bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of copper, cadmium, lead, and arsenic in a live diet on juvenile fish growth
Authors: Erickson Russell J. , Mount David R. , Highland Terry L. , Hockett J. Russell , Leonard Edward N. , Mattson Vincent R. , Dawson Timothy D. , Lott Kevin G. 
Published: November 2010

The effects of diet-borne copper, cadmium, lead, and arsenic on juvenile fish were evaluated using a live diet consisting of the oligochaete Lumbriculus variegatus . In 30 d exposures, no effects were observed on the growth and survival of rainbow trout ( Oncorhynchus mykiss ), fathead minnow ( Pimephales promelas ), and channel catfish ( Ictalurus punctatus ) fed diets contaminated with copper [130–310 µg Cu·(g dm)−1], cadmium [90–540 µg Cd·(g dm)−1], and lead [850–1000 µg Pb·(g dm)−1]. However, rainbow trout growth was reduced in a dose-dependent manner for diets contaminated with arsenic [26–77 µg As·(g dm)−1]. These effects of arsenic on fish growth were accompanied by slower feeding rate, reduced food conversion efficiency, liver cell abnormalities, and fecal matter changes suggestive of digestive effects, and occurred to a similar extent whether the diet was exposed to arsenate or arsenite. Effects from these dietary levels of arsenic, and the absence of effects from these dietary levels of metals, were generally consistent with literature reports using laboratory diets amended with toxicant salts. These results also indicated that reported growth effects on rainbow trout fed diets of invertebrates collected from mining-contaminated areas of the Clark Fork River (Montana, USA) or exposed in the laboratory to Clark Fork River sediments are likely more attributable to the arsenic than the metals in those diets.
Testing the environmental prediction hypothesis for mast-seeding in California oaks
Authors: Koenig Walter D. , Knops Johannes M.H. , Carmen William J. 
Published: November 2010

We analyzed 29 years of acorn production by five species of California oaks (genus Quercus ) to test the hypothesis that trees produce large seed crops prior to wet years, conditions facilitating seedling germination and survival. The mean crop of three of the species correlated positively and nontrivially with the following year’s rainfall, but none was statistically significant. Including the acorn crop 1 and 2 years earlier yielded several significant relationships between the acorn crop and future rainfall, but none held up when applied to a second, independent site. Across individuals, acorn production by 7% of trees correlated significantly with subsequent rainfall. Although these trees differed from other trees in several characters, differences were not sufficient to discriminate between trees that correlated significantly with subsequent rainfall from those that did not. We conclude that acorn production by California oaks does not forecast wet years and does not support the environmental prediction hypothesis.
Silencing Kinase-Interacting Stathmin Gene Enhances Erlotinib Sensitivity by Inhibiting Ser10 p27 Phosphorylation in Epidermal Growth Factor Receptor–Expressing Breast Cancer
Authors: Zhang Dongwei , Tari Ana M. , Akar Ugur , Arun Banu K. , LaFortune Tiffany A. , Nieves-Alicea Rene , Hortobagyi Gabriel N. , Ueno Naoto T. 
Published: November 2010

Abstract
The epidermal growth factor receptor (EGFR) signaling pathway has emerged as a promising target for cancer therapy. EGFR tyrosine kinase inhibitors (TKI) such as erlotinib have been approved for cancer treatment but have shown very limited activity in breast cancer patients. Clarifying the molecular mechanism underlying resistance to EGFR TKIs could lead to more effective treatment against breast cancer. We previously reported that the sensitivity of breast cancer cells to erlotinib is partially dependent on p27 and that cytoplasmic localization of p27 is associated with erlotinib resistance. In the present study, we found that erlotinib induces p27 phosphorylation at Ser10 (S10), and S10 p27 phosphorylation leads to erlotinib resistance in EGFR-expressing breast cancer. Inhibiting S10 phosphorylation of p27 by knocking down human kinase-interacting stathmin (KIS), a nuclear protein that can phosphorylate p27 at S10, led to p27 accumulation in the nucleus and enhanced erlotinib-mediated cytotoxicity. Further, in vivo KIS gene silencing enhanced the antitumor activity of erlotinib in an orthotopic breast cancer xenograft model. KIS depletion also enhanced erlotinib sensitivity in erlotinib-resistant EGFR-expressing triple-negative breast cancer cells. Our study provides a rationale for the development of combinations of erlotinib with KIS inhibition to overcome EGFR TKI resistance in EGFR-expressing breast cancer. Mol Cancer Ther; 9(11); 3090–9. ©2010 AACR.
Exon 7 Deletion in the bcr-abl Gene Is Frequent in Chronic Myeloid Leukemia Patients and Is Not Correlated with Resistance against Imatinib
Authors: Gaillard Jean-Baptiste , Arnould Cécile , Bravo Sophie , Donadio Daniel , Exbrayat Carole , Jourdan Eric , Reboul Dorothée , Chiesa Jean , Lavabre-Bertrand Thierry 
Published: November 2010

