bluuebunny/crossref_metadata_2025_split huggingface dataset:
The (9,5) HOC formulation for the transient Navier–Stokes equations in primitive variable
Authors: Kalita Jiten C. , Sen Shuvam 
Published: March 2007

AbstractWe recently proposed an improved (9,5) higher order compact (HOC) scheme for the unsteady two‐dimensional (2‐D) convection–diffusion equations. Because of using only five points at the current time level in the discretization procedure, the scheme was seen to be computationally more efficient than its predecessors. It was also seen to capture very accurately the solution of the unsteady 2‐D Navier–Stokes (N–S) equations for incompressible viscous flows in the stream function–vorticity (ψ – ω) formulation.In this paper, we extend the scope of the scheme for solving the unsteady incompressible N–S equations based on primitive variable formulation on a collocated grid. The parabolic momentum equations are solved for the velocity field by a time‐marching strategy and the pressure is obtained by discretizing the elliptic pressure Poisson equation by the steady‐state form of the (9,5) scheme with the Neumann boundary conditions. In particular, for pressure, we adopt a strategy on the collocated grid in conjunction with ideas borrowed from the staggered grid approach in finite volume. We first apply this extension to a problem having analytical solution and then to the famous lid‐driven square cavity problem. We also apply our formulation to the backward‐facing step problem to see how the method performs for external flow problems. The results are presented and are compared with established numerical results. This new approach is seen to produce excellent comparison in all the cases. Copyright © 2007 John Wiley & Sons, Ltd.
A continuous second‐order sensitivity equation method for time‐dependent incompressible laminar flows
Authors: Ilinca F. , Pelletier D. , Borggaard J. 
Published: March 2007

AbstractThis paper presents a general formulation of the continuous sensitivity equation method (SEM) for computing first‐ and second‐order sensitivities of time‐dependent, incompressible laminar flows. The formulation accounts for complex parameter dependence and is suitable for a wide range of problems. The SEM formulation is verified on a problem with a closed‐form solution. Systematic grid convergence studies confirm the theoretical rates of convergence in both space and time. The methodology is then applied to uniform flow around a circular cylinder. The flow starts with a symmetrical solution and transitions to the traditional Von Karman street (alternate vortex shedding). Sensitivities are used to demonstrate fast evaluation of nearby flows. The accuracy of nearby flows is much improved when second‐order sensitivities are used. The sensitivity of the Strouhal number with respect to the Reynolds number agrees well with the computed and experimentalSt–Rerelationship. Copyright © 2007 John Wiley & Sons, Ltd.
A comparative study of inflow conditions for two‐ and three‐dimensional spatially developing mixing layers using large eddy simulation
Authors: McMullan W. A. , Gao S. , Coats C. M. 
Published: March 2007

AbstractA series of spatially developing mixing layers are simulated using the large eddy simulation (LES) technique. A hyperbolic tangent function and data derived from boundary layer simulations are used to generate the inflow condition, and their effects on the flow are compared. The simulations are performed in both two and three dimensions. In two‐dimensional simulations, both types of inflow conditions produce a layer that grows through successive pairings of Kelvin–Helmholtz (K–H) vortices, but the composition ratio is lower for the hyperbolic tangent inflow simulations. The two‐dimensional simulations do not undergo a transition to turbulence. The three‐dimensional simulations produce a transition to turbulence, and coherent structures are found in the post‐transition region of the flow. The composition ratio of the three‐dimensional layers is reduced in comparison to the counterpart two‐dimensional runs. The mechanisms of growth are investigated in each type of simulation, and amalgamative pairing interactions are found in the pre‐transition region of the three‐dimensional simulations, and throughout the entire computational domain of those carried out in two‐dimensions. The structures beyond the post‐transition region of the three‐dimensional simulations appear to behave in a much different manner to their pre‐transition cousins, with no pairing‐type interactions observed in the turbulent flow. In order to accurately simulate spatially developing mixing layers, it is postulated that the inflow conditions must closely correspond to the conditions present in the reference experiment. Copyright © 2007 John Wiley & Sons, Ltd.
Assessment of the clinical and molecular impact of different cytogenetic subgroups in a series of 272 lipomas with abnormal karyotype
Authors: Bartuma Hammurabi , Hallor Karolin H. , Panagopoulos Ioannis , Collin Anna , Rydholm Anders , Gustafson Pelle , Bauer Henrik C. F. , Brosjö Otte , Domanski Henryk A. , Mandahl Nils , Mertens Fredrik 
Published: March 2007

