bluuebunny/crossref_metadata_2025_split huggingface dataset:
Thermodynamics of Hydrogen Generation from Methane for Domestic Polymer Electrolyte Fuel Cell Systems
Authors: Barz D.P.J. , Trägner U.K. , Schmidt V.M. , Koschowitz M. 
Published: February 2004

AbstractLow temperature fuel cells such as the Polymer Electrolyte Fuel Cell (PEFC) are preferably used for domestic applications because of their moderate operating conditions. Using the existing distribution system, natural gas is used as a source for a hydrogen rich gas to power this fuel cell type. The high requirements on the fuel gas quality as well as high conversion efficiencies for the small local gas processing units are critical aspects in the evaluation of decentralized fuel cell systems. In the present paper, three typical gas processing methods are evaluated for the supply of a hydrogen rich gas for PEFCs: steam reforming, partial oxidation, and autothermic conversion. All three processes are studied in detail by varying the relevant process parameters: temperature, pressure, steam to fuel ratio, and oxygen to fuel ratio. The results are graphically displayed in numerous nomograms. With the help of these graphs, regions of stable operation and the sensitivity to the operational parameters are discussed. For all three gas processing methods, the graphs generated display methane conversion, the hydrogen yield, and the yields of unwanted components, i.e., carbon monoxide and solid carbon. Although only steady‐state operating conditions were simulated, critical modes of operation, which might occur during start‐up or transient operation can easily be identified. For instance, operating conditions where soot is generated have to be avoided under all circumstances. All simulations were done with the Gibb's reactor model of a commercial simulation program. The Gibb's reactor model was found to be a suitable tool, since the simulated results compared well with reported literature data. According to the simulation results, the methane‐steam‐reforming process appears to be favorable for application to PEFCs. Methane conversion and hydrogen yields are highest for this process while the yield of CO is relatively low.
Electrochemical Reduction of Oxygen on Carbon Supported Pt and Pt/Ru Fuel Cell Electrodes in Alkaline Solutions
Authors: Yu E.H. , Scott K. , Reeve R.W. 
Published: February 2004

AbstractA study of O2 reduction in 1 M NaOH solution at gas diffusion electrodes made from carbon supported Pt and Pt/Ru catalysts is reported. Two Tafel regions were observed for both the Pt and Pt/Ru electrodes. Although the same mechanism was suggested for oxygen reduction on both Pt and Pt/Ru catalysts, the O2 reduction activity was lower on Ru. Electrochemical Impedance Spectroscopy (EIS) analysis was carried out at different potentials and showed the significant contribution of diffusion on the reaction process and kinetics. The effect of methanol on O2 reduction was investigated in solutions containing various concentrations of methanol. The electrode performance deteriorated with increasing methanol concentration because of a mixed cathode potential. The methanol tolerance, i. e., the methanol concentration which polarises the O2 reduction reaction for O2 reduction, at the Pt/C electrode with a Pt loading of 1.2 mg cm–2 is 0.2 M methanol in 1 M NaOH.
Analysis of Direct Methanol Fuel Cell (DMFC)‐Performance via FTIR Spectroscopy of Cathode Exhaust
Authors: Meier F. , Denz S. , Weller A. , Eigenberger G. 
Published: February 2004

AbstractWater and methanol flux through Nafion™ and polyaryl‐blend membranes prepared at ICVT were studied under DMFC operation. The water, methanol, and CO2 content in the cathode exhaust were measured by FTIR spectroscopy. Both the water and methanol flux turned out to be strongly dependent on the operating temperature and thus on membrane swelling. Apart from this, water flux through the membrane is primarily affected by the gas volume flux on the cathode side. A coupling between water flux and methanol flux was observed, which leads to the conclusion that methanol is transported both by diffusion and by convection caused by the superimposed water flux. Polyaryl‐blend membranes showed a reduced diffusive methanol transport when compared to Nafion™ due to their different internal microstructure. The impact of methanol cross‐over on cathode losses at high current density needs further clarification with respect to the prevailing mechanism of methanol oxidation at the cathode.
−160C/A polymorphism in the E‐cadherin gene promoter and risk of hereditary, familial and sporadic prostate cancer
Authors: Jonsson Björn‐Anders , Adami Hans‐Olov , Hägglund Maria , Bergh Anders , Göransson Ingela , Stattin Pär , Wiklund Fredrik , Grönberg Henrik 
Published: February 2004

