bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preparation of MgO Nanosheets with Polar (111) Surfaces by Ligand Exchange and Esterification – Synthesis, Structure, and Application as Catalyst Support
Authors: Zhu Kake , Hua Weiming , Deng Wei , Richards Ryan M. 
Published: April 2012

AbstractMetastable magnesium hydroxymethoxide [Mg(OH)(OCH3)] powder with nanosheet morphology was derived from a direct bottom‐up synthesis using magnesium acetate tetrahydrate as precursor under solvothermal conditions, with benzyl alcohol as structure‐directing agent. The synthesis is driven by esterification of magnesium acetate to the corresponding methyl acetate, namely, ligand exchange and esterification of CH3COO– with CH3O–. A MgO powder featuring a Tasker III type (111) surface as its main exposed surface was produced after decomposition of the as‐prepared Mg(OH)(OCH3) intermediate. X‐ray diffraction (XRD) shows that the as‐formed intermediate is Mg(OH)(OCH3), and methyl acetate is identified in the mother liquor by GC–MS measurements. XRD, SEM, and TEM images also show that the surface of the MgO nanosheets is covered by a Tasker III (111) surface. The vanadia supported on this MgO (111) nanosheet surface is more active than the conventional MgO‐supported system for the oxidative dehydrogenation of ethylbenzene with carbon dioxide, which is attributed to the oxygen‐rich nature and intermediate basicity of the MgO (111) surface.
Protective effect of dietary perilla oil on allergic inflammation in asthmatic mice
Authors: Chang Hui‐Hsiang , Chen Chin‐Shuh , Lin Jin‐Yuarn 
Published: April 2012

AbstractPerilla oil (PER) is rich in α‐linolenic acid (n‐3 fatty acid). To unravel the effects of dietary PER on allergic asthmatic inflammation, three kinds of dietary oil, including PER, corn oil (COR), and perilla compound oil (50% PER and 50% COR), were used for replacing the oil in an AIN76 feed consumed by ovalbumin (OVA)‐sensitized and challenged mice continuously for 5 wk. T‐helper type 1 lymphocyte (Th1)/T‐helper type 2 lymphocyte (Th2) and pro‐/anti‐inflammatory cytokines secreted by the cells from the airway, the lungs, and the spleen of experimental mice were determined by ELISA. The results showed that dietary PER inhibited interleukin (IL)‐1β and tumor necrosis factor (TNF)‐α secretions by lipopolysaccharide (LPS)‐stimulated lung cells, as well as interferon (IFN)‐γ and IL‐6 secretions by LPS‐stimulated splenocytes. Perilla compound oil increased the secretion ratio of IFN‐γ/IL‐5 (Th1/Th2 cytokines) in LPS‐stimulated bronchoalveolar lavage fluid cells, but decreased the ratio of IL‐6/IL‐10 (pro‐/anti‐inflammatory cytokines) in LPS‐stimulated splenocytes. The present study demonstrated that dietary PER and its compound oil protected the airways, the lungs, and the spleen from allergic inflammation in OVA‐challenged asthmatic mice, suggesting that an appropriate n‐6/n‐3 fatty acid ratio at a ratio of 1:1 or less in dietary oil may be beneficial to improve the Th2‐skewed allergic asthmatic inflammation.Practical applications:The present study demonstrated that dietary PER and its compound oil protected the airways, the lungs, and the spleen from allergic inflammation in OVA‐challenged asthmatic mice, suggesting that an appropriate n‐6/n‐3 fatty acid ratio at a ratio of 1:1 or less in dietary oil may be beneficial to improve the Th2‐skewed allergic asthmatic inflammation.
Versatile Synthesis of 2‐(Substituted phenyl)‐6,7‐dihydro‐1H‐indol‐4(5H)‐ones from Morita–Baylis–Hillman Acetates of 2‐Oxo‐2‐(substituted phenyl)acetaldehyde
Authors: Batchu Harikrishna , Batra Sanjay 
Published: April 2012

