bluuebunny/crossref_metadata_2025_split huggingface dataset:
Appetite‐focused dialectical behavior therapy for the treatment of binge eating with purging: A preliminary trial
Authors: Hill Diana M. , Craighead Linda W. , Safer Debra L. 
Published: March 2010

AbstractObjective:This treatment development study investigated the acceptability and efficacy of a modified version of dialectical behavior therapy (DBT) for bulimia nervosa (BN), entitled appetite focused DBT (DBT‐AF).Method:Thirty‐two women with binge/purge episodes at least one time per week were randomly assigned to 12 weekly sessions of DBT‐AF (n = 18) or to a 6‐week delayed treatment control (n = 14). Participants completed the EDE interview and self‐report measures at baseline, 6 weeks, and posttreatment.Results:Treatment attrition was low, and DBT‐AF was rated highly acceptable. At 6 weeks, participants who were receiving DBT‐AF reported significantly fewer BN symptoms than controls. At posttest, 26.9% of the 26 individuals who entered treatment (18 initially assigned and 8 from the delayed treatment control) were abstinent from binge/purge episodes for the past month; 61.5% no longer met full or subthreshold criteria for BN. Participants demonstrated a rapid rate of response to treatment and achieved clinically significant change.Discussion:Results suggest that DBT‐AF warrants further investigation as an alternative to DBT or cognitive behavior therapy for BN. © 2010 by Wiley Periodicals, Inc. (Int J Eat Disord 2011; 44:249–261)
Biaryl Peptides from 4‐Iodophenylalanine by Solid‐Phase Borylation and Suzuki–Miyaura Cross‐Coupling (Eur. J. Org. Chem. 8/2010)
Authors: Afonso Ana , Rosés Cristina , Planas Marta , Feliu Lidia 
Published: March 2010

AbstractThe cover picture shows the skyline of the old part of Girona in northeast Catalonia, Spain. In the foreground is one of the many bridges that span the river Onyar from the new part of the town to the Jewish quarter. This bridge, named the Pont de Sant Feliu, is the usual starting point for visiting this quarter. It offers a nice view of the narrow colourful houses that back onto the river and allows an impressive view of the Cathedral and the Sant Feliu church. Built in different styles (11th–17th century AD), the Cathedral preserves a Gothic nave with the widest arched span in the world. In this picture, the Pont de Sant Feliu serves as a means to depict the synthesis of a 4‐arylphenylalanine tripeptide from a resin‐bound phenylalanine boronate. Details can be found in the article by L. Feliu et al. on p. 1461 ff, and results on the formation of the boronate through a solid‐phase Miyaura borylation are also discussed.
Analysis of the alcohol biomarker phosphatidylethanol by NACE with on‐line ESI‐MS
Authors: Nalesso Alessandro , Viel Guido , Cecchetto Giovanni , Frison Giampietro , Ferrara Santo Davide 
Published: March 2010

AbstractPhosphatidylethanol (Peth), a group of aberrant phospholipids formed in cell membranes in the presence of ethanol, has been recently proposed as biomarker of chronic alcohol abuse. The aim of this study was to develop a new analytical method, based on NACE online coupled with a mass spectrometer for the analysis of Peth in blood. For this purpose an ion‐trap mass spectrometer equipped with an orthogonal ESI source operating in negative ion mode was used. An alkaline solution of ammonium acetate 5 mM (pH 9) in water/methanol (MeOH) (80:20 v/v) was delivered as coaxial sheath liquid. All experiments were performed using an uncoated fused‐silica capillary (90 cm×75 μm id). The effects of variable percentages of ACN, MeOH, 2‐propanol, dichloromethane, along with variable concentrations of ammonium acetate were investigated for the separation of Peth. Collectively, a separation medium composed of ACN (45% v/v), 2‐propanol (20% v/v), dichloromethane (20% v/v), MeOH (10% v/v), water (5% v/v), and ammonium acetate (25 mM) was chosen. The estimated LOD was 0.1 μM, while LOQ was 0.4 μM. Within‐run (intra‐day) and between‐run (inter‐day) precision was always lower than 15%. The method proved to be robust and reliable. The MS detector allowed the simultaneous identification of several Peth homologues, and the use of an internal standard (phosphatidylbutanol) with similar electrophoretic properties of that of Peth increased quantitation effectiveness.
Poly (ADP‐ribose) polymerase‐1 deficiency does not affect ethylnitrosourea mutagenicity in liver and testis of lacZ transgenic mice
Authors: Louro Henriqueta , Faustino Inês , Dias Anabela , Boavida Maria G. , Silva Maria J. 
Published: March 2010

