bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electrochemical Biosensor for the Detection of Interaction Between Arsenic Trioxide and DNA Based on Guanine Signal
Authors: Ozsoz Mehmet , Erdem Arzum , Kara Pinar , Kerman Kagan , Ozkan Dilsat 
Published: May 2003

AbstractThe interaction of arsenic trioxide (As2O3) with calf thymus double‐stranded DNA (dsDNA), calf thymus single‐stranded DNA (ssDNA) and also 17‐mer short oligonucleotide (Probe A) was studied electrochemically by using differential pulse voltammetry (DPV) with carbon paste electrode (CPE) at the surface and also in solution. Potentiometric stripping analysis (PSA) was employed to monitor the interaction of As2O3 with dsDNA in solution phase by using a renewable pencil graphite electrode (PGE). The changes in the experimental parameters such as the concentration of As2O3, and the accumulation time of As2O3 were studied by using DPV; in addition, the reproducibility data for the interaction between DNA and As2O3 was determined by using both electrochemical techniques. After the interaction of As2O3 with dsDNA, the DPV signal of guanine was found to be decreasing when the accumulation time and the concentration of As2O3 were increased. Similar DPV results were also found with ssDNA and oligonucleotide. PSA results observed at a low DNA concentration such as 1 ppm and a different working electrode such as PGE showed that there could be damage to guanine bases. The partition coefficients of As2O3 after interaction with dsDNA and ssDNA in solution by using CPE were calculated. Similarly, the partition coefficients (PC) of As2O3 after interaction with dsDNA in solution was also calculated by PSA at PGE. The features of this proposed method for the detection of DNA damage by As2O3 are discussed and compared with those methods previously reported for the other type of DNA targeted agents in the literature.
Sphere‐Cap Mercury Microelectrodes for Scanning Electrochemical Microscopy Above an Insulating Substrate
Authors: Daniele Salvatore , Bragato Carlo , Ciani Ilenia , Baldo M. Antonietta 
Published: May 2003

AbstractSphere‐cap mercury microelectrodes, fabricated onto platinum microdisks 1 and 10 μm radius, were employed as tips in scanning electrochemical microscopy (SECM). Experimental current vs distance curves were acquired above an insulating substrate with a series of sphere caps whose aspect ratio h/a (h is the height of mercury deposit, a is the disk basal radius) varied between 0.28 and 2.14. It was found that the hindered diffusion effect of the insulating surface was the less pronounced the higher was the h/a parameter of the sphere cap. Comparison of experimental and theoretical approach curves displayed a fairly good agreement for subhemisphere caps (h<a), and a less satisfactory agreement for hemispherical (h=a) and superhemispherical (h>a) caps. Preliminary coupled anodic stripping voltammetry and SECM measurements were also performed for the investigation on local chemical equilibria involving heavy metals at sediment/water interfaces.
Modeling of PAH Elimination by Adiabatic Steam Stripping and Intraparticle Desorption
Authors: Frishfelds V. , Niemeyer B. , Hoehne J. , Jakovics A. 
Published: May 2003

AbstractThe decontamination process of solids loaded with PAH in a pilot plant is modeled. This process is separated into two main stages: fast steam stripping at the entrance of the separation tube and the subsequent slow desorption of PAH from the interior of the soil particles. The stripping process also occurs in two stages: fast diffusion controlled saturation of the partial pressures followed by the heat transfer controlled evaporation. The phase diagram of PAH/water is constructed using both the microscopic model and empirical relationships for systems with wide miscibility gaps. The numerical basis for the calculations describing desorption from the soil particles is discussed. The model for multiple PAH components is based on Langmuir type isotherms which include surface diffusion terms. The obtained results are contrasted with analytical data for systems displaying linear isotherms by dispersive approximation.
Theoretical Characterization of Slurry Fermentation
Authors: Glover K. , Kunz B. 
Published: May 2003

AbstractThis is an extensive study of the three classical fermentation systems (emerged, submerged and solid‐state fermentations), thus uncovering, a system that is an intrinsically concomitant overlap of submerged and solid‐state fermentations – slurry fermentation. It is a convenient method of fermentation with hardly any theoretical characterization. This paper details the specifics of this system and its potential fields of application.
Virtual reality in eating disorders
Authors: Perpiñá C. , Botella C. , Baños R. M. 
Published: May 2003