AbstractA versatile synthesis of 2‐(substituted phenyl)‐6,7‐dihydro‐1H‐indol‐4(5H)‐ones from adducts of the Morita–Baylis–Hillman reaction between 2‐oxo‐2‐(substituted phenyl)acetaldehydes and cyclohex‐2‐enone under mild conditions is described.
On the nature of sexist ambivalence: Profiling ambivalent and univalent sexists
Authors: Sibley Chris G. , Becker Julia C. 
Published: April 2012

AbstractThis study examined the proportion of people who held ambivalent versus univalent sexist attitudes, that is, those who simultaneously endorsed benevolent sexism (BS) and hostile sexism (HS). We examined this by capitalizing on recent innovations in latent class analysis to model latent types of sexists, or response profiles to BS and HS, in a nationally representative New Zealand sample (n = 6450). Our results show, for the first time, that by far, the most common pattern was for people to hold similar levels of BS and HS. Strongly ambivalent sexists, however, constituted only 8%–9% of the population. Most were classified as mild or moderate ambivalent sexists (28% and 44%, respectively). Univalent sexism was exceedingly rare, with between 2% and 5% of people solely endorsing HS but not BS, or BS but not HS. We validated the model by showing theoretically predicted differences across sexist types in demographics (gender, age), ideology (social dominance orientation, right‐wing authoritarianism), and relationship satisfaction. Strongly ambivalent sexists also held the highest levels of gender‐specific system justification, invariant of gender. This provides novel evidence for the premise that strong sexist ambivalence promotes support for and faith in the patriarchical system. Copyright © 2012 John Wiley & Sons, Ltd.
Just ignore or counterattack? On the effects of different strategies for dealing with political attacks
Authors: Carraro Luciana , Castelli Luigi , Breazu Ioana , Campomizzi Giulia , Cerruto Antonella , Mariani Massimiliano , Toto Ivano 
Published: April 2012

AbstractDuring political races, candidates have to decide how to deal with the negative remarks from opposing candidates: just ignore or counterattack? In two studies, we investigated some of the consequences of this choice. In Study 1, participants were presented with a political candidate who systematically attacked his opponent and with the reactions of the attacked candidate: across conditions, the attacked candidate only focused on his political program or counterattacked. Results showed an overt condemnation of the choice to counterattack but a higher spontaneous conformity toward the candidate who counterattacked. Study 2 replicated and extended these results indicating that the gender of the attacked candidate did not affect the results. Moreover, Study 2 showed that conformity toward the attacked candidate was positively related to the predicted chances of winning the election. Results are discussed in relation to their theoretical and applied implications. Copyright © 2012 John Wiley & Sons, Ltd.
Influence of arylamine n‐acetyltransferase, sex, and age on 4‐aminobiphenyl‐induced in vivo mutant frequencies and spectra in mouse liver
Authors: Wang Shuang , Sugamori Kim S. , Brenneman Debbie , Hsu Ivy , Calce Adriana , Grant Denis M. 
Published: April 2012

AbstractOne model for cancer initiation by 4‐aminobiphenyl (ABP) involves N‐oxidation by cytochrome P450 CYP1A2 followed by O‐conjugation by N‐acetyltransferase(s) NAT1 and/or NAT2 and decomposition to a DNA‐binding nitrenium ion. We recently observed that neonatal ABP exposure produced liver tumors in male but not in female mice, and that NAT deficiency reduced liver tumor incidence. However, ABP‐induced liver tumor incidence did not correlate with liver levels of N‐(deoxyguanosin‐8‐yl)‐ABP adducts 24 hr after exposure. In this study, we compared in vivo ABP‐induced DNA mutant frequencies and spectra between male and female wild‐type and NAT‐deficient Muta™Mouse using both the tumor‐inducing neonatal exposure protocol and a 28‐day repetitive dosing adult exposure protocol. ABP produced an increase in liver DNA mutant frequencies in both neonates and adults. However, we observed no sex or strain differences in mutant frequencies in neonatally exposed mice, and higher frequencies in adult females than males. Neonatal ABP exposure of wild‐type mice increased the proportion of G‐T transversions in both males and females, while exposure of Nat1/2(‐/‐) mice produced increased G‐T transversions in males and a decrease in females, even though females had higher levels of N‐(deoxyguanosin‐8‐yl)‐4‐ABP adducts. There was no correlation of mutant frequencies or spectra between mice dosed as neonates or as adults. These results suggest that observed sex‐ and NAT‐dependent differences in ABP‐induced liver tumor incidence in mice are not due to differences in either mutation rates or mutational spectra, and that mechanisms independent of carcinogen bioactivation, covalent DNA binding and mutation may be responsible for these differences. Environ. Mol. Mutagen., 2012. © 2012 Wiley Periodicals, Inc.
Mutagenicity and DNA adduct formation by aristolochic acid in the spleen of Big Blue® rats
Authors: McDaniel L. Patrice , Elander Elizabeth R. , Guo Xiaoqing , Chen Tao , Arlt Volker M. , Mei Nan 
Published: April 2012

