bluuebunny/crossref_metadata_2025_split huggingface dataset:
Starting Out on the Right Foot: Negotiation Schemas When Cultures Collide
Authors: Adair Wendi L. , Taylor Masako S. , Tinsley Catherine H. 
Published: April 2009

AbstractWe investigate the intercultural negotiation schemas of 100 experienced Japanese and U.S. negotiators. Specifically, we examine the assumptions negotiators make about appropriate behavior when primed to negotiate with an intercultural (vs. intracultural) counterpart. We find that intercultural negotiation schemas clash on six of nine elements, meaning U.S. and Japanese negotiators have significantly different expectations about what it is like to negotiate with the other. This clash occurs not because negotiators stay anchored on their own cultural assumptions about negotiating, but rather because they try to adjust to their counterpart’s cultural assumptions about negotiating. But negotiators adjust their schemas by thinking about how their counterpart negotiates in an intracultural rather than intercultural setting. That is, they fail to account for the fact that their counterpart would also adjust expectations for the intercultural context. The phenomenon we uncover is one of schematic overcompensation, whereby negotiators’ intercultural schemas do not match because each negotiator expects the encounter to be just like the counterpart’s within‐culture negotiations. Our theory of schematic overcompensation receives some support, and negotiators’ perceived knowledge and experience with the other culture somewhat attenuates the phenomenon. Implications for negotiator cognition, intercultural negotiation, and global management are discussed.
Identification of Anguilla anguilla (L.) and Anguilla rostrata (Le Sueur) and their hybrids based on a diagnostic single nucleotide polymorphism in nuclear 18S rDNA
Authors: FRANKOWSKI JENS , BASTROP RALF 
Published: April 2009

AbstractThe variability of the nuclear 18S rDNA was examined for 10 species of freshwater eels: Anguilla anguilla, A. australis, A. dieffenbachii, A. japonica, A. marmorata, A. mossambica, A. nebulosa labiata, A. obscura, A. reinhardtii and A. rostrata. We observed that a single nucleotide polymorphism (SNP) separated A. anguilla and A. japonica from the remaining taxa. While this SNP marker may be used to identify hypothetical hybrids of A. japonica and sympatric eel species, we focused on Atlantic eels to evaluate the potential for this diagnostic chromosomal marker to discriminate between individuals of A. anguilla, A. rostrata and their hybrids.
Urinary bile acid sulfate levels in patients with hepatitis C virus‐related chronic liver diseases
Authors: Negoro Shinichiro , Tanaka Atsushi , Takikawa Hajime 
Published: April 2009

Aim:  Urinary bile acids are mainly conjugated with sulfuric acid, and urinary sulfated bile acid (USBA) levels in hepatobiliary diseases have been reported. However, the relationship between USBA and fasting serum total bile acid (TBA) has not been studied in hepatobiliary diseases. In the present study, we measured USBA levels in patients with hepatitis C virus‐related chronic liver diseases, and the relationship between TBA and various laboratory tests was studied.Methods:  USBA was measured using an automatic assay kit in 66 patients with chronic hepatitis and 28 patients with liver cirrhosis, and its relationship between TBA and various laboratory tests was studied.Results:  The median USBA level was 10.7 µmol/g creatinine in patients with chronic hepatitis and 41.1 µmol/g creatinine in liver cirrhosis (P = 0.000). More patients with chronic hepatitis had elevated USBA levels (61%) compared to TBA level (39%) (P = 0.002). USBA level was well correlated with TBA (rs = 0.680), and negatively correlated with albumin (rs = −0.488), prothrombin time (rs = −0.385) and platelet counts (rs = −0.394). In patients with liver cirrhosis, USBA was significantly elevated in Child–Pugh class B compared to Child–Pugh class A (P = 0.036).Conclusion:  Although the metabolic pathways of USBA and TBA are different, these levels correlated very well, and USBA is considered to be a useful indicator of hepatic function like TBA in patients with chronic hepatitis C.
A Cumulative Review of the Range and Incidence of Significant Adverse Events Associated with Acupuncture
Authors: White Adrian 
Published: April 2009

