bluuebunny/crossref_metadata_2025_split huggingface dataset:
Betel quid not containing tobacco and oral cancer: A report on a case–control study in Papua New Guinea and a meta‐analysis of current evidence
Authors: Thomas Steven J. , Bain Christopher J. , Battistutta Diana , Ness Andrew R. , Paissat Darius , Maclennan Robert 
Published: December 2006

AbstractSmoking and betel quid chewing are associated with increased risk of oral cancer but few studies have reported on associations in populations where betel quid does not contain tobacco. We conducted a case–control study in Papua New Guinea and a systematic review. Our case–control study recruited 143 cases with oral cancer and 477 controls. We collected information on smoking and betel quid chewing. Current smoking was associated with an increased risk of oral cancer with an adjusted odds ratio (OR) for daily smokers of 2.63 (95% confidence intervals (95% CI) 1.32, 5.22) and amongst heaviest smokers of 4.63 (95% CI 2.07, 10.36) compared to never‐smokers. Betel chewing was associated with increased risk of oral cancer with an adjusted OR for current chewers of 2.03 (95% CI 1.01, 4.09) and in the heaviest chewers of 2.47 (95% CI 1.13, 5.40) compared to nonchewers. The OR in those who both smoked tobacco and chewed betel quid was 4.85 (95% 1.10, 22.25), relative to those who neither smoked nor chewed. The systematic review identified 10 previous studies that examined risk of oral cancer associated with betel quid chewing that controlled for smoking in populations where betel quid did not contain tobacco. In studies that reported results for non‐smokers the combined OR was 2.14 (95% CI 1.06, 4.32) in betel quid chewers and in studies that adjusted for smoking the combined OR was 3.50 (95% CI 2.16, 5.65) in betel quid chewers. Preventive efforts should discourage betel quid chewing as well as smoking. © 2006 Wiley‐Liss, Inc.
Complete loss of PTEN expression as a possible early prognostic marker for prostate cancer metastasis
Authors: Schmitz Martine , Grignard Gérard , Margue Christiane , Dippel Walter , Capesius Catherine , Mossong Joël , Nathan Michel , Giacchi Sandro , Scheiden René , Kieffer Nelly 
Published: December 2006

AbstractThe EGF/IGF growth factors are potent mitogens that regulate cell proliferation and cell survival and are involved in prostate cancer development. Using laser microdissection technology and real‐time PCR, together with immunohistochemistry, we have explored the growth factor and integrin dependent PI3‐kinase/PTEN/Akt signalling pathway in prostate cell lines and tumour samples by analysing EGF‐R, IGF1‐R, ILK, β3 integrin, PTEN and p‐Akt protein expression. We provide evidence that loss of PTEN expression rather than upregulated EGF/IGF1 receptor expression was responsible for increased p‐Akt in neoplastic prostate cells. We therefore compared PTEN expression in patient biopsies at first time diagnosis recruited prospectively (Study I, 112 patients) and patients with confirmed metastasis recruited retrospectively from the Luxembourg cancer registry (Study II, 42 patients). In Study I, loss of PTEN expression at first time diagnosis was found in 26 of 112 patients (23%). In Study II, 25 of the 42 patients (59%) with lymph node metastasis had complete loss of PTEN expression in both the neoplastic glands of the prostate and the invasive prostate cancer cells in the lymph node, and of these 13 (52%) exhibited already loss of PTEN expression at first diagnosis. These findings demonstrate that loss of PTEN expression is an important factor in progression towards metastatic disease and could potentially serve as an early prognostic marker for prostate cancer metastasis. © 2006 Wiley‐Liss, Inc.
High level of messenger RNA for BRMS1 in primary breast carcinomas is associated with poor prognosis
Authors: Lombardi Grazia , Di Cristofano Claudio , Capodanno Alessandra , Iorio Maria Carla , Aretini Paolo , Isola Patrizia , Tancredi Mariella , Collecchi Paola , Naccarato Antonio Giuseppe , Porta Romana Prosperi , Bevilacqua Generoso , Caligo Maria Adelaide 
Published: December 2006