AbstractAristolochic acid (AA) is a potent human nephrotoxin and carcinogen. We previously reported that AA treatment resulted in DNA damage and mutation in the kidney and liver of rats. In this study, we have determined the DNA adducts and mutations induced by AA in rat spleen. Big Blue® transgenic rats were gavaged with 0, 0.1, 1.0, and 10.0 mg AA/kg body weight five‐times/week for 3 months. Three DNA adducts, [7‐(deoxyadenosin‐N6‐yl)‐aristolactam I, 7‐(deoxyadenosin‐N6‐yl)‐aristolactam II and 7‐(deoxyguanosin‐N2‐yl)‐aristolactam I], were identified by 32P‐postlabeling. Over the dose range studied, there were strong linear dose‐responses for AA‐DNA adduct formation in the treated rat spleens, ranging from 4.6 to 217.6 adducts/108 nucleotides. Spleen cII mutant frequencies also increased in a dose‐dependent manner, ranging from 32.7 to 286.2 × 10−6 in the treated animals. Mutants isolated from the different treatment groups were sequenced; analysis of the resulting spectra indicated that there was a significant difference between the pattern of mutation in the 10 mg/kg AA‐treated and the vehicle control rats. A:T → T:A transversion was the major type of mutation in AA‐treated rats, whereas G:C → A:T transition was the main type of mutation inthe vehicle controls. These results indicate that AA is genotoxic in the spleen of rats exposed under conditions that result in DNA adduct formation and mutation induction in kidney and liver. Environ. Mol. Mutagen., 2012. © 2012 Wiley Periodicals, Inc.
Mitogen‐activated protein kinase p38 regulates krox‐20 to direct schwann cell differentiation and peripheral myelination
Authors: Hossain Shireen , de la Cruz‐Morcillo Miguel‐Angel , Sanchez‐Prieto Ricardo , Almazan Guillermina 
Published: April 2012

AbstractWe previously reported that addition of extracellular matrix (ECM) extracts to rat Schwann cell‐dorsal root ganglion neuron (DRGN) co‐cultures activated mitogen‐activated protein kinase (MAPK) p38, whereas inhibition blocked myelination. Here, we used p38 pharmacological inhibitors and gene silencing to assess their effects on downstream kinases and key transcription factors. We show that p38α regulates expression of the master transcription factor, Krox‐20, required for the onset of myelination in Schwann cell‐DRGNs, as assessed by immunocytochemistry and qRT‐PCR. p38 activity is also required for the expression of the cell cycle inhibitor p27kip1, associated with Schwann cell differentiation. Three potential effectors of p38 were explored: MAPK‐activated protein kinase‐2 (MK2), mitogen and stress‐activated protein kinase‐1 (MSK‐1), and the transcription factor cAMP response element‐binding protein (CREB). Inhibition of MK2 with CMPD1 or gene knockdown with siRNAs reduced numbers of Krox‐20‐positive Schwann cells and expression of myelin proteins MBP and MAG. ECM activated CREB and increased Krox‐20 expression, whereas CREB1 gene silencing reduced Krox‐20. Furthermore, two nonselective inhibitors of MSK‐1 (H89 and R0‐318820) decreased ECM‐induced CREB phosphorylation and, similar to anti‐MSK‐1 siRNAs, reduced Krox‐20‐positive cells. In addition, p38 modulated the expression of two transcription factors involved in the regulation of Krox‐20 [suppressed cAMP‐inducible protein (SCIP) and Sox10], but not Sox2, an antagonist of Krox‐20. Collectively, our results show that p38 primarily directs Schwann cell differentiation and peripheral myelination by regulating Krox‐20 expression through its downstream effectors, MK2 and MSK‐1/CREB, and transcription factors SCIP and Sox10. © 2012 Wiley Periodicals, Inc.
TGF‐β signaling through SMAD2/3 induces the quiescent microglial phenotype within the CNS environment
Authors: Abutbul Shai , Shapiro Jenny , Szaingurten‐Solodkin Irit , Levy Nitzan , Carmy Yaron , Baron Rona , Jung Steffen , Monsonego Alon 
Published: April 2012

