bluuebunny/crossref_metadata_2025_split huggingface dataset:
Voice and Data Solutions (India)
Authors: Mishra Sumita , Gupta Rajen K. 
Published: April 2008

VDS Inc., based in California, US, was founded by three Indian entrepreneurs in January 2000. The company provided VoIP (Voice over Internet Protocol) solutions to wireless, wire line and cable service providers in the US, Europe, and recently, Asia. VDS India, based in Noida, India, was established in September 2000 as the offshore product development base of VDS Inc. The product portfolio of VDS Inc. was steadily growing and gaining recognition in the industry. As a result, the product development base in India was becoming more important than ever. A new CEO, David Joseph was appointed in October 2003 to head VDS India. To standardize work processes to cope with growth in demand and to control attrition rates, David undertook initiatives such as the establishment of a human resources team, setting up of a technical documentation team, the tightening of team processes pertaining to induction and job allocation, and the initiation of organizational processes of employee performance appraisals. David noticed that changes were not easy to implement. Outsourcing of the human resources team and problems of coordination between the technical documentation team and the engineers posed major challenges to David. Integration of communication and information with VDS Inc. also was another area of concern. The case is useful for the examination of human elements in the implementation process.
Whether or Not to Disinvest: The Case of Gujarat State Fertilizers & Chemicals Limited
Authors: Dholakia Ravindra H. , Gandhi Shailesh 
Published: April 2008

India became independent in 1947. Its central planning model emphasized the development of core sectors of Indian economy through Public Sector Undertakings (PSUs). PSUs played an active role in economic development for more than four decades. The process of liberalization and globalization began in 1991. The Central and State Governments initiated process of disinvestment and decontrol in various PSUs. Gujarat State Fertilizers & Chemicals Limited (GSFC) was one of such PSUs. It was promoted in 1962 by the State Government of Gujarat (GoG) with its 49% equity share, as a joint sector fertilizer company. The objective of the Government was to promote agricultural growth by providing chemical fertilizers and other inputs along with extension services to the farmers. Over the years, it diversified into industrial products. It was also instrumental in promotion of other PSUs in Gujarat through equity participation. It had a strong brand image among the farmers. In 2004, GoG appointed an Expert Committee (EC) to review the performance and sustainability of various PSUs in the State of Gujarat including GSFC and to recommend whether or not the Government should continue to hold its investment in them. The task of EC in providing recommendations on GSFC was very challenging because GSFC incurred losses for the first time during 2000–1 to 2002–3 since its inception but showed dramatic turnaround in 2003–4 and further improved its financial performance in 2004–5 and 2005–6. EC had to reassess the developmental role of GSFC and the need for GoG to continue its involvement. It had to assess the sustainability of improved financial performance in future and decide whether or not GoG should disinvest its stake.
Optimistic parallelism benefits from data partitioning
Authors: Kulkarni Milind , Pingali Keshav , Ramanarayanan Ganesh , Walter Bruce , Bala Kavita , Chew L. Paul 
Published: April 2008

Recent studies of irregular applications such as finite-element mesh generators and data-clustering codes have shown that these applications have a generalized data parallelism arising from the use of iterative algorithms that perform computations on elements of worklists. In some irregular applications, the computations on different elements are independent. In other applications, there may be complex patterns of dependences between these computations.
The Galois system was designed to exploit this kind of irregular data parallelism on multicore processors. Its main features are (i) two kinds of set iterators for expressing worklist-based data parallelism, and (ii) a runtime system that performs optimistic parallelization of these iterators, detecting conflicts and rolling back computations as needed. Detection of conflicts and rolling back iterations requires information from class implementors.
In this paper, we introduce mechanisms to improve the execution efficiency of Galois programs: data partitioning, data-centric work assignment, lock coarsening, and over-decomposition. These mechanisms can be used to exploit locality of reference, reduce mis-speculation, and lower synchronization overhead. We also argue that the design of the Galois system permits these mechanisms to be used with relatively little modification to the user code. Finally, we present experimental results that demonstrate the utility of these mechanisms.
Client-server HTTP communications made easy
Authors: Kutinsky Vladimir 
Published: April 2008

