bluuebunny/crossref_metadata_2025_split huggingface dataset:
An examination of the use of high‐investment human resource systems for core and support employees
Authors: Lepak David P. , Taylor M. Susan , Tekleab Amanuel G. , Marrone Jennifer A. , Cohen Debra J. 
Published: May 2007

AbstractIn this study, we examine two competing perspectives regarding the relative use of high‐investment human resource (HIHR) systems for core and support employees within establishments. Using data from 420 establishments, we compare a universal perspective suggesting that the level of HIHR exposure core employees receive is always greater than the level of exposure for sup‐port employees, with a contingency perspective suggesting that the relative level of exposure for these employee groups is contingent on strategy, HR philosophy, or industry.The results did not provide support for the universal prediction that core employees always receive higher levels of exposure to HIHR systems than support employees within the same establishment. Moreover, while strategy and HR philosophy were positively related to the level of HIHR system use across establishments, they did not influence the relative level of exposure to HIHR systems for core and support employees. Interestingly, however, industry did exert a unique impact such that core em‐ployees received significantly greater exposure to HIHR systems than sup‐port employees in nonmanufacturing firms.There were no significant differ‐ences in exposure for these two groups in manufacturing industries. Implications of the findings are discussed. © 2007 Wiley Periodicals, Inc.
Externalizing the core: Firms' use of employment intermediaries in the information and communication technology industries
Authors: Nesheim Torstein , Olsen Karen M. , Kalleberg Arne L. 
Published: May 2007

AbstractRecent research suggests that nonstandard employment relations may be a source of innovation for the firm. In this article, we analyze firms' strategic correlates and perceived benefits from using two types of employment in‐termediaries—consulting firms and temporary help agencies—in their core activities. Organizations with an innovation strategy are more likely to use consulting firms in their core activities, while organizations that compete on the basis of low cost are more apt to use temporary help agencies. Moreover, managers say that consulting firms are more likely than temporary help agencies to provide them with special competencies in their core activities. © 2007 Wiley Periodicals, Inc.
To be strategic in the new public sector, HR must remember its operational activities
Authors: Teo Stephen T. T. , Rodwell John J. 
Published: May 2007

AbstractThis article examines the level of operational and strategic involvement by human resource departments, the influence of HR departments, and the level of strategic integration as predictors of human resource management per‐formance. Surveys from 146 senior line managers and HR executives in com‐mercialized and noncommercialized public‐sector agencies in Australia were the basis of organizational‐ and individual‐level analyses. Results indicate positive relationships between the degree to which operational HR activities are transferred to line managers, HR influence, strategic integration, and the performance of the HRM function. Interestingly, no relationship was found between the level of strategic involvement by HR departments and the per‐ceived performance of the function. Analysis of the individual‐level data sup‐ports the multiple‐constituency approach to HRM, with differences in the evaluation of HRM by respondents from different job functions. The study highlights challenges faced by HR practitioners needing to be operational, to be valued strategically. © 2007 Wiley Periodicals, Inc.
Multisource feedback: Lessons learned and implications for practice
Authors: Atwater Leanne E. , Brett Joan F. , Charles Atira Cherise 
Published: May 2007

AbstractOrganizations around the world are using multisource, or 360‐degree, feed‐back. Although many HR practitioners embrace it as an important mecha‐nism for leadership development, organizations must attend to and address several issues in order to maximize the utility of multisource feedback (MSF). We discuss current research findings and highlight issues for managers to consider both before starting a multisource feedback process and after the feedback is given, plus we review potential outcomes of the process. We also describe lessons learned from an intensive three‐year investigation of an MSF implementation in two organizations. © 2007 Wiley Periodicals, Inc.
Evapotranspiration rates and crop coefficients for a restored marsh in the Sacramento–San Joaquin Delta, California, USA
Authors: Drexler Judy Z. , Anderson Frank E. , Snyder Richard L. 
Published: May 2007

