bluuebunny/crossref_metadata_2025_split huggingface dataset:
Empirical correlation of PGA, spectral accelerations and spectrum intensities from active shallow crustal earthquakes
Authors: Bradley Brendon A. 
Published: April 2011

AbstractEmpirical correlation equations between peak ground acceleration, spectral acceleration, spectrum intensity, and acceleration spectrum intensity are developed. The correlation equations are developed for shallow crustal earthquakes using the Next Generation Attenuation (NGA) ground motion database, and four of the NGA ground motion prediction equations (GMPEs). A particularly novel aspect of the present study is the explicit consideration of epistemic uncertainty in the correlation equations due to both the adopted ground motion database and GMPEs. The resulting correlation equations enable the joint consideration of these four ground motion intensity measures in ground motion selection using frameworks such as the generalized conditional intensity measure approach. Copyright © 2011 John Wiley & Sons, Ltd.
Biaxial testing of unbonded post‐tensioned rocking bridge piers with external replacable dissipaters
Authors: Marriott Dion , Pampanin Stefano , Palermo Alessandro 
Published: April 2011

AbstractThe biaxial response of two bridge piers is experimentally investigated. A post‐tensioned precast bridge pier with external replaceable mild‐steel dissipaters is tested under biaxial loading. The performance of the post‐tensioned bridge pier is compared with a conventionally reinforced monolithic bridge pier. The experimental biaxial response is then compared with previous uniaxial experimental testing of identical bridge piers to understand the influence of biaxial loading, specifically concerning post‐tensioned rocking sections. A 3‐dimensional moment–curvature and moment–rotation analysis program is created to generate the monotonic section response of a conventional and post‐tensioned bridge pier. After comparing the accuracy of the section analysis program to the experimental testing of the monolithic pier, the program is validated against the experimental testing of the post‐tensioned bridge pier. This section analysis program is then used in the calibration of a macro‐model to capture the entire cyclic response of the post‐tensioned bridge pier. The macro‐model adopts multiple linear‐elastic compression‐only springs at the rocking interface, combined with non‐linear inelastic springs for each of the mild‐steel dissipaters and returns encouraging results at both local and global levels.The paper concludes with a number of biaxial moment‐interaction design charts for monolithic and post‐tensioned bridge piers as a function of mechanical and geometric section properties. The design charts define the biaxial yield surface at nominal yield and at the design section capacity defined by one of three material limit states. Copyright © 2011 John Wiley & Sons, Ltd.
Personalised caregiver support: effectiveness of psychosocial interventions in subgroups of caregivers of people with dementia
Authors: Van Mierlo Lisa D. , Meiland Franka J. M. , Van der Roest Henriëtte G. , Dröes Rose‐Marie 
Published: April 2011

AbstractObjectiveInsight into the characteristics of caregivers for whom psychosocial interventions are effective is important for care practice. Until now no systematic reviews were conducted into the effectiveness of psychosocial interventions for caregiver subgroups.MethodsTo gain insight into this relationship between caregiver subgroups and intervention outcomes, a first review study was done. This study reviews the personal characteristics of caregivers of people with dementia for whom psychosocial interventions were effective.ResultsElectronic databases and key articles were searched for reviews on psychosocial interventions for caregivers studies published between January 1990 and February 2008. Based on these reviews, twenty‐six studies met the inclusion criteria (i.e. having positive outcomes described in subgroups). Most positive effects were found in caregivers of people with a diagnosis of ‘dementia not otherwise specified’ and in the subgroup of female caregivers. Examples of outcomes were decreased depression and improved self‐efficacy.ConclusionsThis study gives a first overview of successful psychosocial interventions in subgroups of caregivers of people with dementia. It makes clear that until now, relatively little research has been done into subgroups of these caregivers. It also suggests that more research is needed to better understand which psychosocial interventions are effective for specific subgroups of caregivers of people with dementia. Copyright © 2011 John Wiley & Sons, Ltd.
Resting‐state networks in awake five‐ to eight‐year old children
Authors: de Bie Henrica M.A. , Boersma Maria , Adriaanse Sofie , Veltman Dick J. , Wink Alle Meije , Roosendaal Stefan D. , Barkhof Frederik , Stam Cornelis J. , Oostrom Kim J. , Delemarre‐van de Waal Henriette A. , Sanz‐Arigita Ernesto J. 
Published: April 2011

