bluuebunny/crossref_metadata_2025_split huggingface dataset:
APPROXIMATING HYPERCUBES BY INDEX-SHUFFLE GRAPHS VIA DIRECT-PRODUCT EMULATIONS
Authors: OBRENIĆ BOJANA 
Published: January 2005

Index-shuffle graphs are a family of bounded-degree hypercube-like interconnection networks for parallel computers, introduced by [Baumslag and Obrenić (1997): Index-Shuffle Graphs, …], as an efficient substitute for two standard families of hypercube derivatives: butterflies and shuffle-exchange graphs. In the theoretical framework of graph embedding and network emulations, this paper shows that the index-shuffle graph efficiently approximates the direct-product structure of the hypercube, and thereby has a unique potential to approximate efficiently all of its derivatives. One of the consequences of our results is that any member of the following group of standard bounded-degree hypercube derivatives: butterflies, shuffles, tori, meshes of trees, is emulated by the index-shuffle graph with a slowdown in the order of the logarithm of the slowdown of the most efficient emulation achieved by any other member of this group. Emulation algorithms are presented where the emulation host is the n-dimensional index-shuffle graph Ψn, having N=2n nodes. The emulated graph G is a direct product of the form: G=F0×F1×⋯×Fk-1 where k is a power of 2, and each factor Fi is an instance of any of the following three graph families: cycle, complete binary tree, X-tree. Let the size of each factor be |Fi|≤2nf, where k·nf≤n. The index-shuffle graph Ψn, emulates any factor Fi in the product G with slowdown: O( log k) + O( log nf), which is O( log n) = O( log log N). Any collection of 2ℓ copies of the product G, such that: ℓ+k·nf≤n is emulated by the index-shuffle graph Ψn simultaneously, without any additional slowdown. Relaxing the assumption that k is a power of 2 introduces an additional factor of O( lg *N) into the slowdown.
The actin cytoskeleton differentially regulates platelet α-granule and dense-granule secretion
Authors: Flaumenhaft Robert , Dilks James R. , Rozenvayn Nataliya , Monahan-Earley Rita A. , Feng Dian , Dvorak Ann M. 
Published: January 2005

AbstractStimulation of platelets with strong agonists results in centralization of cytoplasmic organelles and secretion of granules. These observations have led to the supposition that cytoskeletal contraction facilitates granule release by promoting the interaction of granules with one another and with membranes of the open canalicular system. Yet, the influence of the actin cytoskeleton in controlling the membrane fusion events that mediate granule secretion remains largely unknown. To evaluate the role of the actin cytoskeleton in platelet granule secretion, we have assessed the effects of latrunculin A and cytochalasin E on granule secretion. Exposure of platelets to low concentrations of these reagents resulted in acceleration and augmentation of agonist-induced α-granule secretion with comparatively modest effects on dense granule secretion. In contrast, exposure of platelets to high concentrations of latrunculin A inhibited agonist-induced α-granule secretion but stimulated dense granule secretion. Incubation of permeabilized platelets with low concentrations of latrunculin A primed platelets for Ca2+- or guanosine triphosphate (GTP)-γ-S-induced α-granule secretion. Latrunculin A-dependent α-granule secretion was inhibited by antibodies directed at vesicle-associated membrane protein (VAMP), demonstrating that latrunculin A supports soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein-dependent membrane fusion. These results indicate that the actin cytoskeleton interferes with platelet exocytosis and differentially regulates α-granule and dense granule secretion.
Allogeneic hematopoietic stem-cell transplantation with reduced-intensity conditioning in intermediate- or high-risk patients with myelofibrosis with myeloid metaplasia
Authors: Rondelli Damiano , Barosi Giovanni , Bacigalupo Andrea , Prchal Josef T. , Popat Uday , Alessandrino Emilio P. , Spivak Jerry L. , Smith B. Douglas , Klingemann Hans G. , Fruchtman Steven , Hoffman Ronald 
Published: January 2005