AbstractPoly (ADP‐ribose) polymerase‐1 (Parp1) has been implicated in DNA base excision repair, single‐ and double‐strand break repair pathways, as well as in cell death by apoptosis or necrosis. We used Parp1−/− lacZ plasmid‐based transgenic mice to investigate whether Parp1 deficiency influences the in vivo mutagenic and clastogenic response to the alkylating agent N‐ethyl‐N‐Nitrosourea (ENU) in somatic and germ‐cell tissues. The comparison of the lacZ mutant frequencies (MFs) between Parp1+/+ and Parp1−/− mice showed that the ablation of Parp1 does not affect the spontaneous or ENU‐induced MFs in liver and testis. In addition, the spectrum of the ENU‐induced mutations was not dependent on the Parp1 status, given that similar spectra, consisting mostly of point mutations and a small fraction of deletions/insertions, wereobserved in organs of both Parp1−/− and Parp1+/+ mice. Sequencing of point mutations revealed a consistent significant increase in A:T → T:A base substitutions, typically induced by ENU. Overall, we observed that neither the frequency nor the spectrum of ENU‐induced mutations demonstrated a specificity that could be attributed to the Parp1 impairment in mice organs. The analysis of micronucleus frequency in peripheral blood reticulocytes showed that ENU was clastogenic in both Parp1−/− and Parp1+/+ mice and had a strong cytotoxic effect in Parp1−/− mice only. The present data suggest that, at a whole‐organism level, Parp1‐independent repair mechanisms may be operative in the removal of ENU‐induced DNA lesions or that highly damaged cells may be preferentially committed to death when Parp1 is inactivated. Environ. Mol. Mutagen. 2010. © 2010 Wiley‐Liss, Inc.
Dimensionality of three versions of the eating disorder inventory in adolescent girls
Authors: García‐Grau Eugeni , Fusté Adela , Mas Natàlia , Gómez Juana , Bados Arturo , Saldaña Carmina 
Published: March 2010

AbstractObjectivesTo analyze the dimensionality of three versions of the Eating Disorder Inventory (EDI) in adolescent girls.MethodThe sample comprised 738 participants. The Spanish adaptation of the EDI‐2 was used. The EDI‐2 contains the 64 items of EDI and has the same items as EDI‐3. The dimensional structures hypothesized by Garner for the three EDI versions were assessed via a series of Confirmatory Factor Analyses (CFAs).ResultsThe CFA did not confirm Garner's proposed structure in any of the three versions. Consequently it was decided to perform Exploratory Factor Analyses (EFA) of the EDI‐2 and the EDI‐3 to try to indentify the underlying structure. The best theoretical and empirical fit was provided by a 7‐factor structure.DiscussionThis article presents a shortened version of the EDI‐2 which may prove more suitable for use with adolescent girls in the general population than the original questionnaire. Certain practical suggestions for optimizing the use of the different versions of the EDI are also presented. Copyright © 2010 John Wiley & Sons, Ltd and Eating Disorders Association.
Food web bioaccumulation model for polychlorinated biphenyls in San Francisco Bay, California, USA
Authors: Gobas Frank A.P.C. , Arnot Jon A. 
Published: March 2010

Abstract
We document the development and application of a food web bioaccumulation model for polychlorinated biphenyls (PCBs) in San Francisco Bay, California, USA. The model calculates spatial distributions of PCB concentrations in a range of invertebrate, fish, avian, and mammalian organisms, including harbor seals, double-crested cormorants, and Forster's terns. The performance of the model is evaluated against independent empirical PCB concentrations and shows a mean deviation between observed and model-calculated concentrations of 36% for female harbor seals and 5% for benthic invertebrates and jack smelt. The model was applied to produce bay-wide PCB concentration distributions in fish and wildlife species, which were compared with threshold effect concentrations to determine ecological risks and human health risks of fish consumption. Because of their high trophic position in the food web, harbor seals exhibited the highest concentrations of ∑PCBs, which exceeded threshold concentrations for potential adverse effects. The model was also applied to derive bay-wide target sediment concentrations for remediation as part of an ongoing total maximum daily loading characterization. The model calculated bay-wide geometric mean concentrations of ∑PCB in sediments of 1.6 to 73 µg/kg dry weight to meet several ecological and human health risk objectives. The bay-wide geometric ∑PCB concentration in the sediments at the time of the study was 11.6 µg/kg dry weight. The model was developed for assessing the behavior and risks of bioaccumulative substances on an ecosystem level. Environ. Toxicol. Chem. 2010;29:1385–1395. © 2010 SETAC
Spatial Distribution of Electrochemical Performance in a Segmented SOFC: A Combined Modeling and Experimental Study
Authors: Bessler W. G. , Gewies S. , Willich C. , Schiller G. , Friedrich K. A. 
Published: March 2010