AbstractDuring the first 6–7 years of life children undergo a period of major neurocognitive development. Higher‐order cognitive functions such as executive control of attention, encoding and retrieving of stored information and goal‐directed behavior are present but less developed compared to older individuals. There is only very limited information from functional magnetic resonance imaging (fMRI) studies about the level of organization of functional networks in children in the early school period. In this study we perform continuous resting‐state functional connectivity MRI in 5‐ to 8‐year‐old children in an awake state to identify and characterize resting‐state networks (RSNs). Temporal concatenation independent component analysis (ICA) approach was applied to analyze the data. We identified 14 components consisting of regions known to be involved in visual and auditory processing, motor function, attention control, memory, and the default mode network (DMN). Most networks, in particular those supporting basic motor function and sensory related processing, had a robust functional organization similar to mature adult patterns. In contrast, the DMN and other RSNs involved in higher‐order cognitive functions had immature characteristics, revealing incomplete and fragmented patterns indicating less developed functional connectivity. We therefore conclude that the DMN and other RSNs involved in higher order cognitive functioning are detectable, yet in an immature state, at an age when these cognitive abilities are mastered. Hum Brain Mapp, 2011. © 2011 Wiley‐Liss, Inc.
Second malignancies after childhood noncentral nervous system solid cancer: Results from 13 cancer registries
Authors: Maule Milena , Scélo Ghislaine , Pastore Guido , Brennan Paul , Hemminki Kari , Olsen Jorgen H. , Tracey Elizabeth , Pukkala Eero , Weiderpass Elisabete , Brewster David H. , Tamaro Sharon , Chia Kee‐Seng , Pompe‐Kirn Vera , Kliewer Erich V. , Tonita Jon M. , Martos Carmen , Jonasson Jon G. , Merletti Franco , Boffetta Paolo 
Published: April 2011

AbstractChildren diagnosed with noncentral nervous system solid cancers (NCNSSC) experience several adverse late effects, including second malignant neoplasm. The aim of our study was to assess the risk of specific second malignancies after a childhood NCNSSC. Diagnosis and follow‐up data on 10,988 cases of NCNSSC in children (0–14 years) were obtained from 13 registries. Standardized incidence ratios (SIRs) with 95% confidence intervals (CI) and cumulative incidence of second malignancies were computed. We observed 175 second malignant neoplasms, yielding a SIR of 4.6, 95% CI: 3.9–5.3. When considering second cancers with at least 10 occurrences, highest relative risks were found for second malignant bone tumors (SIR = 26.4, 16.6–40.0), soft tissue sarcomas (SIR = 14.1, 6.7–25.8) and myeloid leukemia (SIR = 12.7, 6.3–22.8). Significant increased risks for all malignancies combined were observed after sympathetic nervous system tumors (SIR = 11.4, 5.2–21.6), retinoblastomas (SIR = 7.3, 5.4–9.8), renal tumors (SIR = 5.7, 3.8–8.0), malignant bone tumors (SIR = 5.6, 3.7–8.2), soft tissue sarcomas (SIR = 4.7, 3.2–6.8), germ‐cell, trophoblastic and other gonadal neoplasms (SIR = 2.5, 1.1–4.9), carcinomas and other malignant epithelial neoplasms (SIR = 2.2, 1.4–3.3). The highest risk of a second malignancy of any type occurred 5 to 9 years after NCNSSC (SIR = 9.9, 6.8–13.9). The cumulative incidence of second malignancies 10 years after the first neoplasm was eight times higher among NCNSSC survivors than in the general population, with the absolute difference between observed and expected cumulative incidence still increasing after 50 years of follow‐up. Children who survived a NCNSSC experience a large increased risk of developing a new malignancy, even many years after their initial diagnosis.
Evaluation of predictive models in daily practice for the identification of patients with Lynch syndrome
Authors: Tresallet Christophe , Brouquet Antoine , Julié Catherine , Beauchet Alain , Vallot Céline , Ménégaux Fabrice , Mitry Emmanuel , Radvanyi François , Malafosse Robert , Rougier Philippe , Nordlinger Bernard , Laurent‐Puig Pierre , Boileau Catherine , Emile Jean‐François , Muti Christine , Penna Christophe , Hofmann‐Radvanyi Hélène 
Published: April 2011

