bluuebunny/crossref_metadata_2025_split huggingface dataset:
L'histoire oubliée des horaires individualisés : de la désynchronisation choisie à la flexibilité pour l'entreprise
Authors: Thoemmes Jens 
Published: May 2013

Les horaires individualisés au choix du salarié ont été inventés dans les entreprises au cours des années 1960. Les raisons de leur introduction étaient liées au marché du travail, à la gestion du personnel et à la fluidification des trafics urbains. La désynchronisation des temporalités selon les individus n’a pas manqué d’interpeller les employeurs et les organisations syndicales, critiques à l’égard de cette mesure. Cette innovation sociale a suscité des débats entre les partisans et les opposants de l’individualisation. Elle a conduit à des innovations techniques sur la manière d’enregistrer le temps. La tendance de fond sur un demi-siècle a conduit à la généralisation d’une codétermination des horaires de travail par les salariés eux-mêmes, mais elle n’a pas empêché l’existence de désaccords majeurs sur leur mise en œuvre : la maîtrise de l’emploi du temps pour soi-même ou la flexibilité pour l’entreprise.
Le développement des pratiques d'encadrement de la relation d'emploi dites « responsables » : essai d'analyse critique
Authors: Dubrion Benjamin 
Published: May 2013

Partant de la question du conflit d’intérêts entre employeur et employé, cet article propose un cadre d’analyse visant à clarifier le sens des pratiques d’encadrement de la relation d’emploi présentées comme « responsables » et qui se développent depuis quelques années avec l’essor de la responsabilité sociale de l’entreprise (RSE). À la lumière de développements économiques et gestionnaires mobilisés dans le champ de la théorie des organisations et de travaux empiriques menés ces dernières années sur ces pratiques, nous montrons en quoi celles-ci sont ambivalentes et peuvent ne pas toujours être porteuses de changements radicaux en matière de gestion des ressources humaines.
HLA Class I Antibodies Trigger Increased Adherence of Monocytes to Endothelial Cells by Eliciting an Increase in Endothelial P-Selectin and, Depending on Subclass, by Engaging FcγRs
Authors: Valenzuela Nicole M. , Mulder Arend , Reed Elaine F. 
Published: May 2013

Abstract
Ab-mediated rejection (AMR) of solid organ transplants is characterized by intragraft macrophages. It is incompletely understood how donor-specific Ab binding to graft endothelium promotes monocyte adhesion, and what, if any, contribution is made by the Fc region of the Ab. We investigated the mechanisms underlying monocyte recruitment by HLA class I (HLA I) Ab–activated endothelium. We used a panel of murine mAbs of different subclasses to crosslink HLA I on human aortic, venous, and microvascular endothelial cells and measured the binding of human monocytic cell lines and peripheral blood monocytes. Both anti–HLA I murine (m)IgG1 and mIgG2a induced endothelial P-selectin, which was required for monocyte adhesion to endothelium irrespective of subclass. mIgG2a but not mIgG1 could bind human FcγRs. Accordingly, HLA I mIgG2a but not mIgG1 treatment of endothelial cells significantly augmented recruitment, predominantly through FcγRI, and, to a lesser extent, FcγRIIa. Moreover, HLA I mIgG2a promoted firm adhesion of monocytes to ICAM-1 through Mac-1, which may explain the prominence of monocytes during AMR. We confirmed these observations using human HLA allele-specific mAbs and IgG purified from transplant patient sera. HLA I Abs universally elicit endothelial exocytosis leading to monocyte adherence, implying that P-selectin is a putative therapeutic target to prevent macrophage infiltration during AMR. Importantly, the subclass of donor-specific Ab may influence its pathogenesis. These results imply that human IgG1 and human IgG3 should have a greater capacity to trigger monocyte infiltration into the graft than IgG2 or IgG4 due to enhancement by FcγR interactions.
Metabolic Adaptation of Neutrophils in Cystic Fibrosis Airways Involves Distinct Shifts in Nutrient Transporter Expression
Authors: Laval Julie , Touhami Jawida , Herzenberg Leonore A. , Conrad Carol , Taylor Naomi , Battini Jean-Luc , Sitbon Marc , Tirouvanziam Rabindra 
Published: May 2013

