bluuebunny/crossref_metadata_2025_split huggingface dataset:
The impact of regulatory focus on affective responses to social discrimination
Authors: Sassenberg Kai , Hansen Nina 
Published: August 2006

AbstractThe impact of individuals' regulatory focus and the domain of outcomes (non‐gains vs. losses) on the target's affective responses to social discrimination were tested. Based on regulatory focus theory (Higgins, 1997), it was predicted that a prevention focus would lead to more anger and agitation after social discrimination, because experiencing social discrimination is similar to experiencing failure. This pattern was predicted to be more pronounced when social discrimination was based on losses than when social discrimination was based on non‐gains (i.e., when the in‐group was evaluated more negatively vs. less positively compared to the out‐group). The results of three studies using chronic and situationally induced regulatory focus confirmed these predictions. No effect was found for the promotion focus. Copyright © 2006 John Wiley & Sons, Ltd.
Retracted:When different is better: performance following upward comparison
Authors: Johnson Camille S. , Stapel Diederik A. 
Published: August 2006

AbstractThe attainability of upward social comparisons is known to affect self‐evaluative responses. The consequences for performance, however, are less well understood. We suggest that demoralizing upward comparisons with unattainable targets may lead to improved performance when the target and performance domains are mismatched. For example, comparison with a target that has been successful in an analytic domain should lead to better performance in a verbal domain. This improvement in performance occurs because increased performance in alternative domains provides an opportunity for self‐evaluation maintenance. In three studies, we demonstrate that upward comparisons to targets whose successes are perceived as threatening lead to improved performance when the task and performance domain do not match, but no improvements when the domains match. Copyright © 2006 John Wiley & Sons, Ltd.
Altruism and egoism: prosocial motivations for helping depend on relationship context
Authors: Maner Jon K. , Gailliot Matthew T. 
Published: August 2006

AbstractFindings from the current study suggest that the link between helping and empathic concern—a hypothesized motivator of altruistic behavior—may be more pronounced in the context of kinship relationships than among strangers. Participants expressed their willingness to help a kin‐member or stranger in specific need situations. Putative mediators of helping (empathic concern, general negative affect, perceptions of oneness) were measured. Empathic concern appeared to partially mediate effects of relationship context on willingness to help. Moreover, while controlling for egoistic motivators (negative affect, oneness), empathic concern was linked to participants' willingness to help a kin‐member but not a stranger. Findings suggest that factors motivating prosocial action in close relationships may be different from those that motivate helping among strangers. Copyright © 2006 John Wiley & Sons, Ltd.
When the rich contribute more in public good dilemmas: the role of provision point level
Authors: De Cremer David 
Published: August 2006

AbstractThe present research examined the effects of endowment size, provision point level and the opportunity to voice one's opinion on contributions in asymmetric public good dilemmas. Results from a first experiment showed that group members endowed with more resources contributed more when the required threshold for obtaining a public good was high rather than low. ‘Rich’ participants who reported that their personal contribution was more critical for success contributed more. However, most groups failed to surpass the high provision point threshold level. Results from a second experiment reveal that ‘rich’ participants given voice, contributed more than ‘rich’ participants not given a voice. Voice contributed to greater feelings of inclusiveness, higher contributions and increased the likelihood that the group surpassed the high provision point level. Copyright © 2006 John Wiley & Sons, Ltd.
Considering reasons for a value influences behaviour that expresses related values: an extension of the value‐as‐truisms hypothesis
Authors: Karremans Johan C. 
Published: August 2006

AbstractPrevious research has demonstrated that value‐congruent behaviour is increased after people have considered reasons for or against the value (since values typically lack cognitive support). The present research importantly extends these previous findings. Specifically, based on the reasoning that values can be categorised into different motivational types, it was predicted that considering reasons (i.e. providing cognitive support) for or against a specific value should increase behaviour that expresses a related value. Two studies provided strong support for this central prediction. In Study 1, participants who were asked to consider reasons for or against the values of honesty and loyalty were especially likely to engage in helping behaviour. In Study 2, participants who considered reasons for the value of helpfulness were especially likely to behave in an egalitarian manner (compared to participants who did not consider reasons, and participants who were merely primed with helpfulness). The implications of these findings for when and why considering reasons for a value influences value‐expressive behaviour, as well as some practical implications, are discussed. Copyright © 2006 John Wiley & Sons, Ltd.
DNA damage in Pakistani pesticide‐manufacturing workers assayed using the Comet assay
Authors: Bhalli Javed A. , Khan Q.M. , Nasim A. 
Published: August 2006

