bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multi‐layer interleave‐division multiple access: theory and practice
Authors: Hoeher Peter A. , Schoeneich Hendrik , Fricke Justus Ch. 
Published: January 2008

AbstractDirect‐sequence code‐division multiple access(DS‐CDMA) is often put on the same level with CDMA, ignoring the fact that many different CDMA techniques exist. A special CDMA technique which has recently become popular isinterleave‐division multiple access(IDMA). In this semi‐tutorial, focus is on a generalisation of IDMA referred to asinterleave‐division multiplexing(IDM)/IDMA ormulti‐layer IDMAfor short. Multi‐layer IDMA is a special form of superposition coding, and can be interpreted as ajoint modulation, channel coding and multiple access scheme. Motivated by information theoretical arguments and practical functionalities, a wide range of subjects (such as capacity bounds, power allocation, receiver analysis, quality of service aspects, multi‐layer ARQ and possible applications) are covered. This semi‐tutorial consists of three parts: in the first part, an introduction to IDMA (Section 1) and multi‐layer IDMA (Section 2) is given. In the second part, practical issues such as functionalities of multi‐layer IDMA (Section 3) and multi‐layer ARQ (Section4) are studied. In the third part, information theoretical bounds in conjunction with power allocation (Section 5) and a receiver analysis (Section 6) are provided, before conclusions are drawn in Section 7. Copyright © 2008 John Wiley & Sons, Ltd.
Estimation of predictive uncertainties in flood wave propagation in a river channel using adjoint sensitivity analysis
Authors: Elhanafy Hossam , Copeland Graham J. M. , Gejadze Igor Yu. 
Published: January 2008

AbstractThis paper applies adjoint sensitivity analysis to flash flood wave propagation in a river channel. A numerical model, based on the St‐Venant equations and the corresponding adjoint equations, determines the sensitivities of predicted water levels to uncertainties in key controls such as inflow hydrograph, channel topography, frictional resistance and infiltration rate. Sensitivities are calculated in terms of a measuring function that quantifies water levels greater than certain safe threshold levels along the channel. The adjoint model has been verified by means of an identical twin experiment. The method is applied to a simulated flash flood in a river channel. The sensitivities to key controls are evaluated and ranked and the effects of individual and combined uncertainties on the predicted flood impact are also quantified. Copyright © 2008 John Wiley & Sons, Ltd.
A Lagrangian vortex method for unbounded flows
Authors: Moussa C. , Carley M. J. 
Published: January 2008

AbstractA technique is presented for velocity calculations on the highly distorted node distributions typical of those found in Lagrangian vortex methods. The method solves the partial differential equation for streamfunction directly on the nodes, via a sparse, symmetric system of equations that can be solved using standard iterative solvers. When implemented in a triangulated vortex method, the technique gives computation times which scale as N1.23, where N is the number of nodes. The computation scheme is derived for two‐dimensional problems and applied to the prediction of the evolution of perturbed multipolar vortices. Due to the numerical performance of the method, it has been possible to examine such evolution at higher and lower Reynolds numbers than have been considered in published numerical studies. Copyright © 2008 John Wiley & Sons, Ltd.
Gene expression analysis of BCR/ABL1‐dependent transcriptional response reveals enrichment for genes involved in negative feedback regulation
Authors: Håkansson Petra , Nilsson Björn , Andersson Anna , Lassen Carin , Gullberg Urban , Fioretos Thoas 
Published: January 2008