AbstractSpatially inhomogeneous distribution of current density and temperature in solid oxide fuel cells (SOFC) contributes to accelerated electrode degradation, thermomechanical stresses, and reduced efficiency. This paper presents a combined experimental and modeling study of the distributed electrochemical performance of a planar SOFC. Experimental data were obtained using a segmented cell setup that allows the measurement of local current‐voltage characteristics, gas composition and temperature in 4 × 4 segments. Simulations were performed using a two‐dimensional elementary kinetic model that represents the experimental setup in a detailed way. Excellent agreement between model and experiment was obtained for both global and local performance over all investigated operating conditions under varying H2/H2O/N2 compositions at the anode, O2/N2 compositions at the cathode, temperature, and fuel utilization. A strong variation of the electrochemical performance along the flow path was observed when the cell was operated at high fuel utilization. The simulations predict a considerable gradient of gas‐phase concentrations along the fuel channel and through the thickness of the porous anode, while the gradients are lower at the cathode side. The anode dominates polarization losses. The cell may operate locally in critical operating conditions (low H2/H2O ratios, low local segment voltage) without notably affecting globally observed electrochemical behavior.
Characterisation of Nanocarbon‐Based Gas Diffusion Media by Electrochemical Impedance Spectroscopy
Authors: Gallo Stampino P. , Omati L. , Cristiani C. , Dotelli G. 
Published: March 2010

AbstractA multi‐wall carbon nanotubes (MWCNTs)‐based gas diffusion medium (GDM) was prepared, where carbon black was partially substituted by carbon nanotube (CNT) in the formulation of the micro‐porous layer (MPL). A rheological analysis of the ink used to coat the gas diffusion layer (GDL) was previously performed to correlate viscosities with the slurry composition. Shear thinning inks with viscosity of 0.4 (Pa s–1) were obtained for a composition containing 10 wt.‐% of CNT and 12 wt.‐% of fluorinated polymer. Using the doctor‐blade technique, a coating thickness of about 100–150 μm was obtained.Moreover, electrochemical performance of a single cell assembled with the CNT‐based GDM was compared with that obtained with a sample without CNTs. In order to better understand the role of CNTs, electrochemical impedance spectroscopy (EIS) of the running fuel cell (FC) was also performed. As a result, it was found that the addition of CNTs sensibly improves single cell performances.
Integrated genomic profiling identifies candidate genes implicated in glioma‐genesis and a novel LEO1‐SLC12A1 fusion gene
Authors: Bralten Linda B. C. , Kloosterhof Nanne K. , Gravendeel Lonneke A. M. , Sacchetti Andrea , Duijm Elza J. , Kros Johan M. , van den Bent Martin J. , Hoogenraad Casper C. , Sillevis Smitt Peter A. E. , French Pim J. 
Published: March 2010

AbstractWe performed genotyping and exon‐level expression profiling on 21 glioblastomas (GBMs) and 19 oligodendrogliomas (ODs) to identify genes involved in glioma initiation and/or progression. Low‐copy number amplifications (2.5 < n < 7) and high‐copy number amplifications (n > 7) were more frequently observed in GBMs; ODs generally have more heterozygous deletions per tumor. Four high‐copy amplicons were identified in more than one sample and resulted in overexpression of the known oncogenes EGFR, MDM2, and CDK4. In the fourth amplicon, RBBP5, a member of the RB pathway, may act as a novel oncogene in GBMs. Not all hCNAs contain known genes, which may suggest that other transcriptional and/or regulatory elements are the target for amplification. Regions with most frequent allelic loss, both in ODs and GBMs, resulted in a reduced expression of known tumor suppressor genes. We identified a homozygous deletion spanning the Pragmin gene in one sample, but direct sequencing of all coding exons in 20 other glioma samples failed to detect additional genetic changes. Finally, we screened for fusion genes by identifying aberrant 5′‐3′ expression of genes that lie over regions of a copy number change. A fusion gene between exon 11 of LEO1 and exon 10 of SLC12A1 was identified. Our data show that integrated genomic profiling can identify genes involved in tumor initiation, and/or progression and can be used as an approach to identify novel fusion genes. © 2010 Wiley‐Liss, Inc.
Characterization of the 12q15 MDM2 and 12q13‐14 CDK4 amplicons and clinical correlations in osteosarcoma
Authors: Mejia‐Guerrero Salvador , Quejada Michael , Gokgoz Nalan , Gill Mona , Parkes Robert K. , Wunder Jay S. , Andrulis Irene L. 
Published: March 2010