AbstractConventional lipomas harbor karyotypic changes that could be subdivided into four, usually mutually exclusive, categories: rearrangement, in particular through translocations, of chromosome bands 12q13‐15, resulting in deregulation of the HMGA2 gene, loss of material from or rearrangement of chromosome 13, supernumerary ring or giant marker chromosomes, and aberrations of chromosome band 6p21. In the present study, 272 conventional lipomas, two‐thirds of them deep‐seated, with acquired clonal chromosome changes were assessed with regard to karyotypic and clinical features. A nonrandom distribution of breakpoints and imbalances could be confirmed, with 83% of the cases harboring one or more of the previously known cytogenetic hallmarks. Correlation with clinical features revealed that lipomas with rings/giant markers were larger, occurred in older patients, were more often deep‐seated, and seemed to have an increased tendency to recur locally, compared with tumors with other chromosome aberrations. The possible involvement of the HMGA2 gene in cases that did not show any of the characteristic cytogenetic changes was further evaluated by locus‐specific metaphase fluorescence in situ hybridization (FISH) and RT‐PCR, revealing infrequent cryptic disruption of the gene but abundant expression of full length or truncated transcripts. By FISH, we could also show that breakpoints in bands 10q22‐23 do not affect the MYST4 gene, whereas breakpoints in 6p21 or 8q11‐12 occasionally target the HMGA1 or PLAG1 genes, respectively, also in conventional lipomas. © 2007 Wiley‐Liss, Inc.
Delineation of a 1Mb breakpoint region at 1p13 in Wilms tumors by fine‐tiling oligonucleotide array CGH
Authors: Natrajan Rachael , Williams Richard D. , Grigoriadis Anita , Mackay Alan , Fenwick Kerry , Ashworth Alan , Dome Jeffrey S. , Grundy Paul E. , Pritchard‐Jones Kathy , Jones Chris 
Published: March 2007

AbstractWilms tumor karyotypes frequently exhibit recurrent, large‐scale chromosomal imbalances, among the most common of which are concurrent loss of 1p and gain of 1q. We have previously identified a novel breakpoint at 1p13 by 1 Mb‐spaced array CGH, and have now undertaken a fine‐tiling oligonucleotide array approach to map the region accurately in four tumors exhibiting rearrangements at this locus. The use of a 10 bp‐spaced platform revealed that all four tumors in fact harbored different breakpoints, which targeted intragenic sequences in PHTF1, DCLRE1B, and NRAS, and an intergenic region immediately downstream of TRIM33. All four genes and breakpoints were within the 1.78 Mb intervals identified by the genome‐wide BAC arrays. The precise breakpoint interval was in each case mapped to a 200–1,200 bp region and was confirmed for one case to lie within intron 3 of DCLRE1B by quantitative PCR. Analysis of local genome architecture revealed no convincing conservation of repetitive sequences or specific translocation/recombination‐associated elements within the breakpoint regions. This study highlights the power of fine‐tiling oligonucleotide arrays to delineate breakpoint regions identified by genome‐wide screens. © 2007 Wiley‐Liss, Inc.
Extrahippocampal gray matter atrophy and memory impairment in patients with medial temporal lobe epilepsy
Authors: Bonilha Leonardo , Alessio Andréa , Rorden Chris , Baylis Gordon , Damasceno Benito P. , Min Li Li , Cendes Fernando 
Published: March 2007