AbstractBRMS1 is regarded as a metastasis suppressor gene for its ability to reduce metastatic potential of human and murine breast cancer cells as well as human melanoma cells. However, BRMS1 association to human tumor progression is not clearly understood. In the present study we analyzed BRMS1 mRNA expression in tumor progression and its potential prognostic value for breast carcinoma. BRMS1 mRNA expression level was quantified by real‐time PCR in 47 tumoral, in 14 peritumoral and in 15 metastatic microdissected cellular populations from 47 breast cancer patients with 10‐year follow up. We found BRMS1 expression to be higher in carcinoma cells than in matching normal epithelial cell populations in 10 out of 14 cases (p = 0.0005), while lymph‐nodal carcinoma cells showed lower BRMS1 expression in 9 out of 15 cases (p = 0.001). Using both in vivo (human mammary breast carcinomas) and in vitro systems (breast cancer cell lines) we were able to demonstrate that BRMS1 overexpression was not a bias effect induced by cell proliferation rate. BRMS1 expression levels did not correlate with standard breast cancer prognostic factors but BRMS1 higher expression was associated with patient shorter disease‐free and overall survival. Our findings are apparently inconsistent with the concept of BRMS1 as a metastasis suppressor gene. One possible explanation is that epithelial cells increase their BRMS1 expression as a compensatory response to tumor formation or metastasis progression, which is elevated in proportion to tumor aggressiveness, whereas those cells of the primary tumor that cannot upregulate BRMS1 escape to form metastasis. © 2006 Wiley‐Liss, Inc.
FOXA1: Growth inhibitor and a favorable prognostic factor in human breast cancer
Authors: Wolf Ido , Bose Shikha , Williamson Elizabeth A. , Miller Carl W. , Karlan Beth Y. , Koeffler H. Phillip 
Published: December 2006

AbstractThe transcription factor Forkhead‐box A1 (Foxa1), a member of the FOX class of transcription factors, has been implicated in the pathogenesis of lung, esophageal and prostate cancers. We have recently identified transcriptional activation of p27 by FOXA1. In this study, we analyzed the activities and expression pattern of FOXA1 in breast cancer. Forced expression of FOXA1 inhibited clonal growth of breast cancer cell lines, and FOXA1 levels inversely correlated with growth stimuli. In the estrogen receptor (ER)‐positive MCF‐7 cells, FOXA1 increased p27 promoter activity and inhibited the ER pathway activity. Analysis of FOXA1 expression in breast tissue arrays revealed significantly higher expression in pure ductal carcinomas in situ compared to invasive ductal carcinomas (IDC); and in IDC, high expression of FOXA1 was associated with favorable prognostic factors. Yet, FOXA1 expression was noted in a subset of the ER‐negative tumors. Taken together, our findings suggest a growth inhibitory role for FOXA1, and identify it as a novel, potential prognostic factor in breast cancer. © 2006 Wiley‐Liss, Inc.
Prospective study of vitamins C, E, and A and carotenoids and risk of oral premalignant lesions in men
Authors: Maserejian Nancy Nairi , Giovannucci Edward , Rosner Bernard , Joshipura Kaumudi 
Published: December 2006

AbstractCase–control studies indicate that vitamins C, E, A and carotenoids decrease risk of oral premalignant lesions (OPLs) and oral cancer, but clinical trials have failed to find protective effects of β‐carotene and suggest that vitamin E may increase risk. The authors prospectively evaluated the association between intake of vitamins C, E, A and carotenoids and incidence of OPL. Participants were 42,340 men in the Health Professionals Follow‐up Study who provided information on supplement use and diet every 2–4 years by food frequency questionnaire. The authors confirmed 207 clinically or histopathologically diagnosed OPL events occurring between 1986 and 2002 by medical record review. Multivariate‐adjusted relative risks (RR) of OPL were calculated with proportional hazards models. Total intake of vitamin C, vitamin A or carotenoids was not significantly associated with OPL risk. Dietary vitamin C was significantly associated with reduced risk (quintile 5 vs. 1, RR = 0.52, 95% CI 0.31–0.85, ptrend = 0.04), but no association with supplemental vitamin C was observed. Inverse associations were apparent for β‐cryptoxanthin and α‐carotene intake. No clear relationship emerged with β‐carotene, lycopene or lutein/zeaxanthin. Vitamin E was associated with increased risk (quintile 5 vs. 1, RR = 1.86, 95% CI 1.06–3.19), particularly among current smokers and with supplemental intake (current‐smokers, supplement dose tertile 3 vs. 1, RR = 3.07, 95% CI 1.28–7.34, ptrend = 0.01). For current smokers, β‐carotene also increased risk. Vitamin C from dietary sources, but not supplements, was associated with a reduced risk of OPL. The observed increased risk for current smokers with high vitamin E or β‐carotene intake should be explored further. © 2006 Wiley‐Liss, Inc.
Lipophilin B: A gene preferentially expressed in breast tissue and upregulated in breast cancer
Authors: Culleton Jane , O'Brien Neil , Ryan Bríd M. , Hill Arnold D.K. , McDermott Enda , O'Higgins Niall , Duffy Michael J. 
Published: December 2006