AbstractThe surface renewal method was used to estimate evapotranspiration (ET) for a restored marsh on Twitchell Island in the Sacramento–San Joaquin Delta, California, USA. ET estimates for the marsh, together with reference ET measurements from a nearby climate station, were used to determine crop coefficients over a 3‐year period during the growing season. The mean ET rate for the study period was 6 mm day−1, which is high compared with other marshes with similar vegetation. High ET rates at the marsh may be due to the windy, semi‐arid Mediterranean climate of the region, and the permanently flooded nature of the marsh, which results in very low surface resistance of the vegetation. Crop coefficient (Kc) values for the marsh ranged from 0·73 to 1·18. The mean Kc value over the entire study period was 0·95. The daily Kc values for any given month varied from year to year, and the standard deviation of daily Kc values varied between months. Although several climate variables were undoubtedly responsible for this variation, our analysis revealed that wind direction and the temperature of standing water in the wetland were of particular importance in determining ET rates and Kc values. Published in 2007 by John Wiley & Sons, Ltd.
Interferon‐γ regulation of TNFα‐induced matrix metalloproteinase 3 expression and migration of human glioma T98G cells
Authors: Cheng Sherman M. , Xing Bing , Li James C.B. , Cheung Benny K.W. , Lau Allan S.Y. 
Published: May 2007

AbstractInduction of proinflammatory cytokines in response to malignant cells is an integral component of immune response to control tumor development. However, recent evidences have suggested that tumor cells may evade the immune system and exploit inflammatory responses to enhance its own growth. An exemplary example is the highly invasive and tumor necrosis factor (TNF)α‐resistant glioblastoma, whose growth is associated with TNFα expression. We thus examined whether the tumor takes advantage of TNFα overexpression to enhance its invasiveness. To delineate the contribution of inflammation in tumor migration, we demonstrated that the role of proinflammatory cytokines on matrix metalloproteinases‐3 (MMP‐3) expression, and its consequent effects on the invasiveness of a human glioma cell‐line, T98G. By using Matrigel Invasion Chamber, T98G cell migration was significantly enhanced in response to TNFα. In contrast, interferon‐γ (IFNγ) reduced both basal and TNFα‐enhanced cell invasion. To investigate the mechanisms involved, we demonstrated that TNFα upregulated mRNA and protein expression of MMP‐3 in T98G cells, whereas IFNγ downregulated the MMP‐3 expression. The role of MMP‐3 in glioma invasiveness was further confirmed by transfecting MMP‐3 siRNA in T98G to abrogate the TNFα‐enhanced cell invasion. To delineate the mechanisms further, we showed that IFNγ exerts an inhibitory effect on the binding of TNFα‐activated Ets‐1 and NFκB to their respective enhancer elements found in MMP‐3 promoter. In summary, our results indicated that TNFα enhances the invasiveness of T98G glioma cells through MMP‐3 induction, and such enhancement of cell migration can be inhibited by IFNγ. © 2007 Wiley‐Liss, Inc.
Methylseleninic acid enhances the effect of etoposide to inhibit prostate cancer growth in vivo
Authors: Gonzalez‐Moreno Oscar , Segura Victor , Serrano Diego , Nguewa Paul , de las Rivas Javier , Calvo Alfonso 
Published: May 2007

AbstractNew therapeutic agents are needed for the treatment of androgen‐independent prostate cancer (PrCa). We have investigated the effect of methylseleninic acid (MSA) on tumor stage‐specific prostate cells derived from the C3 (1)/Tag model for PrCa: Pr111, a slow‐growing and nontumorigenic cell line isolated from a prostate intraepithelial neoplasia lesion; Pr14, a tumorigenic line derived from a primary tumor; and Pr14C1, a sub‐clone of Pr14 explanted from a lung metastasis. We demonstrate that MSA strongly inhibits cell growth and induces apoptosis in C3 (1)/Tag tumor cells, in a dose‐dependent manner. A decrease in phosphorylated ERK1/2 and AKT was also found in tumor cells, but not in Pr111. Microarray analysis using affymetrix showed that the number of genes with an altered expression in tumor cells is significantly higher (p < 0.01) than in nontumoral cells. Pathways analyses revealed a decrease in the expression of genes involved in metabolism (Fabp5, Cyba), signal transduction (ERK, AKT), angiogenesis (neuropilin‐1, Flt‐4) and transcription (cAMP response element‐binding protein) in tumor cells. The expression of neuropilin‐1, a protein involved in VEGF signaling and tumor angiogenesis, was 97‐fold repressed in Pr14 cells treated with MSA. Combination treatments using low doses of etoposide or taxotere (docetaxel), plus low doses of MSA revealed a strong enhancement of cell growth inhibition and apoptosis in tumor cells. Our in vivo studies using Pr14 cells xenografted into nude mice demonstrated that MSA significantly enhances the chemotherapeutical effect of etoposide, resulting in 78.3% tumor growth inhibition. These results suggest that MSA could be used against PrCa to enhance the effect of etoposide. © 2007 Wiley‐Liss, Inc.
The combined actions of NK and T lymphocytes are necessary to reject an EGFP+ mesenchymal tumor through mechanisms dependent on NKG2D and IFNγ
Authors: Arina Ainhoa , Murillo Oihana , Hervás‐Stubbs Sandra , Azpilikueta Arantza , Dubrot Juan , Tirapu Iñigo , Huarte Eduardo , Alfaro Carlos , Pérez‐Gracia Jose L. , González‐Aseguinolaza Gloria , Sarobe Pablo , Lasarte Juan J. , Jamieson Amanda , Prieto Jesús , Raulet David H. , Melero Ignacio 
Published: May 2007

