bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relating the sediment phase speciation of arsenic, cadmium, and chromium with their bioavailability for the deposit-feeding polychaete Nereis succinea
Authors: Baumann Zofia , Fisher Nicholas S 
Published: December 2010

Abstract
We studied the influence of sediment geochemistry on bioavailability of As, Cd, and Cr in deposit-feeding polychaetes. Metal phase speciation in sediments was determined with a sequential extraction scheme, and assimilation efficiencies (AEs) of ingested metals were determined by pulse-chase feeding experiments using γ-emitting isotopes. Worms were fed sediments collected from geochemically diverse estuaries that were labeled by sorbing dissolved radiotracers or mixing with radiolabeled algae. Uptake of sediment-bound metals was compared with that from labeled algae or goethite. Metal AEs showed a positive relationship with the exchangeable and carbonate sedimentary fractions, whereas metals in iron and manganese oxides and acid-volatile sulfides, or in pyrite and other refractory material, were inversely correlated with AEs. Arsenic was most bioavailable from algae (72%), less from sediments mixed with algae (24–70%) and least from sediments labeled directly (1–12%). Arsenic AEs in sediments labeled directly showed a positive correlation with sedimentary Mn and Al and negative correlation with Fe. Cadmium AEs were positively correlated with salinity and negatively correlated with sedimentary organic C. The AEs of Cr from sediments or algae were less than 5%, but they were 34% from pure goethite. By quantifying the relationship of metal speciation in sediments with their bioavailability for deposit-feeding polychaetes, the present study provides new insight into understanding metal bioaccumulation in benthic invertebrates. Environ. Toxicol. Chem. 2011; 30:747–756. © 2011 SETAC
ℋ︁‐LU factorization in preconditioners for augmented Lagrangian and grad‐div stabilized saddle point systems
Authors: Börm Steffen , Le Borne Sabine 
Published: December 2010

AbstractThe (mixed finite element) discretization of the linearized Navier–Stokes equations leads to a linear system of equations of saddle point type. The iterative solution of this linear system requires the construction of suitable preconditioners, especially in the case of high Reynolds numbers. In the past, a stabilizing approach has been suggested which does not change the exact solution but influences the accuracy of the discrete solution as well as the effectiveness of iterative solvers. This stabilization technique can be performed on the continuous side before the discretization, where it is known as ‘grad‐div’ (GD) stabilization, as well as on the discrete side where it is known as an ‘augmented Lagrangian’ (AL) technique (and does not change the discrete solution). In this paper, we study the applicability of ℋ︁‐LU factorizations to solve the arising subproblems in the different variants of stabilized saddle point systems. We consider both the saddle point systems that arise from the stabilization in the continuous as well as on the discrete setting. Recently, a modified AL preconditioner has been proposed for the system resulting from the discrete stabilization. We provide a straightforward generalization of this approach to the GD stabilization. We conclude the paper with numerical tests for a variety of problems to illustrate the behavior of the considered preconditioners as well as the suitability of ℋ︁‐LU factorization in the preconditioners. Copyright © 2010 John Wiley & Sons, Ltd.
A linearity‐preserving cell‐centered scheme for the heterogeneous and anisotropic diffusion equations on general meshes
Authors: Gao Zhiming , Wu Jiming 
Published: December 2010

AbstractIn this paper a finite volume scheme for the heterogeneous and anisotropic diffusion equations is proposed on general, possibly nonconforming meshes. This scheme has both cell‐centered unknowns and vertex unknowns. The vertex unknowns are treated as intermediate ones and are expressed as a linear weighted combination of the surrounding cell‐centered unknowns, which reduces the scheme to a completely cell‐centered one. We propose two types of new explicit weights which allow arbitrary diffusion tensors, and are neither discontinuity dependent nor mesh topology dependent. Both the derivation of the scheme and that of new weights satisfy the linearity‐preserving criterion which requires that a discretization scheme should be exact on linear solutions. The resulting new scheme is called as the linearity‐preserving cell‐centered scheme and the numerical results show that it maintain optimal convergence rates for the solution and flux on general polygonal distorted meshes in case that the diffusion tensor is taken to be anisotropic, at times heterogeneous, and/or discontinuous. Copyright © 2010 John Wiley & Sons, Ltd.
An improved progressive preconditioning method for steady non‐cavitating and sheet‐cavitating flows
Authors: Esfahanian Vahid , Akbarzadeh Pooria , Hejranfar Kazem 
Published: December 2010