AbstractPhiladelphia (Ph) chromosome‐positive leukemia is characterized by the BCR/ABL1 fusion protein that affects a wide range of signal transduction pathways. The knowledge about its downstream target genes is, however, still quite limited. To identify novel BCR/ABL1‐regulated genes we used global gene expression profiling of several Ph‐positive and Ph‐negative cell lines treated with imatinib. Following imatinib treatment, the Ph‐positive cells showed decreased growth, viability, and reduced phosphorylation of BCR/ABL1 and STAT5. In total, 142 genes were identified as being dependent on BCR/ABL1‐mediated signaling, mainly including genes involved in signal transduction, e.g. the JAK/STAT, MAPK, TGFB, and insulin signaling pathways, and in regulation of metabolism. Interestingly, BCR/ABL1 was found to activate several genes involved in negative feedback regulation (CISH, SOCS2, SOCS3, PIM1, DUSP6, and TNFAIP3), which may act to indirectly suppress the tumor promoting effects exerted by BCR/ABL1. In addition, several genes identified as deregulated upon BCR/ABL1 expression could be assigned to the TGFB and NFkB signaling pathways, as well as to reflect the metabolic adjustments needed for rapidly growing cells. Apart from providing important pathogenetic insights into BCR/ABL1‐mediated leukemogenesis, the present study also provides a number of pathways/individual genes that may provide attractive targets for future development of targeted therapies. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045–2257/suppmat. © 2008 Wiley‐Liss, Inc.
The expression of BIRC5 is correlated with loss of specific chromosomal regions in breast carcinomas
Authors: Boidot Romain , Vegran Frédérique , Jacob Delphine , Chevrier Sandy , Gangneux Nicolas , Taboureau Johann , Oudin Claire , Rainville Vinciane , Mercier Liliane , Lizard‐Nacol Sarab 
Published: January 2008

AbstractExpression of BIRC5 (survivin), a member of the inhibitor of apoptosis protein (IAP) family, is elevated in fetal tissues and in various human cancers. Mechanisms up‐regulating BIRC5 in cancer are poorly understood. Here, we show that overexpression of BIRC5 induces a high proliferation level in MCF‐7 breast tumor cells. In a population of 191 breast carcinomas, BIRC5 expression is not affected by BIRC5 promoter polymorphism at −31, or BIRC5 gene copy number. However, a significant correlation was found between expression of demethylase (dMTase) and expression of BIRC5. In addition, among 13 chromosomal regions tested for allelic loss [loss of heterozygosity (LOH)], two regions close to D3S1478 and D6S264 were related to BIRC5 expression. In tumors with LOH at D3S1478 and/or D6S264, BIRC5 expression was significantly increased. These regions have been suggested to harbor tumor suppressor genes and/or common fragile sites that may play a role in increasing genetic instability. These results suggest that genes located near D3S1478 and D6S264 might work by inhibiting, directly or indirectly, BIRC5 expression and thus their loss leads to its up‐regulation. In addition, BIRC5 expression may induce breast tumor proliferation by promoting genetic instability. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045‐2257/suppmat. © 2008 Wiley‐Liss, Inc.
Genipin‐induced changes in collagen gels: Correlation of mechanical properties to fluorescence
Authors: Sundararaghavan Harini G. , Monteiro Gary A. , Lapin Norman A. , Chabal Yves J. , Miksan Jennifer R. , Shreiber David I. 
Published: January 2008