AbstractLipophilin B (LPB), which is also known as BU101, is a secretoglobin which exists in vivo as a complex with the mammary‐specific protein, mammaglobin A (MGA). The aim of our study was to investigate the expression of LPB in a panel of breast and nonbreast tissues and compare its expression with that of MGA. Using RT‐PCR, LPB mRNA was detected in 16/25 (64%) of normal breast specimens, 23/30 (77%) of fibroadenomas, 102/156 (65%) of primary breast cancers and in 8/36 (22%) nonbreast tissues. Levels of expression of LPB mRNA were significantly higher in breast cancers compared to both normal breast tissues (p = 0.02) and nonbreast tissue (p < 0.001). In the primary breast cancers, expression of LPB mRNA was positively correlated with the estrogen receptor (p = 0.045) but inversely related to both tumor grade (p < 0.001) and proliferation rates (p = 0.0345). Compared to MGA, expression of LPB was more sensitive but less specific for breast cancer. Using Western blotting, LPB migrated with an approximate molecular mass of 7–8 kDa, the expected molecular mass of free LPB. Immunohistochemical analysis of breast cancers showed that LPB expression was predominantly confined to the cytoplasm of tumor cells. We conclude that expression of LPB is preferentially but not exclusively restricted to breast tissue. Since LPB was expressed relatively specifically in breast tissue and was significantly upregulated in breast carcinomas, it is a promising candidate biomarker for breast cancer. © 2006 Wiley‐Liss, Inc.
An empirical model of the multi‐unit, sequential, clock auction
Authors: Donald Stephen G. , Paarsch Harry J. , Robert Jacques 
Published: December 2006

AbstractWe construct a model of participation and bidding at multi‐unit, sequential, clock auctions when bidders have multi‐unit demand. We describe conditions sufficient to characterize a symmetric, perfect‐Bayesian equilibrium and then demonstrate that this equilibrium induces an efficient allocation. We propose an algorithm, based on the generalized Vickrey auction, to calculate the expected winning bid for each unit sold. This algorithm allows us to construct a simulation‐based estimator of the parameters for both the participation process and the distribution of latent valuations. We apply our method to data from 37 multi‐lot, sequential, English auctions of export permits for timber held in Russia. Copyright © 2006 John Wiley & Sons, Ltd.
A re‐interpretation of the linear quadratic model when inventories and sales are polynomially cointegrated
Authors: Banerjee Anindya , Mizen Paul 
Published: December 2006

AbstractEstimation of the linear quadratic model, the workhorse of the inventory literature, traditionally takes inventories and sales to be first‐difference stationary series, and the ratio of the two variables to be stationary. However, these assumptions do not always match the properties of the data for the last two decades in the United States. We propose a model that allows for the non‐stationary characteristics of the data, using polynomial cointegration. We show that the closed‐form solution has other recent models as special cases. The resulting model performs well on aggregate and disaggregated data. Copyright © 2006 John Wiley & Sons, Ltd.
Nonlinear dynamics of interest rate and inflation
Authors: Lanne Markku 
Published: December 2006

AbstractAccording to several empirical studies US inflation and nominal interest rates as well as the real interest rate can be described as unit root processes. These results imply that nominal interest rates and expected inflation do not move one‐for‐one in the long run, which is incongruent with theoretical models. In this paper we introduce a new nonlinear bivariate mixture autoregressive model that seems to fit quarterly US data (1953 : II–2004 : IV) reasonably well. It is found that the three‐month Treasury bill rate and inflation share a common nonlinear component that explains a large part of their persistence. The real interest rate is devoid of this component, indicating one‐for‐one movement of the nominal interest rate and inflation in the long run and, hence, stationarity of the real interest rate. Copyright © 2006 John Wiley & Sons, Ltd.
Inter‐state dynamics of invention activities, 1930–2000
Authors: Co Catherine Y. , Landon‐Lane John S. , Yun Myeong‐Su 
Published: December 2006