AbstractAn improved progressive preconditioning method for analyzing steady inviscid and laminar flows around fully wetted and sheet‐cavitating hydrofoils is presented. The preconditioning matrix is adapted automatically from the pressure and/or velocity flow‐field by a power‐law relation. The cavitating calculations are based on a single fluid approach. In this approach, the liquid/vapour mixture is treated as a homogeneous fluid whose density is controlled by a barotropic state law. This physical model is integrated with a numerical resolution derived from the cell‐centered Jameson's finite volume algorithm. The stabilization is achieved via the second‐and fourth‐order artificial dissipation scheme. Explicit four‐step Runge–Kutta time integration is applied to achieve the steady‐state condition. Results presented in the paper focus on the pressure distribution on hydrofoils wall, velocity profiles, lift and drag forces, length of sheet cavitation, and effect of the power‐law preconditioning method on convergence speed. The results show satisfactory agreement with numerical and experimental works of others. The scheme has a progressive effect on the convergence speed. The results indicate that using the power‐law preconditioner improves the convergence rate, significantly. Copyright © 2010 John Wiley & Sons, Ltd.
Mental and psychological conditions, medical comorbidity and functional limitation: differential associations in older adults with cognitive impairment, depressive symptoms and co‐existence of both
Authors: Millán‐Calenti José C. , Maseda Ana , Rochette Sophie , Vázquez Gustavo A. , Sánchez Alba , Lorenzo Trinidad 
Published: December 2010

AbstractObjectiveCognitive impairment and depressive symptoms are common among the geriatric population but the co‐occurrence of both is rarely studied. The purpose of this study was to identify and compare the factors associated with three groups of elderly people: those assessed with cognitive impairment alone (COG), depressive symptoms alone (DEP) or co‐existence of both (COG‐DEP).MethodsThe cross‐sectional study included 600 community‐dwellers ages 65 and older. All participants underwent a comprehensive evaluation. Global cognition was measured by the Mini‐Mental State Examination (MMSE) and depressive symptoms were defined by the Geriatric Depression Scale (GDS). Specific chronic illnesses relevant to the Charlson comorbidity index (CCI) were self‐reported. Functional status was evaluated by the Katz' basic (ADL) and Lawton's instrumental (IADL) activities of daily living scales.ResultsCOG‐DEP was explained by IADL dependence (OR: 11.9, 95% CI: 4.59–30.78), ADL dependence (OR: 11.5, 95% CI: 5.59–23.69), cerebrovascular disease (OR: 3.6, 95% CI: 1.48–8.68), congestive heart failure (OR: 3.4, 95% CI: 1.77–6.59) and diabetes (OR: 2.6, 95% CI: 1.30–5.18), but it was best predicted by functional limitations in the adjusted model. Being functionally dependent and medically ill with shorter life expectancy was shown to significantly increase the odds of being DEP. Functional limitation in IADL was without distinction associated to COG, DEP and COG‐DEP.ConclusionThe present results on COG, DEP and COG‐DEP show the particular relevance of certain medical comorbidities and functional limitations to those three distinct groups of elderly people. Copyright © 2010 John Wiley & Sons, Ltd.
Limitation of physical performance in a muscle fatiguing handgrip exercise is mediated by thalamo‐insular activity
Authors: Hilty Lea , Jäncke Lutz , Luechinger Roger , Boutellier Urs , Lutz Kai 
Published: December 2010

AbstractIn this study, we investigated central/supraspinal processes mediating cessation of a muscle fatiguing exercise. Fifteen male subjects performed 39 intermittent, isometric handgrip contractions (13 s on, 5–6 s off) with the dominant right hand while brain activation was assessed by means of functional magnetic resonance imaging (fMRI). An adaptive, partly stochastic protocol was designed such that in approximately 50% of the contraction trials the required force could not be held until the end of the trial (task failure trial). Trials performed in compliance with the force requirements (succeeded trial) were compared with task failure trials concerning neural activity during a small time window before task failure occurred. The data revealed significantly increased activation contralaterally in both the mid/anterior insular cortex and the thalamus during the investigated time window in the case of subsequent task failure. In accordance with other studies investigating sensations that alert the organism to urgent homeostatic imbalance such as air hunger, hunger for food, and pain, we assume that an increased thalamo‐insular activation in the context of a fatigue‐induced handgrip exercise could reflect increased homeostatic disturbance in the exercising muscle and may be of essential importance by mediating task failure to maintain the integrity of the organism. Hum Brain Mapp, 2011. © 2010 Wiley Periodicals, Inc.
3,3′‐diindolylmethane enhances taxotere‐induced growth inhibition of breast cancer cells through downregulation of FoxM1
Authors: Ahmad Aamir , Ali Shadan , Wang Zhiwei , Ali Ashhar S. , Sethi Seema , Sakr Wael A. , Raz Avraham , Rahman KM Wahidur 
Published: December 2010