Abstract
Inflammatory conditions can profoundly alter human neutrophils, a leukocyte subset generally viewed as terminally differentiated and catabolic. In cystic fibrosis (CF) patients, neutrophils recruited to CF airways show active exocytosis and sustained phosphorylation of prosurvival, metabolic pathways. Because the CF airway lumen is also characterized by high levels of free glucose and amino acids, we compared surface expression of Glut1 (glucose) and ASCT2 (neutral amino acids) transporters, as well as that of PiT1 and PiT2 (inorganic phosphate transporters), in blood and airway neutrophils, using specific retroviral envelope-derived ligands. Neither nutrient transporter expression nor glucose uptake was altered on blood neutrophils from CF patients compared with healthy controls. Notably, however, airway neutrophils of CF patients had higher levels of PiT1 and Glut1 and increased glucose uptake compared with their blood counterparts. Based on primary granule exocytosis and scatter profiles, CF airway neutrophils could be divided into two subsets, with one of the subsets characterized by more salient increases in Glut1, ASCT2, PiT1, and PiT2 expression. Moreover, in vitro exocytosis assays of blood neutrophils suggest that surface nutrient transporter expression is not directly associated with primary (or secondary) granule exocytosis. Although expression of nutrient transporters on CF blood or airway neutrophils was not altered by genotype, age, gender, or Pseudomonas aeruginosa infection, oral steroid treatment decreased Glut1 and PiT2 levels in blood neutrophils. Thus, neutrophils recruited from blood into the CF airway lumen display augmented cell surface nutrient transporter expression and glucose uptake, consistent with metabolic adaptation.
Monocyte-Derived IL-5 Reduces TNF Production byMycobacterium tuberculosis–specific CD4 T Cells during SIV/M. tuberculosisCoinfection
Authors: Diedrich Collin R. , Mattila Joshua T. , Flynn JoAnne L. 
Published: May 2013

AbstractHIV-infected individuals are significantly more susceptible to tuberculosis (TB) than uninfected individuals. Although it is established that HIV reduces Mycobacterium tuberculosis–specific T cell responses, the causes of this dysfunction are not known. We used the cynomolgus macaque model of TB to demonstrate that ex vivo SIV reduces the frequency of M. tuberculosis–specific TNF and IFN-γ–producing T cells within 24 h after infection. In vivo, T cell IFN-γ responses in granulomas from animals with SIV/M. tuberculosis coinfection were lower than SIV-negative animals with active TB. The SIV effects on the inhibition of T cell responses were primarily on APCs and not the T cells directly. Specifically, reductions in the frequency of TNF-producing M. tuberculosis–specific CD4 T cells were caused, at least in part, by SIV-induced production of monocyte derived IL-5.
Mutated PPP1R3B Is Recognized by T Cells Used To Treat a Melanoma Patient Who Experienced a Durable Complete Tumor Regression
Authors: Lu Yong-Chen , Yao Xin , Li Yong F. , El-Gamil Mona , Dudley Mark E. , Yang James C. , Almeida Jorge R. , Douek Daniel C. , Samuels Yardena , Rosenberg Steven A. , Robbins Paul F. 
Published: May 2013

