bluuebunny/crossref_metadata_2025_split huggingface dataset:
A simple algebraic interface capturing scheme using hyperbolic tangent function
Authors: Xiao F. , Honma Y. , Kono T. 
Published: April 2005

AbstractThis paper presents a simple and practical scheme for capturing moving interfaces or free boundaries in multi‐fluid simulations. The scheme, which is called THINC (tangent of hyperbola for interface capturing), makes use of the hyperbolic tangent function to compute the numerical flux for the fluid fraction function, and gives a conservative, oscillation‐less and smearing‐less solution to the fluid fraction function even for the extremely distorted interfaces of arbitrary complexity. The numerical results from the THINC scheme possess adequate quality for practical applications, which make the extra geometric reconstruction, such as those in most of the volume of fluid (VOF) methods unnecessary. Thus the scheme is quite simple. The numerical tests show that the THINC scheme has competitive accuracy compared to most exiting methods. Copyright © 2005 John Wiley & Sons, Ltd.
Impaired capacity for upregulation of MHC class II in tumor‐associated microglia
Authors: Schartner Jill M. , Hagar Aaron R. , Van Handel Michelle , Zhang Leying , Nadkarni Nivedita , Badie Behnam 
Published: April 2005

AbstractImmunotherapy for malignant gliomas is being studied as a possible adjunctive therapy for this highly fatal disease. Thus far, inadequate understanding of brain tumor immunology has hindered the design of such therapies. For instance, the role of microglia and macrophages, which comprise a significant proportion of tumor‐infiltrating inflammatory cells, in the regulation of the local anti‐tumor immune response is poorly understood. To study the response of microglia and macrophages to known activators in brain tumors, we injected CpG oligodeoxynucleotide (ODN), interferon‐γ (IFN‐γ), and IFN‐γ/LPS into normal and intracranial RG2 glioma‐bearing rodents. Microglia/macrophage infiltration and their surface expression of MHC class II B7.1 and B7.2 was examined by flow cytometry. Each agent evaluated yielded a distinct microglia/macrophage response: CpG ODN was the most potent inducer of microglia/macrophage infiltration and B7.1 expression, while IFN‐γ resulted in the highest MHC‐II expression in both normal and tumors. Regardless of the agent injected, however, MHC‐II induction was significantly muted in tumor microglia/macrophage as compared with normal brain. These data suggest that microglia/macrophage responsiveness to activators can vary in brain tumors when compared with normal brain. Understanding the mechanism of these differences may be critical in the development of novel immunotherapies for malignant glioma. © 2005 Wiley‐Liss, Inc.
Pattern of cannabis use in ecstasy polydrug users: moderate cannabis use may compensate for self‐rated aggression and somatic symptoms
Authors: Milani R. M. , Parrott A. C. , Schifano F. , Turner J. J. D. 
Published: April 2005

AbstractCannabis is one of the most common ‚co‐drugs’︁ for ecstasy users. The aim of the present study was to explore self‐reported psychobiological problems in ecstasy polydrug users in relation to their pattern of cannabis use. Two hundred and eighty ecstasy polydrug users were allocated into five cannabis groups according to the frequency of their cannabis use. The control group comprised 121 alcohol‐tobacco users. There were no significant group differences with regard to age, diagnosed family psychiatric history and level of self‐rated stress experienced during 6 months prior to the study. The present study produced three main findings: (a) Ecstasy users with no concomitant use of cannabis displayed more self‐rated aggression and somatic symptoms compared with ecstasy users who were smoking cannabis on a monthly or weekly basis. (b) Ecstasy users who reported heavy cannabis use in the past displayed higher paranoid symptoms compared with ecstasy weekly and daily cannabis users. (c) Former heavy cannabis users were the most likely to complain of a variety of ecstasy related long‐term problems. In conclusion, moderate cannabis use may help to ameliorate or mask MDMA‐induced aggressivity and somatic symptoms. However, this study confirms that heavy cannabis and ecstasy use is associated with several psychobiological problems, which may emerge after a period of abstinence from both drugs. Copyright © 2005 John Wiley & Sons, Ltd.
Transactivation of cyclin E gene by EWS‐Fli1 and antitumor effects of cyclin dependent kinase inhibitor on Ewing's family tumor cells
Authors: Li Xu , Tanaka Kazuhiro , Nakatani Fumihiko , Matsunobu Tomoya , Sakimura Riku , Hanada Masuo , Okada Takamitsu , Nakamura Tomoyuki , Iwamoto Yukihide 
Published: April 2005

