bluuebunny/crossref_metadata_2025_split huggingface dataset:
Thermo‐Economic Modelling and Optimisation of Fuel Cell Systems
Authors: Marechal F. , Palazzi F. , Godat J. , Favrat D. 
Published: February 2005

AbstractThis paper describes and illustrates the application of a methodology for thermo‐economic design and optimisation of fuel cell systems. This methodology combines the use of process simulation and process integration techniques to compute thermo‐economic performances of fuel cell systems that will be used in a multi‐objective optimisation framework. The method allows the generation of integrated fuel cell system configurations and their corresponding optimal operating conditions. It should be used as a preliminary design methodology, allowing the identification of promising system configurations, which would be further analysed. The methodology and the thermo‐economic models are described and demonstrated for the design of PEMFC hybrid systems, combining fuel cell and gas turbine technologies.
Model‐Based Analysis for the Control of Molten Carbonate Fuel Cell Systems
Authors: Lukas M. D. , Lee K. Y. 
Published: February 2005

AbstractA first principles‐based non‐linear dynamic model for a Molten Carbonate Fuel Cell system is presented, analysed, and further developed for model‐based control applications. Transient validation results, using a laboratory‐scale test stack, are provided in support of the cell stack model. Physical arguments and time scale separation are used to derive simpler, reduced‐order, model structures useful for control analysis and design. Reduced‐order models are derived for the cell stack alone as well as for the cell stack integrated with Balance‐of‐Plant. The results are compared with the full‐order models and used in control system design.
Air Supply System of a PEMFC Stack Dynamic Model
Authors: Rodatz P. , Onder C. , Guzzella L. 
Published: February 2005

AbstractA typical air supply system for a Proton Exchange Membrane Fuel Cell (PEMFC) stack consists of a compressor, a humidification device, the fuel cell stack, and a pressure control valve. In this paper, a dynamic model for such an air supply system is developed. The model considers the filling/emptying dynamics of the manifolds (which represent the volumes between compressor, fuel cell stack, and valve), the dynamics of the compressor/E‐motor unit, and the inertial effects in the inlet manifold. Validation of the model is performed with measurements obtained from a 6 kWe 100‐cell stack test bench, which was designed and constructed with the objective of reproducing typical operating conditions for automotive applications. On the basis of this model, a model‐based controller can be designed to reduce the system response time to load changes. Furthermore, in this paper an empirical model is proposed, which describes the cell voltage variation across the stack for different operating conditions.
Modelling of Pressurised Hybrid Systems Based on Integrated Planar Solid Oxide Fuel Cell (IP‐SOFC) Technology
Authors: Magistri L. , Traverso A. , Cerutti F. , Bozzolo M. , Costamagna P. , Massardo A. F. 
Published: February 2005

AbstractThis work describes different models, developed by the Thermochemical Power Group at the University of Genoa (Italy), for the simulation of solid oxide fuel cell and gas turbine hybrid systems. The paper focuses on both “cores” of the system: the fuel cell stack on the one hand and the turbomachinery and the auxiliaries on the other hand. Therefore, in the first part of the paper the models developed for the analysis of the Rolls‐Royce Integrated Planar SOFC cells are presented; the results are compared to experimental data, and carefully analysed and discussed. In the second part of the paper, design and off design models of IP‐SOFC pressurised hybrid systems in the range 250 kW–20 MW are presented; the hybrid performance results are presented and discussed, also taking ambient condition effects and a possible control strategy into account. Finally, using an in‐house general purpose transient system analysis code (TRANSEO code), where chemical composition, heat transfer, and fluid dynamic influences vs. time are considered in detail, a preliminary time dependent investigation of a pressurised hybrid system behaviour is presented.
Suppression of accelerated tumor growth in surgical wounds by celecoxib and indomethacin
Authors: Roh Jong‐Lyel , Sung Myung‐Whun , Kim Kwang Hyun 
Published: February 2005