Abstract
Chronic myeloid leukemia (CML) patients treated with imatinib develop frequent resistance generally due to a point mutation. Recently, large rearrangements of abl sequence have also been described. In this study, we focused on the complete deletion of exon 7. We screened for bcr-abldelexon7 in 63 resistant patients by high-resolution melting (HRM) analysis and direct sequencing. Moreover, we analyzed expression of abldelexon7 and bcr-abldelexon7 in 17 CML patients at diagnosis, 32 patients at resistance, and 20 negative controls by quantitative PCR or fragment length analysis. bcr-abldelexon7 was detected on 34 (54%) among 63 resistant patients by HRM, showing an increase in the sensitivity of screening, because only 3.2% could be detected by direct sequencing. This deletion was not associated with a point mutation (P = 0.3362). In addition, abldelexon7 was found in all tested samples with the same pattern of expression, suggesting an alternative splicing mechanism. In the bcr-abl component, there was no statistical difference between CML patients at diagnosis and resistant patients (P = 0.2815) as regarding bcr-abldelexon7 proportion, thus arguing against involvement of deletion in resistance. Moreover, among two patients harboring bcr-abldelexon7 at diagnosis, one experienced a complete disappearance of this transcript, and the other decreased &gt;75% at resistance. In conclusion, bcr-abldelexon7 is frequently observed in CML patients when using sensitive techniques. It seems to be the result of an alternative splicing mechanism and to be independent from the occurrence of resistance. Mol Cancer Ther; 9(11); 3083–9. ©2010 AACR.
HOXC8 Inhibits Androgen Receptor Signaling in Human Prostate Cancer Cells by Inhibiting SRC-3 Recruitment to Direct Androgen Target Genes
Authors: Axlund Sunshine Daddario , Lambert James R. , Nordeen Steven K. 
Published: November 2010

Abstract
HOX (homeobox) genes encode homeodomain-containing transcription factors critical to development, differentiation, and homeostasis. Their dysregulation has been implicated in a variety of cancers. Previously, we showed that a subset of genes of the HOXC cluster is upregulated in primary prostate tumors, lymph node metastases, and malignant prostate cell lines. In the present study, we show that HOXC8 inhibits androgen receptor (AR)-mediated gene induction in LNCaP prostate cancer cells and HPr-1 AR, a nontumorigenic prostate epithelial cell line. Mechanistically, HOXC8 blocks the AR-dependent recruitment of the steroid receptor coactivators steroid receptor coactivator-3 (SRC-3), and CREB binding protein to the androgen-regulated prostate-specific antigen gene enhancer and inhibits histone acetylation of androgen-regulated genes. Inhibition of androgen induction by HOXC8 is reversed upon expression of SRC-3, a member of the SRC/p160 steroid receptor cofactor family. Coimmunoprecipitation studies show that HOXC8 expression inhibits the hormone-dependent interaction of AR and SRC-3. Finally, HOXC8 expression increases invasion in HPr-1 AR nontumorigenic cells. These data suggest a complex role for HOXC8 in prostate cancer, promoting invasiveness while inhibiting AR-mediated gene induction at androgen response element–regulated genes associated with differentiated function of the prostate. A greater understanding of HOXC8 actions in the prostate and its interactions with androgen signaling pathways may elucidate mechanisms driving the onset and progression of prostate cancer. Mol Cancer Res; 8(12); 1643–55. ©2010 AACR.
Black Raspberries Inhibit Intestinal Tumorigenesis in Apc1638+/− and Muc2−/− Mouse Models of Colorectal Cancer
Authors: Bi Xiuli , Fang Wenfeng , Wang Li-Shu , Stoner Gary D. , Yang Wancai 
Published: November 2010