Abstract
Adoptive cell therapy with tumor-infiltrating lymphocytes (TILs) represents an effective treatment for patients with metastatic melanoma. However, most of the Ag targets recognized by effective melanoma-reactive TILs remain elusive. In this study, patient 2369 experienced a complete response, including regressions of bulky liver tumor masses, ongoing beyond 7 y following adoptive TIL transfer. The screening of a cDNA library generated from the autologous melanoma cell line resulted in the isolation of a mutated protein phosphatase 1, regulatory (inhibitor) subunit 3B (PPP1R3B) gene product. The mutated PPP1R3B peptide represents the immunodominant epitope recognized by tumor-reactive T cells in TIL 2369. Five years following adoptive transfer, peripheral blood T lymphocytes obtained from patient 2369 recognized the mutated PPP1R3B epitope. These results demonstrate that adoptive T cell therapy targeting a tumor-specific Ag can mediate long-term survival for a patient with metastatic melanoma. This study also provides an impetus to develop personalized immunotherapy targeting tumor-specific, mutated Ags.
Superantigen-Induced Steroid Resistance Depends on Activation of Phospholipase Cβ2
Authors: Verhaar Auke P. , Wildenberg Manon E. , Duijvestein Marjolijn , Vos Anne Christine W. , Peppelenbosch Maikel P. , Löwenberg Mark , Hommes Daniel W. , van den Brink Gijs R. 
Published: May 2013

Abstract
The glucocorticoid receptor is present in a TCR-associated complex, which includes the Src family tyrosine kinase Lck. Glucocorticoids rapidly dissociate this complex, resulting in the inhibition of canonical Lck-phospholipase C (PLC)γ–dependent TCR signaling. The relative importance of this nongenomic role for the glucocorticoid receptor compared with its direct transcriptional effects is not known. Superantigens induce a state of steroid resistance in activated T cells. It was reported that, in addition to canonical Lck-PLCγ signaling, superantigens can activate a noncanonical G protein–PLCβ–dependent signaling pathway. In this study, we show that staphylococcal enterotoxin B activates a Gαq and PLCβ2–dependent pathway in human T cells. We find that this pathway bypasses the need for canonical Lck-PLCγ signaling in T cell activation and renders superantigen-stimulated T cells insensitive to glucocorticoids in vitro. We show that the PLCβ inhibitor U-73122 sensitizes staphylococcal enterotoxin B–treated mice to dexamethasone in vivo. In conclusion, we find that effects of glucocorticoids on TCR-induced T cell proliferation are mainly nongenomic and can be bypassed by the activation of an Lck-independent signaling pathway.
Pleiotropic Potential of Dehydroxymethylepoxyquinomicin for NF-κB Suppression via Reactive Oxygen Species and Unfolded Protein Response
Authors: Nakajima Shotaro , Kato Hironori , Gu Liubao , Takahashi Shuhei , Johno Hisashi , Umezawa Kazuo , Kitamura Masanori 
Published: May 2013

Abstract
Dehydroxymethylepoxyquinomicin (DHMEQ) is a low-m.w. compound that strongly inhibits NF-κB. Previous reports showed that DHMEQ directly binds to specific cysteine residues of NF-κB subunits and thereby inhibits their nuclear translocation and DNA binding. In this work, we describe novel mechanisms by which DHMEQ suppresses cytokine-triggered activation of NF-κB. We found that sustained exposure of renal tubular cells to DHMEQ blocked TNF-α– and IL-1β–induced TGF-β–activated kinase 1 (TAK1) phosphorylation, a crucial event for NF-κB activation upstream of IκB kinase. This inhibition was mediated by reactive oxygen species (ROS), because of the following: 1) DHMEQ caused generation of ROS; 2) pretreatment with ROS generator inhibited cytokine-induced TAK1 phosphorylation and NF-κB activation; and 3) scavenging of ROS attenuated the suppressive effects of DHMEQ on TAK1 and NF-κB. We also found that DHMEQ caused the unfolded protein response (UPR) through generation of ROS. Alleviation of the UPR by chemical and genetic chaperones partially attenuated the suppressive effect of DHMEQ on NF-κB. The UPR-mediated inhibition of NF-κB occurred downstream of degradation of IκBα and phosphorylation of p65. Subsequent experiments revealed the following: 1) DHMEQ caused selective induction of C/EBPβ through the UPR; 2) overexpression of C/EBPβ suppressed activation of NF-κB; 3) knockdown of C/EBPβ attenuated the inhibitory effect of DHMEQ; and 4) DHMEQ-induced expression of C/EBPβ did not affect TNF-α–triggered degradation of IκBα and phosphorylation of p65. These results suggest that, in addition to its known effect on nuclear translocation of NF-κB, DHMEQ interferes with the cytokine-induced NF-κB signaling via generation of ROS at both upstream and downstream of the IκB kinase–IκB level.
Y Chromosome–Linked B and NK Cell Deficiency in Mice
Authors: Sun Shu-lan , Horino Satoshi , Itoh-Nakadai Ari , Kawabe Takeshi , Asao Atsuko , Takahashi Takeshi , So Takanori , Funayama Ryo , Kondo Motonari , Saitsu Hirotomo , Matsumoto Naomichi , Nakayama Keiko , Ishii Naoto 
Published: May 2013