AbstractChromosomal translocation t(11; 22)(q24; q12) is detected in approximately 90% of Ewing's family tumors (EFTs) including Ewing's sarcoma and primitive neuroectodermal tumor. This results in the formation of the EWS‐Fli1 fusion gene, which produces EWS‐Fli1 fusion protein. This chimerical gene product acts as an aberrant transcriptional activator, which may be responsible for the tumorigenesis of EFTs. We have previously reported that cyclin E expression was upregulated in EFT cells and in EWS‐Fli1 transformed fibroblastic cells. However, the mechanism of the overexpression of cyclin E by EWS‐Fli1 is still unknown. In our study, we investigated the mechanism of transactivation of the cyclin E gene in EFT cells. We found that EWS‐Fli1 enhanced the activity of the cyclin E gene promoter partially through E2F binding sites in the promoter. In addition, the basic transcriptional factor, Sp1, might also be involved in the transactivation of the cyclin E gene by EWS‐Fli1. To study the biological significance of cyclin E overexpression in EFT cells, we used flavopiridol, a pan‐cyclin‐dependent kinase (CDK) inhibitor and found that flavopiridol efficiently suppressed the growth of EFT cells in vitro and in vivo by the inhibition of cyclinE/CDK2 kinase activity and the induction of apoptosis. These results suggest that targeting of the cyclin/CDK complex may provide new insight into treatment of EFTs. © 2005 Wiley‐Liss, Inc.
hTERT gene copy number is not associated with hTERT RNA expression or telomerase activity in colorectal cancer
Authors: Palmqvist Richard , Zhang Anju , Xu Dawei , Golovleva Irina , Norrback Karl‐Fredrik , Gruber Astrid , Öberg Åke , Stenling Roger , Roos Göran 
Published: April 2005

AbstractIn a majority of malignant human tumors telomerase activity can be detected, suggesting an immortal phenotype. Expression of the reverse transcriptase subunit, hTERT, in the human telomerase complex is required for telomerase activity. The regulation of hTERT, from gene level to a fully functional protein, is still a poorly understood process. Increased copy number of the hTERT gene has been demonstrated in a significant portion of established cell lines and tumors of different origin but its relevance for telomerase activity levels is unclear. In the present study, we examined the hTERT gene copy number using fluorescence in situ hybridization (FISH) in samples from 64 colorectal carcinomas and an increased copy number (≥ 3 hTERT gene copies/nucleus) was observed in 31 cases (48%). No statistical association existed between hTERT gene copy number and hTERT RNA expression or telomerase activity. However, a significant relationship was found between an increase in hTERT gene copy number and p53 protein accumulation (p = 0.002) and aneuploidy (p = 0.036). Only 4 tumors showed microsatellite instability, 3 of which had a normal hTERT gene copy number. The data indicated that the increased copy number of the hTERT gene in colorectal carcinoma was a result of genomic instability with no obvious consequence for telomerase activity levels. © 2005 Wiley‐Liss, Inc.
Endogenous immune response to gangliosides in patients with confined prostate cancer
Authors: Ravindranath Mepur H. , Muthugounder Sakunthala , Presser Naftali , Ye Xing , Brosman Stanley , Morton Donald L. 
Published: April 2005

AbstractOur study investigated whether endogenous IgM antibodies to gangliosides occur in patients with early stages of prostate cancer (CaP) patients, after defining ganglioside profiles of CaP cell lines. Immune and resorcinol staining detected the presence of gangliosides GM3, GM2, GD3, GD2 and GD1a but not GM1a, GD1b or GT1b in the extracts of normal prostatic epithelial cells (PrEC) and neoplastic androgen‐insensitive (PC‐3, DU145) and ‐sensitive (LNCaP‐FGC and LNCaP‐FGC‐10) CaP cells. Using a sensitive ELISA, developed and validated in our laboratory, the titers of IgM against 8 gangliosides from sera of patients with benign prostatic hyperplasia (BPH) (n = 11), organ‐confined (T1/T2, n = 36) and unconfined (T3/T4, n = 27) CaP and age‐matched healthy men (n = 11) were determined double‐blinded. Using ANOVA and Fisher's least significant difference (LSD) methods, the log‐titers among different groups were compared. CaP patients differed from healthy and BPH patients in increased titers against GD1a and decreased titers against GD3. Titers of antibodies to other gangliosides exhibited no difference between CaP patients and others. The specific augmentation of anti‐GD1a IgM in patients with organ‐confined CaP (stage T1/T2) but not in patients with unconfined CaP (stage T3/T4) or BPH or in healthy controls is striking. This finding together with identification of GD1a as a major ganglioside in CaP cell lines and with the accruing studies on the immunosuppressive nature of GD1a indicates that augmentation of anti‐GD1a IgM in confined CaP may signify an early endogenous immune response to eliminate a “danger signal” from tumor microenvironment and circulation. © 2005 Wiley‐Liss, Inc.
Epidemiology of testicular cancer: An overview
Authors: Garner Michael J. , Turner Michelle C. , Ghadirian Parviz , Krewski Daniel 
Published: April 2005