AbstractThe production and use of chemical pesticides has increased in recent years. Although the increased use of pesticides may benefit agriculture, they are also the potential source of environmental pollution, and exposure to pesticides can have negative consequences for human health. In the present study, we have assessed DNA damage in blood leukocytes from 29 Pakistani pesticide‐factory workers and 35 controls of similar age and smoking history. The workers were exposed to various mixtures of organophosphates, carbamates, and pyrethroids. DNA damage was measured with the single cell gel electrophoresis (SCGE) assay or Comet assay, using the mean comet tail length (μm) as the DNA damage metric. Exposed workers had significantly longer comet tail lengths than the controls (mean ± SD 19.98 ± 2.87 vs. 7.38 ± 1.48, P < 0.001). Of the possible confounding factors, smokers had significantly longer mean comet tail lengths than nonsmokers and exsmokers for both the workers (21.48 ± 2.58 vs.18.37 ± 2.28, P < 0.001) and the controls (8.86 ± 0.56 vs. 6.79 ± 1.31, P < 0.001), while age had a minimal effect on DNA damage (P > 0.05 and P < 0.05 for workers and controls, respectively). The results of this study indicate that occupational exposure to pesticides causes DNA damage. Environ. Mol. Mutagen., 2006. © 2006 Wiley‐Liss, Inc.
Simultaneous estimation of gene‐gene and gene‐environment interactions for numerous loci using double penalized log–likelihood
Authors: Tanck Michael W.T. , Wouter Jukema J. , Zwinderman Aeilko H. 
Published: August 2006

AbstractMany common human diseases are considered to be caused by complex multifactorial processes. For these diseases, it is expected that numerous genetic and environmental factors and, possibly, their interactions play a role. Therefore, simultaneously analyzing the effects of numerous genes and environmental factors is a more realistic approach compared to single gene analyses, but the large number of genes and environmental factors pose a challenge, not in the least due to the limitations created by the tools available for analyzing such high‐dimensional models. In the present manuscript we propose a method that is capable of identifying “true” interactions in a setting where the number of effects to be estimated is very large and can even surpass the number of observations. Basically, all possible (interaction) effects are entered in a double penalized model, where main effects are ridge penalized, whereas the interactions are subjected to a least absolute shrinkage and selection operator (lasso) penalty. Results from the simulations and real data show that the proposed method is capable of detecting interactions even with relative small effect sizes.Genet.Epidemiol. 2006. © 2006 Wiley‐Liss, Inc.
Gene‐dropping vs. empirical variance estimation for allele‐sharing linkage statistics
Authors: Jung Jeesun , Weeks Daniel E. , Feingold Eleanor 
Published: August 2006

AbstractIn this study, we compare the statistical properties of a number of methods for estimating P‐values for allele‐sharing statistics in non‐parametric linkage analysis. Some of the methods are based on the normality assumption, using different variance estimation methods, and others use simulation (gene‐dropping) to find empirical distributions of the test statistics. For variance estimation methods, we consider the perfect variance approximation and two empirical variance estimates. The simulation‐based methods are gene‐dropping with and without conditioning on the observed founder alleles. We also consider the Kong and Cox linear and exponential models and a Monte Carlo method modified from a method for finding genome‐wide significance levels. We discuss the analytical properties of these various P‐value estimation methods and then present simulation results comparing them. Assuming that the sample sizes are large enough to justify a normality assumption for the linkage statistic, the best P‐value estimation method depends to some extent on the (unknown) genetic model and on the types of pedigrees in the sample. If the sample sizes are not large enough to justify a normality assumption, then gene‐dropping is the best choice. We discuss the differences between conditional and unconditional gene‐dropping. Genet. Epidemiol. 2006. © 2006 Wiley‐Liss, Inc.
Estimating haplotype relative risks in complex disease from unphased SNPs data in families using a likelihood adjusted for ascertainment
Authors: Carayol J. , Philippi A. , Tores F. 
Published: August 2006

