bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serially concatenated continuous phase modulation with symbol interleavers: performance, properties and design principles
Authors: Xiao Ming , Aulin Tor M. 
Published: February 2006

AbstractSerially concatenated continuous phase modulation (SCCPM) systems with symbol interleavers are investigated. The transmitted signals are disturbed by additive white Gaussian noise (AWGN). Compared to bit interleaved SCCPM systems, this scheme shows a substantial improvement in the convergence threshold at the price of a higher error floor. In addition to showing this property, we also investigate the underlying reason by error event analysis. In order to estimate bit error rate (BER) performance, we generalise traditional union bounds for a bit interleaver to this non‐binary interleaver. For the latter, both the order and the position of permuted non‐zero symbols have to be considered. From the analysis, some principal properties are identified. Finally, some design principles are proposed. Our paper concentrates on SCCPM, but the proposed analysis methods and conclusions can be widely used in many other systems such as serially concatenated trellis coded modulation (SCTCM) et cetera. Copyright © 2006 AEIT
Dynamic packet allocation scheme for an all‐to‐all transmission schedule in WDM networks
Authors: Wen Jyh‐Horng , Huang Kuo‐Ting , Tsai Tzu‐Chen , Yang Cheng‐Ying 
Published: February 2006

AbstractIn wavelength division multiplexing broadcast‐and‐select star networks, the all‐to‐all transmission schedule is suitable for the uniform traffic pattern. The system performance is seriously degraded for the non‐uniform traffic patterns. Based on the demand assignment control, a dynamic packet allocation algorithm is proposed for the all‐to‐all transmission schedule. The algorithm decomposes the traffic matrix into a transmission matrix, and a residual matrix with a simple procedure. The transmission matrix is with most entries to approach the uniform traffic matrix. Within the transmission matrix, the idle time slots could be shared with the heavy‐load input nodes to increase the packet transmission. The simulation results show that the system with applying the algorithm could efficiently promote the performance on throughput, packet delay and buffer size for non‐uniform traffic patterns. Copyright © 2006 AEIT
A fully 3D finite volume method for incompressible Navier–Stokes equations
Authors: Deponti Alberto , Pennati Vincenzo , Biase Lucia De 
Published: February 2006

AbstractA semi‐implicit numerical method for the three‐dimensional incompressible Navier–Stokes equations is presented. The method describes the velocity and the non‐hydrostatic pressure field and the free surface evolution in time. The governing equations are discretized by means of the finite volume method on a structured non‐uniform grid; for this reason both local and global mass conservation are guaranteed. Convective and diffusive fluxes on the control volume faces, as well as boundary conditions, are approximated by high‐order formulae. Copyright © 2006 John Wiley & Sons, Ltd.
Hedging and value at risk
Authors: Harris Richard D. F. , Shen Jian 
Published: February 2006

AbstractIn this article, it is shown that although minimum‐variance hedging unambiguously reduces the standard deviation of portfolio returns, it can increase both left skewness and kurtosis; consequently the effectiveness of hedging in terms of value at risk (VaR) and conditional value at risk (CVaR) is uncertain. The reduction in daily standard deviation is compared with the reduction in 1‐day 99% VaR and CVaR for 20 cross‐hedged currency portfolios with the use of historical simulation. On average, minimum‐variance hedging reduces both VaR and CVaR by about 80% of the reduction in standard deviation. Also investigated, as an alternative to minimum‐variance hedging, are minimum‐VaR and minimum‐CVaR hedging strategies that minimize the historical‐simulation VaR and CVaR of the hedge portfolio, respectively. The in‐sample results suggest that in terms of VaR and CVaR reduction, minimum‐VaR and minimum‐CVaR hedging can potentially yield small but consistent improvements over minimum‐variance hedging. The out‐of‐sample results are more mixed, although there is a small improvement for minimum‐VaR hedging for the majority of the currencies considered. © 2006 Wiley Periodicals, Inc. Jrl Fut Mark 26:369–390, 2006
Holy mad cow! Facts or (mis)perceptions: A clinical study
Authors: Tse Yiuman , Hackard James C. 
Published: February 2006