AbstractVirtual Reality (VR) is widely used as a therapeutic tool in the field of neuropsychology and also in the treatment of anxiety disorders. In contrast, VR is much less well‐known in the area of the eating disorders. The objective of this paper is to draw attention to possible applications of this technology in the treatment of eating disorders and describe pilot work in the area of body image disturbance and binge eating using VR technology. Copyright © 2003 John Wiley & Sons, Ltd and Eating Disorders Association.
Internet‐based prevention of eating disorders
Authors: Zabinski Marion F. , Celio Angela A. , Jacobs M. Joy , Manwaring Jamie , Wilfley Denise E. 
Published: May 2003

AbstractInternet technology has greatly influenced communication and information transfer worldwide and has also provided novel avenues for psychological research and treatment delivery. Preliminary research with computerized interventions have been promising and several studies have shown support for electronically delivered programmes related to eating disorder prevention among college‐aged women. Acceptability and efficacy findings for two Internet‐based eating disorders prevention programmes, Student Bodies, an asynchronous intervention, and a synchronous chatroom study, are presented. Initial findings indicate that computerized programmes are promising and future directions of research in this emerging field are discussed. Copyright © 2003 John Wiley & Sons, Ltd and Eating Disorders Association.
Mutational events in LMP1 gene of Epstein‐Barr virus in salivary gland lymphoepithelial carcinomas
Authors: Jen Kai Yu , Cheng Jun , Li Jian , Wu Lanyan , Li Yingfang , Yu Shifeng , Lin Hanliang , Chen Zhilong , Gurtsevitch Vladimir , Saku Takashi 
Published: May 2003

AbstractIt is still unknown what kinds of roles Epstein‐Barr virus (EBV) infection that are highly specific to salivary gland lymphoepithelial carcinomas (LECs) play in their tumorigenesis. To clarify the significance of EBV in LECs, we paid particular attention to the LMP1 gene, which is responsible for triggering several pathways for activating transcription factors. Sixty‐one cases of EBV positive LECs confirmed by PCR and in‐situ hybridization were collected from various areas of the world and studied immunohistochemically for latent membrane protein‐1. Furthermore, PCR for the LMP1 carboxyl (C)‐terminus region was performed, and the PCR products were sequenced for detection of other mutational events. LMP1 gene products were immunohistochemically demonstrated in 51% of the cases, while PCR amplification of the LMP1 gene was successful in 41 cases (67%). Among them, a 30 bp deletion in the C‐terminus of the LMP1 gene, which had been shown to be characteristic to EBV in Chinese nasopharyngeal carcinomas, was found in 20 cases (32%). Most of them were from Guangzhou, Chengdu and Taiwan, while most of the cases from Shanghai and other areas exhibited no 30 bp deletion. In addition, several point mutations including codon 338 of LMP1 were commonly shared by the cases with or without the 30 bp deletion. These results indicate that there are 2 major genomic variations of EBV infecting salivary gland LECs. The frequent mutational events in the C‐terminus in addition to the 30 bp deletion also seem to be critical for the pathogenesis because such mutational events may possibly promote cellular proliferation. © 2003 Wiley‐Liss, Inc.
Antisense treatment against Ki‐67 mRNA inhibits proliferation and tumor growth in vitro and in vivo
Authors: Kausch Ingo , Lingnau Anja , Endl Elmar , Sellmann Kirsten , Deinert Irina , Ratliff Timothy L. , Jocham Dieter , Sczakiel Georg , Gerdes Johannes , Böhle Andreas 
Published: May 2003

AbstractThe Ki‐67 protein is tightly regulated and depends on the proliferative status of a cell. It is present in the nuclei of proliferating cells but absent in resting cells. Since transformation of malignant cells is frequently associated with high cell proliferation and since proliferation is tightly associated with the Ki‐67 protein labeling index, this antigen may represent a potential target for cancer therapy. In the present study we determined the ability of a phosphorothioate antisense oligodeoxyribonucleotide (ODN) targeted against Ki‐67 mRNA to inhibit tumor cell proliferation specifically in cell culture, in multicellular 3‐dimensional spheroids (MCS) and in subcutaneous murine tumor models. Antisense treatment of 1 myeloid and different epithelial tumor cell lines in suspension and monolayer culture, respectively, resulted in specific reduction of Ki‐67 mRNA and protein, inhibition of proliferation and increased apoptotic cell death. Multicellular human bladder carcinoma spheroids lost their 3‐dimensional structure and underwent cell death after incubation with antisense oligonucleotides. The growth of subcutaneous syngeneic prostatic (p = 0.05) and transitional cell tumors (p = 0.001) in immunocompetent mice was significantly inhibited in antisense‐treated animals. From these findings we conclude that antisense inhibition of Ki‐67 protein expression may be a rational approach in anticancer therapy. © 2003 Wiley‐Liss, Inc.
Independent and combined effects of tobacco smoking, chewing and alcohol drinking on the risk of oral, pharyngeal and esophageal cancers in Indian men
Authors: Znaor Ariana , Brennan Paul , Gajalakshmi Vendhan , Mathew Aleyamma , Shanta Viswanathan , Varghese Cherian , Boffetta Paolo 
Published: May 2003