AbstractA total of 21 patients with myelofibrosis with myeloid metaplasia (MMM), with a median age of 54 years (range, 27-68 years), were prepared with a reduced-intensity conditioning (RIC) regimen. The patients received an allogeneic marrow (n = 3) or peripheral blood stem-cell (n = 18) transplant from HLA-matched related (n = 18) or unrelated (n = 2), or 1 Ag-mismatched related (n = 1), donors. RIC regimens included fludarabine/total body irradiation 200 cGy (n = 5) or 450 cGy (n = 1), fludarabine/melphalan (n = 7), thiotepa/cyclophosphamide (n = 7), and thiotepa/fludarabine (n = 1). At the time of transplantation, all of the patients were at intermediate (n = 13) or high (n = 8) risk, according to the Dupriez classification. Of the patients, 19 had grade III or IV marrow fibrosis. All of the patients achieved full engraftment but one. Posttransplantation chimerism analysis showed more than 95% donor cells in 18 patients, while 2 patients achieved complete donor chimerism after donor leukocyte infusion (DLI). Acute graft-versus-host disease (GVHD) grades II to IV was observed in 7 patients, grades III to IV in 2, and extensive chronic GVHD in 8 of 18 evaluable patients. There were 3 patients who died from acute GVHD, infection, and relapse. There are 18 patients alive 12 to 122 months (median, 31 months) after transplantation, and 17 are in remission (1 after a second transplantation). The use of RIC regimens in allogeneic stem cell transplantation results in prolonged survival in intermediate/high-risk MMM patients.
Hepcidin in iron overload disorders
Authors: Papanikolaou George , Tzilianos Michalis , Christakis John I. , Bogdanos Dionisios , Tsimirika Konstantina , MacFarlane Julie , Goldberg Y. Paul , Sakellaropoulos Nikos , Ganz Tomas , Nemeth Elizabeta 
Published: January 2005

Abstract
Hepcidin is the principal regulator of iron absorption in humans. The peptide inhibits cellular iron efflux by binding to the iron export channel ferroportin and inducing its internalization and degradation. Either hepcidin deficiency or alterations in its target, ferroportin, would be expected to result in dysregulated iron absorption, tissue maldistribution of iron, and iron overload. Indeed, hepcidin deficiency has been reported in hereditary hemochromatosis and attributed to mutations in HFE, transferrin receptor 2, hemojuvelin, and the hepcidin gene itself. We measured urinary hepcidin in patients with other genetic causes of iron overload. Hepcidin was found to be suppressed in patients with thalassemia syndromes and congenital dyserythropoietic anemia type 1 and was undetectable in patients with juvenile hemochromatosis with HAMP mutations. Of interest, urine hepcidin levels were significantly elevated in 2 patients with hemochromatosis type 4. These findings extend the spectrum of iron disorders with hepcidin deficiency and underscore the critical importance of the hepcidin–ferroportin interaction in iron homeostasis.
Local IL-13 gene transfer prior to immune-complex arthritis inhibits chondrocyte death and matrix-metalloproteinase-mediated cartilage matrix degradation despite enhanced joint inflammation
Authors: Nabbe Karin CAM , van Lent Peter LEM , Holthuysen Astrid EM , Sloëtjes Annet W , Koch Alisa E , Radstake Timothy RDJ , van den Berg Wim B 
Published: January 2005