AbstractThe chromosomal region 12q13‐15 is recurrently amplified in osteosarcoma (OS), but its importance in bone tumor development remains unknown. Although there are two major candidate genes (MDM2, a TP53 downregulator, and CDK4, involved in cell cycle progression) considered to be the driving genes in this region, the size of the amplicon and number of genes involved have not been determined. In this study, we used 130 classical OS and 15 parosteal OS to determine MDM2 and CDK4 amplification frequency in OS. Tumors in which these genes were amplified were used to map the 12q13‐15 amplified region and to determine its correlation with clinical prognosis. The 12q13‐15 amplification was more prevalent in parosteal OS (67% of cases) than in high‐grade classical OS (12%). Quantitative real‐time PCR of MDM2, CDK4, and 25 other genes showed that this region contains two different amplicons: one at 12q15 centered on MDM2 and one at 12q13‐14 centered on CDK4. Both regions were frequently coamplified in both types of OS, and MDM2 and CDK4 amplification was correlated with higher expression levels for both genes. Univariate and multivariate analyses of clinical data indicated that classical OS patients whose tumors exhibited MDM2 amplification were more likely to be older at diagnosis (median age 32.6 vs. 17.8 years) and female (66.7 vs. 33.3%) than those without gene amplification. There was no association with other clinical parameters. In conclusion, coamplification of MDM2 and CDK4 in two separate amplicons occurs frequently in parosteal OS and less so in classical high‐grade OS. © 2010 Wiley‐Liss, Inc.
Individual and combined roles of CYP3A, P‐glycoprotein (MDR1/ABCB1) and MRP2 (ABCC2) in the pharmacokinetics of docetaxel
Authors: van Waterschoot Robert A.B. , Lagas Jurjen S. , Wagenaar Els , Rosing Hilde , Beijnen Jos H. , Schinkel Alfred H. 
Published: March 2010

AbstractDocetaxel is one of the most widely used anticancer drugs. A major problem with docetaxel treatment, however, is the considerable interpatient variability in docetaxel exposure. Another disadvantage of the drug is that it has a very low oral bioavailability and can, therefore, only be administered intravenously. The drug‐metabolizing enzyme CYP3A and the drug transporter MDR1 (P‐glycoprotein) are major determinants of docetaxel pharmacokinetics. In vitro studies have indicated that docetaxel is also a substrate for the drug transporter MRP2, but the in vivo importance of MRP2 for docetaxel is currently unknown. We, therefore, investigated the role of MRP2 in the pharmacokinetics of docetaxel by utilizing Mrp2−/− mice. We also generated and characterized Cyp3a/Mdr1a/b/Mrp2−/− combination knockout mice to get more insight into how these drug‐handling systems work together in determining docetaxel pharmacokinetics. The systemic exposure in Mrp2−/− mice was not significantly different from wild‐type, after either oral or intravenous administration. Strikingly, however, in Cyp3a/Mdr1a/b/Mrp2−/− mice, systemic docetaxel exposure was increased 166‐fold after oral administration when compared with wild‐type mice, and 2.3‐fold when compared with Cyp3a/Mdr1a/b−/− mice. Interestingly, this 166‐fold increase was disproportionate compared with that for the separate Cyp3a (12‐fold) or Mdr1a/b/Mrp2 (4‐fold) knockouts. The oral bioavailability was increased to 73% in the Cyp3a/Mdr1a/b/Mrp2−/− strain, versus only 10% in wild‐type mice. Our data thus indicate that in the absence of CYP3A and Mdr1a/b activity, Mrp2 has a marked impact on docetaxel pharmacokinetics. These findings could have important implications for improving the oral bioavailability and reducing the variability in docetaxel exposure.
Synergistic antitumor activity of the SN‐38‐incorporating polymeric micelles NK012 with S‐1 in a mouse model of non‐small cell lung cancer
Authors: Nagano Tatsuya , Yasunaga Masahiro , Goto Koichi , Kenmotsu Hirotsugu , Koga Yoshikatsu , Kuroda Jun‐ichiro , Nishimura Yoshihiro , Sugino Takashi , Nishiwaki Yutaka , Matsumura Yasuhiro 
Published: March 2010