AbstractThe understanding of complex diseases and insights to improve their medical management may be achieved through the deduction of how specific haplotypes may play a joint effect to change relative risk information. In this paper we describe an ascertainment adjusted likelihood‐based method to estimate haplotype relative risks using pooled family data coming from association and/or linkage studies that were used to identify specific haplotypes. Haplotype‐based analysis tends to require a large amount of parameters to capture all the information that leads to efficiency problems. An adaptation of the Stochastic Expectation Maximization algorithm is used for haplotypes inference from genotypic data and to reduce the number of nuisance parameters for risk estimation. Using different simulations, we show that this method provides unbiased relative risk estimates even in case of departure from Hardy‐Weinberg equilibrium.Genet. Epidemiol. 2006. © 2006 Wiley‐Liss, Inc.
Retroviral lineage analysis of fibroblast growth factor receptor signaling in FGF2 inhibition of oligodendrocyte progenitor differentiation
Authors: Zhou Yong‐Xing , Flint Nicole C. , Murtie Joshua C. , Le Tuan Q. , Armstrong Regina C. 
Published: August 2006

AbstractFibroblast growth factor 2 (FGF2) inhibits oligodendrocyte progenitor cell (OPC) differentiation during development and limits remyelination following chronic demyelination. The current study examines the mechanism underlying this effect of FGF2 expression on OPC differentiation. Retroviral lineage tracing demonstrates a direct in vivo effect of FGF receptor (FGFR) signaling on OPC differentiation. Retrovirus expressing a dominant negative FGFR construct (FGFRdn) and green fluorescent protein (GFP) was injected into the dorsal columns of postnatal day 7 (P7) mice followed by perfusion at P28. Among the GFP‐labeled cells, FGFRdn retrovirus generated a higher proportion of oligodendrocytes than did control infections. This result from FGFRdn expression in OPCs was similar to the result obtained in our previous study using control retrovirus in FGF2 null mice. Further, in vitro retroviral siRNA expression distinguishes the function of specific FGFR isoforms in OPC responses to FGF2. FGF2 inhibition of OPC differentiation was effectively blocked by siRNA targeted to FGFR1, but not FGFR2 or FGFR3. We propose a model of direct FGF2 activation of FGFR1 leading to inhibition of OPC differentiation. This signaling pathway may be an important regulator of oligodendrocyte generation during myelination in development and may perturb OPC generation of remyelinating oligodendrocytes in demyelinating disease. Published 2006 Wiley‐Liss, Inc.
TGF‐β1 potentiates astrocytic nitric oxide production by expanding the population of astrocytes that express NOS‐2
Authors: Hamby Mary E. , Hewett James A. , Hewett Sandra J. 
Published: August 2006

AbstractBoth transforming growth factor‐β1 (TGF‐β1) and nitric oxide synthase‐2 (NOS‐2) are upregulated under various neuropathological states. Evidence suggests that TGF‐β1 can either attenuate or augment NOS‐2 expression, with the prevailing effect dependent on the experimental paradigm employed and the cell‐type under study. The purpose of the present study was to determine the effect of TGF‐β1 on astrocytic NOS‐2 expression. In purified astrocyte cultures, TGF‐β1 alone did not induce NOS‐2 or NO production. However, NO production induced by lipopolysaccharide (LPS) plus IFNγ was enhanced by TGF‐β1 in a concentration‐dependent manner between 10 and 1,000 pg/mL. The presence of IFNγ was not necessary for this effect to occur, as TGF‐β1 enhanced NO production induced by LPS in a similar fashion. In cultures stimulated with LPS plus IFNγ, the enhancement of NO production by TGF‐β1 was associated with a corresponding increase in NOS‐2 mRNA and protein expression. Interestingly, immunocytochemical assessment of NOS‐2 protein expression demonstrated that TGF‐β1 augmented astrocytic NO production, specifically by increasing the pool of astrocytes capable of expressing NOS‐2 induced by either LPS (∼threefold) or LPS plus IFNγ (∼sevenfold). In a broader sense, our results suggest that TGF‐β1 recruits a latent population of astrocytes to respond to stimulation by pro‐inflammatory mediators. © 2006 Wiley‐Liss, Inc.
Hippocampal and cortical place cell plasticity: Implications for episodic memory
Authors: Frank Loren M. , Brown Emery N. , Stanley Garrett B. 
Published: August 2006

