bluuebunny/crossref_metadata_2025_split huggingface dataset:
Discovery of a strong magnetic field on the O star HD 191612: new clues to the future of θ1 Orionis C
Authors: Donati J.-F. , Howarth I. D. , Bouret J.-C. , Petit P. , Catala C. , Landstreet J. 
Published: November 2005

Abstract
From observations made with the ESPaDOnS spectropolarimeter, recently installed on the 3.6-m Canada-France-Hawaii Telescope, we report the discovery of a strong magnetic field in the Of?p spectrum variable HD 191612 - only the second known magnetic O star (following θ1 Ori C). The stability of the observed Zeeman signature over four nights of observation, together with the non-rotational shape of line profiles, argues that the rotation period of HD 191612 is significantly longer than the 9-d value previously proposed. We suggest that the recently identified 538-d spectral variability period is the rotation period, in which case the observed line-of-sight magnetic field of −220 ± 38 G implies a large-scale field (assumed dipolar) with a polar strength of about −1.5 kG. If confirmed, this scenario suggests that HD 191612 is, essentially, an evolved version of the near-zero-age main-sequence magnetic O star θ1 Ori C, but with an even stronger field (about 15 kG at an age similar to that of θ1 Ori C). We suggest that the rotation rate of HD 191612, which is exceptionally slow by accepted O-star standards, could be due to angular momentum dissipation through a magnetically confined wind.
DECOY STATE QUANTUM KEY DISTRIBUTION
Authors: LO HOI-KWONG 
Published: November 2005

Quantum key distribution (QKD) allows two parties to communicate in absolute security based on the fundamental laws of physics. Up till now, it is widely believed that unconditionally secure QKD based on standard Bennett-Brassard (BB84) protocol is limited in both key generation rate and distance because of imperfect devices. Here, we solve these two problems directly by presenting new protocols that are feasible with only current technology. Surprisingly, our new protocols can make fiber-based QKD unconditionally secure at distances over 100km (for some experiments, such as GYS) and increase the key generation rate from O(η2) in prior art to O(η) where η is the overall transmittance. Our method is to develop the decoy state idea (first proposed by W.-Y. Hwang in "Quantum Key Distribution with High Loss: Toward Global Secure Communication", Phys. Rev. Lett. 91, 057901 (2003)) and consider simple extensions of the BB84 protocol. This part of work is published in "Decoy State Quantum Key Distribution", . We present a general theory of the decoy state protocol and propose a decoy method based on only one signal state and two decoy states. We perform optimization on the choice of intensities of the signal state and the two decoy states. Our result shows that a decoy state protocol with only two types of decoy states—a vacuum and a weak decoy state—asymptotically approaches the theoretical limit of the most general type of decoy state protocols (with an infinite number of decoy states). We also present a one-decoy-state protocol as a special case of Vacuum+Weak decoy method. Moreover, we provide estimations on the effects of statistical fluctuations and suggest that, even for long distance (larger than 100km) QKD, our two-decoy-state protocol can be implemented with only a few hours of experimental data. In conclusion, decoy state quantum key distribution is highly practical. This part of work is published in "Practical Decoy State for Quantum Key Distribution", . We also have done the first experimental demonstration of decoy state quantum key distribution, over 15km of Telecom fibers. This part of work is published in "Experimental Decoy State Quantum Key Distribution Over 15km", .
Does a computer have sexual preferences?
Authors: Mazlack Lawrence J. 
Published: November 2005

At the University of Guelph there has been a single significant introductory computer science course. Approximately 50% of the University's full time undergraduate students have taken this course during their academic career. Sectioning and enrollment has generally been done without regard to academic program or semester in school.
An examination of the past two years' results was performed utilizing the records of 1,350 students. Negligible correlations were found between a student's sex, academic program or semester in school when posed against the students' grades (both final and by grade component). All three results are contrary to the normal implicit assumptions regarding competitiveness between sexes, academic programs and student experience in a computer science course.
Learning theory and political socialization
Authors: Swigger Kathleen M. 
Published: November 2005