AbstractOral, pharyngeal and esophageal cancers are 3 of the 5 most common cancer sites in Indian men. To assess the effect of different patterns of smoking, chewing and alcohol drinking in the development of the above 3 neoplasms and to determine the interaction among these habits, we conducted a case‐control study in Chennai and Trivandrum, South India. The cases included 1,563 oral, 636 pharyngeal and 566 esophageal male cancer patients who were compared with 1,711 male disease controls from the 2 centers as well as 1,927 male healthy hospital visitors from Chennai. We observed a significant dose‐response relationship for duration and amount of consumption of the 3 habits with the development of the 3 neoplasms. Tobacco chewing emerged as the strongest risk factor for oral cancer, with the highest odds ratio (OR) for chewing products containing tobacco of 5.05 [95% confidence internal (CI) 4.26–5.97]. The strongest risk factor for pharyngeal and esophageal cancers was tobacco smoking, with ORs of 4.00 (95% CI 3.07–5.22) and 2.83 (95% CI 2.18–3.66) in current smokers, respectively. An independent increase in risk was observed for each habit in the absence of the other 2. For example, the OR of oral cancers for alcohol drinking in never smokers and never chewers was 2.56 (95% CI 1.42–4.64) and that of esophageal cancers was 3.41 (95% CI 1.46–7.99). Furthermore, significant decreases in risks for all 3 cancer sites were observed in subjects who quit smoking even among those who had quit smoking 2–4 years before the interview. © 2003 Wiley‐Liss, Inc.
KLF6, a putative tumor suppressor gene, is mutated in astrocytic gliomas
Authors: Jeng Yung‐Ming , Hsu Hey‐Chi 
Published: May 2003

AbstractGliomas are the most common tumors of the central nervous system and have a grave prognosis. Deletion of chromosome 10p15 is one of the most common chromosomal alterations in gliomas. Recently, a candidate tumor suppressor gene, KLF6, which is mapped to chromosome 10p, was found to be frequently mutated in prostate cancer. KLF6 is a zinc finger transcription factor and transactivates p21/WAF1/CIP expression. To elucidate the role of genetic alterations of KLF6 in gliomas, we analyzed the 4 exons of the gene by direct DNA sequencing in 155 gliomas. Of these, mutations of KLF6 were found in 9 of 76 (11.8%) glioblastomas multiforme, 2 of 28 (7.1%) anaplastic astrocytomas, 2 of 36 (5.5%) low‐grade diffuse astrocytomas and in none of the 15 oligodendrogliomas. All 13 mutations were located in the transactivation domain and most of them affected either serine residues or codons next to serine residues. Of the 13 cases with KLF6 mutation, loss of heterozygosity (LOH) at the KLF6 locus was inferred from the LOH displayed by the flanking microsatellite markers in 11 cases. We conclude that mutations of the KLF6 gene play a role in the pathogenesis of astrocytic gliomas. © 2003 Wiley‐Liss, Inc.
EBV‐encoded EBNA‐5 associates with P14ARF in extranucleolar inclusions and prolongs the survival of P14ARF‐expressing cells
Authors: Kashuba Elena , Mattsson Karin , Pokrovskaja Katja , Kiss Csaba , Protopopova Marina , Ehlin‐Henriksson Barbro , Klein George , Szekely Laszlo 
Published: May 2003

