bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of antibodies induced by a conjugate vaccine on 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone absorptive transport, metabolism, and proliferation of human lung cells
Authors: De Buck Stefan S. , Schellenberger Mario T. , Ensch Corinne , Muller Claude P. 
Published: December 2009

AbstractOne of the most abundant and potent lung carcinogen is the nicotine‐derived tobacco‐specific nitrosamine, 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK). The monoclonal antibody P9D5 induced with a NNK‐conjugate vaccine was used to investigate the ability of NNK‐specific antibodies to modulate NNK‐induced adverse effects as well as its absorptive transport and metabolism in two lung cancer cell lines (Calu‐3 and NCI‐H82). Transport experiments in Calu‐3 cells with a 50‐fold molar excess of apical P9D5 increased the recovery of coadministered apical NNK, with a concomitant decrease in NNK transepithelial transport of more than 50% compared to controls. In contrast, basolateral P9D5 did neither influence transepithelial transport of NNK nor its disappearance from the apical compartment. Calu‐3 cells were also found to reduce NNK to NNAL and a 65‐fold molar excess of NNK‐specific antibody inhibited this metabolic conversion by 46 and 54% compared to irrelevant control antibody after 48 and 72 hr, respectively. The biological relevance of NNK redistribution by antibody was demonstrated by reversion of NNK‐induced cell proliferation in NCI‐H82 cells. Repartitioning of tobacco carcinogens by antibody may reduce their early effective peak concentrations in susceptible target organs and thus relieve overloaded local DNA repair mechanisms and diminish carcinogen‐induced cell proliferation. Thesein vitrodata therefore suggest that a prophylactic antibody response may be associated with a reduced risk of cancer.
The polyamine metabolism genes ornithine decarboxylase and antizyme 2 predict aggressive behavior in neuroblastomas with and without MYCN amplification
Authors: Geerts Dirk , Koster Jan , Albert David , Koomoa Dana‐Lynn T. , Feith David J. , Pegg Anthony E. , Volckmann Richard , Caron Huib , Versteeg Rogier , Bachmann André S. 
Published: December 2009

AbstractHigh polyamine (PA) levels and ornithine decarboxylase (ODC) overexpression are well‐known phenomena in many aggressive cancer types. We analyzed the expression of ODC and ODC‐activity regulating genes antizymes 1‐3 (OAZ1‐3) and antizyme inhibitors
1‐2 (AZ‐IN1‐2) in human neuroblastoma (NB) tumors and correlated these with genetic and clinical features of NB. Since ODC is a known target gene of MYCN, the correlation between ODC and MYCN was of special interest. Data were obtained from Affymetrix micro‐array analysis of 88 NB tumor samples. In addition, mRNA expression levels of ODC, OAZ2 and MYCN in a MYCN‐inducible NB cell line were determined by quantitative real‐time reverse‐transcriptase polymerase chain reaction (RT‐PCR). ODC mRNA expression in NB tumors was significantly predictive of decreased overall survival probability and correlated with several unfavorable clinical NB characteristics (all p < 0.005). Interestingly, high ODC mRNA expression also showed significant correlation with poor survival prognosis in Kaplan‐Meier analyses stratified for patients without MYCN amplification, suggesting an additional role for ODC independent of MYCN. Conversely, high OAZ2 mRNA expression correlated with increased survival and with several favorable clinical NB characteristics (all p < 0.003). In addition, we provide first evidence of a role for MYCN‐associated transcription factors MAD2 and MAD7 in ODC regulation. In NB cell cultures, ectopic overexpression of MYCN altered ODC but not OAZ2 mRNA levels. In conclusion, these data suggest that elevated ODC and low OAZ2 mRNA expression levels correlate with several unfavorable genetic and clinical features in NB, offering new insights into PA pathways and PA metabolism‐targeting therapy in NB.
Mammographic density, plasma vitamin D levels and risk of breast cancer in postmenopausal women
Authors: Green Angela K. , Hankinson Susan E. , Bertone‐Johnson Elizabeth R. , Tamimi Rulla M. 
Published: December 2009