AbstractBackground.Tumor growth is accelerated in surgical wounds. However, few experiments seeking to prevent such accelerated tumor growth have been performed.Methods.We created surgical wounds in three syngeneic mice for the implantation of three murine cancer cell lines, SCC VII, CT‐26, and B16F10. The tumor growth in the wound group was compared with that in non‐wound–control mice. Celecoxib or indomethacin was administered to the mice that had tumor implanted into the surgical wound to observe the tumor‐suppressive effect.Results.The surgical wounds promoted tumor growth with different degrees, depending on the type of tumor. Such an accelerated tumor growth did not seem to be affected by cyclooxygenase‐2 expression of tumors per se, but its mechanism needs to be explained by further studies. Celecoxib and indomethacin had a significant inhibitory effect on the tumor growth in the surgical wound. This suppressive effect is most obvious when celecoxib is administered daily from 1 day before surgical wounding and tumor implantation.Conclusion.Our results can justify that the preventive use of celecoxib in patients in whom local recurrence by tumor contamination is predicted. © 2005 Wiley Periodicals, Inc. Head Neck 27: XXX–XXX, 2005
Altered extent, pattern and characteristics of microvascular density are indicators of neoplastic progression in the endometrium
Authors: Näyhä Veera , Viitanen Tea , Stenbäck Frej 
Published: February 2005

AbstractThe occurrence, structure and extent of microvascular density were examined in normal endometria, hyperplasia of different types and adenocarcinomas of different degrees of differentiation to determine their biologic and clinical significance in tumor development and progression. Computer‐assisted quantitative image analysis was carried out on 12,500 vessels in regard to vessel number, vessel volume, size, shape and extent of vessel antibody staining, with sensitivity and reproducibility exceeding 99%. The results showed the extent, pattern and characteristics of microvascular density to be intimately associated with extent of tumor development and degree of differentiation of the tumor. Vessel number increased with superficial location in normal endometrium, with increased degree of hyperplasia and atypia and with increased degree of dedifferentiation of adenocarcinoma. Increased vessel shape alterations were characteristic of atypical complex hyperplasia when compared to other types of hyperplasia. Vessel number, size and shape were similar in proliferative endometrium and simplex type hyperplasia, and microvascular density in atypical complex hyperplasia was similar to that in well‐differentiated adenocarcinoma. The results indicated that vessel shape alterations occur during progression of hyperplasia and vessel size increase occurs in complex‐type hyperplasia and in moderately differentiated adenocarcinomas. We conclude that microvascular density is associated with endometrial location and with specific patterns of alteration in different stages of endometrial disease. The results suggest potential clinical applications of vessel analysis for determination of clinical behavior of endometrial preneoplastic and neoplastic alterations. © 2005 Wiley‐Liss, Inc.
Fecal and urinary excretion of aflatoxin B1 metabolites (AFQ1, AFM1 and AFB‐N7‐guanine) in young Chinese males
Authors: Mykkänen Hannu , Zhu Huilian , Salminen Eeva , Juvonen Risto Olavi , Ling Wenhua , Ma Jing , Polychronaki Nektaria , Kemiläinen Heidi , Mykkänen Otto , Salminen Seppo , El‐Nezami Hani 
Published: February 2005

AbstractOur study was designed to assess the fecal and urinary excretion of 3 aflatoxin B1 (AFB1) metabolites, aflatoxins M1 (AFM1) and Q1 (AFQ1) and aflatoxin B1‐N7‐guanine (AFB‐N7‐guanine) that are produced by the predominant forms of cytochrome P450 enzymes responsible for the biotransformation of AFB1. Fecal and urinary AFM1, AFQ1 and urinary AFB‐N7‐guanine were assessed in 83 young Chinese males selected from a larger population (n = 300) based on detectable urinary AFM1. The concentration of fecal AFQ1 (median 137 ng/g fresh weight, IQR 9.1 to 450) was approximately 60 times higher than that of AFM1 (2.3 ng/g, IQR 0.0 to 7.3). In urine, the median AFQ1 was 10.4 ng/ml (IQR 3.4 to 23.3), and the median AFM1 and AFB‐N7‐guanine 0.04 ng/ml (IQR 0.01 to 0.33) and 0.38 ng/ml (IQR 0.0 to 2.15), respectively. A subgroup (n = 14) with hepatitis B virus (HBV) infection had significantly higher fecal concentrations of AFQ1 (p = 0.043) and AFM1 (p = 0.001) than those who were hepatitis B‐virus antigen (HBsAg) negative, and the respective differences in urinary AFQ1 and AFM1 concentrations approached statistical significance (p = 0.054, p = 0.138). Our study demonstrates that AFQ1 is excreted in urine and feces at higher levels than AFM1, and feces are an important route of excretion of these AFB1 metabolites. AFQ1 should be further assessed for its predictive value as a marker for exposure and risk of dietary aflatoxins. © 2005 Wiley‐Liss, Inc.
Response of malignant B lymphocytes to ionizing radiation: Gene expression and genotype
Authors: Lyng Heidi , Landsverk Kirsti S. , Kristiansen Elin , DeAngelis Paula M. , Ree Anne H. , Myklebost Ola , Hovig Eivind , Stokke Trond 
Published: February 2005