AbstractTesticular cancer is a rare disease, accounting for 1.1% of all malignant neoplasms in Canadian males. Despite the low overall incidence of testicular cancer, it is the most common malignancy among young men. The incidence rate of testicular cancer has been increasing since the middle of the 20th century in many western countries. However, the etiology of testicular cancer is not well understood. A search of the peer‐reviewed literature was conducted to identify important articles for review and inclusion in this overview of the epidemiology of testicular cancer. Most of the established risk factors are related to early life events, including cryptorchidism, carcinoma in situ and in utero exposure to estrogens. Occupational, lifestyle, socioeconomic and other risk factors have demonstrated mixed associations with testicular cancer. Although there are few established risk factors for testicular cancer, some appear to be related to hormonal balance at various life stages. Lifestyle and occupational exposures occurring later in life may play a role in promoting the disease, although they are not likely involved in cancer initiation. In addition to summarizing the current epidemiologic evidence on risk factors for testicular cancer, we suggest future research directions that may elucidate the etiology of testicular cancer. © 2005 Wiley‐Liss, Inc.
Family history as a co‐factor for adenocarcinoma and squamous cell carcinoma of the uterine cervix: Results from two studies conducted in Costa Rica and the United States
Authors: Zelmanowicz Alice de M. , Schiffman Mark , Herrero Rolando , Goldstein Alisa M. , Sherman Mark E. , Burk Robert D. , Gravitt Patti , Viscidi Ray , Schwartz Peter , Barnes Willard , Mortel Rodrigue , Silverberg Steven G. , Buckland Julie , Hildesheim Allan 
Published: April 2005

AbstractPrevious work suggests that cervical cancer may aggregate in families. We evaluated the association between a family history of gynecological tumors and risk of squamous cell and adenocarcinomas of the cervix in 2 studies conducted in Costa Rica and the United States. The Costa Rican study consisted of 2,073 women (85 diagnosed with CIN3 or cancer, 55 diagnosed with CIN2 and 1,933 controls) selected from a population‐based study of 10,049 women. The U.S. study consisted of 570 women (124 with in situ or invasive adenocarcinomas, 139 with in situ or invasive squamous cell carcinomas of the cervix and 307 community‐based controls) recruited as part of a multicentric case‐control study in the eastern part of the United States. Information on family history of cervical and other cancers among first‐degree relatives was ascertained via questionnaire. Information on other risk factors for cervical cancer was obtained via questionnaire. Human papillomavirus (HPV) exposure was assessed in both studies using broad spectrum HPV L1‐based PCR testing of exfoliated cervicovaginal cells and in Costa Rica by additional testing of plasma collected from participants for antibodies against the L1 protein of HPV types 16, 18, 31 and 45 by ELISA. A family history of cervical cancer in a first‐degree relative was associated with increased risk of squamous tumors in both studies (odds ration [OR] = 3.2 for CIN3/cancer vs. controls; 95% confidence interval [CI] = 1.1–9.4 in Costa Rica; OR = 2.6 for in situ/invasive squamous cell carcinoma cases vs. controls, 95% CI = 1.1–6.4 in the Eastern United States study). These associations were evident regardless of whether the affected relative was a mother, sister or daughter of the study participant. Furthermore, observed effects were not strongly modified by age. In Costa Rica, the effect persisted in analysis restricted to HPV‐exposed individuals (OR = 3.0; 95% CI = 1.0–9.0), whereas in the Eastern United States study there was evidence of attenuation of risk in analysis of squamous carcinoma cases restricted to HPV positive women (OR = 1.4; 95% CI = 0.29–6.6). No significant association was observed between a family history of cervical cancer in a first‐degree relative and adenocarcinomas (OR = 1.3; 95% CI = 0.43–3.9). History of gynecological tumors other than cervical cancer in a first‐degree relative was not significantly associated with risk of disease in either study. These results are consistent with a role of host factors in the pathogenesis of squamous cell cervical cancer, although familial aggregation due to shared environmental exposures cannot be ruled out. © 2005 Wiley‐Liss, Inc.
Intracellular anti‐E7 human antibodies in single‐chain format inhibit proliferation of HPV16‐positive cervical carcinoma cells
Authors: Accardi Luisa , Donà M. Gabriella , Di Bonito Paola , Giorgi Colomba 
Published: April 2005