AbstractThe E‐cadherin (CDH1) gene has been associated with prostate carcinogenesis. The C/A polymorphism −160 base pairs relative to the transcription start site has been shown to decrease gene transcription. We analyzed the association between this polymorphism and the risk of sporadic, familial (2 close relatives) and hereditary (3 or more close relatives) prostate cancer. We combined data from 3 population‐based epidemiologic studies in Sweden encompassing altogether 1,036 prostate cancer cases and 669 controls that were genotyped for the short nucleotide polymorphism. Odds ratios with 95% confidence intervals were estimated through unconditional logistic regression. We found no significant association between the A‐allele and sporadic (OR = 1.0; 95% CI = 0.8–1.2) or familial (OR = 1.4; 95% CI = 0.9–2.2) prostate cancer. In contrast, risk of hereditary cancer was increased among heterozygote CA carriers (OR = 1.7; 95% CI = 1.0–2.7) and particularly among homozygote AA carriers (OR = 2.6; 95% CI = 1.4–4.9). Our data indicate that the −160 single nucleotide polymorphism in CDH1 is a low‐penetrant prostate cancer susceptibility gene that might explain a proportion of familial and notably hereditary prostate cancer. © 2004 Wiley‐Liss, Inc.
Genetic downregulation of pregnancy‐associated plasma protein‐A (PAPP‐A) by bikunin reduces IGF‐I‐dependent Akt and ERK1/2 activation and subsequently reduces ovarian cancer cell growth, invasion and metastasis
Authors: Tanaka Yoshiko , Kobayashi Hiroshi , Suzuki Mika , Hirashima Yasuyuki , Kanayama Naohiro , Terao Toshihiko 
Published: February 2004

AbstractA Kunitz‐type protease inhibitor, bikunin, downregulates expression of uPA and its receptor uPAR at the mRNA and protein levels in several types of tumor cells. Our recent work showed that, using a cDNA microarray analysis, pregnancy‐associated plasma protein‐A (PAPP‐A) is a candidate bikunin target gene. To clarify how reduced levels of PAPP‐A may confer repressed invasiveness, we transfected human ovarian cancer cell line HRA with antisense (AS)‐PAPP‐A cDNA and compared the properties of the transfected cells to those of parental HRA cells. Here, we show that regulation of uPA mRNA and protein by IGF‐I depends on the PI3K and MAPK signaling pathways and phosphorylation of Akt and ERK1/2 is required for IGF‐I‐mediated cell invasion; that IGFBP‐4 protease in HRA cells is identified as PAPP‐A; that reduced PAPP‐A expression is associated with the upregulation of IGFBP‐4 expression; that higher intact IGFBP‐4 levels were associated with low invasive potential and growth rate in AS‐PAPP‐A cells in response to IGF‐I; that IGF‐I stimulates Akt and ERK1/2 activation of both the control and antisense cells, but the relative potency and efficacy of IGF‐I were lower in the antisense cells compared to the control; and that genetic downregulation of PAPP‐A reduces the proliferation, invasion and metastasis of HRA cells. In conclusion, our data identify a novel role for PAPP‐A as a bikunin target gene. IGF‐I‐induced IGFBP‐4 proteolysis by PAPP‐A may enhance cell growth and invasion through IGF‐I‐dependent Akt and ERK1/2 activation and subsequently upregulation of uPA. © 2004 Wiley‐Liss, Inc.
Tumor necrosis factor‐α augmented tumor response in B16BL6 melanoma‐bearing mice treated with stealth liposomal doxorubicin (Doxil®) correlates with altered Doxil® pharmacokinetics
Authors: Brouckaert Peter , Takahashi Nozomi , van Tiel Sandra T. , Hostens Jeroen , Eggermont Alexander M.M. , Seynhaeve Ann L.B. , Fiers Walter , ten Hagen Timo L.M. 
Published: February 2004