This article covers the problem of making client requests to Web servers over HTTP. More specifically, this article addresses two interrelated problems, sending data to a Web server using the POST method and processing the request with a CGI script at the server side. The purpose of this work is to provide a basis for understanding how these tasks can be performed in APL. While the proposed solutions are of a general form, the discussion is oriented around working examples, instead of simply providing reference material.
The APL code discussed in the article uses a number of .Net libraries that greatly assist the task of programming and do most of the drudgery work for us, hence the name of the article.
A generic language for application-specific flow sampling
Authors: Madhyastha Harsha V. , Krishnamurthy Balachander 
Published: April 2008

Flow records gathered by routers provide valuable coarse-granularity traffic information for several measurement-related network applications. However, due to high volumes of traffic, flow records need to be sampled before they are gathered. Current techniques for producing sampled flow records are either focused on selecting flows from which statistical estimates of traffic volume can be inferred, or have simplistic models for applications. Such sampled flow records are not suitable for many applications with more specific needs, such as ones that make decisions across flows
As a first step towards tailoring the sampling algorithm to an application's needs, we design a generic language in which any particular application can express the classes of traffic of its interest. Our evaluation investigates the expressive power of our language, and whether flow records have sufficient information to enable sampling of records of relevance to applications. We use templates written in our custom language to instrument sampling tailored to three different applications--BLINC, Snort, and Bro. Our study, based on month-long datasets gathered at two different network locations, shows that by learning local traffic characteristics we can sample relevant flow records near-optimally with low false negatives in diverse applications
Fixed Point Methods for the Generalized Stability of Functional Equations in a Single Variable
Authors: Cădariu Liviu , Radu Viorel 
Published: March 2008

AbstractWe discuss on the generalized Ulam-Hyers stability for functional equations in a single variable, including the nonlinear functional equations, the linear functional equations, and a generalization of functional equation for the square root spiral. The stability results have been obtained by a fixed point method. This method introduces a metrical context and shows that the stability is related to some fixed point of a suitable operator.
Hypoxia Down-regulates CCAAT/Enhancer Binding Protein-α Expression in Breast Cancer Cells
Authors: Seifeddine Ramzi , Dreiem Anne , Blanc Etienne , Fulchignoni-Lataud Marie-Claude , Belda Marie-Aude Le Frère , Lecuru Fabrice , Mayi Thérèse Hervèe , Mazure Nathalie , Favaudon Vincent , Massaad Charbel , Barouki Robert , Massaad-Massade Liliane 
Published: April 2008

Abstract
The transcription factor CCAAT/enhancer binding protein-α (C/EBPα) is involved in the control of cell differentiation and proliferation, and has been suggested to act as a tumor suppressor in several cancers. By using microarray analysis, we have previously shown that hypoxia and estrogen down-regulate C/EBPα mRNA in T-47D breast cancer cells. Here, we have examined the mechanism by which the down-regulation by hypoxia takes place. Using the specific RNA polymerase II inhibitor 5,6-dichlorobenzimidazole-1-β-d-ribofuranoside, the mRNA stability was analyzed under normoxia or hypoxia by quantitative reverse transcription-PCR. Hypoxia reduced the half-life of C/EBPα mRNA by ∼30%. C/EBPα gene promoter studies indicated that hypoxia also repressed the transcription of the gene and identified a hypoxia-responsive element (−522; −527 bp), which binds to hypoxia-inducible factor (HIF)-1α, as essential for down-regulation of C/EBPα transcription in hypoxia. Immunocytochemical analysis showed that C/EBPα was localized in the nucleus at 21% O2, but was mostly cytoplasmic under 1% O2. Knockdown of HIF-1α by RNAi restored C/EBPα to normal levels under hypoxic conditions. Immunohistochemical studies of 10 tumor samples did not show any colocalization of C/EBPα and glucose transporter 1 (used as a marker for hypoxia). Taken together, these results show that hypoxia down-regulates C/EBPα expression in breast cancer cells by several mechanisms, including transcriptional and posttranscriptional effects. The down-regulation of C/EBPα in hypoxia is mediated by HIF-1. [Cancer Res 2008;68(7):2158–65]
Conjugation of Human Topoisomerase 2α with Small Ubiquitin-like Modifiers 2/3 in Response to Topoisomerase Inhibitors: Cell Cycle Stage and Chromosome Domain Specificity
Authors: Agostinho Marta , Santos Vera , Ferreira Fernando , Costa Rafael , Cardoso Joana , Pinheiro Inês , Rino José , Jaffray Ellis , Hay Ronald T. , Ferreira João 
Published: April 2008