AbstractThe human malignant B‐lymphocyte cell lines Reh and U698 show arrest in G2 phase after ionizing radiation (IR), but only Reh cells arrest in G1 phase and die by apoptosis. We have used cDNA microarrays to measure changes in gene expression at 2, 4 and 6hr after irradiation of Reh and U698 cells with 0.5 and 4 Gy in order to begin exploring the molecular mechanisms underlying the phenotypic changes. We also investigated whether gene expression changes could be caused by possible aberrations of genes, as measured by comparative genomic hybridization. Reh cells showed upregulation of CDKN1A that likely mediated the G1 arrest. In contrast, U698 cells have impaired function of TP53 protein and no activation of CDKN1A, suppressing the arrest in G1. The G2 arrest in both cell lines was likely due to repression of PLK1 and/or CCNF. IR‐induced apoptosis in Reh cells was probably mediated by TP53 and CDKN1A, whereas a high expression level of MCL1, caused by gene amplification, and activation of the NFKB pathway may have suppressed the apoptotic response in U698 cells. Genes suggested to be involved in apoptosis were activated long before this phenotype was detectable and showed the same temporal expression profiles as genes involved in cell cycle arrest. Our results suggest that differences in functionality and/or copy number of several genes involved in IR‐regulated pathways contributed to the phenotypic differences between Reh and U698 cells after IR, and that multiple molecular factors control the radiation response of malignant B lymphocytes. © 2005 Wiley‐Liss, Inc.
Recombinant adeno‐associated virus (rAAV) expressing TFPI‐2 inhibits invasion, angiogenesis and tumor growth in a human glioblastoma cell line
Authors: Yanamandra Niranjan , Kondraganti Shakuntala , Gondi Christopher S. , Gujrati Meena , Olivero William C. , Dinh Dzung H. , Rao Jasti S. 
Published: February 2005

AbstractRecombinant adeno‐associated viruses (rAAV) have become the vector of choice for many gene therapy protocols. rAAVs have a number of attractive features including long‐term transgene expression and the ability to transduce both dividing and non‐dividing cells. We have shown previously the anti‐cancer role of tissue factor pathway inhibitor‐2 (TFPI‐2), a matrix‐associated serine protease inhibitor, in human glioblastomas. As a result of our present study, in which 0.8‐kb fragment of human TFPI‐2 was cloned into the adeno‐associated viral vectors (rAAA‐TFPI‐2), rAAV‐TFPI‐2 infection of SNB19 cells significantly increased TFPI‐2 as determined by Western blotting. As assessed by spheroid and Matrigel assays, infection of SNB19 cells with rAAV‐TFPI‐2 significantly reduced migration and invasion in a dose‐dependent manner. Tumor spheroids infected with rAAV‐TFPI‐2 and co‐cultured with fetal rat brain aggregates did not invade rat brain aggregates, whereas 90–95% of the mock and AAV‐CMV infected cells invaded rat brain aggregates. In vitro angiogenesis studies (tumor cells co‐cultured with endothelial cells or endothelial cells seeded on matrigel) showed reduction of capillary‐like structure formation in rAAV‐TFPI‐2‐treated cells as compared to parental and mock‐transfected cells. In in vivo angiogenesis results demonstrated the formation of microvessels in SNB19 parental cells and this formation was inhibited when the SNB19 cells were infected with rAAV‐TFPI‐2. Further, we observed a large reduction of tumor growth in SNB19 cells treated with rAAV‐TFPI‐2 virus injected intracerebrally when compared to controls. Our study demonstrates that rAAV‐TFPI‐2‐mediated gene therapy offers a novel tool for the treatment of brain tumors. © 2005 Wiley‐Liss, Inc.
Regulation of CTL responses to MHC‐restricted class I peptide of the gp70 tumour antigen by splenic parenchymal CD4+ T cells in mice failing immunotherapy with DISC–mGM‐CSF
Authors: Ahmad Murrium , Rees Robert C. , McArdle Stephanie E. , Li Geng , Mian Shahid , Entwisle Claire , Loudon Peter , Ali Selman A. 
Published: February 2005