AbstractIn humans, the hippocampus is essential for storing episodic memories. These event memories require the rapid storage of novel associations, but little is known about the cellular correlates of such rapid plasticity. We studied patterns of activity and plasticity in the CA1 region of the hippocampus and in anatomically adjacent cortical regions as rats explored a novel arm of a maze to identify the neural correlates of hippocampally dependent memory formation. We found that hippocampal place fields exhibited three phenomena that may have direct relevance to the encoding of episodic memories: (1) very rapid plasticity upon exposure to the new environment, (2) instability in representations formed after short periods of exploration, and (3) a dissociation between the stability of a hippocampal representation and the apparent familiarity of a location. In contrast, cortical regions showed less dramatic changes. Taken together, these findings suggest that hippocampal activity undergoes a period of rapid reorganization during the encoding of novel information, and that even after this reorganization is complete, areas outside the hippocampus have not yet formed stable memories. © 2006 Wiley‐Liss, Inc.
Alcohol consumption and ovarian cancer risk in a population‐based case–control study
Authors: Peterson Neeraja B. , Trentham‐Dietz Amy , Newcomb Polly A. , Chen Zhi , Hampton John M. , Willett Walter C. , Egan Kathleen M. 
Published: August 2006

AbstractAlcohol consumption has been investigated as a possible risk factor for ovarian cancer in several epidemiological studies, with inconsistent findings. Recent studies have suggested that the association between alcohol consumption and ovarian cancer may vary according to histologic subtype of ovarian cancer and type of alcohol consumed (e.g., wine, beer, or liquor). We examined these associations in a population‐based case‐control study comprised of 762 incident cases of epithelial ovarian cancer and 6,271 population controls from Massachusetts and Wisconsin aged 40–79 years. Women reported their usual alcohol consumption as young adults (20–30 years of age) and in the recent past. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. There was no significant association of ovarian cancer with increasing alcohol consumption either during ages 20–30 years (p trend 0.42) or in the recent past (p trend 0.83). Regular drinking of beer (1 drink/day or more) during ages 20–30 (OR 1.55, 95% CI 1.07–2.26), though not liquor (OR 1.35, 95% CI 0.86–2.11) or wine (OR 0.99, 95% CI 0.49–2.00), was associated with a statistically significant increase in risk of invasive tumors, whereas no significant relationships were observed for recent drinking, regardless of alcohol type. The elevated risk for early adult regular drinking was confined to serous invasive tumors (OR 1.52, 95% CI 1.01–2.30), though results for other subtypes were based on sparse data and results were imprecise. In this study, neither total alcohol consumption as a young adult nor recently was associated with an increase in the risk of ovarian cancer. © 2006 Wiley‐Liss, Inc.
What are cyclooxygenases and lipoxygenases doing in the driver's seat of carcinogenesis?
Authors: Fürstenberger G. , Krieg P. , Müller‐Decker K. , Habenicht A.J.R. 
Published: August 2006

AbstractSubstantial evidence supports a functional role for cyclooxygenase‐ and lipoxygenase‐catalyzed arachidonic and linoleic acid metabolism in cancer development. Genetic intervention studies firmly established cause‐effect relations for cyclooxygenase‐2, but cyclooxygenase‐1 may also be involved. In addition, pharmacologic cyclooxygenase inhibition was found to suppress carcinogenesis in both experimental mouse models and several cancers in humans. Arachidonic acid‐derived eicosanoid or linoleic acid‐derived hydro[peroxy]fatty acid signaling are likely to be involved impacting fundamental biologic phenomina as diverse as cell growth, cell survival, angiogenesis, cell invasion, metastatic potential and immunomodulation. However, long chain unsaturated fatty acid oxidation reactions indicate antipodal functions of distinct lipoxygenase isoforms in carcinogenesis, i.e., the 5‐ and platelet‐type 12‐lipoxygenase exhibit procarcinogenic activities, while 15‐lipoxygenase‐1 and 15‐lipoxygenase‐2 may suppress carcinogenesis. © 2006 Wiley‐Liss, Inc.
Usefulness of EGFR mutation screening in pleural fluid to predict the clinical outcome of gefitinib treated patients with lung cancer
Authors: Soh Junichi , Toyooka Shinichi , Aoe Keisuke , Asano Hiroaki , Ichihara Syuji , Katayama Hideki , Hiraki Akio , Kiura Katsuyuki , Aoe Motoi , Sano Yoshifumi , Sugi Kazuro , Shimizu Nobuyoshi , Date Hiroshi 
Published: August 2006