AbstractThe E7 tumor antigen of human papillomavirus type 16 (HPV16) is a validated target for immunodiagnosis and immunotherapy of HPV‐associated cervical cancer. Anti‐HPV16 E7 antibodies in scFv format were isolated from a human antibody phage display library and characterized. With the aim of interfering with the oncogenic activity of E7 protein, the most reactive of the selected antibody fragments was expressed by eukaryotic vectors in different compartments of the HPV16‐positive cervical carcinoma SiHa cell line. The intracellular antibodies (intrabodies) were tested for their ability of inhibiting cell proliferation. A significant inhibition was obtained targeting the intrabodies to the nuclear and secretory compartments whereas no significant effect was observed in case of cytoplasmic localization. Inhibition was highly specific as no antiproliferative effect was obtained either with the E7‐specific intrabodies in HPV‐negative cells nor with irrelevant intrabodies in SiHa cells. © 2005 Wiley‐Liss, Inc.
Identification of 20 genes aberrantly methylated in human breast cancers
Authors: Miyamoto Kazuaki , Fukutomi Takashi , Akashi‐Tanaka Sadako , Hasegawa Tadashi , Asahara Toshimasa , Sugimura Takashi , Ushijima Toshikazu 
Published: April 2005

AbstractAberrant methylation of CpG islands (CGI) not only plays a role in gene silencing, but is also a potential cancer biomarker. To identify more CGI aberrantly methylated in human breast cancers, we carried out a genome‐wide search for aberrant methylation, using methylation‐sensitive‐representational difference analysis. CGI in 5′ upstream regions of 20 genes, TSPAN‐2, AK5, LOC284999, HOXD11, FLJ25161, XT3, PCDH10, PCDHGB6, SIM1, LOC346978, COE2, TDH (FLJ25033), LOC346419, FLJ33790, GJB2, AMN, LOC201164, DLX4, DCC and FOXA2, were found to be methylated in at least one of 8 breast cancer cell lines. Fifteen of the 20 genes were methylated in more than one of 21 primary breast cancers in Stages I or II, and especially, those of LOC346978, HOXD11, SIM1, PCDHGB6 and FLJ25161 were methylated in more than 10 cancers. All the breast cancers had some aberrant methylation. Among the 13 genes whose CGI were completely methylated in one or more cell lines, FOXA2 and XT3 were expressed in normal human mammary epithelial cells (HMEC) and were not expressed in cancer cell lines with complete methylation. The other 11 genes examined were barely expressed, or not expressed even in HMEC. Our results showed that breast cancer cells accumulate aberrant methylation of the CGI identified here. This may serve as markers for early‐stage breast cancers and suggests that aberrant methylation targets transcriptionally inactive genes in vivo. © 2005 Wiley‐Liss, Inc.
Serum matrix metalloproteinase‐9 in head and neck squamous cell carcinomais a prognostic marker
Authors: Ruokolainen Henni , Pääkkö Paavo , Turpeenniemi‐Hujanen Taina 
Published: April 2005

AbstractThe aim of this study was to determine whether serum matrix metalloproteinase‐9 (MMP‐9) could predict cause‐specific and relapse‐free survival in patients with squamous cell carcinoma of head and neck. Furthermore, this study was designed to investigate whether there is an association between MMP‐9 immunohistochemical staining and serum MMP‐9 levels. Pretreatment serum levels of MMP‐9 were quantitatively measured by ELISA assay in 67 patients presenting with a primary head and neck squamous cell carcinoma. The results were compared with the corresponding immunohistochemical staining results, clinical data and the patients' outcome. The follow‐up time for all of the patients was at least 5 years. There was a statistically significant correlation between circulating MMP‐9 and MMP‐9 immunohistochemical staining in the corresponding tumors (p = 0.028). The cause‐specific and relapse‐free survival rates were clearly lower among patients with high MMP‐9 serum levels (> 73 ng/ml). The 5‐year cause‐specific survival‐rate was 40% in a patient group with high serum MMP‐9, and 69% for patients with a low MMP‐9 level (p = 0.027). In the same follow‐up period, the cumulative relapse‐free survival rate was 36% in patients presenting with a high serum MMP‐9 and 66% in those with a low MMP‐9 level. No correlation was found between MMP‐9 serum levels and the traditional clinical or histopathologic factors. The results suggest for the first time that pretreatment serum MMP‐9 level could serve as a prognostic factor in head and neck squamous cell carcinoma. © 2005 Wiley‐Liss, Inc.
Ribonucleotide reductase inhibitors enhance cidofovir‐induced apoptosis in EBV‐positive nasopharyngeal carcinoma xenografts
Authors: Wakisaka Naohiro , Yoshizaki Tomokazu , Raab‐Traub Nancy , Pagano Joseph S. 
Published: April 2005