AbstractThe optimal strategy for identifying patients with Lynch syndrome among patients with newly diagnosed colorectal cancer (CRC) is still debated. Several predictive models (e.g., MMRpredict, PREMM1,2 and MMRpro) combining personal and familial data have recently been developed to quantify the risk that a given patient with CRC carries a Lynch syndrome‐causing mutation. Their clinical applicability to patients with CRC from the general population requires evaluation. We studied a consecutive series of 214 patients with newly diagnosed CRC characterized for tumor microsatellite instability (MSI), somatic BRAF mutation, MLH1 promoter methylation and mismatch repair (MMR) gene germline mutation status. The performances of the models for identifying MMR mutation carriers (8/214, 3.7%) were evaluated and compared to the revised Bethesda guidelines and a molecular strategy based on MSI testing in all patients followed by the exclusion of MSI‐positive sporadic cases from mutational testing by screening for BRAF mutation and MLH1 promoter methylation. The sensitivities of the three models, at the lowest thresholds proposed, were identical (75%), with similar numbers of probands eligible for further MSI testing (almost half the patients). In our dataset, the prediction models gave no better discrimination than the revised Bethesda guidelines. Both approaches failed to identify two of the eight mutation carriers (the same two patients, aged 67 and 81 years, both with no family history). Thus, like the revised Bethesda guidelines, predictive models did not identify all patients with Lynch syndrome in our series of consecutive CRC. Our results support systematic screening for MMR deficiency in all new CRC cases.
A biparatopic anti‐EGFR nanobody efficiently inhibits solid tumour growth
Authors: Roovers Rob C. , Vosjan Maria J.W.D. , Laeremans Toon , el Khoulati Rachid , de Bruin Renée C.G. , Ferguson Kathryn M. , Verkleij Arie J. , van Dongen Guus A.M.S. , van Bergen en Henegouwen Paul M.P. 
Published: April 2011

AbstractThe epidermal growth factor receptor (EGFR) has been shown to be a valid cancer target for antibody‐based therapy. At present, several anti‐EGFR monoclonal antibodies have been successfully used, such as cetuximab and matuzumab. X‐ray crystallography data show that these antibodies bind to different epitopes on the ecto‐domain of EGFR, providing a rationale for the combined use of these two antibody specificities. We have previously reported on the successful isolation of antagonistic anti‐EGFR nanobodies. In our study, we aimed to improve the efficacy of these molecules by combining nanobodies with specificities similar to both cetuximab and matuzumab into a single biparatopic molecule. Carefully designed phage nanobody selections resulted in two sets of nanobodies that specifically blocked the binding of either matuzumab or cetuximab to EGFR and that did not compete for each others' binding. A combination of nanobodies from both epitope groups into the biparatopic nanobody CONAN‐1 was shown to block EGFR activation more efficiently than monovalent or bivalent (monospecific) nanobodies. In addition, this biparatopic nanobody potently inhibited EGF‐dependent cell proliferation. Importantly, in an in vivo model of athymic mice bearing A431 xenografts, CONAN‐1 inhibited tumour outgrowth with an almost similar potency as the whole mAb cetuximab, despite the fact that CONAN‐1 is devoid of an Fc portion that could mediate immune effector functions. Compared to therapy using bivalent, monospecific nanobodies, CONAN‐1 was clearly more potent in tumour growth inhibition. These results show that the rational design of biparatopic nanobody‐based anticancer therapeutics may yield potent lead molecules for further development.
Intestinal inflammation induces genotoxicity to extraintestinal tissues and cell types in mice
Authors: Westbrook Aya M. , Wei Bo , Braun Jonathan , Schiestl Robert H. 
Published: April 2011

AbstractChronic intestinal inflammation leads to increased risk of colorectal and small intestinal cancers and is also associated with extraintestinal manifestations such as lymphomas, other solid cancers and autoimmune disorders. We have previously found that acute and chronic intestinal inflammation causes DNA damage to circulating peripheral leukocytes, manifesting a systemic effect in genetically and chemically induced models of intestinal inflammation. Our study addresses the scope of tissue targets and genotoxic damage induced by inflammation‐associated genotoxicity. Using several experimental models of intestinal inflammation, we analyzed various types of DNA damage in leukocyte subpopulations of the blood, spleen, mesenteric and peripheral lymph nodes and in intestinal epithelial cells, hepatocytes and the brain. Genotoxicity in the form of DNA single‐ and double‐stranded breaks accompanied by oxidative base damage was found in leukocyte subpopulations of the blood, diverse lymphoid organs, intestinal epithelial cells and hepatocytes. The brain did not demonstrate significant levels of DNA double‐stranded breaks as measured by γ‐H2AX immunostaining. CD4+ and CD8+ T‐cells were most sensitive to DNA damage versus other cell types in the peripheral blood. In vivo measurements and in vitro modeling suggested that genotoxicity was induced by increased levels of systemically circulating proinflammatory cytokines. Moreover, genotoxicity involved increased damage rather than reduced repair, as it is not associated with decreased expression of the DNA double‐strand break recognition and repair protein, ataxia telangiectasia mutated. These findings suggest that levels of intestinal inflammation contribute to the remote tissue burden of genotoxicity, with potential effects on nonintestinal diseases and cancer.
Analysis of the cellular uptake and nuclear delivery of insulin‐like growth factor binding protein‐3 in human osteosarcoma cells
Authors: Micutkova Lucia , Hermann Martin , Offterdinger Martin , Hess Michael W. , Matscheski Andrea , Pircher Haymo , Mück Christoph , Ebner Hannes‐Leonhard , Laich Andreas , Ferrando‐May Elisa , Zwerschke Werner , Huber Lukas A. , Jansen‐Dürr Pidder 
Published: April 2011

