bluuebunny/crossref_metadata_2025_split huggingface dataset:
Optimizing layer‐based scheduling algorithms for parallel tasks with dependencies
Authors: Kunis R. , Rünger G. 
Published: December 2010

AbstractProgramming with parallel tasks leads to task graphs with dependencies representing a parallel program. Scheduling algorithms are employed to find an efficient execution order of the parallel tasks. A large variety of scheduling algorithms exist, including layer‐based scheduling algorithms for homogeneous target platforms that build consecutive layers of independent parallel tasks and schedule each layer separately. Although these scheduling algorithms provide good results in terms of scheduling algorithm runtime and schedule execution time, the resulting schedules leave room for optimization. This article proposes an optimization for arbitrary layer‐based scheduling algorithms, which is called Move‐blocks algorithm. Given a layer‐based schedule of the parallel tasks, this algorithm moves blocks of parallel tasks into preceding layers in order to reduce the overall execution time of a task‐based application. Suitable blocks of parallel tasks are identified by the algorithm Find‐blocks, which is employed together with the Move‐blocks algorithm. The algorithm Move‐blocks is applied to four well‐known scheduling algorithms. A detailed evaluation for a wide range of test cases is given. Copyright © 2010 John Wiley & Sons, Ltd.
Personal goals and prolonged grief disorder symptoms
Authors: Boelen Paul A. 
Published: December 2010

AbstractProlonged grief disorder (PGD, previously called complicated grief) is a debilitating condition that can develop following the loss of a loved one. The present study investigated the relationship between different features of personal goals of bereaved individuals and PGD symptom severity. To this end, 160 bereaved people were asked to write down seven important personal goals and to complete self‐report measures of PGD and depression symptom severity. With respect to the form of goals, the findings showed that more severe PGD symptomatology was associated with lower specificity of goals, a reduced sense of control over achieving goals and a lower perceived likelihood of achieving goals. With respect to the content of the goals, it was found that mourners with more severe levels of PGD symptoms reported more goals that were associated with loss (compared with goals unrelated to the loss), more goals related to feeling states and less goals related to work/education and close relationships. Implications of these findings are discussed. Copyright © 2010 John Wiley & Sons, Ltd.Key Practitioner Message:• The severity of prolonged grief disorder (PGD) symptoms after bereavement is associated with different features of personal goals, including reduced specificity of goals, lower perceived probability and controllability of achieving goals and an enhanced focus on loss‐related goals and goals related to feeling states.• In the treatment of PGD, it could be useful to change the negative beliefs that patients have about the probability and controllability of achieving goals and to help them in finding ways to achieve valued goals.• As recovery from loss hinges (in part) on the person's ability to continue (or restore) activities that are satisfying and meaningful, it could furthermore be fruitful to help patients to reduce their focus on ‘inward‐directed’ goals (associated with their own feelings) and to increase their focus on ‘outward‐directed’ goals (related to social, recreational and occupational activities).
Molecularly imprinted polymer‐based potentiometric sensor for 2‐aminopyridine as a potential impurity in piroxicam
Authors: Najafi Mostafa , Mehdipour Rasoul 
Published: December 2010

AbstractA molecularly imprinted polymer‐based potentiometric sensor was fabricated for determination of 2‐aminopyridine (2‐AP). The electroactive component is the 2‐APH+. To form this specie the determination is carried out in a bufferic solution at pH 4.5 in which 2‐AP is prevalently monoprotonated. Under these conditions, the membrane potential, increases with 2‐AP concentration over a wide range of concentration (5 µM to 100 mM) with a near Nernstian response of 54.1 mV/decade and detection limit of 2.0 µM. The response time is less than 5 s and the sensor can be used for more than 3 months without any significant divergence in response. The selectivity coefficients of the proposed sensor were evaluated and exhibited good selectivity to 2‐AP with respect to the electrode based on a non‐imprinted polymer. The utility of the sensor was successfully tested by examining of 2‐AP in piroxicam (PX) as a potential impurity. Copyright © 2010 John Wiley & Sons, Ltd.
Simultaneous activation of SHR and ATHB8 expression defines switch to preprocambial cell state in Arabidopsis leaf development
Authors: Gardiner Jason , Donner Tyler J. , Scarpella Enrico 
Published: December 2010