AbstractControlled crosslinking of collagen gels has important applications in cell and tissue mechanics as well as tissue engineering. Genipin is a natural plant extract that has been shown to crosslink biological tissues and to produce color and fluorescence changes upon crosslinking. We have characterized the effects of genipin concentration and incubation duration on the mechanical and fluorigenic properties of type I collagen gels. Gels were exposed to genipin (0, 1, 5, or 10 mM) for a defined duration (2, 4, 6, or 12 h). Mechanical properties were characterized using parallel plate rheometry, while fluorigenic properties were examined with a spectrofluorimetric plate reader and with a standard, inverted epifluorescent microscope. Additionally, Fourier transform infrared spectroscopy was used to characterize and track the crosslinking reaction in real‐time. Genipin produced significant concentration‐ and incubation‐dependent increases in the storage modulus, loss modulus, and fluorescence intensity. Storage modulus was strongly correlated to fluorescence exponentially. Minimal cytotoxicity was observed for exposure of L929 fibroblasts cultured within collagen gels to 1 mM genipin for 24 h, but significant cell death occurred for 5 and 10 mM genipin. We conclude that genipin can be used to stiffen collagen gels in a relatively short time frame, that low concentrations of genipin can be used to crosslink cell‐populated collagen gels to affect cell behavior that is influenced by the mechanical properties of the tissue scaffold, and that the degree of crosslinking can be reliably assayed optically via simple fluorescence measurements. © 2008 Wiley Periodicals, Inc. J Biomed Mater Res, 2008
Microtopography of titanium suppresses osteoblastic differentiation but enhances chondroblastic differentiation of rat femoral periosteum‐derived cells
Authors: Kubo Katsutoshi , Att Wael , Yamada Masahiro , Ohmi Kuzuhiro , Tsukimura Naoki , Suzuki Takeo , Maeda Hatsuhiko , Ogawa Takahiro 
Published: January 2008

AbstractDespite the clinical fact that endosseous titanium implants directly contacts periosteum, the behavior and response of the periosteum‐derived cells to surface topography of titanium have rarely been studied. This study examines the effect of titanium surface microtopography on osteoblastic and possibly‐modulated chondroblastic phenotypes of femoral periosteum‐derived cells. Rat femoral periosteum‐derived cells were cultured on either relatively smooth, machined titanium surface or acid‐etched, micro‐roughened titanium surface. The osteoblastic gene expressions, including collagen I, osteopontin and osteocalcin, were downregulated on the acid‐etched surface, compared with the machined surface. Alkaline phosphatase and mineralization activities on the acid‐etched surface were ∼20% of those on the machined surface. Instead, chondroblastic specific genes, including collagen II and IX, and sox 9, were exclusively expressed or highly upregulated on the acid‐etched surface. Alcian blue stain revealed an extensive deposition of glycosaminoglycan on the acid‐etched surface. The cultured matrix on the acid‐etched surface lacked the submicron globular structures that were extensively seen on the machined surface, and contained a remarkably increased percentage of sulfur relative to calcium compared with the culture on the machined surface. These results indicated that titanium microroughness suppresses the osteoblastic phenotype and induces or at least considerably enhances the chondroblastic phenotype of the periosteal cells, suggesting the unique role of titanium surface topography in regulating the periosteal cell differentiation. The suppressive effect of titanium microroughness on the periosteal cells toward the osteoblastic linage was contrasted to the known promotive effect on the bone marrow‐derived osteoblasts. © 2008 Wiley Periodicals, Inc. J Biomed Mater Res 2008
The anti‐apoptosis protein, survivin, mediates gastric epithelial cell cytoprotection against ethanol‐induced injury via activation of the p34cdc2 cyclin‐dependent kinase
Authors: Jones Michael K. , Padilla Oscar R. , Webb Nicole A. , Norng Manith 
Published: January 2008