AbstractWe study the dynamics of the cross‐section distribution of patents per capita for the 48 continental US states from 1930 to 2000 using a discrete‐state Markov chain. We test for and find evidence in favor of the (knowledge) convergence hypothesis. The distribution of patents is converging to a limiting distribution that is significantly more concentrated than its initial distribution. States in the extreme are more mobile than states in the middle of the cross‐sectional distribution and are likely to move to the middle. However, the rate of convergence to the limiting distribution is ‘slow’. Copyright © 2006 John Wiley & Sons, Ltd.
Is there a risk–return trade‐off? Evidence from high‐frequency data
Authors: Bali Turan G. , Peng Lin 
Published: December 2006

AbstractThis paper examines the intertemporal relation between risk and return for the aggregate stock market using high‐frequency data. We use daily realized, GARCH, implied, and range‐based volatility estimators to determine the existence and significance of a risk–return trade‐off for several stock market indices. We find a positive and statistically significant relation between the conditional mean and conditional volatility of market returns at the daily level. This result is robust to alternative specifications of the volatility process, across different measures of market return and sample periods, and after controlling for macro‐economic variables associated with business cycle fluctuations. We also analyze the risk–return relationship over time using rolling regressions, and find that the strong positive relation persists throughout our sample period. The market risk measures adopted in the paper add power to the analysis by incorporating valuable information, either by taking advantage of high‐frequency intraday data (in the case of realized, GARCH, and range volatility) or by utilizing the market's expectation of future volatility (in the case of implied volatility index). Copyright © 2006 John Wiley & Sons, Ltd.
Metabolism of chlorpyrifos and chlorpyrifos oxon by human hepatocytes*
Authors: Choi Kyoungju , Joo Hyun , Rose Randy L. , Hodgso Ernest 
Published: December 2006

AbstractThe metabolism of chlorpyrifos (CPS) and chlorpyrifos oxon (CPO) by human hepatocytes and human liver S9 fractions was investigated using LC‐MS/MS. Cytochrome P450 (CYP)‐dependent and phase II‐related products were determined following incubation with CPS and CPO. CYP‐related products, 3,5,6‐trichloro‐2‐pyridinol (TCP), diethyl thiophosphate, and dealkylated CPS, were found following CPS treatment and dealkylated CPO following CPO treatment. Diethyl phosphate was not identified because of its high polarity and lack of retention with the chromatographic conditions employed. Phase II‐related conjugates, including O‐ and S‐glucuronides as well as 11 GSH‐derived metabolites, were identified in CPS‐treated human hepatocytes, although the O‐sulfate of TCP conjugate was found only when human liver S9 fractions were used as the enzyme source. O‐Glucuronide of TCP was also identified in CPO‐treated hepatocytes. CPS and CPO were identified using HPLC–UV after CPS metabolism by the human liver S9 fraction. However, CPO was not found following treatment of human hepatocytes with either CPS or CPO. These results suggest that human liver plays an important role in detoxification, rather than activation, of CPS. © 2006 Wiley Periodicals, Inc. J Biochem Mol Toxicol 20:279–291, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20145
670 nanometer light treatment attenuates dioxin toxicity in the developing chick embryo
Authors: Yeager Ronnie L. , Lim Jinhwan , Millsap Deborah S. , Jasevicius Ashley V. , Sanders Ruth A. , Whelan Harry T. , Watkins John B. , Eells Janis T. , Henshel Diane S. 
Published: December 2006

Abstract2,3,7,8‐Tetrachlorodibenzo‐p‐dioxin (TCDD) is an acutely toxic anthropogenic chemical. Treatment with a red to near‐infrared (630–1000 nm) light‐emitting diode (LED) attenuates the toxicant‐induced oxidative stress and energy deficit in neuronal cell culture. For this study, fertile chicken (Gallus gallus) eggs were injected once at the start of incubation with sunflower oil vehicle or 200 pg TCDD/g egg (200 parts per trillion), an environmentally relevant dose. Daily LED treatment after TCDD exposure reduced embryonic mortality by 47%. LED treatment of TCDD‐exposed eggs also decreased the hepatic oxidized‐to‐reduced glutathione ratio by 88%. Activities of other hepatic indicators of oxidative stress, such as glutathione reductase and catalase, were increased after LED treatment of TCDD‐exposed eggs. Our study demonstrates that 670 nm phototherapy can mitigate the oxidative stress and energy deficit resulting from developmental exposure to TCDD while reducing TCDD‐induced embryo mortality. Moreover, LED treatment restores hepatic enzyme activities to control levels in TCDD‐exposed embryos. The effective attenuation of TCDD‐induced embryo toxicity by LED treatment could extend to mitigating the effects of other teratogens that induce oxidative and energy stress. © 2006 Wiley Periodicals, Inc. J Biochem Mol Toxicol 20:271–278, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20146
Hepatic chemoprotective enzyme responses to 2‐substituted selenazolidine‐4(R)‐carboxylic acids
Authors: El‐Sayed Wael M. , Franklin Michael R. 
Published: December 2006