Abstract
Freeze-dried black raspberries (BRB) produce chemopreventive effects in a rat model of colon carcinogenesis; however, the mechanisms of inhibition were not determined. Herein, we used two mouse models of human colorectal cancer to determine if dietary BRBs would inhibit colorectal tumor development and to investigate the underlying mechanisms. We found that a 12-week feeding of BRBs significantly inhibited intestinal tumor formation in both models; reducing tumor incidence by 45% and tumor multiplicity by 60% in Apc1638+/− mice and tumor incidence and multiplicity by 50% in Muc2−/− mice. Mechanistic studies revealed that BRBs inhibit tumor development in Apc1638+/− mice by suppressing β-catenin signaling and in Muc2−/− mice by reducing chronic inflammation. Intestinal cell proliferation was inhibited by BRBs in both animal models; however, the extent of mucus cell differentiation was not changed in either model. Collectively, our data suggest that BRBs are highly effective in preventing intestinal tumor development in both Apc1638+/− and Muc2−/− mice through targeting multiple signaling pathways. Cancer Prev Res; 3(11); 1443–50. ©2010 AACR.
Description of Ruehmaphelenchus thailandae n. sp. (Nematoda: Aphelenchoididae) found in dunnage from Thailand
Authors: Gu Jianfeng , Wang Jiangling 
Published: November 2010

AbstractRuehmaphelenchus thailandae n. sp., isolated from deciduous dunnage from Thailand, is described and figured. The new species is characterised by the relatively stout body (a = 28.6 and 27.6 for males and females, respectively), three lines in the lateral field, spicules relatively small (12.0-13.3 μm) with weakly developed condylus and rostrum, bursa absent, vulva located at 79.5% of body length, vulval lips slightly swollen, length of post-uterine branch more than half of vulva to anus distance, female tail conoid, ca two anal body diam. long and with a broad terminal process up to 12 μm long. The new species is the third known for the genus. It can be distinguished from R. martinii and R. asiaticus mainly by the different shape and size of its spicules and different shape of the female tail terminus. The separate species status is also supported by ITS-RFLP pattern. Additional measurements of paratype R. asiaticus are appended.
One Market, Two Courts: Legal Pluralism vs. Homogeneity in the European Economic Area
Authors: Fredriksen Halvard Haukeland 
Published: November 2010

AbstractIn this article the apparent incompatibility between the judicial architecture of the European Economic Area (EEA) and the overall goal of uniform interpretation and application of the common rules in all EEA States is examined. In practice, homogeneity appears achievable only if the European Free Trade Association (EFTA) Court succumbs to the European Court of Justice (ECJ), granting the latter the final word on the interpretation of the EEA Agreement. It is argued that, as far as substantive EEA law is concerned, this is exactly what the EFTA Court has done over the past 17 years of the EEA's existence. The result is a well-functioning EEA Agreement. The price to pay for the EFTA States is the revelation of the perhaps inconvenient truth that the de facto supreme authority on the interpretation of EEA law rests with the ECJ.
A comparative study of piano curricula in Egypt and the USA (with specific reference to the School of Music at the University of Illinois)
Authors: Sahar Abdel Moneim Hanafy Eid  
Published: November 2010