AbstractThe processes underlying the formation of leaf vascular networks have long captured the attention of developmental biologists, especially because files of elongated vascular‐precursor procambial cells seem to differentiate from apparently equivalent, isodiametric ground cells. In Arabidopsis leaves, ground cells that have been specified to vascular fate engage expression of ARABIDOPSIS THALIANA HOMEOBOX8 (ATHB8). While definition of the transcriptional state of ATHB8‐expressing ground cells would be particularly informative, no other genes have been identified whose expression is initiated at this stage. Here we show that expression of SHORT‐ROOT (SHR) is activated simultaneously with that of ATHB8 in leaf development. Congruence between SHR and ATHB8 expression domains persists under conditions of manipulated vein patterning, suggesting that inception of expression of SHR and ATHB8 identifies transition to a preprocambial cell state that presages vein formation. Our observations further characterize the molecular identity of cells at anatomically inconspicuous stages of leaf vein development. Developmental Dynamics, 2011. © 2010 Wiley‐Liss, Inc.
Regioselectivity in the Aryne Cross‐Coupling of Aryllithiums with Functionalized 1,2‐Dibromobenzenes
Authors: Diemer Vincent , Begaud Manon , Leroux Frédéric R. , Colobert Françoise 
Published: December 2010

AbstractTri‐ and tetrasubstitutedortho‐bromobiaryls have been synthesized in good‐to‐excellent yields by aryne cross‐coupling reactions starting from 1,3‐dimethoxybenzene and functionalized 1,2‐dibromobenzenes. This study outlines the influence of the 1,2‐dibromobenzene precursor as well as the reaction temperature on the outcome of the aryl–aryl bond formation and indicates, in the case of dissymmetrical benzyne precursors, how structural parameters (electronic effects, steric hindrance, temperature, etc.) control the regioselectivity of the aryne cross‐coupling reactions.
Pesticide has asymmetric effects on two tadpole species across density gradient
Authors: Distel Christopher A , Boone Michelle D 
Published: December 2010

Abstract
Northern leopard frogs (Rana pipiens) have been disappearing throughout their range. The causes for extirpations have been elusive, although habitat alteration appears to be a major factor. Pesticides have been implicated in declines in western amphibians, but no mechanism has been identified. We tested the hypothesis that leopard frog tadpoles would be eliminated from insecticide-exposed ponds when they were less abundant than a competitor (American toads, Bufo americanus) by manipulating toad and leopard frog density (16, 50, or 150 of each species) with or without the insecticide carbaryl. Insecticide exposure did not interact with density on either species, indicating that contaminant effects were similar despite drastic differences in competition. The survival of both species decreased with increasing conspecific density, but not heterospecific density. Leopard frogs produced more metamorphs at intermediate densities, whereas toads produced more metamorphs at high density. Leopard frog mass at and time to metamorphosis responded negatively to density. Carbaryl did not affect leopard frog survival but positively affected mass at and time to metamorphosis. In contrast, toad survival was reduced after exposure, but mass at metamorphosis was greater. Pesticide-induced survival reductions may not affect population size if reductions are slight (as in toads, whose fitness may be compensated by increased mass). Management strategies aimed at ameliorating the effects of carbaryl in systems with these two species may not need to consider density. Environ. Toxicol. Chem. 2011; 30:650–658. © 2011 SETAC
Pesticide distributions and population declines of California, USA, alpine frogs,Rana muscosaandRana sierrae
Authors: Bradford David F , Knapp Roland A , Sparling Donald W , Nash Maliha S , Stanley Kerri A , Tallent-Halsell Nita G , McConnell Laura L , Simonich Staci M 
Published: December 2010