AbstractEmerging evidence suggests that the transcription factor Forkhead Box M1 (FoxM1) is associated with aggressive human carcinomas, including breast cancer. Because elevated expression of FoxM1 has been observed in human breast cancers, FoxM1 has attracted much attention in recent years as a potential target for the prevention and/or therapeutic intervention in breast cancer. However, no information is currently available regarding how downregulation of FoxM1 could be achieved for breast cancer prevention and therapy. Here, we report for the first time that 3,3′‐diindolylmethane (DIM), a nontoxic dietary chemopreventive agent could effectively downregulate FoxM1 in various breast cancer cell lines. Using gene transfection, real‐time reverse transcription‐PCR, Western blotting, invasion and 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assays, we found that DIM could enhance Taxotere‐induced growth inhibition of breast cancer cells, and decreased invasive capacity of breast cancer cells was observed after either treatment alone or the combination. These effects were associated with downregulation of FoxM1. We also found that knock down of FoxM1 expression by small interfering RNA (siRNA) transfection increased DIM‐induced cell growth inhibition, whereas over‐expression of FoxM1 by cDNA transfection attenuated DIM‐induced cell growth inhibition, suggesting the mechanistic role of FoxM1. Most importantly, the combination treatment significantly inhibited tumor growth in severe combined immunodeficiency (SCID) mice, and the results were correlated with the downregulation of FoxM1 in tumor remnants. We conclude that inactivation of FoxM1 and its target genes by DIM could enhance the therapeutic efficacy of Taxotere in breast cancer, which could be a useful strategy for the prevention and/or treatment of breast cancer.
Checkpoint kinase inhibitor synergizes with DNA‐damaging agents in G1 checkpoint‐defective neuroblastoma
Authors: Xu Hong , Cheung Irene Y. , Wei Xiao X. , Tran Hoa , Gao Xiaoni , Cheung Nai‐Kong V. 
Published: December 2010

AbstractCheckpoint kinase inhibitors can enhance the cancer killing action of DNA‐damaging chemotherapeutic agents by disrupting the S/G2 cell cycle checkpoints. The in vitro and in vivo effects of the Chk1/2 inhibitor AZD7762 when combined with these agents were examined using neuroblastoma cell lines with known p53/MDM2/p14ARF genomic status. Four of four p53 mutant lines and three of five MDM2/p14ARF abnormal lines were defective in G1 checkpoint, correlating with failure to induce endogenous p21 after treatment with DNA‐damaging agents. In cytotoxicity assays, these G1 checkpoint‐defective lines were more resistant to DNA‐damaging agents when compared to G1 checkpoint intact lines, yet becoming more sensitive when AZD7762 was added. Moreover, AZD7762 abrogated DNA damage‐induced S/G2 checkpoint arrest both in vitro and in vivo. In xenograft models, a significant delay in tumor growth accompanied by histological evidence of increased apoptosis was observed, when AZD7762 was added to the DNA‐damaging drug gemcitabine. These results suggest a therapeutic potential of combination therapy using checkpoint kinase inhibitor and chemotherapy to reverse or prevent drug resistance in treating neuroblastomas with defective G1 checkpoints.
Phase II study of sunitinib malate, a multitargeted tyrosine kinase inhibitor in patients with relapsed or refractory soft tissue sarcomas. Focus on three prevalent histologies: Leiomyosarcoma, liposarcoma and malignant fibrous histiocytoma
Authors: Mahmood S. Tariq , Agresta Samuel , Vigil Carlos E. , Zhao Xiuhua , Han Gang , D'Amato Gina , Calitri Ciara E. , Dean Michelle , Garrett Christopher , Schell Michael J. , Antonia Scott , Chiappori Alberto 
Published: December 2010