This research draws a comparison between the School of Music at the University of Illinois, USA and the Faculty of Music Education at Helwan University in Cairo, Egypt (the researcher’s academic appointment is at Menofia University, but she teaches on the faculty of Helwan University). The research answers two important questions: (1) What weaknesses in Egyptian piano curricula lead to students’ poor performance in exams? (2) What steps can be proposed to address these weaknesses and to help improve students’ performances in piano exams? The research comprises three parts: Part 1 presents an overview of music education in Egypt and a detailed description of the Faculty of Music Education, its origin and development over the years. This part addresses music education in general and piano curricula in particular, while focusing on the relevant shortcomings that lead to students’ poor levels of piano performance. Part 2 sheds light on the piano curricula in the School of Music at the University of Illinois. Part 3 compares undergraduate piano curricula in both situations, highlighting relevant strengths and weaknesses. Finally, recommendations are proposed and conclusions stated to address weaknesses in the piano curricula of the Faculty of Music Education at Helwan University.
‘I am an Arab but I live in an English world’: Teaching social work in the United Arab Emirates
Authors: Holtzhausen Leon 
Published: November 2010

• Summary: This article advances a basic model for cross-cultural social work teaching linked to the use of appropriate cultural methodology that is fundamental to the learning success of Arab social work students in the United Arab Emirates (UAE). • Findings: The article’s findings are based on qualitative research methodology and makes use of focus groups and narrative case studies. The article explores Arab social work students’ perception of receiving education in English in a fourth-year Social Work Practice course presented by a Western, English-speaking social work faculty. It also summarizes the self-reflective experiences of the author who lectured social work at a prominent university in the United Arab Emirates over a period of four years in order to generate some practical guidelines for social work educators on cross-cultural teaching and learning success located in a culture other than their own. • Applications: In this regard, the article also shares some suggestions for teaching social work across cultural barriers in the UAE based on student perceptions and self-reflective experiences of the author.
NK-cell education is shaped by donor HLA genotype after unrelated allogeneic hematopoietic stem cell transplantation
Authors: Haas Philippe , Loiseau Pascale , Tamouza Ryad , Cayuela Jean-Michel , Moins-Teisserenc Hélène , Busson Marc , Henry Guylaine , Falk Christine S. , Charron Dominique , Socié Gérard , Toubert Antoine , Dulphy Nicolas 
Published: November 2010

Abstract
The rules governing natural killer (NK)–cell education in the allogeneic environment created by unrelated hematopoietic stem-cell transplantation (HSCT) are still largely elusive, especially in an unrelated donor setting. NK-cell inhibitory receptors for self-human leukocyte antigen (HLA) play a central role in the acquisition or maintenance of NK-cell functional competence. Therefore, the responsiveness of different NK-cell subsets was assessed as a function of their expression or absence of expression of self-HLA–specific inhibitory receptors, in a large cohort (n = 60) of unrelated HSCT recipients. A fully effective NK-cell education process was achieved within the first year after allogeneic HSCT and lasted for at least 3 years thereafter. In addition, HLA-mismatched HSCT led to a stable education pattern that was determined by the donor's HLA ligands. These data suggest that the NK cell's education partner could be of hematopoietic rather than extrahematopoietic origin. This donor-ligand–driven NK-cell education model would suggest a sustained graft-versus-leukemia effect after HLA-mismatched HSCT.
Genetic mapping and developmental timing of transmission ratio distortion in a mouse interspecific backcross
Authors: Eversley Chevonne D , Clark Tavia , Xie Yuying , Steigerwalt Jill , Bell Timothy A , de Villena Fernando PM , Threadgill David W 
Published: November 2010

Abstract

Background
Transmission ratio distortion (TRD), defined as statistically significant deviation from expected 1:1 Mendelian ratios of allele inheritance, results in a reduction of the expected progeny of a given genotype. Since TRD is a common occurrence within interspecific crosses, a mouse interspecific backcross was used to genetically map regions showing TRD, and a developmental analysis was performed to identify the timing of allele loss.