AbstractThe combination therapy of CPT‐11, a prodrug of SN‐38, with S‐1, a dihydropyrimidine dehydrogenase inhibitory fluoropyrimidine, shows a high clinical response rate in non‐small cell lung cancer (NSCLC). However, this combination causes severe toxicities such as diarrhea. Here, we investigated the advantages of treatment with the SN‐38‐incorporating polymeric micelles NK012 over CPT‐11 in combination with S‐1 in mice bearing a NSCLC xenograft in terms of antitumor activity and toxic effects, particularly intestinal toxicity.In vitrocytotoxic effects were examined in human NSCLC cell lines (A549, PC‐9, PC‐14, EBC‐1 and H520).In vivoantitumor effects were evaluated in PC‐14‐ and EBC‐1‐bearing mice after NK012 or CPT‐11 administration on Days 0 and 7 and S‐1 administration on Days 0–13. Pathological changes in the small intestine were also investigated. Thein vitrogrowth inhibitory effects of NK012 were 56.8‐ to 622‐fold more potent than those of CPT‐11. NK012/S‐1 treatment showed significantly higher antitumor activity both in PC‐14‐bearing (p= 0.0007) and EBC‐1‐bearing mice (p< 0.0001) than CPT‐11/S‐1 treatment. The deformity and decrease in the density of intestinal villi were more severe in CPT‐11/S‐1‐treated mice than in NK012/S‐1‐treated mice. NK012/S‐1 combination is a promising candidate regimen against NSCLC without inducing toxicities such as severe diarrhea and therefore warrants clinical evaluation.
Immune evasion of microsatellite unstable colorectal cancers
Authors: Kloor Matthias , Michel Sara , von Knebel Doeberitz Magnus 
Published: March 2010

AbstractColorectal cancers (CRC) develop through 2 major pathways of genetic instability. In contrast to the majority of CRCs, which are characterized by chromosomal instability, high‐level microsatellite unstable (MSI‐H) CRCs arise as a consequence of the loss of DNA mismatch repair (MMR) functions and show accumulation of insertion and deletion mutations particularly in microsatellite sequences. MSI‐H occurs in about 15% of CRCs, and virtually all CRCs occurring in the context of the hereditary cancer‐predisposing Lynch syndrome. These tumors are characterized by a comparably good prognosis and a low frequency of distant metastases. Because of the expression of a defined set of tumor‐specific antigens, MSI‐H CRCs elicit a strong local and systemic antitumoral immune response of the host and therefore use different strategies to evade the control of the immune system. In this review, we will summarize novel molecular mechanisms that at the same time drive pathogenesis, immunogenicity and immune evasion during the development and progression of MSI‐H CRCs. We will focus on the current knowledge about alterations in human leukocyte antigen (HLA) antigen presentation and discuss how immune evasion—while offering protection against local antitumoral immune responses—paradoxically might interfere with the ability of the tumor to form distant organ metastases.
miR‐145, miR‐133a and miR‐133b: Tumor‐suppressive miRNAs target FSCN1 in esophageal squamous cell carcinoma
Authors: Kano Masayuki , Seki Naohiko , Kikkawa Naoko , Fujimura Lisa , Hoshino Isamu , Akutsu Yasunori , Chiyomaru Takeshi , Enokida Hideki , Nakagawa Masayuki , Matsubara Hisahiro 
Published: March 2010

AbstractMicroRNAs (miRNAs), noncoding RNAs 21–25 nucleotides in length, regulate gene expression primarily at the posttranscriptional level. Growing evidence suggests that miRNAs are aberrantly expressed in many human cancers, and that they play significant roles in carcinogenesis and cancer progression. A search for miRNAs with a tumor‐suppressive function in esophageal squamous cell carcinoma (ESCC) was performed using the miRNA expression signatures obtained from ESCC clinical specimens. A subset of 15 miRNAs was significantly downregulated in ESCC. A comparison of miRNA signatures from ESCC and our previous report identified 4 miRNAs that are downregulated in common (miR‐145, miR‐30a‐3p, miR‐133a and miR‐133b), suggesting that these miRNAs are candidate tumor suppressors. Gain‐of‐function analysis revealed that 3 transfectants (miR‐145, miR‐133a and miR‐133b) inhibit cell proliferation and cell invasion in ESCC cells. These miRNAs (miR‐145, miR‐133a and miR‐133b), which have conserved sequences in the 3′UTR of FSCN1 (actin‐binding protein, Fascin homolog 1), inhibited FSCN1 expression. The signal from a luciferase reporter assay was significantly decreased at 2 miR‐145 target sites and 1 miR‐133a/b site, suggesting both miRNAs directly regulate FSCN1. An FSCN1 loss‐of‐function assay found significant cell growth and invasion inhibition, implying an FSCN1 is associated with ESCC carcinogenesis. The identification of tumor‐suppressive miRNAs, miR‐145, miR‐133a and miR‐133b, directly control oncogenic FSCN1 gene. These signal pathways of ESCC could provide new insights into potential mechanisms of ESCC carcinogenesis.