AbstractThe importance of epidermal growth factor receptor (EGFR) gene mutation has been recognized in nonsmall cell lung cancer (NSCLC), requiring the standardization of mutation screening system including the kind of samples. Here, we examined the EGFR mutation status in 61 pleural fluid samples from NSCLC cases using direct sequencing, nonenriched PCR, mutant‐enriched PCR and peptide nucleic acid‐locked nucleic acid (PNA‐LNA) PCR clamp assay. The mutant‐enriched PCR assay detected 16 mutant cases. Among them, the nonenriched PCR assay failed to detect 3 mutant cases. Regarding the discrepancy between mutant‐enriched PCR and PNA‐LNA PCR clamp assays, 3 cases of exon19‐deletions were detected only by mutant‐enriched PCR assay and no difference at the L858R mutation. There was no difference in results between direct sequencing and nonenriched PCR assay. We also correlated the EGFR mutation with clinical outcome of gefitinib‐treated 29 cases. EGFR mutations were present in 10 cases, revealing 7 partial response and 3 no change (NC). In EGFR wild‐type cases, 10 revealed NC and 9 progressive disease. The responders were significantly more frequent among the EGFR mutant cases than among the wild‐type (p < 0.0001). Overall survival (p = 0.0092) and progression‐free survival (p = 0.018) were significantly longer among the EGFR mutant cases than among the wild‐type. In summary, we evaluated the utility of EGFR mutation screening in pleural fluid using 4 assays that showed some discrepancies arising from the designs of the assays. As clinical importance, the EGFR mutation status in pleural fluid can be a biomarker for the favorable outcome of gefitinib‐treated NSCLC cases. © 2006 Wiley‐Liss, Inc.
Maternal dietary exposure to fiber during pregnancy and mammary tumorigenesis among rat offspring
Authors: Yu Bin , Khan Galam , Foxworth Aaron , Huang Kai , Hilakivi‐Clarke Leena 
Published: August 2006

AbstractMaternal diet during pregnancy has been proposed to modify female offspring's later susceptibility to develop breast cancer; however, most of the dietary factors identified thus far have led to increased risk. To identify dietary factors that might reduce offspring's breast cancer risk, pregnant rat dams were fed diets containing 6% fiber originating either from cellulose (control), or oat, whole wheat or defatted flax flour. At birth, dams were switched to the AIN93 semi‐purified diet. Mammary tumor incidence and multiplicity, induced by administering the offspring 5 mg 7,12‐dimethylbenz[a]anthracene (DMBA) at the age of 50 days, was reduced in the whole wheat flour‐exposed offspring and increased in the defatted flax‐exposed offspring. To identify the mechanisms mediating the effects of in utero dietary exposures, changes in mammary gland morphology and gene expression were assessed before puberty onset (3 weeks of age) and at the time rats are most susceptible to malignant transformation (8 weeks of age). The number of terminal end buds (TEBs), i.e., the targets of malignant transformation, was reduced in the mammary glands of whole wheat‐ and oat flour‐exposed offspring, as compared to the controls. Further, the number of apoptotic epithelial cells (based on ISOL assay) was elevated in the whole wheat flour offspring, but no changes in cell proliferation (PCNA), estrogen receptor α (ER‐α) or cyclin D1 mRNA or protein levels were seen. The mRNA and/or protein levels of BRCA1 and p53 were significantly increased in the mammary glands of whole wheat flour offspring. Further, the levels of 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG), a marker of DNA damage, were significantly reduced in these rats, suggesting that maternal dietary exposure to whole wheat during pregnancy may reduce offspring's breast cancer risk by improving DNA damage repair mechanisms. © 2006 Wiley‐Liss, Inc.