Results
Three independent events of statistically significant deviation from the expected 50:50 Mendelian inheritance ratios were observed in an interspecific backcross between the Mus musculus A/J and the Mus spretus SPRET/EiJ inbred strains. At weaning M. musculus alleles are preferentially inherited on Chromosome (Chr) 7, while M. spretus alleles are preferentially inherited on Chrs 10 and 11. Furthermore, alleles on Chr 3 modify the TRD on Chr 11. All TRD loci detected at weaning were present in Mendelian ratios at mid-gestation and at birth.

Conclusions
Given that Mendelian ratios of inheritance are observed for Chr 7, 10 and 11 during development and at birth, the underlying causes for the interspecific TRD events are the differential post-natal survival of pups with specific genotypes. These results are consistent with the TRD mechanism being deviation from Mendelian inheritance rather than meiotic drive or segregation distortion.
Up-regulated expression of type II very low density lipoprotein receptor correlates with cancer metastasis and has a potential link to β-catenin in different cancers
Authors: He Lei , Lu Yanjun , Wang Peng , Zhang Jun , Yin Chuanchang , Qu Shen 
Published: November 2010

AbstractBackgroundVery low density lipoprotein receptor (VLDLR) has been considered as a multiple function receptor due to binding numerous ligands, causing endocytosis and regulating cellular signaling. Our group previously reported that enhanced activity of type II VLDLR (VLDLR II), one subtype of VLDLR, promotes adenocarcinoma SGC7901 cells proliferation and migration. The aim of this study is to explore the expression levels of VLDLR II in human gastric, breast and lung cancer tissues, and to investigate its relationship with clinical characteristics and β-catenin expression status.MethodsVLDLR II expression was examined using immunohistochemistry (IHC) and Western blot in tumor tissues from 213 gastric, breast and lung cancer patients, tumor adjacent noncancerous tissues by same methods. Correlations between VLDLR II and clinical features, as well as β-catenin expression status were evaluated by statistical analysis.ResultsThe immunohistochemical staining of VLDLR II showed statistical difference between tumor tissues and tumor adjacent noncancerous tissues in gastric, breast and lung cancers (P= 0.034, 0.018 and 0.043, respectively). Moreover, using Western, we found higher VLDLR II expression levels were associated with lymph node and distant metastasis in gastric and breast cancer (P< 0.05). Furthermore, highly significant positive correlations were found between VLDLR II and β-catenin in gastric cancer (r= 0.689;P< 0.001)breast cancer (r= 0.594;P< 0.001).ConclusionsAccording to the results of the current study, high VLDLR II expression is correlated with lymph node and distant metastasis in gastric and breast cancer patients, the data suggest that VLDLR II may be a clinical marker in cancers, and has a potential link with β-catenin signaling pathway. This is the first to reveal the closer relationship of VLDLR II with clinical information.
Lessons from genome-wide studies: an integrated definition of the coactivator function of histone acetyl transferases
Authors: Anamika Krishanpal , Krebs Arnaud R , Thompson Julie , Poch Olivier , Devys Didier , Tora Làszlò 
Published: November 2010

Abstract
Histone acetylation is one of the key regulatory mechanisms controlling transcriptional activity in eukaryotic cells. In higher eukaryotes, a number of nuclear histone acetyltransferase (HAT) enzymes have been identified, most of which are part of a large multisubunit complex. This diversity, combined with the large number of potentially acetylable lysines on histones, suggested the existence of a specific regulatory mechanism based on the substrate specificity of HATs. Over the past decade, intensive characterisations of the HAT complexes have been carried out. However, the precise mode of action of HATs, and particularly the functional differences amongst these complexes, remains elusive. Here we review current insights into the functional role of HATs, focusing on the specificity of their action. Studies based on biochemical as well as genetic approaches suggested that HATs exert a high degree of specificity in their acetylation spectra and in the cellular processes they regulate. However, a different view emerged recently from genomic approaches that provided genome-wide maps of HAT recruitments. The careful analysis of genomic data suggests that all HAT complexes would be simultaneously recruited to a similar set of loci in the genome, arguing for a low specificity in their function. In this review, we discuss the significance of these apparent contradictions and suggest a new model that integrates biochemical, genetic and genome-wide data to better describe the functional specificity of HAT complexes.