AbstractIn nasopharyngeal carcinoma (NPC), Epstein‐Barr virus (EBV) infection is mainly latent, and the tumor cells contain episomal viral DNA. We have shown that the acyclic nucleoside phosphonate analog, cidofovir [(S)‐1‐(3‐hydroxy‐2‐(phosphonylmethoxypropyl))cytosine] (HPMPC), inhibits growth of NPC xenografts in nude mice by causing apoptosis. The ribonucleotide reductase (RR) inhibitors, hydroxyurea and didox (3,4‐dihydroxybenzohydroxamic acid), have been demonstrated to inhibit neoplastic growth and are used as antiviral and anticancer agents. Here we show that RR inhibitors enhance the antitumor effect of cidofovir in EBV‐transformed epithelial cells. MTT assays indicate that hydroxyurea and didox enhance cidofovir‐induced cell toxicity in NPC‐KT cells, an EBV‐positive epithelial cell line derived from NPC. The effect is due to enhancement of apoptosis through the caspase cascade as shown by pronounced cleavage of poly(ADP‐ribose) polymerase. Finally, hydroxyurea strikingly enhanced the cidofovir‐induced growth‐inhibitory effect on NPC grown in athymic mice. The results suggest that RR inhibitors should enhance the antitumor effect of acyclic nucleoside phosphonate analogs on NPC. © 2005 Wiley‐Liss, Inc.
Zori 1.0: A parallel quantum Monte Carlo electronic structure package
Authors: Aspuru–Guzik Alán , Salomón–Ferrer Romelia , Austin Brian , Perusquía–Flores Raul , Griffin Mary A. , Oliva Ricardo A. , Skinner David , Domin Dominik , Lester William A. 
Published: April 2005

AbstractThe Zori 1.0 package for electronic structure computations is described. Zori performs variational and diffusion Monte Carlo computations as well as correlated wave function optimization. This article presents an overview of the implemented methods and code capabilities. © 2005 Wiley Periodicals, Inc. J Comput Chem 26: 856–862, 2005
Hamiltonicity and forbidden subgraphs in 4‐connected graphs
Authors: Pfender Florian 
Published: April 2005

AbstractLet T be the line graph of the unique tree F on 8 vertices with degree sequence (3,3,3,1,1,1,1,1), i.e., T is a chain of three triangles. We show that every 4‐connected {T, K1,3}‐free graph has a hamiltonian cycle. © 2005 Wiley Periodicals, Inc. J Graph Theory 49: 262–272, 2005
Posets and planar graphs
Authors: Felsner Stefan , Trotter William T. 
Published: April 2005

AbstractUsually dimension should be an integer valued parameter. We introduce a refined version of dimension for graphs, which can assume a value [t − 1 ↕ t], thought to be between t − 1 and t. We have the following two results: (a) a graph is outerplanar if and only if its dimension is at most [2↕3]. This characterization of outerplanar graphs is closely related to the celebrated result of W. Schnyder [16] who proved that a graph is planar if and only if its dimension is at most 3. (b) The largest n for which the dimension of the complete graph Kn is at most [t − 1 ↕ t] is the number of antichains in the lattice of all subsets of a set of size t − 2. Accordingly, the refined dimension problem for complete graphs is equivalent to the classical combinatorial problem known as Dedekind's problem. This result extends work of Hoşten and Morris [14]. The main results are enriched by background material, which links to a line of research in extremal graph theory, which was stimulated by a problem posed by G. Agnarsson: Find the maximum number of edges in a graph on n nodes with dimension at most t. © 2005 Wiley Periodicals, Inc. J Graph Theory 49: 273–284, 2005