bluuebunny/crossref_metadata_2025_split huggingface dataset:
Education, occupation and vote in Canada, 1965–1984
Authors: Fletcher Joseph F. 
Published: July 2010

Plusiers travaux de recherche sur le comportement électoral canadien ont démontré la faiblesse des effets de la classe sociale sur le vote. Cet article se sert des données de toutes les enquêtes nationales électorates (national election studies) entre les années 1965 et 1984. II cherche à illuminer les rapports statistiques entre d'une part l'appui electoral pour le parti néo‐démocrate et d'autre part l'éducation et le statut socio‐professionel. L'analyse multivariable des données suggère que la faiblesse du rapport classe‐vote s'explique à la fois par les effets contraires des variables culturelles (éducation) et économiques (statut socio‐professionel) et par la façon dont ces effets, qui sont differents dans les cinq régions du pays, se mêlent et se fondent quand on les examine à l'échelle du pays entier. Nos résultats indiquent qu'au Québec et dans les provinces de l'est, il y a une politique de classe basée sur l'éducation, tandis qu'en Ontario et dans les provinces de l'ouest, c'est une politique de classe plus conventionnelle qui prime. Cette étude révèle l'importance d'analyser les divers éléments des programmes électoraux des partis pour une comprehénsion exacte de leur bases sociales dans l'électorat.In an effort to clarity the typical finding of weak class effects on voting in Canada, this article uses data from all the national election studies between 1965 and 1984 in a multivariate investigation of the relations between education, occupation and vote. The major finding is that there are cross‐cutting regional effects for education and occupation on vote for the New Democratic Party (NDP) which effectively obscure one another when viewed from a national perspective. Log‐linear analyses reveal a class politics based on education in Quebec and Atlantic Canada whereas in Ontario, the Prairies and B.C. we find evidence of a more conventional class politics based on occupation. The implications of these findings for understanding the overall pattern of electoral politics in Canada are
Metabolic changes of anterior cingulate cortex in patients with hepatic cirrhosis: A magnetic resonance spectroscopy study
Authors: Zhang Long Jiang , Lu Guang Ming , Yin Jian Zhong , Qi Ji 
Published: July 2010

Aim:  The anterior cingulate cortex (ACC) plays an important role in cognitive functions. The purpose of this study is to compare metabolite concentrations in the ACC of cirrhotic patients with normal controls, and to correlate metabolite changes with Child–Pugh class and with severity of hepatic encephalopathy (HE).Methods:  Fifty‐two cirrhotic patients and 30 healthy volunteers were included in this study. All subjects performed the number connection test type A (NCT‐A) and digital symbol test (DST) before multiple resonance (MR) examinations. Single‐voxel proton MR spectroscopy (MRS) data in the ACC were acquired on a 1.5‐T scanner. The ratios of all metabolites to creatine and phosphocreatine (Cr) were obtained. Statistical analysis was performed to evaluate the difference between control and cirrhotic patients, with respect to metabolite ratios. The correlation between metabolite ratios and Child–Pugh scale, severity of HE, venous ammonia and neuropsychiatric test results was analyzed.Results:  The ratios of choline (Cho)/Cr and myo‐inositol (mIns)/Cr were significantly lower, and the ratio of glutamine– glutamate (Glx)/Cr was significantly higher in cirrhotic patients than those in controls (P < 0.001). mIns/Cr correlated negatively with Child–Pugh scale (r = −0.496, P < 0.001) and HE degree (r = −0.313, P < 0.05). Venous ammonia had a significant correlation with Cho/Cr (r = −0.329, P < 0.05) and mIns/Cr (r = −0.347, P < 0.05). No statistical correlation between metabolite ratios and neuropsychological tests was found for cirrhotic patients, but mIns/Cr did have a statistical correlation with NCT‐A (r = −0.270, P < 0.05) and DST (r = 0.463, P < 0.001) when all subjects were included in the analysis.Conclusion:  Significant metabolite changes were seen in the ACC in cirrhotic patients. Of the metabolites examined, the mIns/Cr level in the ACC was most closely associated with the severity of HE and hepatic functional reserve reflected by Child–Pugh scale.
Iron chelation prevents lung injury after major hepatectomy
Authors: Kalimeris Konstantinos , Nastos Constantinos , Papoutsidakis Nikolaos , Xanthopoulou Marianna N. , Defterevos George , Tympa Aliki , Pafiti Agatha , Andreadou Ioanna , Kostopanagiotou Georgia , Smyrniotis Vassilios , Arkadopoulos Nikolaos 
Published: July 2010