AbstractThe application of tumor necrosis factor‐α (TNF) for the treatment of solid tumors is limited by its severe, life‐threatening, toxicity. Therefore, only low dosages of this cytokine can be applied systemically, which results in poor tumor response. It has been demonstrated previously that administration of high‐dose TNF in a so‐called isolated perfusion system markedly improved tumor response when combined with chemotherapy. It appeared that TNF had a major impact specifically on the tumor‐associated vasculature. At these high concentrations, endothelial cell death is induced by TNF, resulting in complete collapse of the tumor vascular bed. Strikingly, this effect alone is not enough to induce a tumor response, but addition of a chemotherapeutic drug is mandatory to obtain an anti‐tumor effect. We showed that TNF has no anti‐tumor effect by itself but augmented drug accumulation mainly in the tumor, most likely by enhancing vascular leakage. It seems that enhanced vascular leakage, but not endothelial cell death, explains the interaction between TNF and the co‐administered drug. We hypothesized that in a low‐dose setting TNF could induce tumor accumulation of chemotherapeutic drugs and consequently improve tumor response. We demonstrate that free TNF has a strong effect on the pharmacokinetics of co‐administered Doxil® in B16BL6 melanoma‐bearing mice, resulting in strongly augmented drug accumulation in the tumor and improved tumor response. Co‐injection of Stealth® liposomal TNF with Doxil® resulted in comparable or less pronounced tumor responses as compared to free TNF. These results imply that systemic application of clinically tolerable doses of TNF may improve drug distribution and tumor response and could be useful in a number of anti‐cancer therapies. © 2004 Wiley‐Liss, Inc.
Preclinical evaluation of the nonsteroidal anti‐inflammatory agent celecoxib on malignant mesothelioma chemoprevention
Authors: Catalano Alfonso , Graciotti Laura , Rinaldi Luciana , Raffaelli Giorgia , Rodilossi Sabrina , Betta Piergiacomo , Gianni Walter , Amoroso Salvatore , Procopio Antonio 
Published: February 2004

AbstractMalignant mesothelioma (MM) remains the most lethal pleural, peritoneal and pericardial cancer. Here, we characterize the effects of nonsteroidal anti‐inflammatory agents (NSAIDs) on in vitro and in vivo experimental MM models. Unlike primary normal mesothelial cells, the selective cyclooxygenase (COX)‐2 inhibitor celecoxib reduced the in vitro proliferation of several MM cells derived from previously untreated MM patients. Moreover, celecoxib significantly inhibited MM cell colony formation in soft agarose (63–78% at 5 × 10−5 M; p ≤ 0.05) and it elicited remarkable antitumor activity, leading to long‐term survival in >37% of nude mice bearing intraperitoneal MM. Celecoxib was more efficient in inhibiting MM cell growth than acetylsalicylic acid (10−6 M‐10−2 M), indometacin (10−6 M‐10−2 M) and the COX‐2 inhibitor NS‐398 (10−6 M‐10−4 M). Efficacy of these different compounds was not related to the amount of COX‐2 protein levels present on MM cells. Celecoxib, in a dose‐ and time‐dependent manner, induced MM cell apoptosis, which involved decreased Akt phosphorylation, loss of Bcl‐2 and Survivin protein expression and caspase‐3 activation. Furthermore, vascular endothelial growth factor (VEGF), an MM autocrine growth factor and Akt inducer, rescued celecoxib‐induced apoptosis and Akt dephosphorylation. When the VEGF receptor (KDR/Flk‐1) inhibitor, SU‐1498, was used in combination with celecoxib, IC50 of celecoxib in vitro was reduced up to 65%. These data demonstrate that celecoxib may have antitumor properties in MM and provide a rationale for the therapeutic use of celecoxib in combination with a selective VEGF inhibitor. © 2004 Wiley‐Liss, Inc.
Loss of PKR activity in chronic lymphocytic leukemia
Authors: Hii Su Ing , Hardy Lani , Crough Tania , Payne Elizabeth J. , Grimmett Karen , Gill Devinder , McMillan Nigel A.J. 
Published: February 2004