AbstractThe May 20, 2003, announcement confirming diagnosis in a Canadian cow of mad cow disease caused price disturbances in livestock, grain, and stock markets. Price and time data are used to provide a clinical study on the timing, persistency, and rationality of those disturbances in different U.S. markets, showing the three types of uncertainty that C. Avery and P. Zemsky (1998) use to identify herd behavior and the resulting mispricing. Markets react at different times, showing an informational cascading pattern. Misperceptions cause futures contract and stock reactions that are unsupported by the facts. Livestock and grain futures markets reactions suggest that people would replace beef with pork. Biogenetic stocks show price disturbances for companies with no relation to screening or treatment for mad cow disease. The market reactions to the December 23, 2003, announcement of the first incidence of mad cow disease in the United States are examined to see whether the markets have learned from the May event. © 2006 Wiley Periodicals, Inc. Jrl Fut Mark 26:315–341, 2006
An empirical analysis of commodity pricing
Authors: Heaney Richard 
Published: February 2006

AbstractCommodity pricing models generally explain the link between commodity prices and stock levels in terms of a stock‐out constraint or a convenience yield. Analysis of this link is provided using monthly London Metals Exchange copper, lead, and zinc prices obtained for the period November 1964 to December 2003. A Markov model, fitted to these data, supports the existence of two distinct pricing regimes while the impact of convenience yields is also identified. © 2006 Wiley Periodicals, Inc. Jrl Fut Mark 26:391–415, 2006
Nonlinear dynamics and competing behavioral interpretations: Evidence from intra‐day FTSE‐100 index and futures data
Authors: McMillan David G. , Speight Alan E. H. 
Published: February 2006

AbstractExtant empirical research has reported nonlinear behavior within arbitrage relationships. In this article, the authors consider potential nonlinear dynamics within FTSE‐100 index and index‐futures. Such nonlinearity can be rationalized by the existence of transactions costs or through the interaction between informed and noise traders. They consider several empirical models designed to capture these alternative dynamics. Their empirical results provide evidence of a stationary basis term, and thus cointegration between index and index‐futures, and the presence of nonlinear dynamics within that relationship. The results further suggest that noise traders typically engage in momentum trading and are more prone to this behavior type when the underlying market is rising. Fundamental, or arbitrage, traders are characterized by heterogeneity, such that there is slow movement between regimes of behavior. In particular, fundamental traders act more quickly in response to small deviations from equilibrium, but are reluctant to act quickly in response to larger mispricings that are exposed to greater noise trader price risk. © 2006 Wiley Periodicals, Inc. Jrl Fut Mark 26:343–368, 2006
Allelotyping analysis at chromosome arm 8p of high‐grade prostatic intraepithelial neoplasia and incidental, latent, and clinical prostate cancers
Authors: Lu Wei , Takahashi Hiroyuki , Furusato Bungo , Maekawa Suguru , Ikegami Masahiro , Sudo Akemi , Egawa Shin , Hano Hiroshi 
Published: February 2006

AbstractIn this study, we used 7 informative microsatellite markers at 8p22, 23.1, and 23.2 in Japanese patients to compare frequency of loss of heterozygosity (LOH) in 53 lesions of high‐grade prostatic intraepithelial neoplasia (HGPIN), 38 cases (38 lesions) of incidental prostate cancer (IPC), 31 cases (41 lesions) of latent prostate cancer (LPC), and 102 cases (168 lesions) of clinical prostate cancer (CPC). The frequency of LOH at 8p22–23.2 with at least 1 marker was 0%, 33%, 57%, and 51% in the HGPIN, IPC, LPC, and CPC cases, respectively. No statistically significant difference was found at 8p22–23.2 between the types of prostate cancer. However, the frequency of 8p22 deletion was significantly higher in CPC and LPC cases than in IPC cases (P = 0.0003) or lesions (P = 0.0017). The frequency of LOH at 8p22 and 8p23.1 loci in high‐grade tumors was significantly higher than in low‐grade tumors in both the LPCs/IPCs and CPCs (P < 0.05). Allelic loss at 8p22 was significantly more frequent in CPC than in IPC (P = 0.002) and in pT4 CPC than in earlier‐stage CPC (P = 0.038). These findings suggest that deletion of 8p is an important event in both the initiation and metastasis of prostate cancer. The extremely high frequency of LOH at 8p22–23.1 in high‐grade tumors suggests the existence of a novel putative tumor‐suppressor gene associated with the progression of prostate cancer. These results should be useful in identifying the target gene of deletion at 8p. © 2006 Wiley‐Liss, Inc.
Increased seizure duration and slowed potassium kinetics in mice lacking aquaporin‐4 water channels
Authors: Binder Devin K. , Yao Xiaoming , Zador Zsolt , Sick Thomas J. , Verkman Alan S. , Manley Geoffrey T. 
Published: February 2006