Aim:  Oxidative stress has been implicated in lung injury following ischemia/reperfusion and resection of the liver. We tested whether alleviating oxidative stress with iron chelation could improve lung injury after extended hepatectomy.Methods:  Twelve adult female pigs subjected to liver ischemia for 150 min, 65–70% hepatectomy and reperfusion of the remnant liver for 24 h were randomized to a desferrioxamine (DF) group (n = 6) which received i.v. desferrioxamine to a total dose of 100 mg/kg during both ischemia and reperfusion, and a control (C) group (n = 6). We recorded hemodynamic and respiratory parameters, plasma interleukin‐6 and malondialdehyde levels, as well as liver malondialdehyde and protein carbonyls content. Total non‐heme iron was measured in lung and liver. Pulmonary tissue was evaluated histologically for its nitrotyrosine and protein carbonyls content and for superoxide dismutase (SOD) and platelet‐activating factor acetylhydrolase (PAF‐AcH) activities.Results:  Reperfusion of the remnant liver resulted in gradual deterioration of gas‐exchange and pulmonary vascular abnormalities. Iron chelation significantly decreased the oxidative markers in plasma, liver and the lung and lowered activities of pulmonary SOD and PAF‐AcH. The improved liver function was followed by improved arterial oxygenation and pulmonary vascular resistance. DF also improved alveolar collapse and inflammatory cell infiltration, while serum interleukin‐6 increased.Conclusion:  In an experimental pig model that combines liver resection with prolonged ischemia, iron chelation during reperfusion of the remnant liver is associated with improvement of several parameters of oxidative stress, lung injury and arterial oxygenation.
Genetically Abnormal Circulating Cells in Lung Cancer Patients: An Antigen-Independent Fluorescence In situ Hybridization–Based Case-Control Study
Authors: Katz Ruth L. , He Weigong , Khanna Abha , Fernandez Ricardo L. , Zaidi Tanweer M. , Krebs Matthew , Caraway Nancy P. , Zhang Hua-Zhong , Jiang Feng , Spitz Margaret R. , Blowers David P. , Jimenez Carlos A. , Mehran Reza J. , Swisher Stephen G. , Roth Jack A. , Morris Jeffrey S. , Etzel Carol J. , El-Zein Randa 
Published: July 2010

Abstract
Purpose: We performed a study to determine if a fluorescence in situ hybridization (FISH)–based assay using isolated peripheral blood mononuclear cells (PBMCs) with DNA probes targeting specific sites on chromosomes known to have abnormalities in non–small cell lung cancer (NSCLC) cases could detect circulating genetically abnormal cells (CACs).
Experimental Design: We evaluated 59 NSCLC cases with stage I through IV disease and 24 controls. PBMCs and matched tumors were hybridized with 2 two-color [3p22.1/CEP3 and 10q22.3 (SP-A)/CEP10) and 2 four-color [CEP3, CEP7, CEP17, and 9p21.3 (URO); and EGFR, c-MYC, 6p11-q11, and 5p15.2 (LAV)] FISH probes. Percentages of cytogenetically abnormal cells (CACs) in peripheral blood and in matched tumor specimens were quantified by using an automated fluorescent scanner. Numbers of CACs were calculated based on the percentage of CACs (defined as PBMCs with genetic abnormalities) per milliliter of blood and expressed per microliter of blood.
Results: Patients with NSCLC had significantly higher numbers of CACs than controls. Mean number of CACs ranged from 7.23 ± 1.32/μL for deletions of 10q22.3/CEP10 to 45.52 ± 7.49/μL for deletions of 3p22.1/CEP3. Numbers of CACs with deletions of 3p22.1, 10q22.3, and 9p21.3, and gains of URO, increased significantly from early to advanced stage of disease.
Conclusions: We have developed a sensitive and quantitative antigen-independent FISH-based test for detecting CACs in peripheral blood of patients with NSCLC, which showed a significant correlation with the presence of cancer. If this pilot study can be validated in a larger study, CACs may have a role in the management of patients with NSCLC. Clin Cancer Res; 16(15); 3976–87. ©2010 AACR.
A Mutated Soluble Neuropilin-2 B Domain Antagonizes Vascular Endothelial Growth Factor Bioactivity and Inhibits Tumor Progression
Authors: Geretti Elena , van Meeteren Laurens A. , Shimizu Akio , Dudley Andrew C. , Claesson-Welsh Lena , Klagsbrun Michael 
Published: July 2010