AbstractThere are a number of observations that suggest the dsRNA‐activated protein kinase, PKR, may play an active role in formation and maintenance of leukemia, including nonrandom chromosomal deletions in acute leukemia as well as truncations and deletions of the PKR gene in some leukemia cell lines. However, there is little direct evidence from patient material that this is so. Here we show that full‐length PKR is present but not active in 21 of 28 patient samples from B‐cell chronic lymphocytic leukemia (B‐CLL). PKR from these patients was unable to auto‐activate or phosphorylate substrates but was able to bind dsRNA. Furthermore, the lack of PKR activation was not due to differing levels of the PKR activator, PACT nor of the PKR inhibitor, p58IPK. We compared PKR status with clinical parameters and disease staging. No differences were found between the 2 groups in terms of staging (modified Rai or Binet), age, CD38 status, p53 status, 11q23 deletion status or CEP12 deletion status. However, there was a significant correlation between deletion in 13q14.3 and lack of PKR activity. We show that B‐CLL cells appear to contain a soluble inhibitor of PKR, as lysates from cells lacking PKR activity were able to inhibit exogenous PKR in mixing experiments. Finally, we show suppression of PKR activity was still present following ultrafilitration through a 10,000 Da cutoff filter but was lost upon extraction with phenol/chloroform or by high salt washing. This data suggests loss of PKR activity may contribute to the formation and/or maintenance of CLL. © 2004 Wiley‐Liss, Inc.
No ING1 mutations in human brain tumours but reduced expression in high malignancy grades of astrocytoma
Authors: Tallen Gesche , Kaiser Ines , Krabbe Sonja , Lass Ulrike , Hartmann Christian , Henze Günter , Riabowol Karl , von Deimling Andreas 
Published: February 2004

AbstractThe ING1 family of proteins has been shown to have regulatory functions in oncogenesis, apoptosis, DNA repair and cell cycle regulation. Here we present the first report on LOH analysis of the ING1 locus, mutation analysis of the complete coding sequence including intron‐exon boundaries and expression analysis of the different ING1 splice products and protein isoforms in primary brain tumours. No somatic ING1 mutations were detected. Semi‐quantitative analysis revealed higher levels of p33ING1b RNA in benign than in malignant lesions. This correlation was significant in a subset of 37 astrocytic tumours WHO grades I to IV. ING1 protein isoforms p47ING1a, p33ING1b and p24ING1c were found to be expressed variably in this series. Our findings support a regulatory contribution of ING1 to the development or progression of brain tumours. © 2004 Wiley‐Liss, Inc.
Amplification of chromosome 1 sequences in lipomatous tumors and other sarcomas
Authors: Nilsson Malin , Meza‐Zepeda Leonardo A. , Mertens Fredrik , Forus Anne , Myklebost Ola , Mandahl Nils 
Published: February 2004