AbstractThe anti‐apoptosis protein, survivin, promotes cell survival and mitosis. Recent studies have demonstrated that survivin is expressed in normal gastric mucosa. Using an in vitro model, we examined whether survivin plays a role in the cytoprotection produced in gastric mucosa by mild irritant ethanol (ETOH) against subsequent exposure to concentrated ETOH. Pre‐treatment of rat gastric epithelial cells with 1% ETOH reduced cell death, in response to subsequent incubation with 5% ETOH, by 94% (P < 0.005). This pre‐treatment also resulted in increased total and phosphorylated survivin protein levels by 180% (P < 0.0001) and 540% (P < 0.0002), respectively, which required the p34cdc2 cell cycle‐dependent kinase. The cytoprotective effect was abrogated upon siRNA knockdown of survivin protein levels. Further, overexpression of exogenous survivin resulted in significant cytoprotection by 62% (P < 0.02) in the absence of any pre‐treatment. We further examined the in vivo relevance of these findings. In fasted rats, administration of 20% ETOH, which we found to be 93% (P < 0.0001) cytoprotective against 50% ETOH challenge, resulted in increased total and phosphorylated survivin protein levels by 234% (P < 0.001) and 214% (P < 0.02), respectively. Administration of 20% ETOH resulted in increased gastric p34cdc2 activity by 146% (P < 0.01). Inhibition of p34cdc2 by the potent inhibitor, roscovitine, abolished the increased survivin levels in response to pre‐administration of 20% ETOH and reduced the cytoprotection against 50% ETOH challenge by 59% (P < 0.01). These results indicate that survivin is a key mediator of cytoprotection against ETOH‐induced gastric injury, acting at the epithelial cell level, by a mechanism that is dependent, in part, on p34cdc2. J. Cell. Physiol. 215: 750–764, 2008. © 2008 Wiley‐Liss, Inc.
Investigating a clonal human periodontal ligament progenitor/stem cell line in vitro and in vivo
Authors: Fujii Shinsuke , Maeda Hidefumi , Wada Naohisa , Tomokiyo Atsushi , Saito Masahiro , Akamine Akifumi 
Published: January 2008

AbstractThe lifespan of the tooth is influenced by the periodontal ligament (PDL), a specialized connective tissue that connects the cementum with the tooth socket bone. Generation of a cell line from PDL progenitor/stem cells would allow development of tissue engineering‐based regenerative PDL therapy. However, little is known about the characteristics of PDL progenitor/stem cells because PDL tissue consists of a heterogeneous cell population and there are no pure PDL cell lines. Recently, we succeeded in immortalizing primary human PDL fibroblasts (HPLFs) by transfecting them with SV40 T‐antigen and hTERT (Cell Tissue Res 2006; 324: 117–125). In this study, we isolated three clonal cell lines from these immortalized cells (lines 1–4, 1–11, and 1–24) that express RUNX‐2, Col I, ALP, OPN, OCN, RANKL, OPG, scleraxis, periostin, Col XII, and α‐SMA mRNA. Immunocytochemical analysis demonstrated that CD146 was expressed in cell lines 1–4 and 1–11 and that STRO‐1 was expressed in lines 1–11 and 1–24. Lines 1–4 and 1–11 differentiated into osteoblastic cells and adipocytes when cultured in lineage‐specific differentiation media. Four weeks after transplanting cell line 1–11 into immunodeficient mice with β‐tricalcium phosphate (β‐TCP), the transplant produced cementum/bone‐like tissues around the β‐TCP. Eight weeks after transplantation, the 1–11 cell transplant formed PDL‐like structures on the surface of the β‐TCP. These data suggest that cell line 1–11 was derived from a progenitor/stem cell present in the PDL and should be very useful for studying the biology and regeneration of human periodontium. J. Cell. Physiol. 215: 743–749, 2008. © 2008 Wiley‐Liss, Inc.
Ets‐1 triggers and orchestrates the malignant phenotype of mammary cancer cells within their matrix environment
Authors: Furlan Alessandro , Vercamer Chantal , Desbiens Xavier , Pourtier Albin 
Published: January 2008