Objective To summarise the range and frequency of significant adverse events associated with acupuncture in order to provide evidence on which to base continuing efforts to improve the safety of acupuncture practice. Methods Searches were conducted of computerised databases, previous reviews of case reports, population surveys, prospective surveys of acupuncture practice and relevant sections of textbooks for primary and secondary reports to indicate the range of significant adverse events associated with acupuncture. Data from prospective surveys of acupuncture were combined to estimate the incidence of serious adverse events. Results A total of 715 adverse events was included. There were 90 primary reports of trauma, and 186 secondary reports; the most common were pneumothorax and injury to the central nervous system. Infection accounted for 204 primary reports and 91 secondary reports. Over 60% of these cases were hepatitis B. The next most common infection was of the external ear, as a complication of auricular acupuncture. The 144 miscellaneous events mainly comprised seizures and drowsiness judged severe enough to cause a traffic hazard. There were 12 primary reports of deaths. According to the evidence from 12 prospective studies which surveyed more than a million treatments, the risk of a serious adverse event with acupuncture is estimated to be 0.05 per 10 000 treatments, and 0.55 per 10 000 individual patients. Conclusions The risk of serious events occurring in association with acupuncture is very low, below that of many common medical treatments. The range of adverse events reported is wide and some events, specifically trauma and some episodes of infection, are likely to be avoidable.
ANALYZING NONBLOCKING MULTILOG NETWORKS WITH THE KÖNIG–EGEVARÝ THEOREM
Authors: NGO HUNG Q. , NGUYEN THANH-NHAN , HA DUC T. 
Published: April 2009

When analyzing a nonblocking switching network, the typical problem is to find a route for a new request through the network without disturbing existing routes. By solving this problem, we can derive how many hardware components of a certain type (Banyan planes in a multi-log network, for instance) are needed for the network to be nonblocking. This scenario appears in virtually all combinations of switching environments: strictly, widesense or rearrangeably nonblocking, unicast or multicast switching, and circuit, multirate, or photonic switching. In this paper, we show that the König–Egevarý theorem is a very good tool which helps solve the above prototypical problem. The idea is to somehow "represent" the potential blocking connections as edges of a bipartite graph. The maximum number of blocking connections roughly corresponds to the size of a maximum matching in that bipartite graph. The size of any vertex cover, by the König–Egevarý theorem, is an upper bound on the maximum number of blocking connections. Thus, by specifying a small vertex cover, we can derive the sufficient number of hardware components for the network to be nonblocking. We illustrate the technique by analyzing crosstalk-free and non-crosstalk-free widesense nonblocking multicast multi-log networks. Particularly, for the first time in the literature we derive conditions for the d-ary multi-log network to be crosstalk-free multicast widesense nonblocking under the window algorithm for any given window size. Several by-products follow from our approach and results. Firstly, our results allow for computing the best window size minimizing the fabric cost, showing that the multi-log network is a good candidate for crosstalk-free multicast switching architectures. Secondly, the analytical approach also gives a much simpler proof of the known case when the network is not required to be crosstalk-free. Thirdly, we show that several known results for the multi-log multicast networks under the so-called fanout constraints are simple corollaries of our results.
PTTG Overexpression Promotes Lymph Node Metastasis in Human Esophageal Squamous Cell Carcinoma
Authors: Yan Shuang , Zhou Cuiqi , Lou Xiaomin , Xiao Zefen , Zhu Hongxia , Wang Qifeng , Wang Yihua , Lu Ning , He Shun , Zhan Qimin , Liu Siqi , Xu Ningzhi 
Published: April 2009