AbstractAmplifications and gains involving 1q are common abnormalities in solid tumors. Recently, an amplicon originating from 1q21–23, containing the candidate oncogenesCOAS1,COAS2andCOAS3(Chromosome One Amplified Sequence) was identified. The presence, distribution and copy number level of extraCOASsequences were investigated in 48 bone and soft tissue tumor (BSTT) samples using metaphase FISH analysis. Amplification was seen in 27/48 (56%) samples. With few exceptions, all 3 genes were involved, but on averageCOAS2exhibited higher copy numbers. The presence of extraCOASsignals, irrespective of copy numbers, was found at similar frequencies in different histologic tumor subtypes. However, medium or high level amplification was common in lipomatous tumors but rare in other, nonlipomatous tumors (9/21vs. 2/27 samples). The most common localization of extraCOASsignals in lipomatous tumors was in supernumerary ring and giant marker chromosomes. Among nonlipomatous tumors, the distribution of extraCOASgenes was more disperse, being located in various unidentified chromosomal structures, including double minutes, and only rarely in ring chromosomes. BecauseMDM2is known to be amplified frequently in BSTTs, and in particular in atypical lipomatous tumors, cases with extra copies ofCOASwere studied also with anMDM2probe. Twelve out of 18 lipomatous tumors had extra copies of bothCOASandMDM2, and the 2 genes were found to be coamplified and interspersed exclusively in ring and giant marker chromosomes. Also 12 out of 18 nonlipomatous tumors exhibited simultaneous gain ofCOASandMDM2, but colocalization in the same chromosome was less frequent. The role of the frequent coamplification ofCOAS, or some other yet unknown gene in the 1q21–23 region, andMDM2remains to be elucidated. © 2004 Wiley‐Liss, Inc.
Cervical cancer as a priority for prevention in different world regions: An evaluation using years of life lost
Authors: Yang Binh H. , Bray Freddie I. , Parkin D. Maxwell , Sellors John W. , Zhang Zuo‐Feng 
Published: February 2004

AbstractThe relative importance of cancer of the cervix among several important causes of mortality (from cancer and other diseases) has been evaluated by estimating the years of life lost (YLL) by young and middle‐aged women (25–64 years old) in different regions of the world. The life years were weighted to reflect their importance to the individual and to society. On a global basis, cancer of the cervix is responsible for about 2% of the total (weighted) YLL, fewer than for other causes of mortality in this age group. However, it is the most important cause of YLL in Latin America and the Caribbean. It also makes the largest contribution to YLL from cancer in the populous regions of SubSaharan Africa and South‐Central Asia where the actual risk of loss of life from this cause is higher, although overshadowed by noncancer deaths (from AIDS, TB and maternal conditions). The overall picture is not very sensitive to the age weighting function used. The fact that most of the loss of life is preventable, and that simple technologies have been developed that make this practicable, means that cervical cancer has an even higher profile from the perspective of resource allocation in low income settings. © 2004 Wiley‐Liss, Inc.
CD1d is expressed on B‐chronic lymphocytic leukemia cells and mediates α‐galactosylceramide presentation to natural killer T lymphocytes
Authors: Fais Franco , Morabito Fortunato , Stelitano Caterina , Callea Vincenzo , Zanardi Sabrina , Scudeletti Marco , Varese Paola , Ciccone Ermanno , Grossi Carlo Enrico 
Published: February 2004

AbstractGeneration of immune responses against B cell chronic lymphocytic leukemia (B‐CLL) has been the aim of several studies that have demonstrated a poor antigen presenting ability of B‐CLL cells and an inconsistent emergence of T cells capable of killing efficiently the leukemic cells. CD1d is a restriction element structurally related to the major histocompatibility complex (MHC) and capable of presenting lipid antigens to CD1d‐restricted T cells (also defined as natural killer‐T [NKT] cells). The synthetic lipid α‐galactosylceramide (α‐GalCer) has been characterized as a potent stimulator of CD1d‐restricted T cells. We have investigated the expression of CD1d on B‐CLL cells. CD1d was detected by flow cytometric analyses on leukemic cells of all B‐CLL cases studied (n = 38) and was expressed at higher density on cells carrying unmutated immunoglobulin variable region (IgV) genes. In addition, CD1d on B‐CLL cells mediated the presentation of α‐GalCer to CD1d‐restricted T cells, which in turn induced B‐CLL cell death. At variance with another study (Metelitsa et al., Leukemia 2003;17:1068–77), no correlation between expression levels of CD1d and susceptibility to NKT cell lysis was observed. Proliferation and production of interferon‐γ (IFN‐γ) and tumor necrosis factor‐α (TNF‐α) by CD1d‐restricted T cells, in the presence of B‐CLL cells loaded with α‐GalCer, were also observed. Our study demonstrates that B‐CLL cells express a monomorphic restriction element that is functionally capable of antigen presentation and can be useful to design novel B‐CLL immunotherapies. © 2004 Wiley‐Liss, Inc.
Initial results from a randomized trial of cervical visual screening in rural south India
Authors: Sankaranarayanan Rengaswamy , Rajkumar Rajamanickam , Theresa Rajapandian , Esmy Pulikattil Okkaru , Mahe Cedric , Bagyalakshmi Karur R. , Thara Somanathan , Frappart Lucien , Lucas Eric , Muwonge Richard , Shanthakumari S. , Jeevan D. , Subbarao T.M. , Parkin Donald Maxwell , Cherian Jacob 
Published: February 2004