AbstractAtmospherically deposited pesticides from the intensively cultivated Central Valley of California, USA, have been implicated as a cause for population declines of several amphibian species, with the strongest evidence for the frogs Rana muscosa and Rana sierrae at high elevation in the Sierra Nevada mountains. Previous studies on these species have relied on correlations between frog population status and either a metric for amount of upwind pesticide use or limited measurements of pesticide concentrations in the field. The present study tested the hypothesis that pesticide concentrations are negatively correlated with frog population status (i.e., fraction of suitable water bodies occupied within 2 km of a site) by measuring pesticide concentrations in multiple media twice at 28 sites at high elevation in the southern Sierra Nevada. Media represented were air, sediment, and Pseudacris sierra tadpoles. Total cholinesterase (ChE), which has been used as an indicator for organophosphorus and carbamate pesticide exposure, was also measured in P. sierra tadpoles. Results do not support the pesticide-site occupancy hypothesis. Among 46 pesticide compounds analyzed, nine were detected with ≥30% frequency, representing both historically and currently used pesticides. In stepwise regressions with a chemical metric and linear distance from the Central Valley as predictor variables, no negative association was found between frog population status and the concentration of any pesticide or tadpole ChE activity level. By contrast, frog population status showed a strong positive relationship with linear distance from the Valley, a pattern that is consistent with a general west-to-east spread across central California of the amphibian disease chytridiomycosis observed by other researchers. Environ. Toxicol. Chem. 2011; 30:682–691. © 2011 SETAC
Activation of CD47 receptors causes proliferation of human astrocytoma but not normal astrocytes via an Akt‐dependent pathway
Authors: Sick Emilie , Boukhari Abdelaziz , Deramaudt Thérèse , Rondé Philippe , Bucher Bernard , André Philippe , Gies Jean‐Pierre , Takeda Kenneth 
Published: December 2010

AbstractCD47 is a membrane receptor that plays pivotal roles in many pathophysiological processes, including infection, inflammation, cell spreading, proliferation, and apoptosis. We show that activation of CD47 increases proliferation of human U87 and U373 astrocytoma cells but not normal astrocytes. CD47 function‐blocking antibodies inhibit proliferation of untreated U87 and U373 cells but not normal astrocytes, suggesting that CD47 may be constitutively activated in astrocytoma. CD47 expression levels were similar in our three cell types. CD47 couples to G‐proteins in astrocytes and astrocytoma and especially to the Gβγ dimer. Downstream signaling following CD47 activation involves Gβγ dimer‐dependent activation of the PI3K/Akt pathway in astrocytoma cells but not in normal astrocytes. This pathway is known to be deregulated in astrocytoma, leading to cell proliferation and enhanced survival signals. Putative PLIC‐1 interaction with CD47 in astrocytoma cells but not astrocytes may contribute to the proliferative effect observed upon activation of CD47. Our data indicate that CD47 receptors have a stimulatory role in cell proliferation and demonstrate for the first time that CD47 signals via the PI3K/Akt pathway in cancerous cells but not normal cells. © 2010 Wiley‐Liss, Inc.
Drosophila glia use a conserved cotransporter mechanism to regulate extracellular volume
Authors: Leiserson William M. , Forbush Biff , Keshishian Haig 
Published: December 2010

AbstractThe nervous system is protected by blood barriers that use multiple systems to control extracellular solute composition, osmotic pressure, and fluid volume. In the human nervous system, misregulation of the extracellular volume poses serious health threats. Here, we show that the glial cells that form the Drosophila blood–nerve barrier have a conserved molecular mechanism that regulates extracellular volume: the Serine/Threonine kinase Fray, which we previously showed is an ortholog of mammalian PASK/SPAK; and the Na‐K‐Cl cotransporter Ncc69, which we show is an ortholog of human NKCC1. In mammals, PASK/SPAK binds to NKCC1 and regulates its activity. In Drosophila, larvae mutant for Ncc69 develop a peripheral neuropathy, where fluid accumulates between glia and axons. The accumulation of fluid has no detectable impact on action potential conduction, suggesting that the role of Ncc69 is to maintain volume or osmotic homeostasis. Drosophila Ncc69 has kinetics similar to human NKCC1, and NKCC1 can rescue Ncc69, suggesting that they function in a conserved physiological mechanism. We show that fray and Ncc69 are coexpressed in nerve glia, interact in a yeast‐two‐hybrid assay, and have an essentially identical bulging nerve phenotype. We propose that normally functioning nerves generate extracellular solutes that are removed by Ncc69 under the control of Fray. This mechanism may perform a similar role in humans, given that NKCC1 is expressed at the blood–brain barrier. © 2010 Wiley‐Liss, Inc.
Non‐alcoholic fatty liver disease progresses to hepatocellular carcinoma in the absence of apparent cirrhosis
Authors: Ertle Judith , Dechêne Alexander , Sowa Jan‐Peter , Penndorf Volker , Herzer Kerstin , Kaiser Gernot , Schlaak Jörg F. , Gerken Guido , Syn Wing‐Kin , Canbay Ali 
Published: December 2010