Abstract
Human pituitary tumor transforming gene (PTTG) overexpression correlates with metastasis in multiple tumors, and yet its molecular mechanisms of action remain elusive. We detected PTTG overexpression in 66% (111 of 169) of primary esophageal squamous cell carcinoma (ESCC) tumor tissues by in situ hybridization. PTTG overexpression correlated with lymph node metastasis (P &lt; 0.05). Ectopic PTTG overexpression in a representative ESCC cell line, EC9706, increased in vitro cell migration and invasion and promoted in vivo lymph node metastasis. Suppressing PTTG expression by siRNA decreased cell motility in both PTTG-HA/EC9706 and KYSE150 cells. By using mass spectrometric analysis, we identified that PTTG up-regulated S100A4 and galectin-1 secretion and down-regulated tissue inhibitor of metalloproteinase-2 secretion to the culture media. PTTG induced S100A4 and galectin-1 mRNA and protein expression as assessed by Western blot and reverse transcription-PCR. Attenuating galectin-1 expression by siRNA constrained PTTG-HA/EC9706 cell motility (P &lt; 0.05). PTTG activated E-box transcription and induced c-Myc protein expression in EC9706 cells, which in turn may act on an E-box motif within the galectin-1 promoter. Chromatin immunoprecipitation assays further confirmed specific c-Myc binding to galectin-1 promoter. PTTG-induced galectin-1 transactivation and expression were mediated by c-Myc, and both inductions were suppressed by c-Myc RNAi cotranfection. These findings elucidate the molecular mechanisms of PTTG overexpression in promoting tumor metastasis, whereby up-regulated PTTG modulates expression and secretion of metastasis-related factors to facilitate cell motility. [Cancer Res 2009;69(8):3283–90]
Critical Role and Regulation of Transcription Factor FoxM1 in Human Gastric Cancer Angiogenesis and Progression
Authors: Li Qiang , Zhang Nu , Jia Zhiliang , Le Xiangdong , Dai Bingbing , Wei Daoyan , Huang Suyun , Tan Dongfeng , Xie Keping 
Published: April 2009

Abstract
The mammalian forkhead box (Fox) transcription factor FoxM1b is implicated in tumorigenesis. However, the presence of expression and role of FoxM1b in gastric cancer remain unknown. Therefore, we investigated FoxM1b expression in 86 cases of primary gastric cancer and 57 normal gastric tissue specimens. We further investigated the underlying mechanisms of altered FoxM1b expression in and the effect of this altered expression on gastric cancer growth and metastasis using in vitro and animal models of gastric cancer. We found weak expression of FoxM1b protein in the mucous neck region of gastric mucosa, whereas we observed strong staining for FoxM1b in tumor cell nuclei in various gastric tumors and lymph node metastases. A Cox proportional hazards model revealed that FoxM1b expression was an independent prognostic factor in multivariate analysis (P &lt; 0.001). Experimentally, overexpression of FoxM1b by gene transfer significantly promoted the growth and metastasis of gastric cancer cells in orthotopic mouse models, whereas knockdown of FoxM1b expression by small interfering RNA did the opposite. Promotion of gastric tumorigenesis by FoxM1b directly and significantly correlated with transactivation of vascular endothelial growth factor expression and elevation of angiogenesis. Given the importance of FoxM1b to regulation of the expression of genes key to cancer biology overall, dysregulated expression and activation of FoxM1b may play important roles in gastric cancer development and progression. [Cancer Res 2009;69(8):3501–9]
LEF1 in Androgen-Independent Prostate Cancer: Regulation of Androgen Receptor Expression, Prostate Cancer Growth, and Invasion
Authors: Li Yirong , Wang Longgui , Zhang Miao , Melamed Jonathan , Liu Xiaomei , Reiter Robert , Wei Jianjun , Peng Yi , Zou Xuanyi , Pellicer Angel , Garabedian Michael J. , Ferrari Anna , Lee Peng 
Published: April 2009

Abstract
A major obstacle in treating prostate cancer is the development of androgen-independent disease. In this study, we examined LEF1 expression in androgen-independent cancer as well as its regulation of androgen receptor (AR) expression, prostate cancer growth, and invasion in androgen-independent prostate cancer cells. Affymetrix microarray analysis of LNCaP and LNCaP-AI (androgen-independent variant LNCaP) cells revealed 100-fold increases in LEF1 expression in LNCaP-AI cells. We showed that LEF1 overexpression in LNCaP cells resulted in increased AR expression and consequently enhanced growth and invasion ability, whereas LEF1 knockdown in LNCaP-AI cells decreased AR expression and, subsequently, growth and invasion capacity. Chromatin immunoprecipitation, gel shift, and luciferase assays confirmed LEF1 occupancy and regulation of the AR promoter. Thus, we identified LEF1 as a potential marker for androgen-independent disease and as a key regulator of AR expression and prostate cancer growth and invasion. LEF1 is highly expressed in androgen-independent prostate cancer, potentially serving as a marker for androgen-independent disease. [Cancer Res 2009;69(8):3332–8]
A CreER-Based Random Induction Strategy for Modeling Translocation-Associated Sarcomas in Mice
Authors: Haldar Malay , Hedberg Matthew L. , Hockin Matthew F. , Capecchi Mario R. 
Published: April 2009