AbstractThe glial water channel aquaporin‐4 (AQP4) has been hypothesized to modulate water and potassium fluxes associated with neuronal activity. In this study, we examined the seizure phenotype of AQP4 −/− mice using in vivo electrical stimulation and electroencephalographic (EEG) recording. AQP4 −/− mice were found to have dramatically prolonged stimulation‐evoked seizures after hippocampal stimulation compared to wild‐type controls (33 ± 2 s vs. 13 ± 2 s). In addition, AQP4 −/− mice were found to have a higher seizure threshold (167 ± 17 μA vs. 114 ± 10 μA). To assess a potential effect of AQP4 on potassium kinetics, we used in vivo recording with potassium‐sensitive microelectrodes after direct cortical stimulation. Although there was no significant difference in baseline or peak [K+]o, the rise time to peak [K+]o (t1/2, 2.3 ± 0.5 s) as well as the recovery to baseline [K+]o (t1/2, 15.6 ± 1.5 s) were slowed in AQP4 −/− mice compared to WT mice (t1/2, 0.5 ± 0.1 and 6.6 ± 0.7 s, respectively). These results implicate AQP4 in the expression and termination of seizure activity and support the hypothesis that AQP4 is coupled to potassium homeostasis in vivo. © 2006 Wiley‐Liss, Inc.
Induction of parathyroid hormone‐related peptide following peripheral nerve injury: Role as a modulator of Schwann cell phenotype
Authors: Macica Carolyn M. , Liang Guoying , Lankford Karen L. , Broadus Arthur E. 
Published: February 2006

AbstractParathyroid hormone‐related peptide (PTHrP) is widely distributed in the rat nervous system, including the peripheral nervous system, where its function is unknown. PTHrP mRNA expression has recently been shown to be significantly elevated following axotomy of sympathetic ganglia, although the role of PTHrP was not investigated. The role of PTHrP in peripheral nerve injury was investigated in this study using the sciatic nerve injury model and dorsal root ganglion (DRG) explant model of nerve regeneration. We find that PTHrP is a constitutively secreted peptide of proliferating Schwann cells and that the PTHrP receptor (PTH1R) mRNA is expressed in isolated DRG and in sciatic nerve. Using the sciatic nerve injury model, we show that PTHrP is significantly upregulated in DRG and in sciatic nerve. In addition, in situ hybridization revealed significant localization of PTHrP mRNA to Schwann cells in the injured sciatic nerve. We also find that PTHrP causes a dramatic increase in the number of Schwann cells that align with and bundle regrowing axons in explants, characteristic of immature, dedifferentiated Schwann cells. In addition to stimulating migration of Schwann cells along the axonal membrane, PTHrP also stimulates migration on a type 1 collagen matrix. Furthermore, treatment of purified Schwann cell cultures with PTHrP results in the rapid phosphorylation of the cAMP response element protein, CREB. We propose that PTHrP acts by promoting the dedifferentiation of Schwann cells, a critical requirement for successful nerve regeneration and an effect consistent with known PTHrP functions in other cellular differentiation programs. © 2006 Wiley‐Liss, Inc.
Sphingosine‐1‐phosphate is released by cerebellar astrocytes in response to bFGF and induces astrocyte proliferation through Gi‐protein‐coupled receptors
Authors: Bassi Rosaria , Anelli Viviana , Giussani Paola , Tettamanti Guido , Viani Paola , Riboni Laura 
Published: February 2006