AbstractInsulin‐like growth factor (IGF) binding protein‐3 (IGFBP‐3) regulates cell proliferation and survival by extracellular interaction and inactivation of the growth factor IGF‐I. Beyond that, IGF‐independent actions mediated by intracellular IGFBP‐3 including nuclear‐IGFBP‐3, have also been described. We here show, using both confocal and electron microscopy and cell fractionation, that the extracellular addition of IGFBP‐3 to living cells results in rapid uptake and nuclear delivery of IGFBP‐3, by yet partly unknown mechanisms. IGFBP‐3 is internalized through a dynamin‐dependent pathway, traffics through endocytic compartments and is finally delivered into the nucleus. We observed docking of IGFBP‐3 containing structures to the nuclear envelope and found IGFBP‐3 containing dot‐like structures to permeate the nuclear envelope. In summary, our findings establish the pathway by which this tumor suppressor protein is delivered from extracellular space to the nucleus.
Reported behavior of eating anything at anytime and risk of colorectal cancer in women
Authors: Bao Ying , Nimptsch Katharina , Chan Andrew T. , Ng Kimmie , Meyerhardt Jeffrey A. , Willett Walter C. , Giovannucci Edward , Fuchs Charles S. 
Published: April 2011

AbstractAlthough numerous studies have assessed the effect of foods and nutrients on colorectal carcinogenesis, few studies have investigated human eating behavior in relation to risk of colorectal cancer. In our study, we assessed whether the reported behavior of eating anything at anytime influenced colorectal cancer risk and related plasma biomarkers. We prospectively followed up 55,540 women in the Nurses' Health Study who were aged 48–73 years, had no history of cancer, ulcerative colitis or diabetes and responded to the item “I eat anything I want, anytime I want” in the 1994 questionnaire. We also analyzed blood samples for 1,994 women, which were collected in 1989–1990. During 12 years of follow‐up, 552 colorectal cancer cases were documented. After adjusting for age, smoking, body mass index, physical activity, red and processed meat and other known risk factors for colorectal cancer, women who reported eating anything at anytime experienced an increased risk of colorectal cancer (relative risk = 1.28, 95% confidence interval = 1.06–1.56) compared to those who did not report this behavior. In addition, reporting eating anything at anytime was associated with higher fasting plasma levels of insulin (p = 0.04) and C‐peptide (p = 0.05). In conclusion, reports of eating anything at anytime are associated with an increased risk of colorectal cancer in this large prospective cohort study, independent of other potential risk factors for colorectal cancer.
An alternative measure of intergenerational income mobility based on a random coefficient model
Authors: Murtazashvili Irina 
Published: April 2011

SUMMARYWe propose an alternative measure of the degree to which income status is transmitted from one generation to another. Our indicator of intergenerational income mobility is based on a random coefficient model, which allows for variation in intergenerational mobility across families due to multiplicative unobserved family‐specific characteristics. This alternative measure suggests that intergenerational income persistence is typically stronger than when intergenerational income mobility is measured using the standard elasticity of sons' income with respect to fathers' income. Copyright © 2011 John Wiley & Sons, Ltd.
Chromatin interaction networks and higher order architectures of eukaryotic genomes
Authors: Singh Sandhu Kuljeet , Li Guoliang , Sung Wing‐Kin , Ruan Yijun 
Published: April 2011