AbstractMemory impairment observed in patients with medial temporal lobe epilepsy (MTLE) is classically attributed to hippocampal atrophy. The contribution of extrahippocampal structures in shaping memory impairment in patients with MTLE is not yet completely understood, even though atrophy in MTLE extends beyond the hippocampus. We aimed to evaluate the neuropsychological profile of patients with MTLE focusing on memory, and to investigate whether gray matter concentration (GMC) distribution within and outside the medial portion of the temporal lobes would be associated with their neuropsychological performance. We performed a voxel based morphometry study of 36 consecutive patients with MTLE and unilateral hippocampal atrophy. We observed a significant simple regression between general and verbal memory performance based on Wechsler Memory Scale—Revised and the GMC of medial temporal and extratemporal structures in patients with left MTLE. We also performed a “regions of interest analysis” of the medial temporal lobe, and we observed that the GMC of the hippocampus, entorhinal, and perirhinal cortices were consistently associated with general and verbal memory performance in patients with MTLE. We also observed that the GMC of the cingulate and orbito‐frontal cortex are independently associated with verbal and general memory performances. Our results suggest that general and verbal memory impairments in patients with left MTLE are associated with atrophy of the hippocampus, the entorhinal, and the perirhinal cortex. We also suggest that atrophy and dysfunction of limbic and frontal structures such as the cingulate and the orbito‐frontal cortex contribute to memory impairment in MTLE. Hum Brain Mapp 2007. © 2007 Wiley‐Liss, Inc.
Neuromagnetic functional coupling during dichotic listening of speech sounds
Authors: Brancucci Alfredo , Penna Stefania Della , Babiloni Claudio , Vecchio Fabrizio , Capotosto Paolo , Rossi Davide , Franciotti Raffaella , Torquati Kathya , Pizzella Vittorio , Rossini Paolo M. , Romani Gian Luca 
Published: March 2007

AbstractThe present magnetoencephalography (MEG) study tested the hypothesis of a phase synchronization (functional coupling) of cortical alpha rhythms (about 6–12 Hz) within a “speech” cortical neural network comprising bilateral primary auditory cortex and Wernicke's areas, during dichotic listening (DL) of consonant‐vowel (CV) syllables. Dichotic stimulation was done with the CV‐syllable pairs /da/‐/ba/ (true DL, yielded by stimuli having high spectral overlap) and /da/‐/ka/ (sham DL, obtained with stimuli having poor spectral overlap). Whole‐head MEG activity (165 sensors) was recorded from 10 healthy right‐handed non‐musicians showing right ear advantage in a speech DL task. Functional coupling of alpha rhythms was defined as the spectral coherence at the following bands: alpha 1 (about 6–8 Hz), alpha 2 (about 8–10 Hz), and alpha 3 (about 10–12) with respect to the peak of individual alpha frequency. Results showed an inverse pattern of functional coupling: during DL of speech sounds, spectral coherence of the high‐band alpha rhythms increased between left auditory and Wernicke's areas with respect to sham DL, whereas it decreased between left and right auditory areas. The increase of functional coupling within the left hemisphere would underlie the processing of the syllable presented to the right ear, which arrives to the left auditory cortex without the interference of the other syllable presented to the left ear. Conversely, the decrease of inter‐hemispherical coupling of the high‐band alpha might be due to the fact that the two auditory cortices do not receive the same information from the ears during DL. These results suggest that functional coupling of alpha rhythms can constitute a neural substrate for the lateralization of auditory stimuli during DL. Hum Brain Mapp 2008. © 2007 Wiley‐Liss, Inc.
Breast cancer associated transcriptional repressor PLU‐1/JARID1B interacts directly with histone deacetylases
Authors: Barrett Angela , Santangelo Samantha , Tan Keith , Catchpole Steve , Roberts Kevin , Spencer‐Dene Bradley , Hall Debbie , Scibetta Angelo , Burchell Joy , Verdin Eric , Freemont Paul , Taylor‐Papadimitriou Joyce 
Published: March 2007

