bluuebunny/crossref_metadata_2025_split huggingface dataset:
What happened to the ones who dropped out? Outcome in eating disorder patients who complete or prematurely terminate treatment
Authors: Björk Tabita , Björck Caroline , Clinton David , Sohlberg Staffan , Norring Claes 
Published: January 2009

AbstractIntroductionThere is a lack of knowledge about the outcome of eating disorder patients who terminate treatment prematurely. The present study followed‐up eating disorder patients who had previously dropped out of treatment and examined clinical status 36 months after intake.MethodDropouts (n = 30) were compared with treatment completers (n = 52) on diagnostic status, clinical symptoms, psychosocial adjustment and treatment satisfaction at follow‐up. Patterns of change from intake to follow‐up within groups, as well as between groups, were explored.ResultsNo significant differences were found between groups at follow‐up, except for more treatment dissatisfaction reported among dropouts. When patterns of change were examined between groups, patients who completed treatment were found to have made significantly greater changes (less eating disorder symptoms, less psychological problems and more positive self‐image) compared to dropouts.DiscussionAlthough no significant differences in outcome were found between dropouts and completers, greater clinical improvement was found among those who completed treatment. The dropouts examined in this study did well despite premature termination of treatment. Clinical and research implications are discussed. Copyright © 2009 John Wiley & Sons, Ltd and Eating Disorders Association.
Transient analysis of the 161 kU Taiwan‐PengHu submarine power cable system
Authors: Ho Ping‐Heng , Wu Chi‐Jui 
Published: January 2009

AbstractThe 58.9 km, 161 kU Taiwan PengHu submarine power cable system (T‐P‐Cable), the first submarine project of the Taiwan Power Company (Taipower) in this level, will be commercially operated in 2012. It is important to analyze the transient behaviors before operation. It is necessary to find the operation strategy to deal with the transients in advance. The EMTP‐ATP was used in this paper to analyze (1) the switched over voltage (SOV) in normal operation, (2) the slow front transients (SFT) voltage in fault contingency, (3) the transient inrush current (TIC) in energizing of the no‐load transformers and shunt reactors, and (4) the transient recover voltage (TRV) in de‐energizing the shunt reactors. The appropriate set of the surge protective device (SPD) to avoid the SOV and SFT has also been investigated. The results show that there is no TIC in energizing the no‐load transformers and shunt reactors. The TRV across the current breaker (CB) contactors is higher than the system TRV when the shunt reactors are de‐energized without using SPD. There is no re‐strike on the CB contactors. The results of this study provide tremendous prior operation experience and advice for the Taipower. Copyright © 2009 John Wiley & Sons, Ltd.
Using DCE and ranking data to estimate cardinal values for health states for deriving a preference‐based single index from the sexual quality of life questionnaire
Authors: Ratcliffe Julie , Brazier John , Tsuchiya Aki , Symonds Tara , Brown Martin 
Published: January 2009

AbstractThere is an increasing interest in using data derived from ordinal methods, particularly data derived from discrete choice experiments (DCEs), to estimate the cardinal values for health states to calculate quality adjusted life years (QALYs). Ordinal measurement strategies such as DCE may have considerable practical advantages over more conventional cardinal measurement techniques, e.g. time trade‐off (TTO), because they may not require such a high degree of abstract reasoning. However, there are a number of challenges to deriving the cardinal values for health states using ordinal data, including anchoring the values on the full health–dead scale used to calculate QALYs. This paper reports on a study that deals with these problems in the context of using two ordinal techniques, DCE and ranking, to derive the cardinal values for health states derived from a condition‐specific sexual health measure. The results were compared with values generated using a commonly used cardinal valuation technique, the TTO. This study raises some important issues about the use of ordinal data to produce cardinal health state valuations. Copyright © 2009 John Wiley & Sons, Ltd.
Effects of resveratrol analogs on cell cycle progression, cell cycle associated proteins and 5fluoro‐uracil sensitivity in human derived colon cancer cells
Authors: Colin Didier , Gimazane Amandine , Lizard Gérard , Izard Jean‐Claude , Solary Eric , Latruffe Norbert , Delmas Dominique 
Published: January 2009