AbstractDuring immune-complex-mediated arthritis (ICA), severe cartilage destruction is mediated by Fcγ receptors (FcγRs) (mainly FcγRI), cytokines (e.g. IL-1), and enzymes (matrix metalloproteinases (MMPs)). IL-13, a T helper 2 (Th2) cytokine abundantly found in synovial fluid of patients with rheumatoid arthritis, has been shown to reduce joint inflammation and bone destruction during experimental arthritis. However, the effect on severe cartilage destruction has not been studied in detail. We have now investigated the role of IL-13 in chondrocyte death and MMP-mediated cartilage damage during ICA. IL-13 was locally overexpressed in knee joints after injection of an adenovirus encoding IL-13 (AxCAhIL-13), 1 day before the onset of arthritis; injection of AxCANI (an empty adenoviral construct) was used as a control. IL-13 significantly increased the amount of inflammatory cells in the synovial lining and the joint cavity, by 30% to 60% at day 3 after the onset of ICA. Despite the enhanced inflammatory response, chondrocyte death was diminished by two-thirds at days 3 and 7. The mRNA level of FcγRI, a receptor shown to be crucial in the induction of chondrocyte death, was significantly down-regulated in synovium. Furthermore, MMP-mediated cartilage damage, measured as neoepitope (VDIPEN) expression using immunolocalization, was halved. In contrast, mRNA levels of MMP-3, -9, -12, and -13 were significantly higher and IL-1 protein, which induces production of latent MMPs, was increased fivefold by IL-13. This study demonstrates that IL-13 overexpression during ICA diminished both chondrocyte death and MMP-mediated VDIPEN expression, even though joint inflammation was enhanced.
Coronary artery bypass surgery and longitudinal evaluation of the autonomic cardiovascular function
Authors: Soares Pedro PauloS , Moreno Adalgiza M , Cravo Sérgio LD , Nóbrega Antonio ClaudioL 
Published: January 2005

Abstract
Introduction
Imbalance in autonomic cardiovascular function increases the risk for sudden death in patients with coronary artery disease (CAD), but the time course of the impact of coronary artery bypass grafting (CABG) on autonomic function has been little studied. Thus, the purpose of the present study was to determine the effects of the CABG on the cardiovascular autonomic function.

Methods
Patients undergoing CABG (n = 13) and two matched control groups (patients with CAD who refused surgical treatment [n = 9], and healthy volunteers [n = 9]) underwent a prospective longitudinal study consisting of autonomic evaluation before and after (3, 6, 15, 30, 60, and 90 days) surgery, including measurement of heart rate variability (HRV), respiratory sinus arrhythmia (RSA), and Valsalva maneuver.

Results
After CABG there was a decrease in, and a later recovery of, (1) the HRV in the time domain and in the frequency domain, (2) RSA, and (3) Valsalva maneuver.

Conclusions
CABG caused an impairment, reversible after 60 days, of cardiovascular autonomic function, with a maximal decrease on about the sixth day after surgery.
Behavioral profiles and symptoms of autism in CHARGE syndrome: Preliminary Canadian epidemiological data
Authors: Smith Isabel M. , Nichols Shana L. , Issekutz Karina , Blake Kim 
Published: February 2005

AbstractIndividuals with CHARGE syndrome were identified through the Canadian Pediatric Surveillance Program (CPSP). From this population‐based cohort (n = 78), we present data on developmental and behavioral characteristics for the first 13 individuals (eight males, five females) for whom assessments are complete. Standardized parent questionnaires on development and behavior were followed by a structured telephone interview, with a specific emphasis on symptoms of autistic spectrum disorder (ASD). Preliminary results confirm that individuals with CHARGE syndrome have relatively low adaptive behavior skills, motor impairments being particularly significant. Most individuals did not present with significant behavior problems; however, evidence of ASD symptoms was judged to be moderate to strong in six of the ten children who were above the age of 4–5 years. Results are discussed with reference to the challenges inherent in the diagnosis of autism in individuals with sensory impairments, and to the implications for understanding the etiology of CHARGE syndrome and of ASD. © 2005 Wiley‐Liss, Inc.
Dual substrate biodegradation of a nonionic surfactant and pentachlorophenol by Sphingomonas chlorophenolica RA2
Authors: Bielefeldt Angela R. , Cort Todd 
Published: February 2005