AbstractThe PLU‐1/JARID1B nuclear protein, which is expressed in a high proportion of breast cancers, but shows restricted expression elsewhere, belongs to the ARID family of proteins, known to play important roles in development, differentiation, transcriptional regulation and chromatin remodeling. PLU‐1/JARID1B is a strong transcriptional repressor, and here we show that the protein localizes in MAD bodies when cotransfected with class IIa histone deacetylases (HDACs) or N‐CoR. Direct binding to class I and class IIa HDACs is demonstrated, while the interaction with N‐CoR appears to be indirect. The domains involved in the HDAC4‐PLU‐1/JARID1B interaction were investigated in detail, and the data show that 2 PHD domains in PLU‐1/JARID1B, which are involved in transcriptional repression, are also crucial for binding to a domain in the 5′ region of HDAC4, overlapping the MEF‐2 binding region. Physiological relevance of this interaction in the mammary gland is suggested from the observation that HDAC4 and PLU‐1/JARID1B are coexpressed in the pregnant and involuting mouse mammary gland and are both silenced at lactation. Significantly, the expression of both proteins is seen in breast cancers. © 2007 Wiley‐Liss, Inc.
Mutations of the Wnt antagonist AXIN2 (Conductin) result in TCF‐dependent transcription in medulloblastomas
Authors: Koch Arend , Hrychyk Aksana , Hartmann Wolfgang , Waha Anke , Mikeska Thomas , Waha Andreas , Schüller Ulrich , Sörensen Nils , Berthold Frank , Goodyer Cynthia G. , Wiestler Otmar D. , Birchmeier Walter , Behrens Jürgen , Pietsch Torsten 
Published: March 2007

AbstractMedulloblastomas (MBs) represent the most common malignant brain tumors in children. Most MBs develop sporadically in the cerebellum, but their incidence is highly elevated in patients with familial adenomatous polyposis coli. These patients carry germline mutations in the APC tumor suppressor gene. APC is part of a multiprotein complex involved in the Wnt signaling pathway that controls the stability of β‐catenin, the central effector in this cascade. Previous genetic studies in MBs have identified mutations in genes coding for β‐catenin and its partners, APC and AXIN1, which cause activation of Wnt signaling. The pathway is negatively controlled by the tumor suppressor AXIN2 (Conductin), a scaffold protein of this signaling complex. To investigate whether alterations in AXIN2 may also be involved in the pathogenesis of sporadic MBs, we performed a mutational screening of the AXIN2 gene in 116 MB biopsy samples and 11 MB cell lines using single‐strand conformation polymorphism and sequencing analysis. One MB displayed a somatic, tumor‐specific 2 bp insertion in exon 5, leading to carboxy‐terminal truncation of the AXIN2 protein. This tumor biopsy showed nuclear accumulation of β‐catenin protein, indicating an activation of Wnt signaling. In 2 further MB biopsies, mutations were identified in exon 5 (Glu408Lys) and exon 8 (Ser738Phe) of the AXIN2 gene, which are due to predicted germline mutations and rare polymorphisms. mRNA expression analysis in 22 MBs revealed reduced expression of AXIN2 mRNA compared to 8 fetal cerebellar tissues. Promoter hypermethylation could be ruled out as a major cause for transcriptional silencing by bisulfite sequencing. To study the functional role of AXIN2 in MBs, wild‐type AXIN2 was overexpressed in MB cell lines in which the Wnt signaling pathway was activated by Wnt‐3a. In this assay, AXIN2 inhibited Wnt signaling demonstrated in luciferase reporter assays. In contrast, overexpression of mutated AXIN2 with a deleted C‐terminal DIX‐domain resulted in an activation of the Wnt signaling pathway. These findings indicate that mutations of AXIN2 can lead to an oncogenic activation of the Wnt pathway in MBs. © 2007 Wiley‐Liss, Inc.
Improved detection of bladder carcinoma cells in voided urine by standardized microsatellite analysis
Authors: Frigerio Simona , Padberg Barbara C. , Strebel Räto T. , Lenggenhager Daniela M. , Messthaler Angelika , Abdou Marie‐Therese , Moch Holger , Zimmermann Dieter R. 
Published: March 2007