AbstractMammographic density is a strong risk factor for breast cancer, but the underlying biology for this association is unknown. Studies suggest that vitamin D may reduce breast cancer risk and dietary vitamin D intake has been associated with reduced breast density. We conducted a case–control study nested within the Nurses' Health Study cohort consisting of 463 and 497 postmenopausal cases and controls, respectively. We examined the association between mammographic density and plasma levels of 25‐hydroxyvitamin D [25(OH)D] and 1,25‐dihydroxyvitamin D [1,25(OH)2D]. We assessed whether plasma vitamin D metabolites modify the association between breast density and breast cancer. Percent mammographic density was measured from digitized film mammograms. Generalized linear models were used to determine mean percent breast density per quartile of vitamin D metabolite. Logistic regression models were used to calculate relative risks and confidence intervals. All models were adjusted for matching variables and potential confounders. We found no cross‐sectional association between circulating levels of 25(OH)D or 1,25(OH)2D with mammographic density. Women in the highest tertile of mammographic density and lowest tertile of plasma 25(OH)D had 4 times greater risk of breast cancer than women with the lowest mammographic density and highest plasma 25(OH)D levels (RR = 3.8; 95% CI: 2.0–7.3). The overall interaction between mammographic density and plasma 25(OH)D was nonsignificant (p‐het = 0.20). These results indicate that the association between mammographic density and breast cancer is independent of plasma vitamin D metabolites in postmenopausal women. Further research examining vitamin D, mammographic density and breast cancer risk is warranted.
Alcohol consumption‐associated breast cancer incidence and potential effect modifiers: the Japan Public Health Center‐based Prospective Study
Authors: Suzuki Reiko , Iwasaki Motoki , Inoue Manami , Sasazuki Shizuka , Sawada Norie , Yamaji Taiki , Shimazu Taichi , Tsugane Shoichiro 
Published: December 2009

AbstractEpidemiological studies have evaluated whether the impact of alcohol intake on breast cancer risk is modified by use of exogenous estrogens, folate intake, body weight and smoking status, but results have been inconsistent. Further, effect modification by intake of isoflavones and alcohol‐induced facial flushing, which are prevalent in Asian populations, have not been investigated. We investigated the association between alcohol intake and breast cancer risk and whether the association is modified by these factors among 50,757 premenopausal and postmenopausal women (aged 40–69 years) in the population‐based Japan Public Health Center‐based Prospective Study. Alcohol consumption and other related factors were assessed using self‐reported questionnaires. Through to the end of 2006, 572 patients were identified. Relative risks (RRs) and 95% confidence intervals (CIs) were estimated by hazard ratios derived from Cox proportional hazards regression models. Compared with never‐drinkers, regular alcohol drinkers (>150 g of ethanol/week) had a higher risk of the development of breast cancer; the multivariable‐adjusted RRs were 1.75 (95% CI = 1.16–2.65; ptrend = 0.035) for overall, 1.78 (95% CI = 1.09–2.90) for premenopausal and 1.21 (95% CI = 0.53–2.75) for postmenopausal women. There was no statistical evidence for effect modification by menopausal status, use of exogenous estrogens, intakes of isoflavone and folate, body weight, alcohol‐induced facial flushing or smoking (All pinteractions ≥ 0.15). Excessive alcohol intake was associated with an increase in the risk of breast cancer in this population. There was no statistical evidence for effect modification.
Immunosuppressive disorders and risk of anal squamous cell carcinoma: A nationwide cohort study in Denmark, 1978–2005
Authors: Sunesen Kåre G. , Nørgaard Mette , Thorlacius‐Ussing Ole , Laurberg Søren 
Published: December 2009