AbstractEpidemiological studies suggested that trans‐resveratrol, a wine grape component, could prevent malignant tumor development. This compound also demonstrated cytostatic and cytotoxic effects on tumor cells in vitro. To obtain trans‐resveratrol derivatives with a better cellular uptake and enhanced antiproliferative effects, we synthesized a triacetate derivative as well as an oligomer, ε‐viniferin and its acetylated form, ε‐viniferin penta‐acetate. We also obtained vineatrol, a wine grape shoot extract that associates several polyphenols that may act synergistically, including trans‐resveratrol and ε‐viniferin. We show here that resveratrol triacetate and vineatrol are as efficient as trans‐resveratrol in inducing the accumulation of human colon cancer cells in early S phase of the cell cycle. This effect is associated with a nuclear redistribution of cyclin A and the formation of a cyclin A/cyclin‐dependent kinase 2 complex whose kinase activity is increased. In contrast, ε‐viniferin and its acetylated form do not demonstrate any significant activity on these cells when tested alone. Interestingly, resveratrol triacetate and vineatrol dramatically enhance 5‐Fluoro‐Uracil‐mediated inhibition of colon cancer cell proliferation. Thus, acetylated derivatives of resveratrol have retained the cytostatic and cytotoxic activities of the parental molecule and thus deserve to be tested as chemosensitizers in animal models. © 2009 UICC
Overexpression of WWP1 is associated with the estrogen receptor and insulin‐like growth factor receptor 1 in breast carcinoma
Authors: Chen Ceshi , Zhou Zhongmei , Sheehan Christine E. , Slodkowska Elzbieta , Sheehan Christopher B. , Boguniewicz Ann , Ross Jeffrey S. 
Published: January 2009

AbstractWWP1, a HECT type E3 ubiquitin ligase frequently amplified and overexpressed in breast cancer, has the potential to become a useful clinical biomarker and therapeutic target in breast cancer. Here, we performed immunohistochemical staining in formalin‐fixed and paraffin‐embedded tissue sections from 187 cases of primary invasive mammary carcinoma [137 ductal carcinomas (IDC) and 50 lobular carcinomas (ILC)] by using a monoclonal anti‐WWP1 antibody. The normal breast epithelium and adjacent benign epithelium are essentially negative for WWP1. Cytoplasmic WWP1 immunoreactivity was observed in 76/187 (40.6%) tumors and showed a positive correlation with ERα (p = 0.05) and IGF‐1R proteins (p = 0.001) in this cohort. The positive correlations between WWP1 and ER/IGF‐1R were also observed in a panel of 12 breast cancer cell lines by Western blot. Interestingly, the ER levels are decreased when WWP1 is silenced in ER positive MCF7 and T47D breast cancer cell lines. Finally, WWP1 ablation collectively inhibits cell proliferation with tamoxifen in MCF7 and T47D, as measured by 3H‐thymidine incorporation assays. These findings suggest that WWP1 may play an important role in ER positive breast cancer. © 2009 UICC
Construction of oncogenetic tree models reveals multiple pathways of oral cancer progression
Authors: Pathare Swapnali , Schäffer Alejandro A. , Beerenwinkel Niko , Mahimkar Manoj 
Published: January 2009

AbstractOral cancer develops and progresses by accumulation of genetic alterations. The interrelationship between these alterations and their sequence of occurrence in oral cancers has not been thoroughly understood. In the present study, we applied oncogenetic tree models to comparative genomic hybridization (CGH) data of 97 primary oral cancers to identify pathways of progression. CGH revealed the most frequent gains on chromosomes 8q (72.4%) and 9q (41.2%) and frequent losses on 3p (49.5%) and 8p (47.5%). Both mixture and distance‐based tree models suggested multiple progression pathways and identified +8q as an early event. The mixture model suggested two independent pathways namely a major pathway with −8p and a less frequent pathway with +9q. The distance‐based tree identified three progression pathways, one characterized by −8p, another by −3p and the third by alterations +11q and +7p. Differences were observed in cytogenetic pathways of node‐positive and node‐negative oral cancers. Node‐positive cancers were characterized by more non‐random aberrations (n= 11) and progressed via −8p or −3p. On the other hand, node‐negative cancers involved fewer non‐random alterations (n= 6) and progressed along −3p. In summary, the tree models for oral cancers provided novel information about the interactions between genetic alterations and predicted their probable order of occurrence. © 2009 UICC
Functional evidence for Eme1 as a marker of cisplatin resistance
Authors: Tomoda Yoshitaka , Katsura Mari , Okajima Miyuki , Hosoya Noriko , Kohno Nobuoki , Miyagawa Kiyoshi 
Published: January 2009