AbstractSuccessful treatment of bladder cancer depends largely on early diagnosis of primary and recurrent disease. Sensitive, specific and noninvasive procedures for detection are especially needed for grade 1 and 2 bladder tumors, because of the relatively low sensitivity of cytology. Here we introduce a novel strategy to improve the sensitivity and reliability of microsatellite analyses by employing marker‐specific threshold values for loss‐of‐heterozygosity (LOH) at 10 loci. These individual cut‐offs were experimentally determined with 35 normal control tissues and subsequently validated in a retrospective study with bladder cancer biopsies from 86 patients. In a prospective analysis of voided urines samples and matched blood probes from 91 patients, LOH‐analysis, UroVysion FISH and conventional urine cytology were compared with histological findings of consecutive transurethral biopsies. Whereas all samples could be analyzed by our LOH assay, only 56 samples were suitable for all 3 analyses. The highest sensitivity was obtained with our LOH‐assay/cytology approach (G1–2: 72%; G3: 96%) being only surpassed by a combination of all 3 techniques (G1–2: 83%; G3: 100%). Since over 93% of the patients with recurrent disease were identified by LOH/cytology‐analyses of their voided urine samples, a monitoring scheme alternating cystoscopy with LOH/cytology‐examination could now be envisioned to reduce invasive interventions and consequently improve follow‐up compliance, especially in patients with low grade tumors. © 2007 Wiley‐Liss, Inc.
TNF potentiates anticancer activity of bortezomib (Velcade®) through reduced expression of proteasome subunits and dysregulation of unfolded protein response
Authors: Nowis Dominika , McConnell Elizabeth J. , Dierlam Lindsey , Palamarchuk Alla , Lass Agnieszka , Wójcik Cezary 
Published: March 2007

AbstractBortezomib (Velcade®) exploits proteasome inhibition as a unique mechanism of anticancer activity. The effectiveness of bortezomib is, however, limited, therefore, the search for therapeutic regimens combining bortezomib with other agents. In the present work we demonstrate enhanced anticancer activity of bortezomib by its combination with tumor necrosis factor (TNF) in the experimental model of C‐26 colon carcinoma in mice. This interaction likely relies on the induction of a dysregulated response to ER stress, leading to apoptosis of cancer cells, evidenced by caspase‐3 cleavage, p53 accumulation as well as increased SAPK/JNK phosphorylation. ER stress induced by the combination of TNF and bortezomib is corroborated by upregulation of BiP, PDI and calnexin as well as cleavage of caspase‐12; however, in contrast to the classic pathway, it is also associated with decreased phosphorylation of eIF2α and prevention of XBP‐1 splicing. TNF prevented the upregulation of Hsp27 induced by bortezomib, which may contribute to enhanced ER stress. Moreover, TNF interfered with bortezomib‐induced upregulation of distinct subunits of the 26S proteasome. Bortezomib concentration used in this study was not sufficient to prevent TNF from inducing nuclear translocation of p65/RelA; however, the combination of both agents reduced total p65/RelA levels. Combined treatment of tumor‐bearing mice with bortezomib and TNF not only inhibited tumor growth but also significantly prolonged animal survival. Therefore, combination of bortezomib with TNF is an attractive option for further clinical studies. © 2007 Wiley‐Liss, Inc.
δ‐, but not µ‐, opioid receptor stabilizes K+ homeostasis by reducing Ca2+ influx in the cortex during acute hypoxia
Authors: Chao Dongman , Bazzy‐Asaad Alia , Balboni Gianfranco , Xia Ying 
Published: March 2007