AbstractCompromised immune function may increase the risk of anal squamous cell carcinoma (SCC). We examined the risk of anal SCC in patients with HIV infection and other chronic disorders associated with immunosuppression. A population‐based cohort study was conducted using the Danish National Patient Registry and the Danish Cancer Registry (DCR). We identified all patients with a first‐time hospital contact or procedure for HIV infection, solid organ transplantation or autoimmune disease or a first‐time record of haematologic malignancy in the DCR, 1978–2005, and followed these for a subsequent anal SCC, starting follow‐up 1 year after diagnosis of the index disease. Standardised incidence ratios (SIRs) were computed as the ratio of observed to expected numbers of anal SCCs, based on national age‐, sex‐ and period‐specific rates. Among 4,488 patients with HIV, we observed 21 anal SCCs with 0.3 expected (SIR: 81.1 (95% confidence interval (CI): 51.6–121.9)). Risk of anal SCC was markedly increased among 5,113 solid organ recipients (SIR: 14.4 (CI: 7.0–26.4)) and 30,165 patients with haematologic malignancies (SIR: 2.3 (CI: 1.1–4.2)) but only moderately increased among 242,114 patients with autoimmune diseases (SIR: 1.3 (CI: 1.0–1.6)). SIRs varied according to type of autoimmune disease and were high in patients with Crohn's disease (SIR: 3.1 (CI: 1.2–6.4)), psoriasis (SIR: 3.1 (CI: 1.8–5.1)), polyarteritis nodosa (SIR: 8.8 (CI: 1.5–29.0)) and Wegener's granulomatosis (SIR: 12.4 (CI: 2.1–40.8)). In conclusion, we found HIV infection, solid organ transplantation, haematologic malignancies and a range of specific autoimmune diseases strongly associated with increased risk of anal SCC.
The T‐box transcription factor Tbx2: Its role in development and possible implication in cancer
Authors: Abrahams Amaal , Parker M. Iqbal , Prince Sharon 
Published: December 2009

AbstractTbx2 is a member of the T‐box family of transcription factors that are crucial in embryonic development. Recent studies suggest that T‐box factors may also play a role in controlling cell cycle progression and in the genesis of cancer. Tbx2 has been implicated in several developmental processes such as coordinating cell fate, patterning and morphogenesis of a wide range of tissues and organs including limbs, kidneys, lungs, mammary glands, heart, and craniofacial structures. Importantly, Tbx2 is overexpressed in several cancers including melanoma, small cell lung carcinoma, breast, pancreatic, liver, and bladder cancers and can suppress senescence, a cellular process, which serves as a barrier to cancer development. This review presents a state of the art overview of the role and regulation of Tbx2 in early embryonic development and in cancer. © 2009 IUBMB IUBMB Life, 62(2): 92–102, 2010
Fertility and female employment dynamics in Europe: the effect of using alternative econometric modeling assumptions
Authors: Michaud Pierre‐Carl , Tatsiramos Konstantinos 
Published: December 2009

AbstractWe investigate the direct and long‐run effects of fertility on employment in Europe, estimating dynamic models of labor supply under different assumptions regarding the exogeneity of fertility and modeling assumptions related to initial conditions, unobserved heterogeneity and serial correlation in the error terms. We find overall large direct and long‐run effects of giving birth on employment probabilities, and these effects differ considerably across countries. We find that within countries the results are sensitive to the statistical assumption made on initial conditions, the inclusion of serial correlation and the assumption of strict exogeneity of children. However, the pattern across countries is robust to these assumptions. We show that such patterns are largely consistent with prevailing institutional differences related to the flexibility of the labor markets and family policies. Copyright © 2009 John Wiley & Sons, Ltd.
Micropillar substrate influences the cellular attachment and laminin expression
Authors: Su Wen‐Ta , Liao Yung‐Feng , Lin Chuang‐Yu , Li Li‐Tzu 
Published: December 2009

AbstractFibroblasts alter their mode of attachment and focal contact when placed on square arrays of silicon pillars. The pillars had 1‐μm diameters with identical surface chemistry. Distance between pillars is 9 μm and height of pillars is 1, 5, or 10 μm on substrates. We found that these micropillars, rather than specific interactions, provided more opportunities for mechanical interlocking of the fibroblasts and acted as physical barriers that restrained cell migration. The cellular morphology and behavior is guidable by the height of pillars. In some cases, the fibroblasts filled in the intervals among several pillars; in others, a pillar protruded visibly through the cell body but did not pierce it, the cells were survived. Therefore, fibroblasts were immobilized upon in situ and the cytoplasma migrated outward to the bottom of the substrate subsequently. Laminin plays a critical role in cell attachment to the basement membrane. The results of laminin expression in fibroblasts suggest that pillar pattern appears to change cellular behavior and affect laminin expression significantly. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res, 2010
Increased integrin α5β1 heterodimer formation and reduced c‐Jun expression are involved in integrin β1 overexpression‐mediated cell growth arrest
Authors: Fang Zhengyu , Yao Wantong , Fu Yi , Wang Li‐Ying , Li Zengxia , Yang Yong , Shi Yinghong , Qiu Shuangjian , Fan Jia , Zha Xiliang 
Published: December 2009