AbstractAcquisition of invasive characteristics is a hallmark of breast carcinoma progression. During this phenomenon, Ets‐1 transcription factor overexpression is induced and associated with breast cancer invasiveness, and poor prognosis. We hypothesized that Ets‐1 transcription factor could be the orchestrator of a genetic program inducing the expression of genes necessary for cell motility, as postulated by the tumor microenvironment invasion model. We aimed at elucidating the role of Ets‐1 in the molecular control of mammary cancer cell invasion and aggressiveness within their matrix environment. To that purpose, mouse mammary tumor MMT epithelial cells were engineered to stably overexpress Ets‐1, or the dominant negative Ets‐1 DNA Binding domain. The biological function of Ets‐1 was assessed in three‐dimensional extracellular matrix systems recreating a microenvironmental architecture resembling in vivo geometric constraints. Ets‐1 overexpression provided MMT cells with a motile and invasive phenotype, leading to cell scattering, and impairing multicellular organization in matrix‐mimicking gels. We evidenced that Ets‐1 promoted HGF/SF activation, and the expression of its receptor, c‐Met. Ets‐1 also orchestrated switches in integrin expression pattern, towards a pro‐migratory and malignant phenotype. Moreover, Ets‐1 concomitantly triggered matrix metalloproteinases (MMP) expression and activation, thus contributing to cell scattering. Functional relevance of these observations was confirmed with blocking antibodies or MMP inhibitors. Our data highlight a critical role for Ets‐1 in the orchestration of a network of molecular and phenotypic events, converging to enhance malignant features and invasion by mammary cancer cells of their environment. Ets‐1 overexpression hence appears as a probable key step for breast cancer progression. J. Cell. Physiol. 215: 782–793, 2008. © 2008 Wiley‐Liss, Inc.
The x cystine/glutamate antiporter: A potential target for therapy of cancer and other diseases
Authors: Lo Maisie , Wang Yu‐Zhuo , Gout Peter W. 
Published: January 2008

AbstractThe x cystine/glutamate antiporter is a major plasma membrane transporter for the cellular uptake of cystine in exchange for intracellular glutamate. Its main functions in the body are mediation of cellular cystine uptake for synthesis of glutathione essential for cellular protection from oxidative stress and maintenance of a cystine:cysteine redox balance in the extracellular compartment. In the past decade it has become evident that the x transporter plays an important role in various aspects of cancer, including: (i) growth and progression of cancers that have a critical growth requirement for extracellular cystine/cysteine, (ii) glutathione‐based drug resistance, (iii) excitotoxicity due to excessive release of glutamate, and (iv) uptake of herpesvirus 8, a causative agent of Kaposi's sarcoma. The x transporter also plays a role in certain CNS and eye diseases. This review focuses on the expression and function of the x transporter in cells and tissues with particular emphasis on its role in disease pathogenesis. The potential use of x inhibitors (e.g., sulfasalazine) for arresting tumor growth and/or sensitizing cancers is discussed. J. Cell. Physiol. 215: 593–602, 2008. © 2008 Wiley‐Liss, Inc.
On a conjecture about edge irregular total labelings
Authors: Brandt Stephan , Miškuf Jozef , Rautenbach Dieter 
Published: January 2008

AbstractAs our main result, we prove that for every multigraph G = (V, E) which has no loops and is of order n, size m, and maximum degree $\Delta < {{{10}}^{-{{3}}}{{m}}\over \sqrt{{{8}}{{n}}}}$ there is a mapping ${{f}}:{{V}}\cup {{E}}\to \big\{{{1}},{{2}},\ldots,\big\lceil{{{m}}+{{2}}\over {{3}}}\big\rceil\big\}$ such that ${{f}}({{u}})+{{f}}({{uv}})+{{f}}({{v}})\not={{f}}({{u}}')+{{f}}({{u}}'{{v}}')+{{f}}({{v}}')$ for every ${{uv}},{{u}}'{{v}}'\in {{E}}$ with ${{uv}}\not={{u}}'{{v}}'$. Functions with this property were recently introduced and studied by Bača et al. and were called edge irregular total labelings. Our result confirms a recent conjecture of Ivančo and Jendrol′ about such labelings for dense graphs, for graphs where the maximum and minimum degree are not too different in terms of the order, and also for large graphs of bounded maximum degree. © 2008 Wiley Periodicals, Inc. J Graph Theory 57: 333–343, 2008
On conjectures of Frankl and El‐Zahar
Authors: Llano Bernardo , Montellano‐Ballesteros Juan José , Rivera‐Campo Eduardo , Strausz Ricardo 
Published: January 2008