AbstractSoft tissue sarcomas (STS) represent a diverse group of histologic subtypes with targetable molecular alterations, often treated as a single disease. Sunitinib malate is a multitargeted receptor tyrosine kinase inhibitor active in other solid tumors carrying similar alterations (i.e., imatinib mesylate‐refractory gastrointestinal stromal tumors). This single‐institution phase II study investigated the safety and efficacy of sunitinib malate in three common STS subtypes. Patients with documented unresectable or metastatic STS (liposarcoma, leiomyosarcoma and malignant fibrous histiocytoma [MFH]), measurable disease, and 3 or less prior lines of therapy were eligible. Treatment consisted of sunitinib malate, 50 mg daily, for 4 weeks every 6 weeks. Forty‐eight patients were enrolled, and 35% were heavily pretreated (≥2 prior lines of chemotherapy). The safety profile resembled previously known sunitinib malate toxicities. Median progression‐free and overall survivals for liposarcoma, leiomyosarcoma, and MFH were 3.9 and 18.6, 4.2 and 10.1 and 2.5 and 13.6 months, respectively. The 3‐month progression‐free rates in the untreated and pretreated (chemotherapy) patients with liposarcoma, leiomyosarcoma and MFH were 75% and 69.2%, 60%, and 62.5% and 25% and 44.4%, respectively. With the caveats that a minority of patients with potentially indolent or low‐grade disease could have been included and the small numbers, a 3‐month progression‐free rate of >40% suggests activity for sunitinib malate at least in liposarcomas and leiomyosarcomas. Thus, we believe that further investigation in these susceptible STS subtypes is warranted.
High‐frequency microwave ablation method for enhanced cancer treatment with minimized collateral damage
Authors: Yoon Jeonghoon , Cho Jeiwon , Kim Namgon , Kim Dae‐Duk , Lee Eunsook , Cheon Changyul , Kwon Youngwoo 
Published: December 2010

AbstractTo overcome the limits of conventional microwave ablation, a new frequency spectrum above 6 GHz has been explored for low‐power and low collateral damage ablation procedure. A planar coaxial probe‐based applicator, suitable for easy insertion into the human body, was developed for our study to cover a wideband frequency up to 30 GHz. Thermal ablations with small input power (1–3 W) at various microwave frequencies were performed on nude mice xenografted with human breast cancer. Comparative study of ablation efficiencies revealed that 18‐GHz microwave results in the largest difference in the temperature rise between cancer and normal tissues as well as the highest ablation efficiency, reaching 20 times that of 2 GHz. Thermal profile study on the composite region of cancer and fat also showed significantly reduced collateral damage using 18 GHz. Application of low‐power (1 W) 18‐GHz microwave on the nude mice xenografted with human breast cancer cells resulted in recurrence‐free treatment. The proposed microwave ablation method can be a very effective process to treat small‐sized tumor with minimized invasiveness and collateral damages.
Vascular effects dominate solid tumor response to treatment with combretastatin A‐4‐phosphate
Authors: Jane Lunt Sarah , Akerman Simon , Hill Sally A. , Fisher Matthew , Wright Victoria J. , Reyes‐Aldasoro Constantino C. , Tozer Gillian M. , Kanthou Chryso 
Published: December 2010

AbstractVascular‐targeted therapeutics are increasingly used in the clinic. However, less is known about the direct response of tumor cells to these agents. We have developed a combretastatin‐A‐4‐phosphate (CA4P) resistant variant of SW1222 human colorectal carcinoma cells to examine the relative importance of vascular versus tumor cell targeting in the ultimate treatment response. SW1222Res cells were generated through exposure of wild‐type cells (SW1222WT) to increasing CA4P concentrations in vitro. Increased resistance was confirmed through analyses of cell viability, apoptosis and multidrug‐resistance (MDR) protein expression. In vivo, comparative studies examined tumor cell necrosis, apoptosis, vessel morphology and functional vascular end‐points following treatment with CA4P (single 100 mg/kg dose). Tumor response to repeated CA4P dosing (50 mg/kg/day, 5 days/week for 2 weeks) was examined through growth measurement, and ultimate tumor cell survival was studied by ex vivo clonogenic assay. In vitro, SW1222Res cells showed reduced CA4P sensitivity, enhanced MDR protein expression and a reduced apoptotic index. In vivo, CA4P induced significantly lower apoptotic cell death in SW1222Res versus SW1222WT tumors indicating maintenance of resistance characteristics. However, CA4P‐induced tumor necrosis was equivalent in both lines. Similarly, rapid CA4P‐mediated vessel disruption and blood flow shut‐down were observed in both lines. Cell surviving fraction was comparable in the two tumor types following single dose CA4P and SW1222Res tumors were at least as sensitive as SW1222WT tumors to repeated dosing. Despite tumor cell resistance to CA4P, SW1222Res response in vivo was not impaired, strongly supporting the view that vascular damage dominates the therapeutic response to this agent.
Biology of Krüppel‐like factor 6 transcriptional regulator in cell life and death
Authors: Andreoli Verónica , Gehrau Ricardo C. , Bocco Jose Luis 
Published: December 2010