AbstractThe impact of a single round of screening of visual inspection with acetic acid (VIA) on cervical cancer incidence and mortality was investigated in a cluster randomized trial in south India. Women 30–59 years of age in 113 clusters in Dindigul District were randomized to VIA screening (57 clusters, 48,225 women) by nurses and to a control group (56 clusters, 30,167 women). 30,577 eligible women were screened between May 2000 and April 2003; 2,939 (9.6%) screen‐positive women were investigated with colposcopy by nurses and 2,777 (9.1%) women had biopsy. CIN 1 was diagnosed in 1,778 women, CIN 2‐3 lesions were found in 222, and there were 69 screen detected invasive cervical cancers. The detection rates of lesions per 1,000 screened women were 58.2 for CIN 1, 7.3 for CIN 2‐3, and 2.3 for invasive cancer. The detection rate of high‐grade lesions in our study was 2–3‐fold higher than those observed in repeatedly screened populations in developed countries. 71% of women with CIN 1 and 80% of those with CIN 2‐3 lesions accepted cryotherapy provided by nurses and surgical treatment by mid‐level clinicians. Overall, 97 and 34 incident cervical cancer cases were observed in the intervention and control arms, respectively. The intervention arm accrued 124,144 person years and the control arm accrued 90,172 during the study period. The age standardized cervical cancer incidence rates were 92.4/100,000 person‐years in the intervention and 43.1/100,000 in the control arms. In the screened arm, 35.0% of cases were in Stage I as opposed to none in the control arm. The preliminary findings from our study indicate that not only is a VIA‐based screening programme feasible, safe and acceptable to a population in rural settings, it also results in early detection of cervical neoplasia. © 2004 Wiley‐Liss, Inc.
Analysis of the natural killer mediated immune response in metastatic renal cell carcinoma patients
Authors: Gati Asma , Da Rocha Sylvie , Guerra Nadia , Escudier Bernard , Moretta Alessandro , Chouaib Salem , Angevin Eric , Caignard Anne 
Published: February 2004

AbstractMetastatic renal cell carcinomas (MRCC) are considered as immunogeneic tumors on the basis of the clinical responses observed in patients treated by IL‐2. However, renal cell carcinoma patients are also characterized by alterations of the immune response that may compromise the immunotherapeutic approaches. In our study, we have studied the phenotype and the functional capacities of peripheral NK cells in a panel of neprectomized metastatic renal cell carcinoma patients. NK cells were harvested by negative immunoselection from fresh peripheral blood samples. In most of MRCC patients analysed (23/28), the expression of NCR (NKp46 and NKp30) was similar to that of donors. Lytic capacities by activated immunoselected NK cells from MRCC patients assessed against K562 and 3 renal tumor cell lines were in the range of that observed in NK cells from normal donors. HLA‐I− renal tumor cells UOK23 were killed with a good efficiency, whereas HLA‐I renal tumor cells were more resistant. Although LFA‐1/ICAM‐1 interaction potentiates RCC cell lysis, HLA‐I/NKR interaction clearly decreased RCC cell susceptibility to NK cells. In addition, proliferation of NK cells from MRCC patients in response to cytokines was altered. © 2004 Wiley‐Liss, Inc.