Abstract
Type 2 topoisomerases, in particular the α isoform in human cells, play a key role in cohesion and sister chromatid separation during mitosis. These enzymes are thus vital for cycling cells and are obvious targets in cancer chemotherapy. Evidence obtained in yeast and Xenopus model systems indicates that conjugation of topoisomerase 2 with small ubiquitin-like modifier (SUMO) proteins is required for its mitotic functions. Here, we provide biochemical and cytologic evidence that topoisomerase 2α is conjugated to SUMO-2/3 during interphase and mitosis in response to topoisomerase 2 inhibitors and “poisons” (ICRF-187, etoposide, doxorubicin) that stabilize catalytic intermediates (cleavage complexes, closed clamp forms) of the enzyme onto target DNA. During mitosis, SUMO-2/3–modified forms of topoisomerase 2α localize to centromeres and chromosome cores/axes. However, centromeres are unresponsive to inhibitors during interphase. Furthermore, formation of topoisomerase 2α–SUMO-2/3 conjugates within mitotic chromosomes strongly correlates with incomplete chromatid decatenation and decreases progressively as cells approach the metaphase-anaphase transition. We also found that the PIASy protein, an E3 ligase for SUMO proteins, colocalizes with SUMO-2/3 at the mitotic chromosomal cores/axes and is necessary for both formation of SUMO-2/3 conjugates and proper chromatid segregation. We suggest that the efficacy of topoisomerase inhibitors to arrest cells traversing mitosis may relate to their targeting of topoisomerase 2α–SUMO-2/3 conjugates that concentrate at mitotic chromosome axes and are directly involved in chromatid arm separation. [Cancer Res 2008;68(7):2409–18]
MCF7 Side Population Cells with Characteristics of Cancer Stem/Progenitor Cells Express the Tumor Antigen MUC1
Authors: Engelmann Katja , Shen Hongmei , Finn Olivera J. 
Published: April 2008

Abstract
Chemotherapy, radiation, and growth inhibitory drugs preferentially eliminate actively growing cancer cells. Cancer recurrence is currently thought to be due to nondividing cancer stem/progenitor cells that are resistant to these therapies. Different therapeutic approaches need to be considered for the elimination of the cancer stem cell population. Immunotherapy is one such approach. In addition to specificity and lack of toxicity, immunotherapy targets cancer cells irrespective of their state of proliferation, as long as they express particular tumor antigens. For that reason, it is important to examine if the tumor antigens that are currently being tested as immunotherapeutic agents are also present on cancer stem cells. This study aimed to determine if one well-known tumor antigen, MUC1, which is being tested as an immunotherapy target on tumor cells, is also expressed on the quiescent cancer stem/progenitor cells. We used the so-called side population (SP) cells found in the MCF7 breast cancer cell line, which we first confirmed by cell surface markers and gene profiling to be highly enriched in cells that fulfill specific functional, phenotypic, and molecular criteria for being tumor stem/progenitor cells. We show that these cells express MUC1 and give rise to MUC1+ tumors in vivo, which maintain the MUC1+ SP population. MUC1 on SP cells is hypoglycosylated and heavily sialylated; the characteristics of the tumor-specific form were expressed on mature cancer cells and recognized by tumor-specific T cells and antibodies. This suggests that stem/progenitor cells, like mature tumor cells, would be targets of MUC1-directed immunotherapy. [Cancer Res 2008;68(7):2419–26]
DNA Damage Signaling in Hematopoietic Cells: A Role for Mre11 Complex Repair of Topoisomerase Lesions
Authors: Morales Monica , Liu Yan , Laiakis Evagelia C. , Morgan William F. , Nimer Stephen D. , Petrini John H.J. 
Published: April 2008