AbstractMicroglia are myeloid‐derived cells that colonize the central nervous system (CNS) at early stages of development and constitute up to 20% of the glial populations throughout life. While extensive progress has been recently made in identifying the cellular origin of microglia, the mechanism whereby the cells acquire the unique ramified and quiescent phenotype within the CNS milieu remains unknown. Here, we show that upon co‐culturing of either CD117+/Lin− hematopoietic progenitors or CD11c+ bone marrow derived cells with organotypic hippocampal slices or primary glia, the cells acquire a ramified morphology concomitant with reduced levels of CD86, MHCII, and CD11c and up‐regulation of the microglial cell–surface proteins CX3CR1 and Iba‐1. We further demonstrate that the transforming growth factor beta (TGF‐β) signaling pathway via SMAD2/3 phosphorylation is essential for both primary microglia and myeloid‐derived cells in order to acquire their quiescent phenotype. Our study suggests that the abundant expression of TGF‐β within the CNS during development and various inflammatory processes plays a key role in promoting the quiescent phenotype of microglia and may thus serve as a target for therapeutic strategies aimed at modulating the function of microglia in neurodegenerative diseases such as Alzheimer's and prion. © 2012 Wiley Periodicals, Inc.
An 80‐year record of sediment quality in the lower Mississippi River
Authors: Van Metre Peter C. , Horowitz Arthur J. 
Published: April 2012

AbstractIn 1937, the US Army Corps of Engineers cut through the “neck” of a large meander on the lower Mississippi River (below the confluence with the Ohio River) forming the Caulk Neck cutoff and creating Lake Whittington, a 26‐km long oxbow lake, in northern Mississippi. Since 1938, seasonal flooding and a boat channel connecting the lake with the Mississippi River have led to sediment accumulation in the lake, resulting in an 80‐year record of sediment quality in the river. On the basis of an age‐dated sediment core from the lake, trends in trace metals and hydrophobic organic compounds (except polycyclic aromatic hydrocarbons) follow well‐known patterns with upward trends from the 1930s to the ca 1970s, followed by downward trends to the present. Two factors contribute to these patterns: reservoir construction and changes in emissions. The construction of seven large reservoirs on the Missouri River, in particular the closure of the Fort Randall (1953) and Gavins Point (1955) Dams, greatly reduced the load of relatively clean sediment to the Mississippi River, likely contributing to downstream increases in contaminant concentrations in the Mississippi River. Increasing anthropogenic emissions also contributed to upward trends until ca 1970 when major environmental policy actions began resulting in broad decreases in emissions and downward trends in the concentrations of most of the contaminants monitored. Polycyclic aromatic hydrocarbons and phosphorus are partial exceptions to this pattern, with increases to the 1960s and variable concentrations showing no clear trend since. Published 2012. This article is a U.S. Government work and is in the public domain in the USA.
Influence of DNA repair gene polymorphisms on prognosis in inoperable non‐small cell lung cancer patients treated with radiotherapy and platinum‐based chemotherapy
Authors: Butkiewicz Dorota , Drosik Anna , Suwiński Rafał , Krześniak Małgorzata , Rusin Marek , Kosarewicz Agata , Rachtan Jadwiga , Matuszczyk Iwona , Gawkowska‐Suwińska Marzena 
Published: April 2012

