coregulatory proteins required for the formation of productive AR transcriptional complexes is critical for ADI AR activation. Previously, we have shown that the transcriptional coactivator p300 is required for ADI activation of the AR and is up-regulated in prostate cancer, in which its expression is associated with cell proliferation and predicts aggressive tumor features. The mechanism responsible for the deregulated expression of p300, however, remains elusive. Here, we show that p300 expression in prostate cancer cells is subject to androgen regulation. In several prostate cancer model systems, addition of synthetic and natural androgens led to decreased expression of p300 in a time-dependent and dose-dependent manner. Experiments using AR antagonists or small interfering RNA targeting the AR revealed that down-regulation of p300 depends entirely on the presence of a functional AR. It is noteworthy that androgens down-regulated p300 protein expression while leaving messenger levels unaltered. Conversely, both short-term and long-term androgen deprivation resulted in marked up-regulation of p300 expression. The androgen deprivation–induced increase in p300 expression was not affected by the addition of cytokines or growth factors or by cotreatment with antiandrogens. Moreover, increased p300 expression upon androgen starvation is crucial for prostate cancer cell proliferation, as loss of p300 expression severely reduces expression of cyclins governing G1-S and G2-M cell cycle transition and decreases 5-bromo-2′-deoxyuridine incorporation. [Cancer Res 2007;67(7):3422–30]
Two Common Chromosome 8q24 Variants Are Associated with Increased Risk for Prostate Cancer
Authors: Wang Liang , McDonnell Shannon K. , Slusser Joshua P. , Hebbring Scott J. , Cunningham Julie M. , Jacobsen Steven J. , Cerhan James R. , Blute Michael L. , Schaid Daniel J. , Thibodeau Stephen N. 
Published: April 2007

Abstract
Two variants (rs1447295/DG8S737) of chromosome 8q24 were recently reported to be associated with increased risk of prostate cancer (PC). To confirm this finding, we genotyped and compared the frequencies of these polymorphisms among 1,121 Caucasian men with PC (435 men with familial PC, 491 men with sporadic PC, and 195 men with aggressive PC) to 545 population-based controls. For the single nucleotide polymorphism marker rs1447295, frequencies of the minor allele (A) were 10.3% in controls, 11.9% in sporadic cases, 16.7% in familial cases, and 17.2% in aggressive cases. Compared with controls, the A allele was significantly more common in both familial PC [odds ratios (OR), 1.93; 95% confidence intervals (95% CI), 1.37–2.72; P = 0.0004] and aggressive PC (OR, 1.87; 95% CI, 1.28–2.74; P = 0.0005) but not for sporadic PC (OR, 1.16; 95% CI, 0.85–1.58; P = 0.25). Although the A allele was more frequent in aggressive PC cases when compared with controls, the allele frequencies were similar among cases with high- and low-grade PC (Gleason grades &lt;7 and ≥7, respectively). For the microsatellite marker DG8S737, the −8 allele was significantly more frequent in familial PC (OR, 1.68; 95% CI, 1.09–2.60; P = 0.031), whereas the −10 allele was more frequent in aggressive PC (OR, 2.85; 95% CI, 1.52–5.36; P = 0.0004). Haplotype analysis showed significant differences in haplotype frequencies between the familial PC (P = 0.006) and aggressive PC (P = 0.005) cases versus controls. The −8/A haplotype showed the strongest association with familial PC (P = 0.008), whereas the −10/A haplotype was most strongly associated with aggressive PC (P = 0.00005). These results further confirm the importance of these two polymorphic variants (rs1447295 and DG8S737) as risk factors for PC. However, the mechanism explaining this increased risk has not yet been established. [Cancer Res 2007;67(7):2944–50]
Mutant V600E BRAF Increases Hypoxia Inducible Factor-1α Expression in Melanoma
Authors: Kumar Suresh M. , Yu Hong , Edwards Robin , Chen Lianjun , Kazianis Steven , Brafford Patricia , Acs Geza , Herlyn Meenhard , Xu Xiaowei 
Published: April 2007

Abstract
Mutations in the BRAF serine/threonine kinase gene are frequently found in cutaneous melanomas. Activation of hypoxia inducible factor-1α (HIF-1α) in response to both hypoxic stress and oncogenic signals has important implications in cancer development and progression. Here, we report that mutant BRAFV600E increases HIF-1α expression in melanoma cells. Our microarray profiling data in 35 melanoma and melanocyte cell lines showed that HIF-1α gene expression was significantly increased in melanomas harboring BRAFV600E mutation. Stable suppression of mutant BRAFV600E or both wild-type and mutant BRAFV600E by RNA interference in melanoma cells resulted in significantly decreased HIF-1α expression. Knockdown of mutant BRAFV600E induced significant reduction of cell survival and proliferation under hypoxic conditions, whereas knockdown of both wild-type and mutant BRAFV600E resulted in further reduction. The effects of BRAF knockdown can be rescued by reintroducing BRAFV600E into tumor cells. Transfection of BRAFV600E into melanoma cells with wild-type BRAF induced significantly more hypoxic tolerance. Knockdown of HIF-1α in melanoma cells resulted in decreased cell survival under hypoxic conditions. Pharmacologic inhibition of BRAF by BAY 43-9006 also resulted in decreased HIF-1α expression. Although HIF-1α translational rate was not changed, the protein was less stable in BRAF knockdown cells. In additional, von Hippel-Lindau protein expression was significantly increased in BRAF knockdown cells. Our data show for the first time that BRAFV600E mutation increases HIF-1α expression and melanoma cell survival under hypoxic conditions and suggest that effects of the oncogenic V600E BRAF mutation may be partially mediated through the HIF-1α pathway. [Cancer Res 2007;67(7):3177–84]
Relation of a Hypoxia Metagene Derived from Head and Neck Cancer to Prognosis of Multiple Cancers
Authors: Winter Stuart C. , Buffa Francesca M. , Silva Priyamal , Miller Crispin , Valentine Helen R. , Turley Helen , Shah Ketan A. , Cox Graham J. , Corbridge Rogan J. , Homer Jarrod J. , Musgrove Brian , Slevin Nick , Sloan Philip , Price Pat , West Catharine M.L. , Harris Adrian L. 
Published: April 2007