AbstractPast work has shown that δ‐opioid receptor (DOR) activation by [D‐Ala2,D‐Leu5]‐enkephalin (DADLE) attenuated the disruption of K+ homeostasis induced by hypoxia or oxygen‐glucose deprivation (OGD) in the cortex, while naltrindole, a DOR antagonist blocked this effect, suggesting that DOR activity stabilizes K+ homeostasis in the cortex during hypoxic/ischemic stress. However, several important issues remain unclear regarding this new observation, especially the difference between DOR and other opioid receptors in the stabilization of K+ homeostasis and the underlying mechanism. In this study, we asked whether DOR is different from µ‐opioid receptors (MOR) in stabilizing K+ homeostasis and which membrane channel(s) is critically involved in the DOR effect. The main findings are that (1) similar to DADLE (10 µM), H‐Dmt‐Tic‐NH‐CH (CH2COOH)‐Bid (1–10 µM), a more specific and potent DOR agonist significantly attenuated anoxic K+ derangement in cortical slice; (2) [D‐Ala2, N‐Me‐Phe4, glycinol5]‐enkephalin (DAGO; 10 µM), a MOR agonist, did not produce any appreciable change in anoxic disruption of K+ homeostasis; (3) absence of Ca2+ greatly attenuated anoxic K+ derangement; (4) inhibition of Ca2+‐activated K+ (BK) channels with paxilline (10 µM) reduced anoxic K+ derangement; (5) DADLE (10 µM) could not further reduce anoxic K+ derangement in the Ca2+‐free perfused slices or in the presence of paxilline; and (6) glybenclamide (20 µM), a KATP channel blocker, decreased anoxia‐induced K+ derangement, but DADLE (10 µM) could further attenuate anoxic K+ derangement in the glybenclamide‐perfused slices. These data suggest that DOR, but not MOR, activation is protective against anoxic K+ derangement in the cortex, at least partially via an inhibition of hypoxia‐induced increase in Ca2+ entry‐BK channel activity. J. Cell. Physiol. 212: 60–67, 2007. © 2007 Wiley‐Liss, Inc.
Cyclin B1 proteolysis via p38 MAPK signaling participates in G2 checkpoint elicited by arsenite
Authors: Li Ju‐Pi , Yang Jia‐Ling 
Published: March 2007

AbstractTimely induction of cyclin B1 controls mitotic entry, whereas its proteolysis is essential for mitotic exit. By contrast, cyclin B1 transcription is repressed during G2 arrest induced by DNA damage. The p38 mitogen‐activated protein kinase is involved in the G2 checkpoint; yet, its impact on cyclin B1 protein levels remains unclear. Here we show that untimely proteolysis of cyclin B1 following p38 activation contributes to G2 checkpoint. Exposing early G2 cells to arsenite impeded cyclin B1 protein accumulation, Cdk1 activation, and G2‐to‐M progression. Conversely, cyclin B1 was non‐degradable in late G2 and mitotic cells after arsenite. Cyclin B1 proteolysis was enhanced by arsenite in early G2 and asynchronous cells. This rapid destruction of cyclin B1 was mediated via the ubiquitin–proteasome pathway probably in a Cdc20 and Cdh1 independent mechanism. Under arsenite, inhibition of p38 activation or depletion of p38α suppressed cyclin B1 ubiquitination and proteolysis, while forced expression of MKK6‐p38 accelerated these events. Inactivation of p38 in arsenite‐treated early G2 cells allowed G2‐to‐M progression, blocked apoptosis, increased cell viability, and decreased micronucleus formation. Thus, p38 signaling pathway triggering cyclin B1 proteolysis after arsenite may play an important role in connecting G2 arrest with apoptosis or genome instability. J. Cell. Physiol. 212: 481–488, 2007. © 2007 Wiley‐Liss, Inc.