AbstractPolymorphisms in DNA repair genes may modulate not only an individual DNA repair capacity, DNA damage levels and cancer risk but also clinical outcome after DNA damage‐inducing anticancer therapy. In this study, we analyzed the association between the XPA ‐4G>A, XPD Asp312Asn, hOGG1 Ser326Cys, XRCC1 Arg399Gln, XRCC2 ‐4234G>C, XRCC3 ‐4541A>G and Thr241Met polymorphisms and prognosis in 250 inoperable non‐small cell lung cancer (NSCLC) patients treated with radiotherapy and platinum‐based chemotherapy. In univariate model, the XPA‐4A and XRCC1 399Gln alleles alone and in combination influenced survival only in stage III group. In multivariate analysis, the XPA‐4 GA/AA was associated with poor survival (HR 1.55, p = 0.011 overall and HR 1.72, p = 0.008 in stage III). In chemoradiotherapy group, the XPA‐4A carriers were at increased risk of death and progression (HR 1.73, p = 0.013 and HR 1.65, p = 0.016, respectively), especially in stage III (p = 0.008). Moreover, individuals with ≥ 2 XPA/XRCC1 adverse alleles showed a higher risk of death (HR 1.46, p = 0.036 overall; HR 1.85, p = 0.004 in stage III and HR 1.71, p = 0.022 in chemoradiotherapy group) and progression (HR 1.75, p = 0.011 overall and HR 1.93, p = 0.005 in stage III). The XPA‐4 GA/AA genotype individually and together with the XRCC1 399Gln was an independent unfavorable prognostic factor in our study. Thus, our findings indicate a prognostic potential of the XPA‐4G>A in unresected NSCLC treated with radiotherapy and chemoradiotherapy. The results require validation in an independent population.
Small median tumor diameter at cure threshold (<20 mm) among aggressive non‐small cell lung cancers in male smokers predicts both chest X‐ray and CT screening outcomes in a novel simulation framework
Authors: Goldwasser Deborah L. , Kimmel Marek 
Published: April 2012

AbstractThe effectiveness of population‐wide lung cancer screening strategies depends on the underlying natural course of lung cancer. We evaluate the expected stage distribution in the Mayo CT screening study under an existing simulation model of non‐small cell lung cancer (NSCLC) progression calibrated to the Mayo lung project (MLP). Within a likelihood framework, we evaluate whether the probability of 5‐year NSCLC survival conditional on tumor diameter at detection depends significantly on screening detection modality, namely chest X‐ray and computed tomography. We describe a novel simulation framework in which tumor progression depends on cellular proliferation and mutation within a stem cell compartment of the tumor. We fit this model to randomized trial data from the MLP and produce estimates of the median radiologic size at the cure threshold. We examine the goodness of model fit with respect to radiologic tumor size and 5‐year NSCLC survival among incident cancers in both the MLP and Mayo CT studies. An existing model of NSCLC progression under‐predicts the number of advanced‐stage incident NSCLCs among males in the Mayo CT study (p‐value = 0.004). The probability of 5‐year NSCLC survival conditional on tumor diameter depends significantly on detection modality (p‐value = 0.0312). In our new model, selected solution sets having a median tumor diameter of 16.2–22.1 mm at cure threshold among aggressive NSCLCs predict both MLP and Mayo CT outcomes. We conclude that the median lung tumor diameter at cure threshold among aggressive NSCLCs in male smokers may be small (<20 mm).
Quantification of PKC family genes in sporadic breast cancer by qRT‐PCR: Evidence that PKCι/λ overexpression is an independent prognostic factor
Authors: Awadelkarim Khalid Dafaallah , Callens Céline , Rossé Carine , Susini Aurélie , Vacher Sophie , Rouleau Etienne , Lidereau Rosette , Bièche Ivan 
Published: April 2012