AbstractThe simultaneous biodegradation of the nonionic surfactant Tween 20 (Tw20) and pentachlorophenol (PCP) by Sphingomonas chlorophenolica sp. Strain RA2 (RA2) was measured. As a sole substrate, Tw20 biodegradation was best described by the Contois kinetic model. During concurrent biodegradation of Tw20 and PCP, the biodegradation rates of Tw20 were not significantly affected by 50 or 100 mg/L PCP, but were significantly inhibited by 500 mg/L PCP. Decreases in cell yield in the presence of PCP suggest that PCP was acting as an uncoupler. Cultures were pre‐grown on PCP or Tw20 before degradation of PCP to evaluate enzyme induction effects, and long lags before PCP biodegradation after growth on Tw20 occurred. Although biokinetic models could accurately describe some of the data sets of RA2 growth and Tw20 and PCP degradation, finding a single set of kinetic parameters that predicted all dual substrate tests was not achieved. The complicating factors to modeling PCP and Tw20 interactions are described and may be more widely applicable to the biodegradation of toxic organic compounds in the presence of a biodegradable surfactant. ©2005 Wiley Periodicals, Inc.
Production of Desmodus rotundus salivary plasminogen activator α1 (DSPAα1) in tobacco is hampered by proteolysis
Authors: Schiermeyer Andreas , Schinkel Helga , Apel Stefanie , Fischer Rainer , Schillberg Stefan 
Published: February 2005

AbstractThe high fibrin specificity of Desmodus rotundus salivary plasminogen activator α1 (DSPAα1 or desmoteplase (INN)) makes it a promising candidate for the treatment of acute ischemic stroke. In the current study we explored the use of transgenic tobacco plants and BY‐2 suspension cells as alternative production platforms for this drug. Four different N‐terminal signal peptides, from plants and animals, were used to translocate the recombinant DSPAα1 protein to the endomembrane system. Intact recombinant DSPAα1 was produced in transgenic plants and BY‐2 cells, although a certain degree of degradation was observed in immunoblotted extracts. The choice of signal peptide had no major influence on the degradation pattern or recombinant protein accumulation, which reached a maximum level of 38 μg/g leaf material. N‐terminal sequencing of purified, His6‐tagged DSPAα1 revealed only minor changes in the position of signal peptide cleavage compared to the same protein expressed in Chinese hamster ovary cells. However, correctly processed recombinant DSPAα1 was also detected. The enzymatic activity of the recombinant protein was confirmed using an in vitro assay with unpurified and purified samples, demonstrating that plants are suitable for the production of functional DSPAα1. In contrast to whole plant cell extracts, no recombinant DSPAα1 was detected in the culture supernatant of transgenic BY‐2 cells. Further analysis showed that recombinant DSPAα1 is subject to proteolysis and that endogenous secreted BY‐2 proteases are responsible for DSPAα1 degradation in the culture medium. The addition of a highly concentrated protease inhibitor mixture or 5 mM EDTA reduced DSPAα1 proteolysis, improving the accumulation of intact product in the culture medium. Strategies to improve the plant cell suspension system for the production of secreted recombinant proteins are discussed. © 2005 Wiley Periodicals, Inc.
Unifying concept of DNA repair: The polymerase scanning hypothesis
Authors: Heddle John A. , Bielas Jason H. 
Published: January 2005