AbstractAn essential role for the Krüppel‐like transcription factor family has been determined in the regulation of remarkable processes including cell proliferation, differentiation, signal transduction, oncogenesis, and cell death. A member of this group, Krüppel‐like factor 6 (KLF6), identified on the basis of its ability to regulate a group of genes belonging to the carcinoembryonic antigen gene family, has been involved in human carcinogenesis. Early studies proposed a tumor suppressor function for KLF6 because of its ability to reduce cell proliferation through several biochemical mechanisms including regulation of cell cycle components, oncogene products, and apoptosis. Mutations within the klf6 gene, decreased expression and/or loss‐of‐heterozygosity were associated with the development of different human malignancies, and, hence, further supporting the tumor suppressor function of KLF6. This view has been challenged by other studies in distinct types of human cancers describing infrequent genetic alterations of klf6 gene or even enhanced expression in some tumors. The scenario about KLF6 function became still more complex as the description of oncogenic KLF6 splice variant 1 (SV1) with dominant negative activity against the wild type KLF6 (wtKLF6) protein. Additionally, increased evidence is suggesting that KLF6 is a bonafide target of several signaling cascades, which ultimate regulatory effect on this protein could drive decisions of cell life and death, facing the dilemma about how wtKLF6 could be involved in both processes. These apparently conflicting situations, emerged by apparently opposite effects mediated by wtKLF6, may be related, at least in part, to the biological cross‐talk with the c‐Jun oncoprotein. Depending on the stimulus received by the cell, wtKLF6 interaction with c‐Jun determines different cell outcomes such as proliferation control or apoptosis. Thus, KLF6 responsiveness represents a kind of cell warning signal on receiving different stimuli, including oncogenic activation and microbial infections, orchestrating the implementation of proliferation and apoptotic programs. © 2010 IUBMB IUBMB Life, 62(12): 896–905, 2010
MicroRNAs and other small silencing RNAs in cancer
Authors: Rovira Carlos , Güida Maria C. , Cayota Alfonso 
Published: December 2010

AbstractSmall noncoding RNAs are key controllers of cellular function, and their deregulation can lead to cancer development and metastatic evolution. This review summarizes the most important examples of small RNAs involved in human cancer and discusses their clinical use as biomarkers and drug targets for diagnosis, prognosis, and treatment of cancer. We also describe the possible mechanisms underlying small RNA‐mediated transformation and outline the future describing new small RNA families with great potential in cancer biology. © 2010 IUBMB IUBMB Life, 62(12): 859–968
Protective effects of 1,3‐diaryl‐2‐propen‐1‐one derivatives against H2O2‐induced damage in SK‐N‐MC cells
Authors: Bayati Samaneh , Yazdanparast Razieh , Majd Soraya Sajadi , Oh Seikwan 
Published: December 2010

AbstractAlzheimer's disease (AD) is an age‐related neurodegenerative disorder of the central nervous system resulting in memory loss and dementia. Some of the associated pathogenic changes are amyloid peptide aggregation, excitotoxicity, oxidative stress and inflammation. Oxidative stress plays an indispensable role in the pathophysiology of AD. Therefore, antioxidant therapies appear to be promising approaches in dealing with AD patients. In that line, we evaluated the free radical scavenging capabilities of 13 different chalcones (1,3‐diphenyl‐2‐propen‐1‐one) derivatives against the free‐radical damaging effects of hydrogen peroxide (H2O2) on the SK‐N‐MC neuroblastoma cell line. Pretreatment of the cells for 3 h with 20 µ m of each of these derivatives (compounds 8–20) followed by exposure to 300 µ m H2O2 for 24 h indicated that all compounds, except compound 20, were capable of restoring the viabilities of cells relative to the control (H2O2–treated) cells. The destructive effect of H2O2 on the adhesive behavior of the cells was almost totally restored by each of the derivatives. In addition, each of the derivatives except compounds 20 and 14 significantly reduced the extent of lipofuscin formation among the cells time‐dependently. Despite these activities, some of the derivatives, such as compounds 12 and 19, did not reduce the H2O2‐induced intracellular ROS (reactive oxygen species) levels, meaning that these two derivatives act through a different mechanism other than free‐radical scavenging activity. On the other hand, for those derivatives acting as anti‐oxidants, structure–activity evaluation clearly revealed that the hydroxyl group of vanillin ring is required for their free‐radical scavenging activities. Copyright © 2010 John Wiley & Sons, Ltd.