AbstractEukaryotic genome is, not only linearly but also spatially, organized into non‐random architecture. Though the linear organization of genes and their epigenetic descriptors are well characterized, the relevance of their spatial organization is beginning to unfold only recently. It is increasingly being recognized that physical interactions among distant genomic elements could serve as an important mean to eukaryotic genome regulation. With the advent of proximity ligation based techniques coupled with next generation sequencing, it is now possible to explore whole genome chromatin interactions at high resolution. Emerging data on genome‐wide chromatin interactions suggest that distantly located genes are not independent entities and instead cross‐talk with each other in an extensive manner, supporting the notion of “chromatin interaction networks”. Moreover, the data also advance the field to “3‐dimensional (3D) chromatin structure and dynamics”, which would enable molecular biologists to explore the spatiotemporal regulation of genome. In this article, we introduce a stepwise topological transformation of genome from 1‐dimension (1D, linear) to 2‐dimension (2D, networks) to 3‐dimension (3D, architecture) and discuss how such transformations could advance our understanding of genome biology. J. Cell. Biochem. 112: 2218–2221, 2011. © 2011 Wiley‐Liss, Inc.
Fisetin induces Nrf2‐mediated HO‐1 expression through PKC‐δ and p38 in human umbilical vein endothelial cells
Authors: Lee Seung Eun , Jeong Seong Il , Yang Hana , Park Cheung‐Seog , Jin Young‐Ho , Park Yong Seek 
Published: April 2011

AbstractFisetin is a natural flavonoid from fruits and vegetables that exhibits antioxidant, neurotrophic, anti‐inflammatory, and anti‐cancer effects in various disease models. Up‐regulation of heme oxygenase‐1 (HO‐1) expression protects against oxidative stress‐induced cell death, and therefore, plays a crucial role in cytoprotection in a variety of pathological models. In the present study, we investigated the effect of fisetin on the up‐regulation of HO‐1 in human umbilical vein endothelial cells (HUVECs). Small interfering RNA and pharmacological inhibitors of PKC‐δ and p38 MAPK attenuated HO‐1 induction in fisetin‐stimulated HUVECs. Fisetin treatment resulted in significantly increased NF‐E2‐related factor 2 (Nrf2) nuclear translocation, and antioxidant response element (ARE)‐luciferase activity, leading to up‐regulation of HO‐1 expression. In addition, fisetin pretreatment reduced hydrogen peroxide (H2O2)‐induced cell death, and this effect was reversed by ZnPP, an inhibitor of HO‐1. In summary, these findings suggest that induction of HO‐1 expression via Nrf2 activation may contribute to the cytoprotection exerted by fisetin against H2O2‐induced oxidative stress in HUVECs. J. Cell. Biochem. 112: 2352–2360, 2011. © 2011 Wiley‐Liss, Inc.
β‐globin matrix attachment region improves stable genomic expression of the Sleeping beauty transposon
Authors: Sjeklocha Lucas , Chen Yixin , Daly Meghan C. , Steer Clifford J. , Kren Betsy T. 
Published: April 2011

AbstractThe liver is an attractive target for gene therapy due to its extensive capability for protein production and the numerous diseases resulting from a loss of gene function it normally provides. The Sleeping Beauty Transposon (SB‐Tn)1 system is a non‐viral vector capable of delivering and mediating therapeutic transgene(s) insertion into the host genome for long‐term expression. A current challenge for this system is the low efficiency of integration of the transgene. In this study we use a human hepatoma cell line (HuH‐7) and primary human blood outgrowth endothelial cells (BOECs) to test vectors containing DNA elements to enhance transposition without integrating themselves. We employed the human β‐globin matrix attachment region (MAR) and the Simian virus 40 (SV40) nuclear translocation signal to increase the percent of HuH‐7 cells persistently expressing a GFP::Zeo reporter construct by ∼50% for each element; while combining both did not show an additive effect. Interestingly, both elements together displayed an additive effect on the number of insertion sites, and in BOECs the SV40 alone appeared to have an inhibitory effect on transposition. In long‐term cultures the loss of plasmid DNA, transposase expression and mapping of insertion sites demonstrated bona fide transposition without episomal expression. These results show that addition of the β‐globin MAR and potentially other elements to the backbone of SB‐Tn system can enhance transposition and expression of therapeutic transgenes. These findings may have a significant influence on the use of SB transgene delivery to liver for the treatment of a wide variety of disorders. J. Cell. Biochem. 112: 2361–2375, 2011. © 2011 Wiley‐Liss, Inc.