AbstractThe mitogenic role of sphingosine‐1‐phosphate (S1P) and its involvement in basic fibroblast growth factor (bFGF)‐induced proliferation were examined in primary cultures of cerebellar astrocytes. Exposure to bFGF resulted in a rapid increase of extracellular S1P formation, bFGF inducing astrocytes to release S1P, but not sphingosine kinase, in the extracellular milieu. The SK inhibitor N,N‐dimethylsphingosine inhibited S1P release as well as bFGF‐induced growth stimulation. S1P application in quiescent astrocytes caused a dose‐dependent increase in DNA synthesis. This gliotrophic effect was induced by a brief exposure to low nanomolar S1P, mimicked by the S1P receptor agonist dihydro‐S1P, and inhibited by pertussis toxin (PTX), an inactivator of Gi/Go‐proteins. S1P also induced activation of extracellular signal‐regulated kinase that was inhibited again by PTX. Moreover, the S1P lyase inhibitor 4‐deoxypyridoxine induced the cellular accumulation of S1P but did not affect DNA synthesis. These results support the view that S1P exerted a mitogenic effect on cerebellar astrocytes extracellularly, most likely through cell surface S1P receptors. In agreement, mRNAs for S1P1, S1P2, and S1P3 receptors are expressed in cerebellar astrocytes (Anelli et al., 2005. J Neurochem 92:1204–1215). Ceramide, a negative regulator of astrocyte proliferation and down‐regulated by bFGF (Riboni et al., 2002. Cerebellum 1:129–135), efficiently inhibited S1P‐induced proliferation. The S1P action appears to be part of an autocrine/paracrine cascade stimulated by bFGF and, together with ceramide down‐regulation, essential for astrocytes to respond to bFGF. The results suggest that S1P and bFGF/S1P may play an important role in physiopathological glial proliferation, such as brain development, reactive gliosis and brain tumor formation. © 2006 Wiley‐Liss, Inc.
Cyclic AMP synergistically enhances neuregulin‐dependent ERK and Akt activation and cell cycle progression in Schwann cells
Authors: Monje Paula V. , Bartlett Bunge Mary , Wood Patrick M. 
Published: February 2006

AbstractThe elevation of intracellular cAMP synergistically enhances the neuregulin‐dependent proliferation of cultured Schwann cells (SCs); however, the mechanism by which this occurs has not been completely defined. To better understand this mechanism, we investigated the effect of cAMP on the activation of the extracellular signal‐regulated kinase (ERK) and phosphoinositide 3‐kinase (PI3‐K)‐Akt (PKB) pathways by heregulin, a member of the neuregulin family. Using primary cultures of adult SCs, we demonstrated that the adenylyl cyclase activator, forskolin, enhanced heregulin‐dependent SC proliferation by reducing the time required for S‐phase entry. When cAMP levels were increased, using either forskolin or a cell permeable analogue of cAMP, the heregulin‐induced phosphorylation of ERK was converted from transient to sustained and the heregulin‐induced phosphorylation of Akt was synergistically increased. Consistent with these observations, studies in which inhibitors of MEK, the upstream stimulating ERK kinase, and PI3‐K were administered at different times following the onset of stimulation indicated that sustained high levels of both MEK/ERK and PI3‐K/Akt activity before S‐phase initiation were essential for S‐phase entry. Overall, these novel results indicate that in neuregulin‐stimulated SCs the activation of cAMP‐mediated pathways accelerates G1‐S progression by prolonging ERK activation and concurrently enhancing Akt activation. © 2006 Wiley‐Liss, Inc.
Fish consumption and breast cancer risk. The European Prospective Investigation into Cancer and Nutrition (EPIC)
Authors: Engeset Dagrun , Alsaker Elin , Lund Eiliv , Welch Ailsa , Khaw Kay‐Tee , Clavel‐Chapelon Françoise , Thiébaut Anne , Chajès Véronique , Key Timothy J , Allen Naomi E , Amiano Pilar , Dorronsoro Miren , Tjønneland Anne , Stripp Connie , Peeters Petra HM , van Gils Carla H , Chirlaque Maria‐Dolores , Nagel Gabriele , Linseisen Jakob , Ocké Marga C , Bueno‐de‐Mesquita H Bas , Sacerdote Carlotta , Tumino Rosario , Ardanaz Eva , Sánchez Maria‐Jose , Panico Salvatore , Palli Domenico , Trichopoulou Antonia , Kalapothaki Victoria , Benetou Vicky , Quirós J Ramón , Agudo Antonio , Overvad Kim , Bjerregaard Lone , Wirfält Elisabet , Schulz Mandy , Boeing Heiner , Slimani Nadia , Riboli Elio 
Published: February 2006