Abstract
Neuropilins (NRP1 and NRP2) are coreceptors for vascular endothelial growth factor (VEGF) and mediate angiogenesis and tumor progression. VEGF binds to the NRP1 and NRP2 B domains. Previously, it was shown that mutagenesis of the soluble NRP2 B domain (MutB-NRP2) increased affinity to VEGF by 8-fold. Here, we show that MutB-NRP2 inhibited 125I-VEGF binding to NRP1, NRP2, and VEGFR-2. It antagonized VEGF-induced VEGFR-2/NRP2 complex formation and inhibited VEGF-induced activation of AKT, a mediator of cell survival, without affecting activation of VEGFR-2. In three-dimensional embryoid bodies, a model of VEGF-induced angiogenesis, MutB-NRP2 inhibited VEGF-induced sprouting. When overexpressed in human melanoma cells, MutB-NRP2 inhibited tumor growth compared with control tumors. Avastin (bevacizumab), a monoclonal antibody to VEGF, inhibited VEGF interactions with VEGFR-2, but not with NRPs. The combination of MutB-NRP2 and Avastin resulted in an enhanced inhibition of human melanoma tumor growth compared with MutB-NRP2 treatment only or Avastin treatment only. In conclusion, these results indicate that MutB-NRP2 is a novel antagonist of VEGF bioactivity and tumor progression. Mol Cancer Res; 8(8); 1063–73. ©2010 AACR.
Novel Function of Tenascin-C, a Matrix Protein Relevant to Atherosclerosis, in Platelet Recruitment and Activation Under Flow
Authors: Schaff Mathieu , Receveur Nicolas , Bourdon Catherine , Wurtz Virginie , Denis Cécile V. , Orend Gertraud , Gachet Christian , Lanza François , Mangin Pierre H. 
Published: July 2010

Objective—
The identification of platelet-reactive proteins exclusively present in atherosclerotic plaques could provide interesting targets for effective and safe antithrombotic strategies. In this context, we explored platelet adhesion and activation to tenascin-C (TN-C), a matrix protein preferentially found within atheroma.

Methods and Results—

We show that platelets efficiently adhere to TN-C under both static and flow conditions. Videomicroscopy revealed a unique behavior under flow, with platelets exhibiting stationary adhesion to TN-C; in contrast, platelets rolled over von Willebrand factor and detached from fibrinogen. Platelet interaction with TN-C was predominantly supported by integrin α
2
β
1
under static conditions, whereas under high shear, it was dependent on both the α
2
β
1
integrin and the glycoprotein Ib-IX complex. Integrin α
IIb
β
3
appeared to play a secondary role but only at low shear rates. The glycoprotein Ib-IX–dependent interaction was indirect, relying on von Willebrand factor, and increased as a function of wall shear rate. Von Willebrand factor bound directly to TN-C, as shown by ELISA and coimmunoprecipitation, suggesting that it acts as a bridge between TN-C and platelets. The adhesion of platelets to TN-C triggered their activation, as demonstrated by a shape change and increases in intracellular calcium level.

Conclusion—
This study provides evidence that TN-C serves as a novel adhesive matrix for platelets in a context that is relevant to atherothrombosis.
Introduction
Authors: Gregg Benjamin 
Published: July 2010

AbstractI introduce the five articles in this special issue of Comparative Sociology as each applies the theory of enlightened localism. First I outline the theory in question and then highlight those aspects that each of the authors deploys, the criticisms each levels at it, and the suggestions each offers toward its improvement. Lea Ypi applies the theory to human rights in a way that might reconcile universal norms with the need for individual motivation that can only be local. Jonathan White uses the theory to develop a conception of the European Union that would preserve rather than, as now, repress the partisan politicking at the core of democracy. Junmin Wang finds the theory helpful in analyzing the unintended decentralization of political power in China as a consequence of recent economic reforms. Ko Hasegawa seeks an enlightened localist solution to the problematic integration of a minority population into mainstream Japanese society. Manuel Ahedo enlists the theory in combating ghettoized schooling all too typical for immigrant children in Europe with ideas for integrating the children of immigrants with those of long-established residents. I conclude by listing some of the questions raised by the articles and to be addressed by future research ‐ concerns that might move an enlightened localist approach forward.
Gender Justice in a Prayer: American Muslim Women’sExegesis, Authority, and Leadership
Authors: Hammer Juliane 
Published: July 2010