AbstractDirect intratumour injection of the disabled infectious single‐cycle–herpes simplex virus–encoding murine granulocyte/macrophage colony‐stimulating factor (DISC‐HSV–mGM‐CSF) into established colon carcinoma CT26 tumours induced complete tumour rejection in up to 70% of treated animals (regressors), while the remaining mice developed progressive tumours (progressors). This murine Balb/c model was used to dissect the cellular mechanisms involved in tumour regression or progression following immunotherapy. CTLs were generated by coculturing lymphocytes and parenchymal cells from the same spleens of individual regressor or progressor animals in the presence of the relevant AH‐1 peptide derived from the gp70 tumour‐associated antigens expressed by CT26 tumours. Tumour regression was correlated with potent CTL responses, spleen weight and cytokine (IFN‐γ) production. Conversely, progressor splenocytes exhibited weak to no CTL activity and poor IFN‐γ production, concomitant with the presence of a suppressor cell population in the progressor splenic parenchymal cell fraction. Further fractionation of this parenchymal subpopulation demonstrated that cells inhibitory to the activation of AH‐1‐specific CTLs, restimulated in vitro with peptide, were present in the nonadherent parenchymal fraction. In vitro depletion of progressor parenchymal CD3+/CD4+ T cells restored the CTL response of the cocultured splenocytes (regressor lymphocytes and progressor parenchymal cells) and decreased the production of IL‐10, suggesting that CD3+CD4+ T lymphocytes present in the parenchymal fraction regulated the CTL response to AH‐1. We examined the cellular responses associated with tumour rejection and progression, identifying regulatory pathways associated with failure to respond to immunotherapy. © 2005 Wiley‐Liss, Inc.
Diarsenic and tetraarsenic oxide inhibit cell cycle progression and bFGF‐ and VEGF‐induced proliferation of human endothelial cells
Authors: Woo Sang Hyeok , Park Myung‐Jin , An Sungkwan , Lee Hyung‐Chahn , Jin Hyeon‐Ok , Lee Su‐Jae , Gwak Ho‐Shin , Park In‐Chul , Hong Seok‐Il , Rhee Chang Hun 
Published: February 2005

AbstractArsenic trioxide (As2O3, diarsenic oxide) has recently been reported to induce apoptosis and inhibit the proliferation of various human cancer cells derived from solid tumors as well as hematopoietic malignancies. In this study, the in vitro effects of As2O3 and tetraasrsenic oxide (As4O6) on cell cycle regulation and basic fibroblast growth factor (bFGF)‐ or vascular endothelial growth factor (VEGF)‐stimulated cell proliferation of human umbilical vein endothelial cells (HUVEC) were investigated. Significant dose‐dependent inhibition of cell proliferation was observed when HUVEC were treated with either arsenical compound for 48 h, and flow cytometric analysis revealed that these two arsenical compounds induced cell cycle arrest at the G1 and G2/M phases—the increases in cell population at the G1 and G2/M phase were dominantly observed in As2O3‐ and As4O6‐treated cells, respectively. In both arsenical compounds‐treated cells, the protein levels of cyclin A and CDC25C were significantly reduced in a dose‐dependent manner, concomitant to the reduced activities of CDK2‐ and CDC2‐associated kinase. In G1‐synchronized HUVEC, the arsenical compounds prevented the cell cycle progression from G1 to S phase, which was stimulated by bFGF or VEGF, through the inhibition of growth factor‐dependent signaling. These results suggest that arsenical compounds inhibit the proliferation of HUVEC via G1 and G2/M phase arrest of the cell cycle. In addition, these inhibitory effects on bFGF‐ or VEGF‐stimulated cell proliferation suggest antiangiogenic potential of these arsenical compounds. © 2005 Wiley‐Liss, Inc.
Normal human osteoclasts formed from peripheral blood monocytes express PTH type 1 receptors and are stimulated by PTH in the absence of osteoblasts
Authors: Dempster David W. , Hughes‐Begos Christine E. , Plavetic‐Chee Katarina , Brandao‐Burch Andrea , Cosman Felicia , Nieves Jeri , Neubort Simon , Lu Shi Shou , Iida‐Klein Akiko , Arnett Tim , Lindsay Robert 
Published: February 2005