AbstractIntegrins, heterodimers of α and β subunits, are a family of cell surface molecules mediating cell–cell and cell–extracellular matrix interaction. The largest subgroup is formed by the β1 subunit containing integrins which consist of 12 members with different ligand‐binding properties. We previously reported that overexpressed integrin β1 subunit in the hepatocellular carcinoma cell line SMMC‐7721 imposed a growth inhibitory effect through the upregulation of p21cip1 and p27kip1. In this study, we confirmed the growth inhibitory effect of β1 subunit overexpression in different cancer cell lines. The upregulated CDK inhibitors induced by β1 integrin overexpression were essential for this integrin‐mediated growth arrest. Reduced c‐Jun level after integrin β1 overexpression plays an important role in the transcriptional activation of p21 through the Sp1 sites. Solely overexpressed β1 subunit could induce the expression of diverse α subunit in different cell lines, among which α5 subunit was found to be correlated with integrin β1‐mediated growth arrest. Relative lack of ECM–integrin interaction might be a reason for integrin β1 overexpression‐mediated growth arrest. These results helped us understand more about the mechanisms that integrins regulate cell growth. J. Cell. Biochem. 109: 383–395, 2010. © 2009 Wiley‐Liss, Inc.
All‐trans‐retinoic acid intensifies endoplasmic reticulum stress in N‐acetylglucosaminyltransferase V repressed human hepatocarcinoma cells by perturbing homocysteine metabolism
Authors: Xu Ying‐Ying , Guan Dong‐Yin , Yang Min , Wang Hao , Shen Zong‐Hou 
Published: December 2009

AbstractWe previously reported that all‐trans‐retinoic acid (ATRA) induced apoptosis in N‐acetylglucosaminyltransferase V (GnT‐V) repressed human hepatocarcinoma 7721 (GnT‐V‐AS/7721) cells via endoplasmic reticulum (ER) stress. In addition to confirming these findings, we further found that ATRA repressed the expression of betaine‐homocysteine methyltransferase (BHMT) and cystathionine‐β‐synthase (CBS), which are key enzymes that are involved in homocysteine metabolism, increased the level of intracellular homocysteine, and decreased the glutathione (GSH) level in GnT‐V‐AS/7721 cells. To investigate the effect of ATRA on homocysteine metabolism, cells were challenged with exogenous homocysteine. In GnT‐V‐AS/7721 cells with ATRA treatment, a significant elevation of intracellular homocysteine levels suggests that ATRA perturbs homocysteine metabolism in GnT‐V‐AS/7721 cells and, therefore, sensitizes the cells to homocysteine‐induced ER stress. An obvious increase in the levels of GRP78/Bip protein and spliced XBP1 mRNA were observed. Furthermore, we observed that ATRA blunted the homocysteine‐induced increase of GSH only in GnT‐V‐AS/7721 cells. These results demonstrate that ATRA intensifies ER stress and induces apoptosis in GnT‐V‐AS/7721 cells by disturbing homocysteine metabolism through the down‐regulation of CBS and BHMT, depleting the cellular GSH and, in turn, altering the cellular redox status. In addition, we showed that ATRA did not trigger ER stress, induce apoptosis, or affect homocysteine metabolism in L02 cells, which is a cell type that is derived from normal liver tissue. These results provide support for the hypothesis that ATRA is an anticancer agent. J. Cell. Biochem. 109: 468–477, 2010. © 2009 Wiley‐Liss, Inc.
PcG recruitment by the YY1 REPO domain can be mediated by Yaf2
Authors: Wilkinson Frank , Pratt Heather , Atchison Michael L. 
Published: December 2009