AbstractThe 2005 woman-led Friday prayer in New York City generated broad media attention and significant levels of intra-Muslim debates about women’s inclusion in mosques, gender roles, and textual interpretation. This essay examines the prayer event within the larger context of American Muslim women’s contributions to reinterpretations of the Qur’an and their negotiations of religious authority, leadership roles, and mosque spaces in a North American context. The essay is based on the writings of American Muslim women on gender discourses and on media coverage, documentaries, and Internet sources produced by and about them. I argue that some of the initiatives toward gender inclusiveness in American mosques and communities should be read as an embodiment of gender-just interpretations of the Qur’an, and as products of particularly American and transnational constellations of Muslim discourses on gender. Another women’s ‘sit-in’ at the Islamic Center in Washington, D.C., in February of 2010 serves as an epilogue to the essay.
Circumventing Uncertainty in the Moral Economy: West African Shrines in Europe, Witchcraft and Secret Gambling
Authors: Parish Jane 
Published: July 2010

AbstractThis paper examines the moral economy of the African Diaspora through the illicit activities of secret Ghanaian gamblers in Europe. It follows a Ghanaian, Mr. Baba, a gambler, from North West England, who looks to the most unlikely of sources of information and certainty in a fast networked society, the Akan anti-witchcraft shrine located not in Ghana but in the eastern suburbs of Paris, as global bookmaker extraordinaire. In this environment, the anti-witchcraft shrine rather than being a traditional, obsolete relic of a superstitious past is in its supersonic element. It is able to transmit ‘hidden’ data, a valuable exchange commodity in an uncertain and insecure age, about betting odds on an infinite range of topics. At the same time, simultaneously, it protects this commodity from the grasp of witches ‐ immoral, female figures who link fraudulent facts to the relations that people have with one another.
A germline gain-of-function mutation in Ptpn11 (Shp-2) phosphatase induces myeloproliferative disease by aberrant activation of hematopoietic stem cells
Authors: Xu Dan , Wang Siying , Yu Wen-Mei , Chan Gordon , Araki Toshiyuki , Bunting Kevin D. , Neel Benjamin G. , Qu Cheng-Kui 
Published: July 2010

Abstract
Germline and somatic gain-of-function mutations in tyrosine phosphatase PTPN11 (SHP-2) are associated with juvenile myelomonocytic leukemia (JMML), a myeloproliferative disease (MPD) of early childhood. The mechanism by which PTPN11 mutations induce this disease is not fully understood. Signaling partners that mediate the pathogenic effects of PTPN11 mutations have not been explored. Here we report that germ line mutation Ptpn11D61G in mice aberrantly accelerates hematopoietic stem cell (HSC) cycling, increases the stem cell pool, and elevates short-term and long-term repopulating capabilities, leading to the development of MPD. MPD is reproduced in primary and secondary recipient mice transplanted with Ptpn11D61G/+ whole bone marrow cells or purified Lineage−Sca-1+c-Kit+ cells, but not lineage committed progenitors. The deleterious effects of Ptpn11D61G mutation on HSCs are attributable to enhancing cytokine/growth factor signaling. The aberrant HSC activities caused by Ptpn11D61G mutation are largely corrected by deletion of Gab2, a prominent interacting protein and target of Shp-2 in cell signaling. As a result, MPD phenotypes are markedly ameliorated in Ptpn11D61G/+/Gab2−/− double mutant mice. Collectively, our data suggest that oncogenic Ptpn11 induces MPD by aberrant activation of HSCs. This study also identifies Gab2 as an important mediator for the pathogenic effects of Ptpn11 mutations.
How I treat Diamond-Blackfan anemia
Authors: Vlachos Adrianna , Muir Ellen 
Published: July 2010