AbstractDrugs targeting protein kinase C (PKC) show promising therapeutic activity. However, little is known about the expression patterns of the 11 PKC genes in human tumors, and the clinical significance of most PKC genes is unknown. We used qRT‐PCR assays to quantify mRNA levels of the 11 PKC genes in 458 breast tumors from patients with known clinical/pathological status and long‐term outcome. The proportion of tumors in which the expression of the different genes was altered varied widely, from 9.6% for PKN2 to 40.2% for PKCι/λ. In breast tumors, overexpression was the main alteration observed for PKCι/λ (33.4%), PKCδ (29.5%) and PKCζ (9.6%), whereas underexpression was the main alteration observed for PKCα (27.3%), PKCε (11.6%), PKCη (8.7%) and PKN2 (8.1%). Both overexpression and underexpression were observed for PKCβ (underexpression 15.5%, overexpression 13.8%), PKCθ (underexpression 14.8%, overexpression 10.0%) and PKN1 (underexpression 6.6%, overexpression 7.4%). Several links were found between different PKC genes; and also between the expression patterns of PKC genes and several classical pathological and clinical parameters. PKCι/λ alone was found to have prognostic significance (p = 0.043), whereas PKCα showed a trend towards an influence on relapse‐free survival (p = 0.052). PKCι/λ retained its prognostic significance in Cox multivariate regression analysis (p = 0.031). These results reveal very complex expression patterns of PKC genes in breast tumors, and suggest that their expression should be considered together when evaluating anti‐tumoral drugs. PKCι/λ seems to be the most promising therapeutic target in breast cancer.
Body size and risk of differentiated thyroid carcinomas: Findings from the EPIC study
Authors: Rinaldi Sabina , Lise Mauro , Clavel‐Chapelon Françoise , Boutron‐Ruault Marie‐Christine , Guillas Gwenaelle , Overvad Kim , Tjønneland Anne , Halkjær Jytte , Lukanova Annekatrin , Kaaks Rudolf , Bergmann Manuela M. , Boeing Heiner , Trichopoulou Antonia , Zylis Dimosthenis , Valanou Elissavet , Palli Domenico , Agnoli Claudia , Tumino Rosario , Polidoro Silvia , Mattiello Amalia , Bas Bueno‐de‐Mesquita H. , Peeters Petra H. , Weiderpass Elisabete , Lund Eiliv , Skeie Guri , Rodríguez Laudina , Travier Noemie , Sánchez Maria‐José , Amiano Pilar , Huerta José‐María , Ardanaz Eva , Rasmuson Torgny , Hallmans Göran , Almquist Martin , Manjer Jonas , Tsilidis Konstantinos K. , Allen Naomi E. , Khaw Kay‐Tee , Wareham Nick , Byrnes Graham , Romieu Isabelle , Riboli Elio , Franceschi Silvia 
Published: April 2012

AbstractResults from case‐control and prospective studies suggest a moderate positive association between obesity and height and differentiated thyroid carcinoma (TC). Little is known on the relationship between other measures of adiposity and differentiated TC risk. Here, we present the results of a study on body size and risk of differentiated TC based on a large European prospective study (EPIC). During follow‐up, 508 incident cases of differentiated TC were identified in women, and 58 in men. 78% of cases were papillary TC. Cox proportional hazard models were used to estimate hazard ratios (HRs). In women, differentiated TC risk was significantly associated with body mass index (BMI, kg/m2) (HR highest vs lowest quintile = 1.41, 95% CI: 1.03–1.94); height (HR = 1.61; 95% CI: 1.18–2.20); HR highest vs lowest tertile waist (HR = 1.34, 95% CI: 1.00–1.79) and waist‐to‐hip ratio (HR = 1.42, 95% CI: 1.05–1.91). The association with BMI was somewhat stronger in women below age 50. Corresponding associations for papillary TC were similar to those for all differentiated TC. In men the only body size factors significantly associated with differentiated TC were height (non linear), and leg length (HR highest vs. lowest tertile = 3.03, 95% CI: 1.30–7.07). Our study lends further support to the presence of a moderate positive association between differentiated TC risk and overweight and obesity in women. The risk increase among taller individuals of both sexes suggests that some genetic characteristics or early environmental exposures may also be implicated in the etiology of differentiated TC.