The purpose of this C.A.I. module is to introduce students enrolled in undergraduate courses in political science, sociology, and education to aspects of learning theory that have direct application to a study of political socialization. The interactive module demonstrates how various models representing learning theories can be used to describe the process by which individuals acquire their political behavior. The purpose of this C.A.I. module is to describe learning theory in such a way as to guide students in critically constructing and evaluating their own assumptions concerning the nature of the process of political socialization. Thus, it is felt that these lessons can contribute to a better understanding of the prominent literature that deals with questions considered relevant to a discussion of political socialization.
The lessons in the module were written in the Instructional Dialogue Facility (IDF) on a Hewlett-Packard 2000 at the University of Iowa. These lessons call over a dozen BASIC programs specifically written for the module. The lessons allow for self-pacing and freedom of choice concerning the number and type of learning subtasks that the student undertakes at any particular time. The module not only enhances the courses for which they were designed but also adds to the inventory of interactive lessons available to all users of computer assisted instruction.
An interactive program advising system
Authors: Gillett Will 
Published: November 2005

This paper describes components of an Interactive Program Advising System (IPAS) for beginning programming students. The system, being unaware of the algorithm being implemented by the student, is unable to direct the student toward writing a correct program. It instead comments on the programming constructs the student has used in the specific implementing language—in this case FORTRAN.
Beginning programming students often write poorly structured programs (especially in a non-block-structured language like FORTRAN) with constructs which, while legal, indicate that the student doesn't really understand the operation being performed. Data is currently being collected on “conceptual errors” commonly made by beginning students. This paper describes some of these “errors” and what comments can be presented to the student to help him understand and correct his own “errors.” A subsequent paper will present statistics on frequency of errors and plausible student logic which would produce the errors.
A Direct Test of Potential Roles for β3 and β5 Integrins in Growth and Metastasis of Murine Mammary Carcinomas
Authors: Taverna Daniela , Crowley Denise , Connolly Mary , Bronson Roderick T. , Hynes Richard O. 
Published: November 2005

Abstract
αvβ3 or αvβ5 integrins are widely expressed on blood and endothelial cells. Inhibition of the functions of these integrins has been reported to suppress neovascularization and tumor growth, suggesting that they may be critical modulators of angiogenesis. However, mice lacking these integrins exhibit extensive angiogenesis. Tumors arising from s.c. injections of tumor cells into mice lacking one or both integrins show enhanced tumor growth compared with growth in control mice due to both increased angiogenesis and to altered innate immune response. Other data suggest additional roles for these integrins, on either platelets or the tumor cells themselves, in enhancing tumor progression and metastasis. Here, we investigate the involvement of β3 and β5 integrins in the development and progression of mammary carcinomas. We intercrossed mouse mammary tumor virus (MMTV)-c-neu transgenic mice with β3 or β5 or β3β5 integrin-deficient mice and observed that multiple, large mammary tumors developed in 100% of mice on all genetic backgrounds. A statistically significant earlier onset of tumor growth was observed in the MMTV-c-neu/β3β5 integrin-null females compared with control mice. No major differences were observed in tumor size or number, vessel number or vessel structure and lung metastases were observed with similar frequency and size in all strains. MMTV-c-neu/β3β5 integrin-null mice had higher numbers of mammary acini, which may account for the earlier onset of tumors in this strain. These data indicate that αvβ3 or αvβ5 integrins are not essential for tumor growth and progression, although they might play some role in mammary gland development.
The Role of Peroxiredoxin II in Radiation-Resistant MCF-7 Breast Cancer Cells
Authors: Wang Tieli , Tamae Daniel , LeBon Thomas , Shively John E. , Yen Yun , Li Jian Jian 
Published: November 2005

Abstract
Although several signaling pathways have been suggested to be involved in the cellular response to ionizing radiation, the molecular basis of tumor resistance to radiation remains elusive. We have developed a unique model system based upon the MCF-7 human breast cancer cell line that became resistant to radiation treatment (MCF+FIR30) after exposure to chronic ionizing radiation. By proteomics analysis, we found that peroxiredoxin II (PrxII), a member of a family of peroxidases, is up-regulated in the radiation-derived MCF+FIR3 cells but not in the MCF+FIS4 cells that are relatively sensitive to radiation. Both MCF+FIR3 and MCF+FIS4 cell lines are from MCF+FIR30 populations. Furthermore, the resistance to ionizing radiation can be partially reversed by silencing the expression of PrxII by PrxII/small interfering RNA treatment of MCF+FIR3 resistant cells, suggesting that PrxII is not the sole factor responsible for the resistant phenotype. The relevance of this mechanism was further confirmed by the increased radioresistance in PrxII-overexpressing MCF+FIS4 cells when compared with vector control cells. The up-regulation of the PrxII protein in radioresistant cancer cells suggested that human peroxiredoxin plays an important role in eliminating the generation of reactive oxygen species by ionizing radiation. The present finding, together with the observation that PrxII is also up-regulated in response to ionizing radiation in other cell systems, strengthens the hypothesis that the PrxII antioxidant protein is involved in the cellular response to ionizing radiation and functions to reduce the intracellular reactive oxygen species levels, resulting in increased resistance of breast cancer cells to ionizing radiation.
Diminished Expression of Transcription Factors Nuclear Factor κB and CCAAT/Enhancer Binding Protein Underlies a Novel Tumor Evasion Mechanism Affecting Macrophages of Mammary Tumor–Bearing Mice
Authors: Torroella-Kouri Marta , Ma Xiaojing , Perry Giselle , Ivanova Milena , Cejas Pedro J. , Owen Jennifer L. , Iragavarapu-Charyulu Vijaya , Lopez Diana M. 
Published: November 2005