AbstractBetter understanding of the mechanisms that mediate spontaneous immune rejections ought to be important in the quest for improvements in immunotherapy of cancer. A set of intraperitoneal tumors of mesenchymal origin that had been chemically induced in ubiquitously expressing EGFP transgenic mice provided a model in which both T and NK cells were absolutely required for tumor rejection. Tumor cells were traceable because of being fluorescent and readily grafted in RAG1−/− immunodeficient mice, whereas they were rejected in a majority of syngeneic C57BL/6 and EGFP‐transgenic mice. Tumor‐cell clones with the highest EGFP expression tended to be rejected, but a direct involvement of EGFP as the antigen recognized for the immune rejections was ruled out. Rejections were absolutely dependent on NK cells as well as on CD4+ and CD8+ T lymphocytes according to selective depletion studies. Furthermore, CD8+ and CD4+ T lymphocytes as well as NK cells were detected in the inflammatory infiltrate that mediates tumor rejection along with some DC. The effects of IFNγ, produced at the tumor site by T and NK lymphocytes, were only required at the malignant cell level and were necessary for tumor eradication. NK recognition of tumor cells was mediated by the NKG2D‐activating receptor and blocking its function in vivo partially interfered with rejection. Therefore, complete rejection of these mesenchymal tumors requires a concerted set of activities including direct tumor‐cell destruction and IFNγ production that are mediated by both NK and T cells. © 2007 Wiley‐Liss, Inc.
Artesunate attenuates the growth of human colorectal carcinoma and inhibits hyperactive Wnt/β‐catenin pathway
Authors: Li Lin‐Na , Zhang Hua‐Dong , Yuan Shou‐Jun , Tian Zeng‐Yue , Wang Lin , Sun Zhi‐Xian 
Published: May 2007

AbstractArtesunate (ART), a remarkable antimalarial agent, also inhibited the growth of human colorectal carcinoma. As determined by MTT assay, flow cytometry analysis on apoptosis and indirect immunofluorescence analysis on the proliferation‐associated marker Ki67, ART suppressed the proliferation and promoted the apoptosis of colorectal cancer cells in a dose‐dependent manner. Furthermore, immunofluorescence analysis on β‐catenin and RT‐PCR analysis on Wnt/β‐catenin target genes demonstrated ART translocated β‐catenin from nucleus to adherent junctions of membrane and reduced transcription mediated by β‐catenin. These results suggested the anticancer activity of ART correlated with the inhibition of hyperactive Wnt/β‐catenin signaling pathway. In vivo, ART significantly slowed the growth of colorectal tumor xenografts. Bioluminescent imaging also revealed that ART decreased the physiological activity of tumor xenografts and delayed spontaneous liver metastasis. These antitumor effects were related to the membranous translocation of β‐catenin and the inhibition of the unrestricted activation of Wnt/β‐catenin pathway, which was confirmed by the immunohistochemical staining of tumor tissues. These results and the known low toxicity are clues that ART might be a promising candidate drug for the treatment of colorectal carcinoma. © 2007 Wiley‐Liss, Inc.
Increased HIF1α in SDH and FH deficient tumors does not cause microsatellite instability
Authors: Lehtonen Heli J. , Mäkinen Markus J. , Kiuru Maija , Laiho Päivi , Herva Riitta , Minderhout Ivonne van , Hogendoorn Pancras C.W. , Cornelisse Cees , Devilee Peter , Launonen Virpi , Aaltonen Lauri A. 
Published: May 2007