AbstractEpstein‐Barr virus (EBV) carrying lymphoblastoid cells of normal origin express the full program of all 9 virus‐encoded, growth transformation associated proteins. They have an intact p53 pathway as a rule. This raises the question of whether any of the viral proteins impair the pathway functionally. Using a yeast 2‐hybrid system, we have shown that EBNA‐5 but not the other EBNAs interacts with the p14ARF protein, a regulator of the p53 pathway. The interaction was confirmed in vitro using a GST pull‐down assay. Moreover, expression of EBNA‐5 increased the survival of p14ARF‐transfected cells. EBV infection of resting B cells induced the expression of p14ARF mRNA without increased level of the protein. A fraction of the p14ARF localized to the nucleoli but the bulk of the protein accumulated in nuclear but extranucleolar inclusions. Formation of the extranucleolar inclusions led to complete relocalization of EBNA‐5 from nucleoplasm to these structures. The inclusions also contained p53 and HDM2, and were surrounded by PML bodies and proteasomes, which suggests that these inclusions could be targets for proteasome dependent protein degradation. © 2003 Wiley‐Liss, Inc.
Oligogenic segregation analysis of hereditary prostate cancer pedigrees: Evidence for multiple loci affecting age at onset
Authors: Conlon Erin M. , Goode Ellen L. , Gibbs Mark , Stanford Janet L. , Badzioch Michael , Janer Marta , Kolb Suzanne , Hood Lee , Ostrander Elain A. , Jarvik Gail P. , Wijsman Ellen M. 
Published: May 2003

AbstractPrevious studies have suggested strong evidence for a hereditary component to prostate cancer (PC) susceptibility. Here, we analyze 3,796 individuals in 263 PC families recruited as part of the ongoing Prostate Cancer Genetic Research Study (PROGRESS). We use Markov chain Monte Carlo (MCMC) oligogenic segregation analysis to estimate the number of quantitative trait loci (QTLs) and their contribution to the variance in age at onset of hereditary PC (HPC). We estimate 2 covariate effects: diagnosis of PC before and after prostate‐specific antigen (PSA) test availability, and presence/absence of at least 1 blood relative with primary neuroepithelial brain cancer (BC). We find evidence that 2 to 3 QTLs contribute to the variance in age at onset of HPC. The 2 QTLs with the largest contribution to the total variance are both effectively dominant loci. We find that the covariate for diagnosis before and after PSA test availability is important. Our findings for the number of QTLs contributing to HPC and the variance contribution of these QTLs will be instructive in mapping and identifying these genes. © 2003 Wiley‐Liss, Inc.
EBV specific antibody‐based and DNA‐based assays in serologic diagnosis of nasopharyngeal carcinoma
Authors: Chan Kwok H , Gu Yao L , Ng Fai , Ng Park SP , Seto Wing H , Sham Jonathan ST , Chua Daniel , Wei William , Chen Yue L , Luk Winsie , Zong Yong S , Ng Mun H 
Published: May 2003

AbstractWe assessed 5 EBV specific assays for their capacity to effect serologic diagnosis of suspected NPC. The assays were the immunofluorescent assays, VCA IgA and EA IgA, the enzyme‐linked immunosorbent assays specific for EBNA 1 IgA or zta IgG and an EBV DNA assay. Serum samples were taken from 218 symptomatic NPC patients presenting consecutively at a public hospital in Hong Kong, 51 of whom were subsequently diagnosed as having NPC; 4 had EBV‐associated lung cancer with similar serology as NPC. The remaining patients included 23 who had other cancers and 140 who had other diseases. Objectives of serodiagnosis under such clinical settings, therefore, are to both exclude and predict a diagnosis of NPC. None of the assays individually can meet both requirements adequately, however. The difficulty was best overcome by combining EBNA 1 IgA and zta IgG. It was shown that 68.3% of the patients gave a confirmed test results, negative or positive, by both tests. A confirmed negative result was associated with a negative predictive value of 99.1%, providing a clear indication to exclude a diagnosis of NPC; a confirmed positive result was associated with a positive predictive value of 86.8%, providing a clear indication to proceed with diagnostic work‐up of NPC. The remaining patients gave equivocal test results, being positive for one or the other test, which were associated with a positive predictive value of 43.3% and 24.2%, respectively. © 2003 Wiley‐Liss, Inc.
Differential prognostic impact of the cyclins E and B in premenopausal and postmenopausal women with lymph node‐negative breast cancer
Authors: Rudolph Pierre , Kühling Heidi , Alm Per , Fernö Mårten , Baldetorp Bo , Olsson Håkan , Parwaresch Reza 
Published: May 2003