AbstractThe ability to predict cisplatin sensitivity in tumors has been expected to greatly improve the outcome of cancer therapy, because the drug is frequently used in a variety of tumors. Although ERCC1 and other repair proteins have been investigated as markers of cisplatin resistance, reliable markers are still needed. Here, we demonstrate that Eme1 levels can predict cisplatin sensitivity more accurately than ERCC1 or Rad51 levels in a variety of human cancer cell lines. Eme1 forms a heterodimeric protein complex with Mus81 and functions as a structure‐specific endonuclease. Haploinsufficiency of Eme1 led to hypersensitivity to cisplatin in the colon cancer cell line HCT116. On the basis of this finding, we examined the relationships between levels of proteins involved in the repair of interstrand cross‐links and cisplatin sensitivity in human tumor cell lines with a variety of origins. Although ERCC1, Rad51 and Mus81 levels correlated with sensitivity to some extent, the clearest correlation was observed with Eme1. Tumors with low Eme1 levels were more sensitive to the drug than tumors with high levels. This suggests that the measurement of Eme1 in tumors may be more informative for cisplatin‐based chemotherapy than that of the currently available markers. © 2009 UICC
A novel mechanism for anti‐EGFR antibody action involves chemokine‐mediated leukocyte infiltration
Authors: Hoffmann Thomas K. , Schirlau Kerstin , Sonkoly Enikö , Brandau Sven , Lang Stephan , Pivarcsi Andor , Balz Vera , Müller Anja , Homey Bernhard , Boelke Edwin , Reichert Torsten , Friebe‐Hoffmann Ulrike , Greve Jens , Schuler Patrick , Scheckenbach Kathrin , Schipper Jörg , Bas Murat , Whiteside Theresa L. , Bier Henning 
Published: January 2009

AbstractOverexpression of the epidermal growth factor receptor (EGFR) is a hallmark of squamous cell carcinoma of the head and neck (SCCHN). Monoclonal antibodies (mAbs) against EGFR are currently used for therapy of recurrent or metastatic disease; however, their mode of action is not completely understood. To investigate the immunological effects of anti‐EGFR mAb, we generated a three‐dimensional spheroid model of EGFR‐expressing SCCHN and used this model to study the effect of anti‐EGFR mAb on leukocyte migration toward tumors. Pretreatment with the blocking anti‐EGFR mAb EMD 72000, its F(ab′)2 fragments or an EGFR tyrosine kinase inhibitor led to substantially increased leukocyte infiltration into EGFR overexpressing tumor spheroids, but not into those with low EGFR expression. Nonblocking anti‐EGFR mAb or fibroblast‐specific mAb did not affect leukocyte infiltration, suggesting that the observed increase in leukocyte infiltration depends on interference with EGFR activation. Using a human cytokine macroarray, we demonstrated that the blockade of EGFR by anti‐EGFR mAb in EGFR‐overexpressing SCCHN cells leads to differential expression of several cytokines and chemokines, including the chemokine MCP‐1/CCL‐2. The significant upregulation of MCP‐1/CCL2 on exposure to anti‐EGFR mAb was confirmed by quantitative PCR and enzyme‐linked immunospot analyses. Moreover, blocking anti‐MCP‐1 antibody inhibited leukocyte migration toward tumor cells induced by anti‐EGFR mAb, pointing to an important role of MCP‐1/CCL2 in anti‐EGFR mAb‐induced leukocyte migration. Our findings demonstrate that anti‐EGFR mAb induces leukocyte infiltration to tumor spheroids by upregulating chemokine expression. This novel mechanism for anti‐EGFR mAb action may contribute to the antitumor effects of anti‐EGFR mAb in vivo. © 2009 Wiley‐Liss, Inc.
Young children's responses to September 11th: The New York City experience
Authors: Klein Tovah P. , Devoe Ellen R. , Miranda‐Julian Claudia , Linas Keri 
Published: January 2009