Abstract
The Mre11 complex promotes DNA double-strand break repair and regulates DNA damage signaling via activation of the ataxia-telangiectasia mutated (ATM) kinase. The hypermorphic Rad50S allele encodes a variant of Rad50, a member of the Mre11 complex. Cells expressing Rad50S experience constitutive ATM activation, which leads to precipitous apoptotic attrition in hematopoietic cells. In this study, we show that ATM activation by the Rad50S-containing Mre11 complex enhances the proliferation of LSK cells, a population consisting of hematopoietic stem cells and multipotent progenitor cells. In Rad50S/S mice, enhanced LSK proliferation triggers apoptotic attrition. This phenotype is mitigated when Rad50S/S is combined with mutations that alter either LSK cell quiescence (myeloid elf-1–like factor/ELF4–deficient mice) or hematopoietic differentiation (p21- and p27-deficient mice), indicating that the LSK population is a primary target of Rad50S pathology. We show that cells from Rad50S/S mice are hypersensitive to camptothecin, a topoisomerase I inhibitor that causes DNA damage primarily during DNA replication. On this basis, we propose that apoptotic attrition of Rad50S/S hematopoietic cells results from enhanced proliferation in the context of topoisomerase-associated DNA damage. Impairment of apoptosis in Rad50S/S mice promotes hematopoietic malignancy, suggesting that primitive hematopoietic cells serve as a reservoir of potentially oncogenic lesions in Rad50S/S mice. These data provide compelling evidence that the Mre11 complex plays a role in the metabolism of topoisomerase lesions in mammals, and further suggest that such lesions can accumulate in primitive hematopoietic cells and confer significant oncogenic potential. [Cancer Res 2008;68(7):2186–93]
A Cryptic Vascular Endothelial Growth Factor T-Cell Epitope: Identification and Characterization by Mass Spectrometry and T-Cell Assays
Authors: Weinzierl Andreas O. , Maurer Dominik , Altenberend Florian , Schneiderhan-Marra Nicole , Klingel Karin , Schoor Oliver , Wernet Dorothee , Joos Thomas , Rammensee Hans-Georg , Stevanović Stefan 
Published: April 2008

AbstractVascular endothelial growth factor (VEGF) is involved in various physiologic processes, such as angiogenesis or wound healing, but is also crucial in pathologic events, such as tumor growth. Thus, clinical anti-VEGF treatments have been developed that could already show beneficial effects for cancer patients. In this article, we describe the first VEGF-derived CD8+ T-cell epitope. The natural HLA ligand SRFGGAVVR was identified by differential mass spectrometry in two primary renal cell carcinomas (RCC) and was significantly overpresented on both tumor tissues. SRFGGAVVR is derived from a cryptic translated region of VEGF presumably by initiation of translation at the nonclassic start codon CUG499. SRFGGAVVR-specific T cells were generated in vitro using peptide-loaded dendritic cells or artificial antigen-presenting cells. SRFGGAVVR-specific CD8+ T cells, identified by HLA tetramer analysis after in vitro stimulation, were fully functional T effector cells, which were able to secrete IFN-γ on stimulation and killed tumor cells in vitro. Additionally, we have quantitatively analyzed VEGF mRNA and protein levels in RCC tumor and normal tissue samples by gene chip analysis, quantitative reverse transcription-PCR, in situ hybridization, and bead-based immunoassay. In the future, T cells directed against VEGF as a tumor-associated antigen may represent a possible way of combining peptide-based anti-VEGF immunotherapy with already existent anti-VEGF cancer therapies. [Cancer Res 2008;68(7):2447–54]
FGFR2-Amplified Gastric Cancer Cell Lines Require FGFR2 and Erbb3 Signaling for Growth and Survival
Authors: Kunii Kaiko , Davis Lenora , Gorenstein Julie , Hatch Harold , Yashiro Masakazu , Di Bacco Alessandra , Elbi Cem , Lutterbach Bart 
Published: April 2008

Abstract
We have identified a critical role for amplified FGFR2 in gastric cancer cell proliferation and survival. In a panel of gastric cancer cell lines, fibroblast growth factor receptor 2 (FGFR2) was overexpressed and tyrosine phosphorylated selectively in FGFR2-amplified cell lines KatoIII, Snu16, and OCUM-2M. FGFR2 kinase inhibition by a specific small-molecule inhibitor resulted in selective and potent growth inhibition in FGFR2-amplified cell lines, resulting in growth arrest in KatoIII cells and prominent induction of apoptosis in both Snu16 and OCUM-2M cells. FGFR2-amplified cell lines also contained elevated phosphotyrosine in EGFR, Her2, and Erbb3, but the elevated phosphorylation in EGFR could not be inhibited by gefitinib or erlotinib. We show that the elevated EGFR, Her2, and Erbb3 phosphotyrosine is dependent on FGFR2, revealing EGFR family kinases to be downstream targets of amplified FGFR2. Moreover, shRNA to Erbb3 resulted in a loss of proliferation, confirming a functional role for the activated EGFR signaling pathway. These results reveal that both the FGFR2 and EGFR family signaling pathways are activated in FGFR2-amplified gastric cancer cell lines to drive cell proliferation and survival. Inhibitors of FGFR2 or Erbb3 signaling may have therapeutic efficacy in the subset of gastric cancers containing FGFR2 amplification. [Cancer Res 2008;68(7):2340–8]
Skewing the T-Cell Repertoire by Combined DNA Vaccination, Host Conditioning, and Adoptive Transfer
Authors: Jorritsma Annelies , Bins Adriaan D. , Schumacher Ton N.M. , Haanen John B.A.G. 
Published: April 2008