AbstractThe Polycomb Group (PcG) complex of transcriptional repressors is critical for the maintenance of stage‐specific developmental gene expression, stem cell maintenance and for large‐scale chromosomal dynamics. Functional deficiency of a single PcG gene can severely compromise PcG function, leading to developmental defects, embryonic lethality, or a number of malignancies. Despite the critical nature of PcG proteins, the mechanisms by which these complexes mediate their effects are relatively uncharacterized. Nearly all vertebrate PcG proteins lack inherent DNA binding capacity, making it unclear how they are targeted to Polycomb response element (PRE) sequences. Transcription factor YY1 is a functional ortholog of a Drosophila PcG protein, Pleiohomeotic (PHO), one of the few PcG proteins with specific DNA binding capability, and YY1 can recruit PcG proteins to specific DNA sequences. A small 25 amino acid YY1 domain (the REPO domain) is necessary and sufficient for recruitment of PcG proteins to DNA and for transcriptional repression. We show here that the YY1 REPO domain interacts with PcG protein Yaf2 and recruits Yaf2 to DNA. Interaction is lost when the YY1 REPO domain is deleted. In addition we show that Yaf2, when linked to a heterologous DNA binding domain, can recruit PcG proteins to DNA leading to transcriptional repression. When the Drosophila homolog of Yaf2 (dRYBP) is mutated, PcG recruitment to DNA is reduced. Taken together, our results suggest that Yaf2 serves as a molecular bridge between YY1 and other PcG complex proteins. J. Cell. Biochem. 109: 478–486, 2010. © 2009 Wiley‐Liss, Inc.
Use of the glycerol by‐product of biodiesel to modify the surface of expanded vermiculite to produce an efficient oil absorbent
Authors: de Araújo Medeiros Miguel , de Oliveira Danielle Leite , Sansiviero Maria T. C. , Araújo Maria Helena , Lago Rochel Montero 
Published: December 2009

AbstractBACKGROUND: Glycerol (Gly) a by‐product from biodiesel production was impregnated onto the surface of expanded vermiculite (EV) and reacted to produce a highly efficient absorbent to remove oils spilt on water.RESULTS: Expanded vermiculite was impregnated with glycerol at EV/Gly ratios of 1/1, 1/2, 1/3 and 1/4, and treated at 380, 480, 580 or 700 °C. Electrospray ionization mass spectroscopy, thermogravimetry, BET surface area, Hg porosimetry and Raman analyses indicated that residual NaOH from the biodiesel process catalyzed the polymerization of glycerol. At higher temperatures the polymer decomposed to form a carbon layer covering the EV surface. These materials were investigated for the removal of three different oils, i.e. diesel, soybean and engine oil spilt on water.CONCLUSION: This work showed that glycerol from biodiesel production can be used directly to produce a highly efficient absorbent to remediate oil spill accidents. The results obtained showed a remarkable increase on oil removal efficiency with a strong decrease on water absorption. Copyright © 2009 Society of Chemical Industry
Ladungsverteilung und Reaktivität phosphororganischer Verbindungen, IX1) Experimentelle Befunde zur Ladungsverteilung in Arylphosphin‐[p‐nitro‐phenyl]‐iminen2)
Authors: Goetz Horst , Probst Dietrich 
Published: December 2009

AbstractEs werden Dipolmomente, 1H‐NMR‐ und UV‐Spektren einer Reihe von Aryl‐dipropyl‐ (1) und Triaryl(bzw. Trialkyl)‐phosphin‐[p‐nitro‐phenyl]‐iminen (2) untersucht. Eine Merocyaninartige Mesomerie in diesen Verbindungen und das Problem der dπ–pπ‐Konjugation am Phosphor werden diskutiert.
Modelluntersuchungen zur Funktion der Tetrahydropterine als Cofaktoren biologischer Hydroxylierungen
Authors: Wahlefeld August‐Wilhelm , Jaenicke Lothar , Hein Günter 
Published: December 2009