AbstractInteractions between malignant tumors and the host immune system shape the course of cancer progression. The molecular basis of such interactions is the subject of immense interest. Proinflammatory cytokines produced by macrophages are critical mediators of immune responses that contribute to the control of the advancement of neoplasia. We have shown that the expressions of interleukin 12 (IL-12) and inducible nitric oxide synthase (iNOS) are decreased in macrophages from mammary tumor–bearing mice. In this study, we investigated the causes of IL-12 dysregulation and found deficient nuclear factor κB (NFκB) and CCAAT/enhancer binding protein (C/EBP) expression and function in tumor bearers' peritoneal macrophages. The constitutive expressions of NFκB p50, c-rel, p65, and C/EBPα and β, as well as the lipopolysaccharide-induced nuclear translocation and DNA binding of NFκB components and C/EBPα and β, are profoundly impaired in macrophages from mice bearing D1-DMBA-3 tumors. Because similar findings occur with the iNOS gene, it seems that it represents a novel mechanism by which tumor-derived factors interfere with the host immune defenses.
Novel Molecular Signaling and Classification of Human Clinically Nonfunctional Pituitary Adenomas Identified by Gene Expression Profiling and Proteomic Analyses
Authors: Moreno Carlos S. , Evans Chheng-Orn , Zhan Xianquan , Okor Mammerhi , Desiderio Dominic M. , Oyesiku Nelson M. 
Published: November 2005

Abstract
Pituitary adenomas comprise 10% of intracranial tumors and occur in about 20% of the population. They cause significant morbidity by compression of regional structures or the inappropriate expression of pituitary hormones. Their molecular pathogenesis is unclear, and the current classification of clinically nonfunctional tumors does not reflect any molecular distinctions between the subtypes. To further elucidate the molecular changes that contribute to the development of these tumors and reclassify them according to the molecular basis, we investigated 11 nonfunctional pituitary adenomas and eight normal pituitary glands, using 33 oligonucleotide GeneChip microarrays. We validated microarray results with the reverse transcription real-time quantitative PCR, using a larger number of nonfunctional adenomas. We also used proteomic analysis to examine protein expression in these nonfunctional adenomas. Microarray analysis identified significant increases in the expression of 115 genes and decreases in 169 genes, whereas proteomic analysis identified 21 up-regulated and 29 down-regulated proteins. We observed changes in expression of SFRP1, TLE2, PITX2, NOTCH3, and DLK1, suggesting that the developmental Wnt and Notch pathways are activated and important for the progression of nonfunctional pituitary adenomas. We further analyzed gene expression profiles of all nonfunctional pituitary subtypes to each other and identified genes that were affected uniquely in each subtype. These results show distinct gene and protein expression patterns in adenomas, provide new insight into the pathogenesis and molecular classification of nonfunctional pituitary adenomas, and suggest that therapeutic targeting of the Notch pathway could be effective for these tumors.
Steroid Receptor Regulation of Epidermal Growth Factor Signaling through Src in Breast and Prostate Cancer Cells: Steroid Antagonist Action
Authors: Migliaccio Antimo , Di Domenico Marina , Castoria Gabriella , Nanayakkara Merlin , Lombardi Maria , de Falco Antonietta , Bilancio Antonio , Varricchio Lilian , Ciociola Alessandra , Auricchio Ferdinando 
Published: November 2005