Abstract
Previously, we reported modeling synovial sarcomas in mice by conditionally expressing the human t(X;18) translocation–derived SYT-SSX2 fusion protein in Myf5-expressing myoblasts. Using a tamoxifen-inducible CreER system in mice, we show here that sporadic expression of SYT-SSX2 across multiple tissue types leads to exclusive formation of synovial sarcoma–like tumors, whereas its widespread expression is lethal. Certain clinical and histologic features of tumors in this new model suggest additional nonmyoblast origin for synovial sarcoma. CreER-based sporadic expression both avoids the severe early developmental phenotypes associated with widespread SYT-SSX2 expression and better models natural pathogenesis of cancers in which transformed cells usually arise within an environment of largely normal cells. Furthermore, this strategy may recapitulate multiple potential cellular origins within a single model system. [Cancer Res 2009;69(8):3657–64]
Genetic Subgrouping of Melanoma Reveals New Opportunities for Targeted Therapy
Authors: Smalley Keiran S.M. , Nathanson Katherine L. , Flaherty Keith T. 
Published: April 2009

Abstract
The discovery of activating oncogenic BRAF V600E mutations in the majority of melanomas has not yet been translated into more effective therapy. The failure of agents may be due to lack of sufficiently targeted therapeutics, but is more likely based on the activation of multiple oncogenic pathways in melanomas in addition to the mitogen-activated protein kinase signaling pathway. In contrast, there are groups of melanomas that instead rely on either c-KIT or CRAF signaling that may be amenable to single-agent targeted therapy. In the current review, we discuss how knowledge about these new melanoma subgroups may lead to improved strategies for treating melanomas harboring BRAF V600E mutations. [Cancer Res 2009;69(8):3241–4]
The Role of the Mouse Y Chromosome on Susceptibility to Testicular Germ Cell Tumors
Authors: Anderson Philip D. , Lam Man-Yee , Poirier Christophe , Bishop Colin E. , Nadeau Joseph H. 
Published: April 2009

Abstract
Testicular germ cell tumors (TGCT) are sex limited, occurring only in males with a Y chromosome. Recently, the gr/gr deletion on the human Y chromosome was associated with increased risk of TGCTs. In addition, the presence of Y chromosome sequences is associated with TGCTs in cases of gonadal dysgenesis. TGCTs in strain 129 males recapitulate many aspects of testicular cancer in human infants and can be used to evaluate the role of the Y chromosome in TGCT risk. We used chromosome substitution strains and a sex-reversing mutant to test the role of the Y chromosome on TGCT susceptibility. Our results show that a Y-linked gene that does not differ among the tested strains is essential for tumorigenesis. [Cancer Res 2009;69(8):3614–8]
Risk Information Exposure and Direct-to-Consumer Genetic Testing for BRCA Mutations among Women with a Personal or Family History of Breast or Ovarian Cancer
Authors: Gray Stacy W. , O'Grady Cristin , Karp Lauren , Smith Daniel , Schwartz J. Sanford , Hornik Robert C. , Armstrong Katrina 
Published: April 2009

Abstract
Background: Direct-to-consumer (DTC) BRCA testing may expand access to genetic testing and enhance cancer prevention efforts. It is not known, however, if current DTC websites provide adequate risk information for informed medical decision making.
Methods: A total of 284 women with a personal or family history of breast/ovarian cancer were randomly assigned to view a “mock” DTC commercial website [control condition (CC); n = 93] or the same “mock” website that included information on the potential risks of obtaining genetic testing online. Risk information was framed two ways: risk information attributed to expert sources (ES; n = 98) and unattributed risk information (URI; n = 93). Participants completed an online survey. End points were intentions to get BRCA testing, testing site preference, and beliefs about DTC BRCA testing.
Results: The sample was 82% white, had a mean age of 39 years (range, 18-70 years) and had a mean education of 3 years of college. Women exposed to risk information had lower intentions to get BRCA testing than women in the CC [adjusted odds ratio (OR), 0.48; 95% confidence interval (95% CI) 0.26-0.87; P = 0.016], and less positive beliefs about online BRCA testing (adjusted OR, 0.48; 95% CI, 0.27-0.86; P = 0.014). Women in the ES condition were more likely to prefer clinic-based testing than were women in the CC (adjusted OR, 2.05; 95% CI, 1.07-3.90; P = 0.030).
Conclusion: Exposing women to information on the potential risks of online BRCA testing altered their intentions, beliefs, and preferences for BRCA testing. Policy makers may want to consider the content and framing of risk information on DTC websites as they formulate regulation for this rapidly growing industry. (Cancer Epidemiol Biomarkers Prev 2009;18(4):1303–11)
Long-Term Survivors of Childhood Cancers in the United States
Authors: Mariotto Angela B. , Rowland Julia H. , Yabroff K. Robin , Scoppa Steve , Hachey Mark , Ries Lynn , Feuer Eric J. 
Published: April 2009