AbstractGermline mutations in nuclear genes encoding mitochondrial enzymes fumarate hydratase (FH) and succinate dehydrogenase (subunits SDHB/C/D) have been implicated in the development of tumor syndromes referred to as hereditary leiomyomatosis and renal cell cancer (HLRCC) and hereditary paragangliomatosis (HPGL), respectively. FH and SDH are operating in the tricarboxylic acid cycle (the TCA cycle, the Krebs cycle). In the FH and SDH deficient tumors, accumulation of the substrates, fumarate and succinate, has been shown to cause stabilization of hypoxia inducible factor 1α (HIF1α). According to recent studies, HIF1α could contribute to the hypoxia induced genomic instability seen in many cancers, through repression of mismatch repair (MMR) protein MSH2. In this study, in agreement with previous works, we found HIF1α to be moderately or highly stabilized in 67% (16/24) and 77% (48/62) of HLRCC tumors and SDHB/C/D paragangliomas (PGL) and pheochromocytomas (PHEO), respectively. In addition, a set of 54 other familial and nonfamilial PGLs/PHEOs were studied. Moderately or highly stabilized HIF1α was present in 68% (26/38) of the PGLs but in PHEOs (n = 16) no such pattern was observed. We then analyzed the suggested link between HIF1α stabilization and MSH2 repression, in HLRCC and HPGL tumor material. No microsatellite instability (MSI) or lack of MSH2 expression was, however, observed. Thus we failed to provide in vivo evidence for the proposed link between HIF1α stabilization and functional MMR deficiency, in TCAC deficient tumors. © 2007 Wiley‐Liss, Inc.
Cyclin‐dependent kinase inhibitor, flavopiridol, induces apoptosis and inhibits tumor growth in drug‐resistant osteosarcoma and Ewing's family tumor cells
Authors: Li Yan , Tanaka Kazuhiro , Li Xu , Okada Takamitsu , Nakamura Tomoyuki , Takasaki Minoru , Yamamoto Shunsaku , Oda Yoshinao , Tsuneyoshi Masazumi , Iwamoto Yukihide 
Published: May 2007

AbstractMultimodal therapies play important roles in the treatment of osteosarcoma (OS) and Ewing's family of tumors (EFTs), two most frequent malignant bone tumors. Although the clinical outcome of primary OS and EFTs is greatly improved, the relapsed cases often are associated with multidrug resistance of the tumors and the prognosis of these patients is still poor. Flavopiridol, a pan cyclin‐dependent kinase (CDK) inhibitor is a novel antitumor agent that can induce cell cycle arrest and apoptosis in many cancer cells. However, there have been no studies about the effects of flavopiridol on drug‐resistant OS and EFTs. Here, we demonstrated that flavopiridol induced the cleavage of poly‐ADP‐ribose polymerase (PARP) in a time and dose dependent manner in adriamycin‐resistant OS and EFTs cells expressing P‐glycoprotein (P‐gp) and multidrug resistance‐associated protein 1 (MRP1) as effectively as in their parental cells. Our data also showed that flavopiridol caused the release of mitochondrial cytochrome c and the activation of caspase‐9, caspase‐8 and caspase‐3, with an increase ratio of the proapoptotic protein level (Bax) to the antiapoptotic protein level (Bcl‐2 and Bcl‐XL), while apoptosis was inhibited by pan caspase inhibitor (Z‐VAD‐FMK) and caspase‐3 inhibitor (Z‐DEVD‐FMK), not by caspase‐8 inhibitor (Z‐IETD‐FMK). The treatment with flavopiridol further inhibited the tumor growth in mouse models of the drug‐resistant OS and EFTs. These results suggest that flavopiridol might be promising in clinical therapy for the relapsed OS and EFTs. © 2007 Wiley‐Liss, Inc.
Transforming properties of TC‐1 in human breast cancer: Interaction with FGFR2 and β‐catenin signaling pathways
Authors: Yang Zeng‐Quan , Moffa Allison B. , Haddad Ramsi , Streicher Katie L. , Ethier Stephen P. 
Published: May 2007