AbstractSearching for new prognostic factors, we investigated the influence of cyclin expression on breast cancer prognosis. A total of 273 archival tumor specimens from patients with pT1/pT2 N0 breast cancers treated by surgery and local irradiation were immunostained for cyclins E, A and B. Outcome was evaluated as metastasis‐free (MFS) and disease‐specific survival (DSS) over a median observation period of 99 months. In postmenopausal women, DSS was significantly predicted by cyclin E, and in premenopausal patients by cyclin B. No statistical significance was found for cyclin A. When the prognostic impact of cyclins was compared to that of standard prognostic indicators in a multivariate analysis, both cyclin E and cyclin B were selected as independent predictors of survival in postmenopausal and premenopausal patients, respectively. After inclusion of Ki‐67 in the model, cyclin E lost its significance, whereas cyclin B remained the only independent prognostic factor with a hazard ratio of 4.5 (p = 0.026) for tumor‐related death. Assessment of cyclin expression may, therefore, refine current prognostic models if considered in relation to menopausal status. The prognostic relevance of cyclins is likely attributable to an influence on proliferation, cell survival and genetic instability. Awareness of the molecular mechanisms leading to deregulated cyclin expression may guide decisions for risk‐adapted therapy regimens. © 2003 Wiley‐Liss, Inc.
Carboplatin induces Fas (APO‐1/CD95)‐dependent apoptosis of human tongue carcinoma cells: Sensitization for apoptosis by upregulation of FADD expression
Authors: Mishima Koichi , Nariai Yoshiki , Yoshimura Yasuro 
Published: May 2003

AbstractWe examined the apoptosis of tongue carcinoma cells and the effects of anticancer drugs to identify the molecules that mediate apoptotic cascade in the malignancy. Carboplatin (CBDCA) induced apoptosis of SCC‐9 and SCC‐25, human well‐differentiated tongue squamous carcinoma cell lines. Neutralizing anti‐Fas (APO‐1/CD95) and anti‐Fas ligand (FasL) antibodies obliterated the CBDCA‐induced cell death. In the absence of CBDCA, cytotoxic anti‐Fas antibody, which binds to and activates Fas at the cell surface, failed to induce apoptosis. However, in the presence of CBDCA, the cytotoxic antibody markedly enhanced the apoptosis in a dose‐dependent manner. Western blotting and reverse‐transcription (RT) PCR revealed that there were no alterations in Fas or FasL expression upon CBDCA treatment. SCC‐25 induced apoptosis of Jurkat cells, Fas‐sensitive T‐lymphatic leukemia cell line, and the apoptosis was inhibited by neutralizing anti‐Fas or anti‐FasL antibody. These results indicate that the tongue carcinoma cells express nonfunctional Fas and functional FasL, which by themselves fail to induce apoptosis. The expression of FADD in the tongue carcinoma cells was very low and was largely enhanced by CBDCA treatment. Suppression of FADD expression using the specific antisense oligonucleotide resulted in a failure of CBDCA induction of cell death. These results indicate that a deficiency of FADD is involved in the insensitivity of tongue carcinoma cells for Fas activation, and that CBDCA treatment switches nonfunctional Fas to functional Fas by upregulation of FADD expression, resulting in activation of a Fas‐sensitive pathway leading to apoptosis. © 2003 Wiley‐Liss, Inc.
Identification of drug‐regulated genes in osteosarcoma cells
Authors: Fellenberg Jörg , Dechant Markus J. , Ewerbeck Volker , Mau Hans 
Published: May 2003

AbstractThe introduction of systemic chemotherapy improved significantly the prognosis of osteosarcoma. Despite this success, approximately 30–40% of patients will relapse. Cytotoxic drugs have been shown to induce apoptosis in the target cells independent of their primary effects. The underlying molecular mechanisms and the intracellular mediators, however, are still largely unknown. Therefore, the purpose of our study was to identify drug‐regulated genes in osteosarcoma cells useful as prognostic factors and for the development of new therapeutic strategies. Using suppressive subtractive hybridization (SSH) the gene expression pattern of untreated Saos‐2 cells was compared to cells treated with cisplatin, methotrexate and doxorubicin, respectively. We identified 8 genes that are regulated >2‐fold in drug‐treated osteosarcoma cell lines. Expression of ferritin light chain, rhoA, inosine monophosphatdgehydrogenase II, ribonucleotide reductase M2, pro2000 and pro1859 were increased after drug treatment, whereas prohibitin and α‐actinin expressions were significantly downregulated. Differential expression of the identified genes was verified by Northern blot analysis of 3 different osteosarcoma cell lines. In addition, the effects on chemosensitivity of 4 selected genes was analyzed by overexpression of recombinant constructs in Saos‐2 cells and subsequent quantification of drug‐induced apoptosis. Overexpression of prohibitin and rhoA reduced significantly drug sensitivity to approximately 52% and 59% indicating a crucial role in the modulation of drug‐induced cell death. © 2003 Wiley‐Liss, Inc.