AbstractAlthough the knowledge base regarding very young children's responses to trauma has been expanding, descriptions of their responses to terrorism remain sparse. Yet, their vulnerability makes this an important group to study. Recent events in the United States (9/11, Hurricane Katrina) make this question highly relevant. This study aims to provide extensive descriptions of how children 5 years or younger on September 11th who were living in close proximity to Ground Zero responded that day and in the following months. Sixty‐seven New York City parents (with 104 children) participated in focus groups between November 2001 and May 2002. Focus groups also provided a foundation for an in‐depth study examining young children's adaptation following 9/11 and changes in parenting behaviors after the disaster. Findings on children's behavioral and emotional reactions on 9/11 and in the 8 months after as well as their need to return to normalcy are reported. Consistent with current understanding of trauma symptoms in young children, parents reported behaviors including chronic sleep disruptions, fearful reactions, development of new fears, and increased clinginess and separation anxiety following the disaster. On the actual day, children's responses were described as ranging from calm and cooperative to difficult and panicky. Implications for working with parents and young children affected by terrorism or community‐level trauma and directions for future research are discussed.
Neonatal physiological regulation is associated with perinatal factors: A study of neonates born to healthy African American women living in poverty
Authors: Jacob Suma , Byrne Michelle , Keenan Kate 
Published: January 2009

AbstractMaternal mental health and prenatal stress are linked with neurobehavioral differences in the offspring. The majority of studies documenting this effect have been conducted using either predominantly European American infants or minority infants exposed to teratogens in utero. In this study, we focus on healthy African American women from low‐income environments to investigate the earliest individual differences in biobehavioral regulation, including resting heart rate and variability (HRV). In 87 neonates, HRV was significantly lower in those born to mothers reporting past major depressive disorder (p = .01). The number of maternal life stressors also was associated with lower neonatal HRV (p = .03). Obstetrical complications were not associated with significant differences, but breast‐ versus bottle‐feeding in the first few days of life was related to higher HRV (p = .04). Early variation in physiological regulation may be linked to subsequent individual differences in response to stress. Thus, identifying the earliest point in development when such differences can be reliably measured may result in opportunities for prevention of later deficits in regulating response to stress.
Distinct actions of Akt1 and Akt2 in skeletal muscle differentiation
Authors: Rotwein Peter , Wilson Elizabeth M. 
Published: January 2009

AbstractDifferentiation, maturation, and repair of skeletal muscle requires ongoing cooperation between signaling cascades activated by hormones and growth factors, and intrinsic regulatory programs controlled by myogenic transcription factors. The insulin‐like growth factor—phosphatidylinositol‐3 kinase—Akt pathway has been implicated in muscle growth and regeneration after injury, in counteracting sarcopenia during aging, and in maintaining muscle cell viability. Here we present evidence for distinct roles for Akt1 and Akt2 in different phases of muscle differentiation. Targeted knockdown of either Akt had no effect on C2 myoblast proliferation, even though Akt1 concentrations are markedly higher than Akt2 levels under growth‐promoting conditions. Akt2 concentrations rose by nearly an order of magnitude during muscle differentiation, while Akt1 levels remained constant, yet loss of either protein did not increase myoblast death. Rather, knockdown or genetic knockout of Akt1 blocked differentiation at its earliest stages, preventing induction of muscle‐specific proteins and inhibiting formation of multinucleated myofibers, while myoblasts lacking Akt2 differentiated normally, although resultant myofibers were thinner and incorporated fewer nuclei than controls. Forced expression of knockdown‐resistant Akt1 partially reversed the deficit in differentiation seen in myoblasts lacking Akt1. Our results define isoform‐specific Akt actions in muscle cells, and demonstrate that both Akts are necessary for full myoblast differentiation and maturation. J. Cell. Physiol. 219: 503–511, 2009. © 2009 Wiley‐Liss, Inc.
H‐Ras and PI3K are required for the formation of circular dorsal ruffles induced by low‐power laser irradiation
Authors: Gao Xuejuan , Xing Da , Liu Lei , Tang Yonghong 
Published: January 2009