Abstract
Approaches for T-cell–based immunotherapy that have shown substantial effects in clinical trials are generally based on the adoptive transfer of high numbers of antigen-specific cells, and the success of these approaches is thought to rely on the high magnitude of the tumor-specific T-cell responses that are induced. In this study, we aimed to develop strategies that also yield a T-cell repertoire that is highly skewed toward tumor recognition but do not rely on ex vivo generation of tumor-specific T cells. To this end, the tumor-specific T-cell repertoire was first expanded by DNA vaccination and then infused into irradiated recipients. Subsequent vaccination of the recipient mice with the same antigen resulted in peak CD8+ T-cell responses of ∼50%. These high T-cell responses required the presence of antigen-experienced tumor-specific T cells within the graft because only mice that received cells of previously vaccinated donor mice developed effective responses. Tumor-bearing mice treated with this combined therapy showed a significant delay in tumor outgrowth, compared with mice treated by irradiation or vaccination alone. Furthermore, this antitumor effect was accompanied by an increased accumulation of activated and antigen-specific T cells within the tumor. In summary, the combination of DNA vaccination with host conditioning and adoptive transfer generates a marked, but transient, skewing of the T-cell repertoire toward tumor recognition. This strategy does not require ex vivo expansion of cells to generate effective antitumor immunity and may therefore easily be translated to clinical application. [Cancer Res 2008;68(7):2455–62]
Methylation Silencing of Transforming Growth Factor-β Receptor Type II in Rat Prostate Cancers
Authors: Yamashita Satoshi , Takahashi Satoru , McDonell Nathalie , Watanabe Naoko , Niwa Tohru , Hosoya Kosuke , Tsujino Yoshimi , Shirai Tomoyuki , Ushijima Toshikazu 
Published: April 2008

Abstract
To identify methylation-silenced genes in prostate cancers, a microarray analysis for genes up-regulated by treatment with a demethylating agent, 5-aza-2′-deoxycytidine, was performed using three rat prostate cancer cell lines. Eight genes (Aebp1, Dysf, Gas6, LOC361288, Nnat, Ocm, RGD1308119, and Tgfbr2) were re-expressed at 16-fold or more, and their promoter CpG islands were shown to be densely methylated in the cancer cell lines. From the eight genes, Tgfbr2, a key mediator of transforming growth factor-β (TGF-β) signaling that has been strongly implicated in human and rat prostate carcinogenesis, was selected, and its silencing in primary samples was analyzed further. Tgfbr2 was methylated and markedly down-regulated in three of seven 3,2′-dimethyl-4-aminobiphenyl–induced invasive adenocarcinomas in the dorsolateral lobe of the rat prostate. In humans, marked down-regulation of TGFBR2 protein was observed in 12 of 20 high-grade prostatic intraepithelial neoplasia and 36 of 60 prostate cancers. DNA methylation of the human TGFBR2 promoter CpG islands repressed transcription, if present, but neither methylation nor mutation were detected in 27 human prostate cancers analyzed. Methylation silencing of rat Tgfbr2 was associated with histone H3 lysine 9 trimethylation, whereas decreased expression of human TGFBR2 was mainly due to decreased transcription activity, sometimes in concert with histone deacetylation and H3 lysine 27 trimethylation. The identification of methylation silencing of Tgfbr2 in rat prostate cancers, in accordance with TGFBR2 down-regulation in human prostate cancers, will enable us to analyze how aberrant methylation is induced in vivo and identify factors that promote and suppress the induction of aberrant methylation. [Cancer Res 2008;68(7):2112–21]