AbstractIn epidemiology and human supplementation studies, as well as many animal models, selenium has shown antitumorigenic activity. The mechanism of action, however, has not been satisfactorily resolved. Selenium supplementation affects many enzymes in addition to those where selenocysteine is an essential component. Such enzymes include cytoprotective detoxifying enzymes, and the regulation of these enzymes by a set of 2‐substituted selenazolidine‐4(R)‐carboxylic acids (SCAs) has been investigated. Following seven consecutive daily doses of these prodrugs of L‐selenocysteine, changes in hepatic enzyme activities and/or mRNA levels of glutathione transferase (GST), microsomal epoxide hydrolase (mEH), NAD(P)H‐quinone oxidoreductase (NQO), UDP‐glucuronosyltransferase (UGT), glutathione peroxidase (GPx), and thioredoxin reductase (TR) have been observed. Among the enzymes examined, UGTs and GPx were found to be the least affected. Among the compounds, 2‐oxoSCA produced the most changes and 2‐phenylSCA produced the least, none. For no two compounds was the pattern of changes identical, and for a single compound, few changes were reproduced in common by the two routes of administration investigated. In general, more changes were elicited following intraperitoneal (i.p.) administration than with the intragastric (i.g.) route. This dominance was typified by 2‐butylSCA and 2‐cyclohexylSCA where enzyme activity elevations (TR and mEH with both, NQO with 2‐butylSCA) were seen only with the i.p. route. With 2‐oxoSCA, however, GST, TR, and NQO activities were found to be elevated independent of route. Only with GST (both routes) and TR (i.p. route), elevations in mRNAs accompanied the 2‐oxoSCA elicited elevations of activities at the time of sacrifice. For some enzymes, most notably mEH with compounds administered i.p., elevations in mRNAs were not manifest as increased enzyme activity. Thus, although constituting a closely related series of compounds, each 2‐substituted SCA produced its own unique pattern of changes, and for most members, changes were predominant following i.p. administration. © 2006 Wiley Periodicals, Inc. J Biochem Mol Toxicol 20:292–301, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20148
Methyl palmitate inhibits lipopolysaccharide‐stimulated phagocytic activity of rat peritoneal macrophages
Authors: Sarkar Swapna , Khan M. Firoze , Kaphalia Bhupendra S. , Ansari G. A. S. 
Published: December 2006

AbstractMacrophages, in general, are critical effectors of body's immune system. Chemical inhibition of phagocytic activity of such macrophages as Kupffer cells has been extensively studied. We have earlier shown that methyl palmitate (MP) inhibits the activation of Kupffer cells. To evaluate the potential of MP to inhibit the activation of other macrophages, we treated rat peritoneal macrophages with varying concentrations of MP. Its treatment led to a dose‐dependent inhibition of phagocytic activity, which was found to be 34%, 47%, and 66% at 0.25, 0.50, and 1.0 mM MP, respectively, as measured by latex bead uptake. When MP‐treated peritoneal macrophages were stimulated with lipopolysaccharide (LPS), the nitric oxide (.NO) release was inhibited at 6 h, while cyclooxygenase‐2 expression decreased after 24 h. The treatment with MP increased the release of interleukin (IL)‐10 in the LPS‐treated cells at 6 h, while IL‐6 and tumor necrosis factor‐α were significantly increased both at 6 and 24 h. Our data suggest that MP inhibits phagocytic activity and .NO production similar to that observed in isolated Kupffer cells. Therefore, inhibition of phagocytosis by MP may be a general phenomenon, and it could be used as an inhibitor of macrophage function. © 2006 Wiley Periodicals, Inc. J Biochem Mol Toxicol 20:302–308, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20150