Abstract
Affymetrix U133plus2 GeneChips were used to profile 59 head and neck squamous cell cancers. A hypoxia metagene was obtained by analysis of genes whose in vivo expression clustered with the expression of 10 well-known hypoxia-regulated genes (e.g., CA9, GLUT1, and VEGF). To minimize random aggregation, strongly correlated up-regulated genes appearing in &gt;50% of clusters defined a signature comprising 99 genes, of which 27% were previously known to be hypoxia associated. The median RNA expression of the 99 genes in the signature was an independent prognostic factor for recurrence-free survival in a publicly available head and neck cancer data set, outdoing the original intrinsic classifier. In a published breast cancer series, the hypoxia signature was a significant prognostic factor for overall survival independent of clinicopathologic risk factors and a trained profile. The work highlights the validity and potential of using data from analysis of in vitro stress pathways for deriving a biological metagene/gene signature in vivo. [Cancer Res 2007;67(7):3441–9]
N-Cadherin Signaling Potentiates Mammary Tumor Metastasis via Enhanced Extracellular Signal-Regulated Kinase Activation
Authors: Hulit James , Suyama Kimita , Chung Su , Keren Rinat , Agiostratidou Georgia , Shan Weisong , Dong Xinyuan , Williams Terence M. , Lisanti Michael P. , Knudsen Karen , Hazan Rachel B. 
Published: April 2007

Abstract
N-cadherin is up-regulated in aggressive breast carcinomas, but its mechanism of action in vivo remains unknown. Transgenic mice coexpressing N-cadherin and polyomavirus middle T antigen (PyVmT) in the mammary epithelium displayed increased pulmonary metastasis, with no differences in tumor onset or growth relative to control PyVmT mice. PyVmT-N-cadherin tumors contained higher levels of phosphorylated extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) than PyVmT controls, and phosphorylated ERK staining was further increased in pulmonary metastases. Tumor cell isolates from PyVmT-N-cadherin mice exhibited enhanced ERK activation, motility, invasion, and matrix metalloproteinase-9 (MMP-9) expression relative to PyVmT controls. MAPK/ERK kinase 1 inhibition in PyVmT-N-cadherin cells reduced MMP-9 production and invasion but not motility. Furthermore, inactivation of fibroblast growth factor receptor in PyVmT-N-cadherin cells reduced motility, invasion, and ERK activation but had no effect on PyVmT cells. Thus, de novo expression of N-cadherin in mammary ducts enhances metastasis of breast tumors via enhanced ERK signaling. [Cancer Res 2007;67(7):3106–16]
Senescent Human Fibroblasts Increase the Early Growth of Xenograft Tumors via Matrix Metalloproteinase Secretion
Authors: Liu Dan , Hornsby Peter J. 
Published: April 2007

AbstractAlthough cellular senescence is believed to have a tumor suppressor function, senescent cells have been shown to increase the potential for growth of adjacent cancer cells in animal models. Replicatively senescent human fibroblasts increase the growth of cotransplanted cancer cells in vivo, but the role of cells that have undergone damage-mediated stress-induced premature senescence (SIPS) has not been studied in mouse transplant models. Here, we show that human fibroblasts that have undergone SIPS by exposure to the DNA-damaging agent bleomycin increase the growth of cotransplanted cancer cells (MDA-MB-231) in immunodeficient mice. Xenografts containing SIPS fibroblasts (SIPSF) exhibited early tissue damage as evidenced by fluid accumulation (edema). Cancer cells adjacent to the fluid showed increased DNA synthesis. Fluid accumulation, increased xenograft size, and increased cell proliferation were all reduced by the matrix metalloproteinase (MMP) inhibitor GM6001. MMPs and other genes characteristic of inflammation/tissue injury were overexpressed in SIPSF. Inhibition of MMP activity did not affect SIPSF stimulation of cancer cell proliferation in culture. However, another overexpressed product (hepatocyte growth factor) did have a direct mitogenic action on cancer cells. Based on the present results, we propose that senescent cells may promote cancer growth both by a direct mitogenic effect and by an indirect effect via tissue damage. Senescent stromal cells may cause an MMP-mediated increase in permeability of adjacent capillaries, thereby exposing incipient cancer cells to increased levels of mitogens, cytokines, and other plasma products. This exposure may increase cancer cell proliferation and result in promotion of preneoplastic cells. [Cancer Res 2007;67(7):3117–26]