AbstractThe formation of circular dorsal ruffles upon growth factor stimulation facilitates the static cells for subsequent motility. Low‐power laser irradiation (LPLI) has been shown to exert some promotive effects on migration and proliferation in various cell types. It is unclear whether LPLI could induce the formation of circular ruffles. In this study, using confocal fluorescence microscope, we for the first time demonstrated that LPLI could induce the production of circular ruffle structures in COS‐7 cells. These structures were proved to be actin‐based and originated from membrane microdomains enriched in cholesterol. Ras was shown to be activated by LPLI and expression of YFP‐H‐Ras (N17), a dominant negative H‐Ras, blocked the generation of circular ruffles induced by LPLI. Wortmannin, PI3K inhibitor, potently suppressed the formation of LPLI‐induced circular ruffles in a dose‐dependent manner. However, blocking the activation of PKC, which was activated during LPLI‐induced cell proliferation in our previous study, had no effect on the formation of circular ruffles. Thus, both H‐Ras and PI3K were required for the formation of circular ruffles induced by LPLI and the generation of circular ruffles provides new information for the mechanisms of biological effects of LPLI. J. Cell. Physiol. 219: 535–543, 2009. © 2009 Wiley‐Liss, Inc.
Low‐power laser irradiation promotes cell proliferation by activating PI3K/Akt pathway
Authors: Zhang Lingling , Xing Da , Gao Xuejuan , Wu Shengnan 
Published: January 2009

AbstractLow‐power laser irradiation (LPLI) can stimulate cell proliferation through a wide network of signals. Akt is an important protein kinase in modulating cell proliferation. In this study, using real‐time single‐cell analysis, we investigated the activity of Akt and its effects on cell proliferation induced by LPLI in African green monkey SV40‐transformed kidney fibroblast cells (COS‐7). We utilized a recombinant fluorescence resonance energy transfer (FRET) Akt probe (BKAR) to dynamically detect the activation of Akt after LPLI treatment. Our results show that LPLI induced a gradual and continuous activation of Akt. Moreover, the activation of Akt can be completely abolished by wortmannin, a specific inhibitor of PI3K, suggesting that the activation of Akt caused by LPLI is a PI3K‐dependent event. Src family is involved in Akt activation as demonstrated by the part inhibition of Akt activity in samples treated with PP1 (an inhibitor of Src family). In contrast, loading Gö 6983, a PKC inhibitor, did not affect this response. Further experiments performed using GFP‐Akt fluorescence imaging and Western blot analysis demonstrate that, the activation of Akt is a multi‐step process in response to LPLI, involving membrane recruitment, phosphorylation, and membrane detachment. LPLI promotes cell proliferation through PI3K/Akt activation since the cell viability was significantly inhibited by PI3K inhibitor. All these studies create a concernful conclusion that PI3K/Akt signaling pathway is well involved in LPLI triggered cell proliferation that acts as a time‐ and dose‐dependent manner. J. Cell. Physiol. 219: 553–562, 2009. © 2009 Wiley‐Liss, Inc.
Oxidative stress promotes ocular neovascularization
Authors: Dong Aling , Xie Bing , Shen Jikui , Yoshida Tsunehiko , Yokoi Katsutoshi , Hackett Sean F. , Campochiaro Peter A. 
Published: January 2009

AbstractMice deficient in superoxide dismutase 1 (Sod1−/− mice) develop many features seen in patients with age‐related macular degeneration (AMD) including choroidal neovascularization (NV). We sought to determine if the absence of SOD1 contributes to the pro‐angiogenic environment in the subretinal space or whether it is completely secondary to other changes in Bruch's membrane and the retinal pigmented epithelium (RPE) that precede the development of choroidal NV. In an ischemic retinopathy model or a transgenic model in which the rhodopsin promoter drives expression of vascular endothelial growth factor (VEGF) in photoreceptor there was significantly more NV in Sod1−/− compared to Sod1+/+ mice. The compromised antioxidant defense system in Sod1−/− mice contributes to the pro‐angiogenic environment, because treatment of Sod1−/− mice with a mixture of antioxidants caused a significant reduction in ischemia‐induced retinal NV. Wild‐type mice treated with the same antioxidants also showed reduced ischemia‐induced retinal NV, reduced VEGF‐induced subretinal NV, and reduced choroidal NV at Bruch's membrane rupture sites. These data suggest that reactive oxygen species contribute to several types of ocular NV. This could explain why in the Age‐Related Eye Disease Trial, antioxidant treatment reduced conversion from non‐neovascular to neovascular AMD and severe vision loss, and suggest that potent antioxidants should be considered for other diseases complicated by ocular NV. J. Cell. Physiol. 219: 544–552, 2009. © 2009 Wiley‐Liss, Inc.