AbstractThere is current interest in fish consumption and marine omega‐3 (n‐3) fatty acids and breast cancer risk. Some in vitro and animal studies have suggested an inhibitory effect of marine n‐3 fatty acids on breast cancer growth, but the results from epidemiological studies that have examined the association between fish consumption and breast cancer risk in humans are inconsistent. We examined fish consumption and breast cancer risk in 310,671 women aged between 25 and 70 yr at recruitment into the European Prospective Investigation Into Cancer and Nutrition (EPIC). The participants completed a dietary questionnaire between 1992–98 and were followed up for incidence of breast cancer for a median of 6.4 yr. Hazard ratio for breast cancer by intake of total and lean and fatty fish were estimated, stratified by study centre and adjusted for established breast cancer risk factors. During follow‐up, 4,776 invasive incident breast cancers were reported. No significant associations between intake of total fish and breast cancer risk were observed, hazard ratio (HR) 1.01 (95% confidence interval [CI] 0.99–1.02; p = 0.28 per 10 g fish/day). When examining lean and fatty fish separately, we found a positive significant association only in the highest quintile for fatty fish (HR 1.13, 95% CI 1.01–1.26), but test for trend was not significant (p = 0.10). No associations with breast cancer risk were observed when the study participants were subdivided by menopausal status. Although the period of follow‐up is relatively short, the results provide no evidence for an association between fish intake and breast cancer risk. © 2006 Wiley‐Liss, Inc.
Tumor selective replication of Newcastle disease virus: Association with defects of tumor cells in antiviral defence
Authors: Fiola Christoph , Peeters Ben , Fournier Philippe , Arnold Annette , Bucur Mariana , Schirrmacher Volker 
Published: February 2006

AbstractTo investigate tumor‐selective viral replication, we compared several tumorigenic human cell lines to nontumorigenic human cells from the blood for the sensitivity to become infected by a recombinant lentogenic strain of Newcastle Disease Virus (NDV) with incorporated transgene EGFP (NDFL‐EGFP). Although fluorescence signals in nontumorigenic cells were only weak or missing completely, a massive and long‐lasting transgene‐expression was observed in all tumor cell lines. The majority of tumor cells (50–95%) could be infected, and viral replication was associated with an increase in the cell surface density of viral antigens. To clarify the underlying mechanism of the observed difference in virus susceptibility we examined the kinetics of interferon‐induced antiviral enzymes because NDV is a strong type‐I interferon inducer. This analysis revealed several defects of tumor cells in their antiviral defence responses: They showed no response to UV‐inactivated NDV, whereas nontumorigenic cells reacted with induction of high‐levels of the antiviral enzymes PKR and MxA. Upon coincubation with live NDV, tumor cells showed a delayed response in the increased expression of the antiviral enzymes in comparison with PBMC. In nontumorigenic cells the replication cycle of NDV stopped after the production of positive‐strand RNA, while tumor cells continued in the replication cycle and copied viral genomes 10–50 hr after infection. These results can explain the tumor selective replication behavior of this interesting antineoplastic virus. © 2006 Wiley‐Liss, Inc.
Iressa induces cytostasis and augments Fas‐mediated apoptosis in acinic cell adenocarcinoma overexpressing HER2/neu
Authors: Piechocki Marie P. , Yoo George H. , Dibbley Susan K. , Amjad Esmael H. , Lonardo Fulvio 
Published: February 2006

AbstractUnderstanding the role of signal transduction in regulating pathways responsible for cell growth, survival and apoptosis is critical for cancer therapy. We developed and characterized a HER2/neu and Fas overexpressing cell line (BNT.888 ACA2) from a salivary gland adenocarcinoma that arose in a HER2/neu transgenic mouse. We evaluated the effects of Iressa on signal transduction networks downstream of the activated HER2 and the impact on proliferation, cell cycle and apoptosis. Iressa treatment diminished phosphorylation of the HER2/neu and EGFR. Phosphorylation of STAT‐3 also decreased and mitogenic signaling through the MAPK pathways was greatly reduced. Cyclin D1 levels decreased, and cells were arrested in G0 and failed to enter S‐phase because of hypophosphorylation of Rb and to traverse the G2M checkpoint because of degradation of cyclin B1. Cytostasis occurred within 48 hr at 250–500 nM Iressa. Levels of proapoptotic factors (bim and bax) increased and levels of antiapoptotic factors (bcl‐2 and bcl‐xL) decreased in a dose‐dependent manner. Higher doses of Iressa diminished phosphorylation of Akt slightly, but failed to induce apoptosis. Fas antibody was a potent agonist of apoptosis. Pretreatment with Iressa (1 μM, 24 hr) greatly enhanced Fas‐mediated apoptosis as determined by Annexin V binding, cleavage of caspase‐3 and PARP. Augmentation of apoptosis was associated with increased Fas expression and membrane localization. Iressa pretreatment increased bid activation, cleavage of caspases ‐3, ‐9 and ‐12 and stress signaling via c Jun. These data showing that Iressa induces cytostasis and primes the extrinsic (Fas) and intrinsic (mitochondrial and endoplasmic reticulum) apoptotic pathways should lead to the development of novel therapeutic targets and strategies. © 2006 Wiley‐Liss, Inc.