AbstractBreast cancer development is associated with gene amplification and over expression that is believed to have a causative role in oncogenesis. Previous studies have demonstrated that over expression of TC‐1(C8orf4) mRNA occurs in ∼50% of breast cancer cell lines and primary tumor specimens. Here, we show that TC‐1 has transforming properties in human mammary epithelial (HME) cells and its expression is mechanistically linked to FGFR signaling cascades. In vitro experiments demonstrate that TC‐1 over expression mediates both anchorage‐independent and growth factor‐independent proliferation of HME cells. TC‐1 was down regulated by the FGFR inhibitor PD173074 in the breast cancer cell line SUM‐52 that also has an FGFR2 gene amplification and over expression. Furthermore, forced expression of FGFR2 in HME cells increased the level of expression of endogenous TC‐1 mRNA. TC‐1 has been implicated as a modulator of Wnt/β‐catenin signaling in 293 cells and in gastric cancer cells. However, while we did find increased expression of a subset of β‐catenin target genes in TC‐1 over expressing cells, we did not find an association of TC‐1 with global expression of β‐catenin target genes in our cells. Taken together, our data suggest that TC‐1 over expression is transforming and may link with the FGFR pathway in a subset of breast cancer. © 2007 Wiley‐Liss, Inc.
IGF‐I and mammographic density in four geographic locations: A pooled analysis
Authors: Maskarinec Gertraud , Takata Yumie , Chen Zhao , Gram Inger Torhild , Nagata Chisato , Pagano Ian , Hayashi Kentaro , Arendell Leslie , Skeie Guri , Rinaldi Sabina , Kaaks Rudolph 
Published: May 2007

AbstractInsulin‐like growth factor (IGF‐I) and prolactin have been found to be associated with breast cancer risk and with mammographic density. In a pooled analysis from 4 geographic locations, we investigated the association of percent mammographic density with serum levels of IGF‐I, IGFBP‐3 and prolactin. The pooled data set included 1,327 pre‐ and postmenopausal women: Caucasians from Norway, Arizona and Hawaii, Japanese from Hawaii and Japan, Latina from Arizona, and Native Hawaiians from Hawaii. Serum samples were assayed for IGF‐I, IGFBP‐3 and prolactin levels using ELISA assays. Mammographic density was quantified using a computer‐assisted density method. After stratification by menopausal status, multiple regression models estimated the relation between serum analytes and breast density. All serum analytes except prolactin among postmenopausal women differed significantly by location/ethnicity group. Among premenopausal subjects, IGF‐I levels and the molar ratio were highest in Hawaii, intermediate in Japan and lowest in Arizona. For IGFBP‐3, the order was reversed. Among postmenopausal subjects, Norwegian women had the highest IGF‐I levels and women in Arizona had the lowest while women in Japan and Hawaii had intermediate levels. We observed no significant relation between percent density and IGF‐I or prolactin levels among pre‐and postmenopausal women. The significant differences in IGF‐I levels by location but not ethnicity suggest that environmental factors influence IGF‐I levels, whereas percent breast density varies more according to ethnic background than by location. Based on this analysis, the influence of circulating levels of IGF‐I, IGFBP‐3, and prolactin on percent density appears to be very small. © 2007 Wiley‐Liss, Inc.
Re‐expression of sonic hedgehog and reduction of CDX2 after Helicobacter pylori eradication prior to incomplete intestinal metaplasia
Authors: Shiotani Akiko , Uedo Noriya , Iishi Hiroyasu , Tatsuta Masaharu , Ishiguro Shingo , Nakae Yukinori , Kamada Tomoari , Haruma Ken , Merchant Juanita L. 
Published: May 2007

AbstractLoss of Sonic Hedgehog (Shh) and aberrant CDX2 expression are early changes correlating with the presence of intestinal metaplasia that occur in the gastric mucosa prior to neoplastic transformation. The aim of this study was to compare the improvement in corpus gastritis with Shh and CDX2 expression after H. pylori eradication between subjects at high risk for gastric cancer and controls. The usefulness of serum pepsinogen levels as a predictor of resolved corpus gastritis was also examined. Seventy patients with endoscopic resection for early gastric cancer and 30 controls were studied. Expression of Shh and CDX2 were evaluated by immunostaining. Serum levels of pepsinogen I before eradication in the patients scored as having improvement of corpus atrophy were significantly higher than in the patients without improvement (<0.01). Residual inflammation at the corpus lesser curve was more frequently detected in the cancer group than in the controls (OR 4.6 95% C.I. 1.6–13.5) and in the mucosa with incomplete intestinal metaplasia rather than in those without incomplete intestinal metaplasia (OR 7.6 95% C.I. 2.4–24.3). Atrophy, expression of Shh and CDX2 at the corpus lesser curve significantly improved in mucosa without incomplete intestinal metaplasia (p < 0.01), but not in mucosa with incomplete intestinal metaplasia. In conclusion, H. pylori eradication prior to development of incomplete intestinal metaplasia improves corpus gastritis and may prevent gastric cancer. Pepsinogen I may be a useful marker in patients with a residual higher risk of gastric cancer after H. pylori eradication. © 2007 Wiley‐Liss, Inc.