AbstractNon‐alcoholic fatty liver disease (NAFLD) is the most common liver disease in developed countries, and accumulating evidence suggests it as the hepatic manifestation of the metabolic syndrome (MS). Although the published prevalence of hepatocellular carcinoma (HCC) is low in NAFLD/NASH patients, most of these data have been derived from areas endemic for viral hepatitis. We recruited 162 adults with HCC between February 2007 and March 2008, investigated the underlying etiologies and determined the prevalence of the MS and related features within each group. Patients with NAFLD/NASH‐associated HCC exhibited a higher prevalence of metabolic features (Type 2 diabetes mellitus, hypertension, dyslipidemia, coronary artery disease) compared to non‐NAFLD/NASH‐HCC. Intriguingly, a significant number (41.7%; p < 0.005) of individuals with NAFLD/NASH‐HCC had no evidence of cirrhosis. Patients with alcohol‐induced liver disease also displayed many features (14/19, 73.7%) of the MS, although, in contrast to NAFLD/NASH‐HCC, alcohol‐associated HCC was highly associated with cirrhosis (95.0%; p = 0.064). NAFLD/NASH as the hepatic entity of the MS may itself pose a risk factor for HCC, even in the absence of cirrhosis. The MS may also promote development of HCC among those with alcoholic liver disease. Increased awareness of liver manifestations in the MS may instigate early interventions against developing HCC.
Upregulation of p18Ink4c expression by oncogenic HPV E6 via p53‐miR‐34a pathway
Authors: Wang Xiaohong , Meyers Craig , Guo Ming , Zheng Zhi‐Ming 
Published: December 2010

AbstractBinding of p53 to miR‐34a promoter activates the expression of tumor‐suppressive miR‐34a. Oncogenic human papillomavirus (HPV) infection downregulates miR‐34a expression through viral E6 degradation of p53. In our report, we found that miR‐34a specifically targets p18Ink4c, a CDK4 and CDK6 inhibitor induced by E2F transactivation. HPV18+ HeLa cells with ectopic miR‐34a expression or by E6 siRNA knockdown‐induced expression of endogenous miR‐34a exhibited a substantial reduction of p18Ink4c in a dose‐dependent manner, but had no effect on p16Ink4a, another member of CDK4/6 inhibitor family. In contrast, de novo infection by oncogenic HPVs of human keratinocyte‐derived raft tissues increased p18Ink4c expression. Suppression of endogenous miR‐34a in cell lines with a miR‐34a inhibitor also increased p18Ink4c. We found that miR‐34a suppresses the expression of p18Ink4c by binding to a specific seed match in the 5′ UTR of p18Ink4c. Further investigation found remarkable increase of p18Ink4c in cervical precancer lesions and cervical cancer. Immunohistochemical staining of cervical tissue arrays showed increased expression of p18Ink4c in 68% of cervical cancer, 8.3% of chronic cervical inflammation and 4.8% of normal cervix. Although p18Ink4c inhibits cell proliferation in general and regulates E2F1 expression in HCT116 cells, it appears not to function as a tumor suppressor in cervical cancer cells lacking an intact G1 checkpoint because of viral E7 degradation of pRB. In summary, our study demonstrates an intimate connection among oncogenic HPV E6, p53, miR‐34a and p18Ink4c and identifies p18Ink4c as a possible biomarker for cervical cancer.
E‐cadherin expression on human carcinoma cell affects trastuzumab‐mediated antibody‐dependent cellular cytotoxicity through killer cell lectin‐like receptor G1 on natural killer cells
Authors: Yamauchi Chisako , Fujii Satoshi , Kimura Taichi , Kuwata Takeshi , Wada Noriaki , Mukai Hirofumi , Matsumoto Naoki , Fukayama Masashi , Ochiai Atsushi 
Published: December 2010