AbstractAn induced subgraph ${\cal S}$ of a graph ${\cal G}$ is called a derived subgraph of ${\cal G}$ if ${\cal S}$ contains no isolated vertices. An edge e of ${\cal S}$ is said to be residual if e occurs in more than half of the derived subgraphs of ${\cal S}$. In this article, we prove that every simple graph with at least one edge contains a non‐residual edge. This was conjectured by El‐Zahar in 1997. © 2008 Wiley Periodicals, Inc. J Graph Theory 57: 344–352, 2008
Turán's theorem and k‐connected graphs
Authors: Bougard Nicolas , Joret Gwenaël 
Published: January 2008

AbstractThe minimum size of a k‐connected graph with given order and stability number is investigated. If no connectivity is required, the answer is given by Turán's Theorem. For connected graphs, the problem has been solved recently independently by Christophe et al., and by Gitler and Valencia. In this article, we give a short proof of their result and determine the extremal graphs. We settle the case of 2‐connected graphs, characterize the corresponding extremal graphs, and also extend a result of Brouwer related to Turán's Theorem. © 2008 Wiley Periodicals, Inc. J Graph Theory 58: 1–13, 2008
Ore‐type degree conditions for a graph to be H‐linked
Authors: Kostochka Alexandr V. , Yu Gexin 
Published: January 2008

AbstractGiven a fixed multigraph H with V(H) = {h1,…, hm}, we say that a graph G is H‐linked if for every choice of m vertices v1, …, vm in G, there exists a subdivision of H in G such that for every i, vi is the branch vertex representing hi. This generalizes the notion of k‐linked graphs (as well as some other notions). For a family ${\cal H}$ of graphs, a graph G is ${\cal H}$‐linked if G is H‐linked for every $H\in {\cal H}$. In this article, we estimate the minimum integer r = r(n, k, d) such that each n‐vertex graph with $\sigma_{2}(G)\ge {r}$ is ${\cal H}$‐linked, where ${\cal H}$ is the family of simple graphs with k edges and minimum degree at least $d \ge 2$. © 2008 Wiley Periodicals, Inc. J Graph Theory 58: 14–26, 2008
Cartilage repair with osteochondral autografts in sheep: Effect of biophysical stimulation with pulsed electromagnetic fields
Authors: Benazzo Franco , Cadossi Matteo , Cavani Francesco , Fini Milena , Giavaresi Gianluca , Setti Stefania , Cadossi Ruggero , Giardino Roberto 
Published: January 2008

AbstractThe effect of pulsed electromagnetic fields (PEMFs) on the integration of osteochondral autografts was evaluated in sheep. After osteochondral grafts were performed, the animals were treated with PEMFs for 6 h/day or sham‐treated. Six animals were sacrificed at 1 month. Fourteen animals were treated for 2 months and sacrificed at 6 months. At 1 month, the osteogenic activity at the transplant–host subchondral bone interface was increased in PEMF‐treated animals compared to controls. Articular cartilage was healthy in controls and stimulated animals. At 6 months, complete resorption was observed in four control grafts only. Cyst‐like resorption areas were more frequent within the graft of sham‐treated animals versus PEMF‐treated. The average volume of the cysts was not significantly different between the two groups; nevertheless, analysis of the variance of the volumes demonstrated a significant difference. The histological score showed no significant differences between controls and stimulated animals, but the percentage of surface covered by fibrous tissue was higher in the control group than in the stimulated one. Interleukin‐1 and tumor necrosis factor‐α concentration in the synovial fluid was significantly lower, and transforming growth factor‐β1 was significantly higher, in PEMF‐treated animals compared to controls. One month after osteochondral graft implantation, we observed larger bone formation in PEMF‐treated grafts which favors early graft stabilization. In the long term, PEMF exposure limited the bone resorption in subchondral bone; furthermore, the cytokine profile in the synovial fluid was indicative of a more favorable articular environment for the graft. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:631–642, 2008