Abstract
Under conditions of short-term hormone deprivation, epidermal growth factor (EGF) induces DNA synthesis, cytoskeletal changes, and Src activation in MCF-7 and LNCaP cells. These effects are drastically inhibited by pure estradiol or androgen antagonists, implicating a role of the steroid receptors in these findings. Interestingly, EGF triggers rapid association of Src with androgen receptor (AR) and estradiol receptor α (ERα) in MCF-7 cells or ERβ in LNCaP cells. Here, we show that, through EGF receptor (EGFR) and erb-B2, EGF induces tyrosine phosphorylation of ER preassociated with AR, thereby triggering the assembly of ER/AR with Src and EGFR. Remarkably, experiments in Cos cells show that this complex stimulates EGF-triggered EGFR tyrosine phosphorylation. In turn, estradiol and androgen antagonists, through the Src-associated receptors, prevent Src activation by EGF and heavily reduce EGFR tyrosine phosphorylation and the subsequent multiple effects, including DNA synthesis and cytoskeletal changes in MCF-7 cells. In addition, knockdown of ERα or AR gene by small interfering RNA (siRNA) almost abolishes EGFR tyrosine phosphorylation and DNA synthesis in EGF-treated MCF-7 cells. The present findings reveal that steroid receptors have a key role in EGF signaling. EGFR tyrosine phosphorylation, depending on Src, is a part of this mechanism. Understanding of EGF-triggered growth and invasiveness of mammary and prostate cancer cells expressing steroid receptors is enhanced by this report, which reveals novel aspects of steroid receptor action.
Postreplicative Joining of DNA Double-Strand Breaks Causes Genomic Instability in DNA-PKcs–Deficient Mouse Embryonic Fibroblasts
Authors: Martín Marta , Genescà Anna , Latre Laura , Jaco Isabel , Taccioli Guillermo E. , Egozcue Josep , Blasco María A. , Iliakis George , Tusell Laura 
Published: November 2005

Abstract
Combined cytogenetic and biochemical approaches were used to investigate the contributions of the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) in the maintenance of genomic stability in nonirradiated and irradiated primary mouse embryo fibroblasts (MEF). We show that telomere dysfunction contributes only marginally to genomic instability associated with DNA-PKcs deficiency in the absence of radiation. Following exposure to ionizing radiation, DNA-PKcs−/− MEFs are radiosensitized mainly as a result of the associated DNA double-strand break (DSB) repair defect. This defect manifests as an increase in the fraction of DSB rejoining with slow kinetics although nearly complete rejoining is achieved within 48 hours. Fifty-four hours after ionizing radiation, DNA-PKcs−/− cells present with a high number of simple and complex chromosome rearrangements as well as with unrepaired chromosome breaks. Overall, induction of chromosome aberrations is 6-fold higher in DNA-PKcs−/− MEFs than in their wild-type counterparts. Spectral karyotyping-fluorescence in situ hybridization technology distinguishes between rearrangements formed by prereplicative and postreplicative DSB rejoining and identifies sister chromatid fusion as a significant source of genomic instability and radiation sensitivity in DNA-PKcs−/− MEFs. Because DNA-PKcs−/− MEFs show a strong G1 checkpoint response after ionizing radiation, we propose that the delayed rejoining of DNA DSBs in DNA-PKcs−/− MEFs prolongs the mean life of broken chromosome ends and increases the probability of incorrect joining. The preponderance of sister chromatid fusion as a product of incorrect joining points to a possible defect in S-phase arrest and emphasizes proximity in these misrepair events.
Possible Detection of Pancreatic Cancer by Plasma Protein Profiling
Authors: Honda Kazufumi , Hayashida Yasuharu , Umaki Tomoko , Okusaka Takuji , Kosuge Tomoo , Kikuchi Satoru , Endo Mitsufumi , Tsuchida Akihiko , Aoki Tatsuya , Itoi Takao , Moriyasu Fuminori , Hirohashi Setsuo , Yamada Tesshi 
Published: November 2005