AbstractThe prevailing view for many years has been that osteoclasts do not express parathyroid hormone (PTH) receptors and that PTH's effects on osteoclasts are mediated indirectly via osteoblasts. However, several recent reports suggest that osteoclasts express PTH receptors. In this study, we tested the hypothesis that human osteoclasts formed in vitro express functional PTH type 1 receptors (PTH1R). Peripheral blood monocytes (PBMC) were cultured on bone slices or plastic culture dishes with human recombinant RANK ligand (RANKL) and recombinant human macrophage colony‐stimulating factor (M‐CSF) for 16–21 days. This resulted in a mixed population of mono‐ and multi‐nucleated cells, all of which stained positively for the human calcitonin receptor. The cells actively resorbed bone, as assessed by release of C‐terminal telopeptide of type I collagen and the formation of abundant resorption pits. We obtained evidence for the presence of PTH1R in these cells by four independent techniques. First, using immunocytochemistry, positive staining for PTH1R was observed in both mono‐ and multi‐nucleated cells intimately associated with resorption cavities. Second, PTH1R protein expression was demonstrated by Western blot analysis. Third, the cells expressed PTH1R mRNA at 21 days and treatment with 10−7M hPTH (1–34) reduced PTH1R mRNA expression by 35%. Finally, bone resorption was reproducibly increased by two to threefold when PTH (1–34) was added to the cultures. These findings provide strong support for a direct stimulatory action of PTH on human osteoclasts mediated by PTH1R. This suggests a dual regulatory mechanism, whereby PTH acts both directly on osteoclasts and also, indirectly, via osteoblasts. © 2005 Wiley‐Liss, Inc.
N‐cadherin mediated distribution of β‐catenin alters MAP kinase and BMP‐2 signaling on chondrogenesis‐related gene expression
Authors: Modarresi Rozbeh , Lafond Toulouse , Roman‐Blas Jorge A. , Danielson Keith G. , Tuan Rocky S. , Seghatoleslami M. Reza 
Published: February 2005

AbstractWe have examined the effect of calcium‐dependent adhesion, mediated by N‐cadherin, on cell signaling during chondrogenesis of multipotential embryonic mouse C3H10T1/2 cells. The activity of chondrogenic genes, type II collagen, aggrecan, and Sox9 were examined in monolayer (non‐chondrogenic), and micromass (chondrogenic) cultures of parental C3H10T1/2 cells and altered C3H10T1/2 cell lines that express a dominant negative form of N‐cadherin (Δ390‐T1/2) or overexpress normal N‐cadherin (MNCD2‐T1/2). Our findings show that missexpression or inhibition of N‐cadherin in C3H10T1/2 cells results in temporal and spatial changes in expression of the chondrogenic genes Sox9, aggrecan, and collagen type II. We have also analyzed activity of the serum response factor (SRF), a nuclear target of MAP kinase signaling implicated in chondrogenesis. In semi‐confluent monolayer cultures (minimum cell–cell contact) of C3H10T1/2, MNCD2‐T1/2, or Δ390‐T1/2 cells, there was no significant change in the pattern of MAP kinase or bone morphogenetic protein‐2 (BMP‐2) regulation of SRF. However, in micromass cultures, the effect of MAP kinase and BMP‐2 on SRF activity was proportional to the nuclear localization of β‐catenin, a Wnt stabilized cytoplasmic factor that can associate with lymphoid enhancer‐binding factor (LEF) to serve as a transcription factor. Our findings suggest that the extent of adherens junction formation mediated by N‐cadherin can modulate the potential Wnt‐induced nuclear activity of β‐catenin. Published 2005 Wiley‐Liss, Inc.
Effect of resveratrol on high glucose‐induced stress in human leukemia K562 cells
Authors: Chan Wen‐Hsiung 
Published: February 2005

AbstractHyperglycemia, a symptom of diabetes mellitus, induces hyperosmotic responses, including apoptosis, in vascular endothelial cells and leukocytes. Hyperosmotic shock elicits a stress response in mammalian cells, often leading to apoptotic cell death. In a previous report, we showed that hyperosmotic shock induced apoptosis in various mammalian cells. Importantly, apoptotic biochemical changes (i.e., caspase‐3 activation and DNA fragmentation) were blocked by antioxidant pretreatment during hyperosmotic shock‐induced cell death. In the present study, we report that resveratrol, a phytoalexin present in grapes with known antioxidant and anti‐inflammatory properties, attenuates high glucose‐induced apoptotic changes, including c‐Jun N‐terminal kinase (JNK) activation and caspase‐3 activation in human leukemia K562 cells. Experiments with the cell permeable dye, 2′,7′‐dichlorofluorescein diacetate (DCF‐DA), an indicator of reactive oxygen species (ROS) generation, revealed that high glucose treatment directly increased intracellular oxidative stress, which was attenuated by resveratrol. In addition, high glucose‐treated K562 cells displayed a lower degree of attachment to collagen, the major component of vessel wall subendothelium. In contrast, cells pretreated with resveratrol followed by high glucose exhibited higher affinity for collagen. The results of this report collectively imply the involvement of oxidative stress in high glucose‐induced apoptosis and alterations in attachment ability. Moreover, resveratrol blocks these events by virtue of its antioxidant property. © 2005 Wiley‐Liss, Inc.