AbstractDiamond-Blackfan anemia (DBA) is characterized by red cell failure, the presence of congenital anomalies, and cancer predisposition. In addition to being an inherited bone marrow failure syndrome, DBA is also categorized as a ribosomopathy as, in more than 50% of cases, the syndrome appears to result from haploinsufficiency of either a small or large subunit-associated ribosomal protein. Nonetheless, the exact mechanism by which haploinsufficiency results in erythroid failure, as well as the other clinical manifestations, remains uncertain. New knowledge regarding genetic and molecular mechanisms combined with robust clinical data from several international patient registries has provided important insights into the diagnosis of DBA and may, in the future, provide new treatments as well. Diagnostic criteria have been expanded to include patients with little or no clinical findings. Patient management is therefore centered on accurate diagnosis, appropriate use of transfusions and iron chelation, corticosteroids, hematopoietic stem cell transplantation, and a coordinated multidisciplinary approach to these complex patients.
Simultaneous prediction of transcription factor binding sites in a group of prokaryotic genomes
Authors: Zhang Shaoqiang , Li Shan , Pham Phuc T , Su Zhengchang 
Published: July 2010

Abstract

Background
Our current understanding of transcription factor binding sites (TFBSs) in sequenced prokaryotic genomes is very limited due to the lack of an accurate and efficient computational method for the prediction of TFBSs at a genome scale. In an attempt to change this situation, we have recently developed a comparative genomics based algorithm called GLECLUBS for de novo genome-wide prediction of TFBSs in a target genome. Although GLECLUBS has achieved rather high prediction accuracy of TFBSs in a target genome, it is still not efficient enough to be applied to all the sequenced prokaryotic genomes.

Results
Here, we designed a new algorithm based on GLECLUBS called extended GLECLUBS (eGLECLUBS) for simultaneous prediction of TFBSs in a group of related prokaryotic genomes. When tested on a group of γ-proteobacterial genomes including E. coli K12, a group of firmicutes genomes including B. subtilis and a group of cyanobacterial genomes using the same parameter settings, eGLECLUBS predicts more than 82% of known TFBSs in extracted inter-operonic sequences in both E. coli K12 and B. subtilis. Because each genome in a group is equally treated, it is highly likely that similar prediction accuracy has been achieved for each genome in the group.

Conclusions
We have developed a new algorithm for genome-wide de novo prediction of TFBSs in a group of related prokaryotic genomes. The algorithm has achieved the same level of accuracy and robustness as its predecessor GLECLUBS, but can work on dozens of genomes at the same time.
Troglitazone suppresses telomerase activity independently of PPARγ in estrogen-receptor negative breast cancer cells
Authors: Rashid-Kolvear Fariborz , Taboski Michael AS , Nguyen Johnny , Wang Dong-Yu , Harrington Lea A , Done Susan J 
Published: July 2010

Abstract

Background
Breast cancer is one the highest causes of female cancer death worldwide. Many standard chemotherapeutic agents currently used to treat breast cancer are relatively non-specific and act on all rapidly dividing cells. In recent years, more specific targeted therapies have been introduced. It is known that telomerase is active in over 90% of breast cancer tumors but inactive in adjacent normal tissues. The prevalence of active telomerase in breast cancer patients makes telomerase an attractive therapeutic target. Recent evidence suggests that telomerase activity can be suppressed by peroxisome proliferator activated receptor gamma (PPARγ). However, its effect on telomerase regulation in breast cancer has not been investigated.

Methods
In this study, we investigated the effect of the PPARγ ligand, troglitazone, on telomerase activity in the MDA-MB-231 breast cancer cell line. Real time RT-PCR and telomerase activity assays were used to evaluate the effect of troglitazone. MDA-MB-231 cells had PPARγ expression silenced using shRNA interference.

Results
We demonstrated that troglitazone reduced the mRNA expression of hTERT and telomerase activity in the MDA-MB-231 breast cancer cell line. Troglitazone reduced telomerase activity even in the absence of PPARγ. In agreement with this result, we found no correlation between PPARγ and hTERT mRNA transcript levels in breast cancer patients. Statistical significance was determined using Pearson correlation and the paired Student's t test.

Conclusions
To our knowledge, this is the first time that the effect of troglitazone on telomerase activity in breast cancer cells has been investigated. Our data suggest that troglitazone may be used as an anti-telomerase agent; however, the mechanism underlying this inhibitory effect remains to be determined.