Abstract
Purpose: To estimate the number of individuals in the United States diagnosed with cancer as children (ages 0-19 years) as of 2005, with a focus on those surviving for &gt;30 years.
Methods: To estimate the national prevalence of survivors of childhood cancers, we used data from the Surveillance Epidemiology and End Results program from 1975 to 2004. Long-term childhood cancer survivors, diagnosed before 1975, were estimated using incidence and survival models extrapolated into years before 1975.
Results: We estimated that there are a total of 328,652 survivors of childhood cancer in the United States as of January 1, 2005, of these, 24% have survived &gt;30 years since diagnosis. The cancer sites with the largest number of survivors are brain (51,650), acute lymphoblastic leukemia (49,271), germ cell tumors (34,169), and Hodgkin lymphoma (31,598). Sites with higher proportions of survivors diagnosed &gt;30 years ago are germ cell (43%), soft tissue (38%), renal (34%), and bone (26%). Historical trends from Connecticut data show major improvements in survival for all of the childhood cancer sites.
Conclusion: The number of survivors of childhood cancers is expected to increase in the future consequent to the lifesaving advances in treatment introduced after 1970, especially for acute lymphoblastic leukemia. Because this population is at increased risk for illness-related morbidity and mortality, appreciating the number of survivors who were treated as children is important both to determining the national cancer burden and planning for the future health care needs of these individuals. (Cancer Epidemiol Biomarkers Prev 2009;18(4):1033–40)
Association between Glioma and History of Allergies, Asthma, and Eczema: A Case-Control Study with Three Groups of Controls
Authors: Il'yasova Dora , McCarthy Bridget , Marcello Jennifer , Schildkraut Joellen M. , Moorman Patricia G. , Krishnamachari Bhuma , Ali-Osman Francis , Bigner Darell D. , Davis Faith 
Published: April 2009

Abstract
Because glioma etiology is largely unknown, the inverse association of glioma risk with atopic conditions is promising and deserves close scrutiny. We examined the association between a history of allergies, asthma, and eczema, and glioma risk using sibling, friend, and clinic-based controls. This analysis included 388 incident glioma cases and 80 sibling, 191 friend, and 177 clinic-based controls. Each subject's medical history was assessed via a Web-based or telephone survey. Odds ratios (OR) and their 95% confidence intervals (CI) for the associations with allergies, asthma, eczema, and the overall number of these conditions were calculated from conditional (for sibling and friend controls) and unconditional (for clinic-based controls) logistic models. Allergies were consistently inversely associated with the glioma: ORs were 0.53 (95% CI, 0.15-1.84), 0.54 (95% CI, 0.28-1.07), and 0.34 (95% CI, 0.23-0.50) with sibling, friend, and clinic-based controls, respectively. Asthma showed an inverse association only in the comparison with sibling controls (OR, 0.43; 95% CI, 0.19-1.00). Eczema showed an inverse association only in the comparison with friend controls (OR, 0.42; 95% CI, 0.15-1.18). The overall number of these conditions (ordinal score 0, 1, 2, 3) was inversely associated with glioma: The risk decreased 31% to 45% with each addition of an atopic condition. These estimates were the most stable when different control groups were considered. Comparing the prevalence of these conditions in the three control groups with published data, we note that clinic-based controls generally better approximate the prevalence data for population-based groups. These controls seem to present a reasonable choice for clinic-centered case-control studies. (Cancer Epidemiol Biomarkers Prev 2009;18(4):1232–8)