AbstractTrastuzumab is a recombinant antibody drug that is widely used for the treatment of HER2‐overexpressing breast carcinoma. Despite encouraging clinical results, many HER2‐overexpressing carcinomas are primarily resistant to trastuzumab. We attempted to explain trastuzumab resistance and search for solutions. Since the killer cell lectin‐like receptor G1 (KLRG1), an inhibitory receptor expressed on subsets of natural killer (NK) cells recognizes E‐cadherin as ligands and may inhibit immune responses by regulating the effector function of NK cells, we used HER2‐overexpressing carcinoma cells which were expressing E‐cadherin to investigate the role of antibody‐dependent cellular cytotoxicity (ADCC) through KLRG1 on NK cells in vitro and vivo. The results indicated that HER2‐overexpressing carcinoma cells were killed by trastuzumab‐mediated ADCC and the ADCC activity was reflected the degree of E‐cadherin expression on carcinoma cells. We found that expression of E‐cadherin was shown to be a predictor of response to trastuzumab‐based treatment for HER2‐overexpressing carcinomas, furthermore, trastuzumab‐mediated ADCC was markedly enhanced by KLRG1‐negative peripheral blood mononuclear cells (PBMCsKLRG1(−)).
Inhibition of signal transducer and activator of transcription 5 by the inhibitor of janus kinases stimulates dormant human leukemia CD34+/CD38− cells and sensitizes them to antileukemia agents
Authors: Ikezoe Takayuki , Yang Jing , Nishioka Chie , Kojima Shinsuke , Takeuchi Asako , Phillip Koeffler H. , Yokoyama Akihito 
Published: December 2010

AbstractTo verify molecular mechanisms by which leukemia stem cells (LSCs) maintain a dormant state, we explored the activity of the major prosurvival signal pathways in CD34+/CD38− compartment, supposed to contain LSCs, and CD34+/CD38+ counterparts from patients with acute myelogenous leukemia (AML, n = 11) by fluorescence‐activated cell sorting (FACS). CD34+/CD38− cells expressed a greater amount of p‐janus kinase 2 (JAK2) and p‐signal transducer and activator of transcription 5 (STAT5) than CD34+/CD38+ counterparts in all patients except for one case. In addition, we found that CD34+/CD38− cells were relatively resistant to cytarabine‐ and the inhibitor of the fms‐like tyrosine kinase 3 (FLT3)‐mediated growth inhibition, as measured by the clonogenic assay. Interestingly, blockade of JAK2/STAT5 signaling by the specific JAK2 inhibitor AZ960 stimulated cell cycling in CD34+/CD38− cells in conjunction with downregulation of cyclin‐dependent kinase inhibitor p21waf1 and sensitized these cells to the growth inhibition mediated by cytarabine and the FLT3 kinase inhibitor. Moreover, exposure of CD34+/CD38− cells to AZ960 potently induced apoptosis in parallel with downregulation of antiapoptotic protein Bcl‐xL, as measured by Western blot analysis. Taken together, JAK2/STAT5 signaling may be a promising molecular target to eradicate CD34+/CD38− leukemia cells in individuals with AML.
Rapamycin enhances the activity of oncolytic herpes simplex virus against tumor cells that are resistant to virus replication
Authors: Fu Xinping , Tao Lihua , Rivera Armando , Zhang Xiaoliu 
Published: December 2010

AbstractOncolytic herpes simplex virus (HSV) is currently in phase III clinical trials for development as a novel therapeutic agent against a broad range of human tumors. Although results have been promising, clinical outcome is likely to be compromised by intrinsic and acquired resistance to HSV replication, leading us to test agents that may overcome this obstacle. We found that, despite showing no effect on HSV replication in tumor cells fully permissive to the virus growth, the mTOR inhibitor rapamycin markedly increased the yield and dissemination of oncolytic HSVs in semipermissive tumor cells. Similar results were obtained in tumor‐bearing mice. Co‐administration of rapamycin with an HSV‐derived oncolytic virus either blocked or reversed the growth of tumor xenografts established from semipermissive human tumor cells, while use of either agent alone produced only transient inhibitory effect. Together, our results suggest that rapamycin could be used to potentiate the activity of oncolytic HSVs against difficult‐to‐treat human tumors or perhaps to prevent the emergence of resistant tumor cells during virotherapy.