AbstractAccording to a series of experiments on untransformed mouse embryonic fibroblasts, quiescent mouse cells lack global genomic repair (GGR) of premutagenic DNA damage. The gene used to assess mutation and premutagenic DNA damage was the lacI transgene incorporated permanently in the DNA in a λ shuttle vector. The transgene lacks mammalian transcription signals and thus is unexpressed in the cells. Although the cells conducted transcription‐coupled repair (TCR) of UV damage, the transgene was not repaired over a 4‐day interval. These cells are not terminally differentiated and can readily be induced to resume cellular division. In this article, we discuss the interpretation of these results and suggest a new hypothesis for DNA scanning, the mechanism by which cells discover DNA damage and initiate DNA repair. Our hypothesis, which we call the polymerase scanning hypothesis, is that GGR is initiated in very much the same way as TCR, by a polymerase complex encountering the damage. We call the two together polymersase‐coupled repair (PC repair). In the case of GGR, it would be the DNA replication complex during the S‐phase. This is, we suggest, the dominant mechanism of repair of DNA at low doses for untranscribed genes. Evidence contrary to this hypothesis exists, which we discuss, but it should be noted that existing hypotheses about DNA scanning and DNA repair cannot account for the results that we have obtained. Environ. Mol. Mutagen., 2005. © 2005 Wiley‐Liss, Inc.
A high resolution scheme for flows in open channels with arbitrary cross‐section
Authors: Aldrighetti E. , Zanolli P. 
Published: February 2005

AbstractThe aim of this paper is to present a numerical scheme to simulate unsteady, one‐dimensional flows in open channels with arbitrary cross‐section. This scheme is fully conservative of volume and momentum and preserves the non‐negativity of the water depth. The finite difference method derived is semi‐implicit in time and based on a space staggered grid. A high‐resolution technique, the flux limiter method, is implemented to control the accuracy of the proposed scheme. Our purpose is to achieve the precision and the stability of the method with respect to the regularity of the data. A few computational examples on classical test cases are given to illustrate the properties of the present method in terms of stability, accuracy and efficiency. Copyright © 2005 John Wiley & Sons, Ltd.
Energy balance, insulin‐related genes and risk of colon and rectal cancer
Authors: Slattery Martha L. , Murtaugh Maureen , Caan Bette , Ma Khe Ni , Neuhausen Susan , Samowitz Wade 
Published: February 2005

AbstractEnergy balance, or the ability to maintain body weight by balancing energy intake with energy expenditure, appears to be important in the etiology of colon cancer. One possible mechanism whereby energy balance may be associated with colorectal cancer is through its association with insulin. In our study, we evaluate the interaction between polymorphisms in 4 genes thought to be involved in insulin‐related functions and components of energy balance with risk of colorectal cancer. Data from 2 population‐based case‐control studies of colon and rectal cancer conducted in Utah and Northern California were used to evaluate associations between body mass index (BMI), physical activity, energy intake and sucrose‐to‐fiber ratio and a CA repeat polymorphism of the IGF1 gene, the A/C polymorphism at nucleotide ‐202 of the IGFBP3, the G972R polymorphism of the IRS1 gene and the G1057D polymorphism of the IRS2 gene. A total of 1,346 incident colon cancer cases and 1,544 population‐based controls and 952 incident rectal cancer cases and 1,205 controls were available for analysis. Inconsistent associations were identified between BMI, physical activity, energy intake and insulin‐related genes. The 192/192 IGF1 genotype was associated with significant reduction in colon cancer risk among those with high physical activity (odds ratio [OR] 0.57; 95% confidence interval [CI] 0.39–0.83; p interaction 0.01). Although there was no significant pattern of interaction between either BMI or energy intake and polymorphisms assessed, specific sources of energy did appear to be more related to colon cancer risk in the presence of specific IRS2 and IGF1 genotypes. A high sucrose‐to‐fiber ratio increased risk of colon cancer in men who had the IRS2 DD genotype and among men who did not have the 192/192 IGF1 genotype. In summary, these data support the importance of components of energy balance in risk of colorectal cancer. Obesity, physical activity and energy intake appear to alter risk of colorectal cancer; however, the risk appears to be minimally influenced by genetic variants evaluated. © 2005 Wiley‐Liss, Inc.
Resveratrol‐induced apoptosis in MCF‐7 human breast cancer cells involves a caspase‐independent mechanism with downregulation of Bcl‐2 and NF‐κB
Authors: Pozo‐Guisado Eulalia , Merino Jaime M. , Mulero‐Navarro Sonia , Lorenzo‐Benayas M. Jesús , Centeno Francisco , Alvarez‐Barrientos Alberto , Salguero Pedro M. Fernandez 
Published: February 2005