Abstract2‐Amino‐4‐hydroxy‐6.8‐dimethyl‐7.8‐dihydro‐pterin (2) und ‐5.6.7.8‐tetrahydro‐pterin (1) werden synthetisiert und ihre Eigenschaften als Redoxsystem sowie als Metallkomplexbildner untersucht. – Das Tetrahydropterin 1 wird reversibel über ein Trihydropterin‐Radikal 5 bzw. dessen N.N′‐Dimeres zum 7.8‐Dihydro‐pterin 2 oxydiert, wie durch Aufnahme der potentiometrischen Oxydoreduktionskurven, der polarographischen Halbstufenpotentiale und der UV‐Spektren nachgewiesen wird. Entsprechend ist die Metall‐Affinität der Hydrierungsstufen bestimmt worden Es bilden sich aus 1 mit zweiwertigen Übergangsmetallen (Cu2⊕) und aus 2 mit einwertigen Übergansgsmetallen (Cu⊕) die gleichen chargetransfer‐Komplexe, in denen das Pterin in der radikalischen Trihydropterin‐Zwischenstufe stabilisiert ist. – Auf Grund dieser Modelluntersuchungen wird die enzymatische Hydroxylierung aromatischer Ringe als ein Kreisvorgang gedeutet, bei dem 1 das essentielle Metall reduziert, das dann seinerseits mit Sauerstoff über das Peroxid‐Anion das hydroxylierende Hydroxyl‐Radikal oder das Hydroxyl‐Anion bildet.
Zur Stokvis‐Reaktion, XVII1) Vilsmeier‐Reaktion mit Pyrrol‐ und Pyrrolon‐Derivaten
Authors: Schnierle Franz , Reinhard Horst , Dieter Norbert , Lippacher Eberhard , von Dobeneck Henning 
Published: December 2009

AbstractPyrrole mit freier α‐Stellung ergeben bei der Vilsmeier‐Formylierung α‐Formylpyrrole. Besitzt das Ausgangspyrrol oder ‐pyrrolon einen Acetyl‐Substituenten, so entstehen bevorzugt Halogenacroleine 1 oder 2. Δ3‐Pyrrolone geben über Immoniumsalze 4 und innere Immoniumsalze 5 α‐Halogen‐α‐formylpyrrole 3, die sich reduktiv in Formylpyrrole überführen lassen. Am N nicht‐substituierte Bromformylpyrrole kondensieren mit Pyrrolonen in Zn/Natronlauge zu α‐Oxo‐dipyrromethenen (“Neo‐Typ”). – Durch Verwendung von Oxalylchlorid bei der Vilsmeier‐Reaktion erhält man 2.1′‐Dipyrromethene 7.
Azapolyenaldehyde
Authors: Kuhn Richard , Teller Erich 
Published: December 2009

AbstractPyridiniumsalze aus aromatischen Aldehyden, Benzoylchlorid und Pyridin setzen sich mit konz. Alkalien unter Öffnung des Pyridin‐Rings zu Azapolyenaldehyden um. In diesen haben die der Aldehydgruppe folgenden beiden konjugierten Doppelbindungen cis‐Anordnung. Aus dem Pyridiniumsalz 1a erhält man so 7‐Phenyl‐6‐aza‐heptatrien‐(2c.4c6)‐al (3a), aus 16 sein Methylderivat 17. Aus 8 bzw. 11 entstehen 9‐Phenyl‐6‐aza‐nonateraen‐(2.4.6.8)‐al (10) bzw. 13‐Phenyl‐6.12‐diaza‐tridecahexaen‐(2.4.6.8.10.12)‐al (12). Das Bispyridiniumsalz 14 liefert den Bis‐azapolyenaldehyd 15. Aus dem Chinoliniumsalz 19 und dem Isochinoliniumsalz 22 lassen sich Azapolyenaldehyde (21 bzw. 23) gewinnen, die im konjugierten System einen Benzol‐Ring besitzen. Bei den Azapolyenaldehyden 3a (als Anil 7a) und 23a gelingt die Isomerisierung mit Jod zu einer trans‐Form (7b bzw. 23b), wie sich NMR‐spektroskopisch (Tab. 1) erkennen läßt. Die längstwelligen UV‐Maxima der Phenyl‐aza‐polyenaldehyde sind gegenüber denen der analogen Phenylpolynaldehyde hypsochrom verschoben (Tab. 2).