AbstractThe survival rate of pancreatic cancer patients is the lowest among those with common solid tumors, and early detection is one of the most feasible means of improving outcomes. We compared plasma proteomes between pancreatic cancer patients and sex- and age-matched healthy controls using surface-enhanced laser desorption/ionization coupled with hybrid quadrupole time-of-flight mass spectrometry. Proteomic spectra were generated from a total of 245 plasma samples obtained from two institutes. A discriminating proteomic pattern was extracted from a training cohort (71 pancreatic cancer patients and 71 healthy controls) using a support vector machine learning algorithm and was applied to two validation cohorts. We recognized a set of four mass peaks at 8,766, 17,272, 28,080, and 14,779 m/z, whose mean intensities differed significantly (Mann-Whitney U test, P &lt; 0.01), as most accurately discriminating cancer patients from healthy controls in the training cohort [sensitivity of 97.2% (69 of 71), specificity of 94.4% (67 of 71), and area under the curve value of 0.978]. This set discriminated cancer patients in the first validation cohort with a sensitivity of 90.9% (30 of 33) and a specificity of 91.1% (41 of 45), and its discriminating capacity was further validated in an independent cohort at a second institution. When combined with CA19-9, 100% (29 of 29 patients) of pancreatic cancers, including early-stage (stages I and II) tumors, were detected. Although a multi-institutional large-scale study will be necessary to confirm clinical significance, the biomarker set identified in this study may be applicable to using plasma samples to diagnose pancreatic cancer.
Complement-Mediated Mechanisms in Anti-GD2 Monoclonal Antibody Therapy of Murine Metastatic Cancer
Authors: Imai Masaki , Landen Charles , Ohta Rieko , Cheung Nai-Kong V. , Tomlinson Stephen 
Published: November 2005

AbstractThe role of complement in antibody therapy of cancer is in general poorly understood. We used the EL4 syngeneic mouse model of metastatic lymphoma to investigate the role of complement in immunotherapy directed against GD2, a target of clinical relevance. IgG2a and IgM anti-GD2 therapy protected EL4-challenged mice from metastases and prolonged survival. Expression of CD59, an inhibitor of direct complement-mediated cytotoxicity (CMC), effectively protected EL4 cells from CMC in vitro but did not affect the outcome of monoclonal antibody therapy. Protection by IgG therapy was also unaffected in mice deficient in C3 or complement receptor 3 (CR3) but was almost completely abrogated in FcγR I/III–deficient mice. These data indicate a crucial role for antibody-dependent cell-mediated cytoxicity (ADCC). However, at lower doses of IgG, therapeutic effect was partially abrogated in C3-deficient mice, indicating complement-mediated enhancement of ADCC at limiting IgG concentration. In contrast to IgG, the therapeutic effect of IgM was completely abrogated in C3-deficient mice. High level expression of CD59 on EL4 did not influence IgM therapy, suggesting IgM functions by complement-dependent cell-mediated cytotoxicity (CDCC), a mechanism thought to be inactive against tumor cells. Thus, IgG and IgM can operate via different primary mechanisms of action, and CDCC and complement-dependent enhancement of ADCC mechanisms are operative in vivo. The effects of complement can be supplemental to other antibody-mediated mechanisms and likely have increased significance at limiting antibody concentration or low antigen density.
Loss of the hSNF5 Gene Concomitantly Inactivates p21CIP/WAF1 and p16INK4a Activity Associated with Replicative Senescence in A204 Rhabdoid Tumor Cells
Authors: Chai Jingjing , Charboneau Aubri L. , Betz Bryan L. , Weissman Bernard E. 
Published: November 2005

Abstract
hSNF5, the smallest member of the SWI/SNF chromatin remodeling complex, is lost in most malignant rhabdoid tumors (MRT). In MRT cell lines, reexpression of hSNF5 induces G1 cell cycle arrest, elevated p16INK4a, and activated replicative senescence markers, such as β-galactosidase (β-Gal) and plasminogen activator inhibitor-1. To compare the replicative senescence caused by hSNF5 in A204 cells to normal cellular senescence, we examined the activation of both p16INK4a and p21CIP/WAF1. Analogous to normal cellular senescence, both p16INK4a and p21CIP/WAF1 were up-regulated following hSNF5 restoration. Furthermore, we found that hSNF5 bound the p16INK4a and p21CIP/WAF1 promoters, suggesting that it directly regulates transcription of these genes. Using p16INK4a RNA interference, we showed its requirement for the replicative senescence caused by hSNF5 but not the growth arrest. Instead, p21CIP/WAF1 remained activated by hSNF5 in the absence of high p16INK4a expression, apparently causing the growth arrest in A204. Interestingly, we also found that, in the absence of p16INK4a, reexpression of hSNF5 also increased protein levels of a second cyclin-dependent kinase (CDK) inhibitor, p18INK4c. However, our data show that lack of hSNF5 does not abrogate cellular responsiveness to DNA damage or growth-inhibitory factors. In summary, our studies suggest that hSNF5 loss may influence the regulation of multiple CDK inhibitors involved in replicative senescence.