AbstractResveratrol (RES), a chemopreventive molecule, inhibits the proliferation of tumor cells of different etiologies. We previously showed that RES alters the cell cycle and induces apoptosis in MCF‐7 breast tumor cells by interfering with the estrogen receptor (ERaα)–dependent phosphoinositide 3‐kinase (PI3K) pathway. Here, we analyzed signaling downstream of PI3K, to understand the mechanisms of RES‐induced apoptosis. Apoptotic death by RES in MCF‐7 was mediated by Bcl‐2 downregulation since overexpression of this protein abolished apoptosis. Decreased Bcl‐2 levels were not related to cytochrome c release, activation of caspases 3/8 or poly(ADP‐ribose) polymerase proteolysis. However, RES decreased mitochondrial membrane potential and increased reactive oxygen species and nitric oxide production. NF‐κB, a regulator of Bcl‐2 expression, and calpain protease activity, a regulator of NF‐κB, were both inhibited by RES. The patterns for NF‐κB and calpain activities followed that of PI3K and were inhibited by LY294002. NF‐κB inhibition coincided with diminished MMP‐9 activity and cell migration. These data suggest that RES‐induced apoptosis in MCF‐7 could involve an oxidative, caspase‐independent mechanism, whereby inhibition of PI3K signaling converges to Bcl‐2 through NF‐κB and calpain protease activity. Therefore, Bcl‐2 and NF‐κB could be considered potential targets for the chemopreventive activity of RES in estrogen‐responsive tumor cells. © 2005 Wiley‐Liss, Inc.
Methylenetetrahydrofolate reductase polymorphisms and risk of squamous cell carcinoma of the head and neck: A case‐control analysis
Authors: Neumann Ana S. , Lyons Heather J. , Shen Hongbing , Liu Zhensheng , Shi Qiuling , Sturgis Erich M. , Shete Sanjay , Spitz Margaret R. , El‐Naggar Adel , Hong Waun Ki , Wei Qingyi 
Published: February 2005

AbstractFolate deficiency is implicated in cancer risk that may be modulated by a genetic variation in the methylenetetrahydrofolate reductase (MTHFR) gene in folate metabolism. We hypothesized that genetic variants in MTHFR are associated with risk of squamous cell carcinoma of the head and neck (SCCHN). We genotyped 3 MTHFR polymorphisms (C677T, A1298C and G1793A) and estimated their haplotypes in a hospital‐based case‐control study of 537 SCCHN cases and 545 cancer‐free controls. The controls were frequency‐matched to the cases by age (± 5 years), sex, ethnicity and smoking status. We found that the MTHFR 1298AC/CC genotypes were associated with an approximately 35% reduction in risk of SCCHN (adjusted odds ratio = 0.65; 95% CI = 0.51–0.82) compared to the AA genotype. The MTHFR 677CT and 1793GA/AA genotypes were associated with nonsignificant increased risk of SCCHN compared to the 677CC and 1793GG genotypes, respectively. We estimated that there were 8 haplotypes and 16 haplotype genotypes based on these 3 variants. When we used the haplotypes and assumed that the 677T, 1298A and 1793A alleles were risk alleles, the adjusted odds ratios increased as the number of risk alleles increased: 1.00 for 0–1 variant, 1.85 (1.3–2.5) for any 2 risk alleles and 1.93 (1.4–2.7) for any 3 risk alleles. These results suggest that all 3 MTHFR polymorphisms may play a role in the susceptibility to SCCHN among non‐Hispanic whites. Future studies should incorporate detailed data on alcohol consumption, dietary folate intake and related serologic measurements. © 2005 Wiley‐Liss, Inc.