Abstract
There are no primary immunodeficiency diseases linked to the Y chromosome, because the Y chromosome does not contain any vital genes. We have established a novel mouse strain in which all males lack B and NK cells and have Peyer’s patch defects. By 10 wk of age, 100% of the males had evident immunodeficiencies. Mating these immunodeficient males with wild-type females on two different genetic backgrounds for several generations demonstrated that the immunodeficiency is linked to the Y chromosome and is inherited in a Mendelian fashion. Although multicolor fluorescence in situ hybridization analysis showed that the Y chromosome in the mutant male mice was one third shorter than that in wild-type males, exome sequencing did not identify any significant gene mutations. The precise molecular mechanisms are still unknown. Bone marrow chimeric analyses demonstrated that an intrinsic abnormality in bone marrow hematopoietic cells causes the B and NK cell defects. Interestingly, fetal liver cells transplanted from the mutant male mice reconstituted B and NK cells in lymphocyte-deficient Il2rg−/− recipient mice, whereas adult bone marrow transplants did not. Transducing the EBF gene, a master transcription factor for B cell development, into mutant hematopoietic progenitor cells rescued B cell but not NK cell development both in vitro and in vivo. These Y chromosome–linked immunodeficient mice, which have preferential B and NK cell defects, may be a useful model of lymphocyte development.
The Proto-Oncogene c-mycRegulates Antibody Secretion and Ig Class Switch Recombination
Authors: Fernández David , Ortiz Maitane , Rodríguez Lorena , García Arancha , Martinez Dolores , Moreno de Alborán Ignacio 
Published: May 2013

AbstractThe immune response involves the generation of Ab-secreting cells and memory B cells through a process called terminal B lymphocyte differentiation. This program requires the transcriptional repressor Blimp-1, which inhibits c-myc expression and terminates proliferation. Although the role of c-Myc in cell proliferation is well characterized, it is not known whether it has other functions in terminal differentiation. In this study, we show that c-Myc not only regulates cell proliferation, but it is also essential for Ab-secreting cell function and differentiation in vivo. c-Myc–deficient B lymphocytes hypersecrete IgM and do not undergo Ig class switch recombination (CSR). CSR has been previously linked to proliferation, and in this study we mechanistically link class switching and proliferation via c-Myc. We observed that c-Myc regulates CSR by transcriptionally activating the B cell–specific factor activation-induced cytidine deaminase. By linking cell proliferation and CSR, c-Myc is thus a critical component for a potent immune response
K-theory of Furstenberg Transformation Group C*-algebras
Authors: Reihani Kamran 
Published: May 2013

AbstractThis paper studies the K-theoretic invariants of the crossed product C*-algebras associated with an important family of homeomorphisms of the tori Tn called Furstenberg transformations. Using the Pimsner–Voiculescu theorem, we prove that given n, the K-groups of those crossed products whose corresponding n × n integer matrices are unipotent of maximal degree always have the same rank an. We show using the theory developed here that a claim made in the literature about the torsion subgroups of these K-groups is false. Using the representation theory of the simple Lie algebra sl(2;C), we show that, remarkably, an has a combinatorial significance. For example, every a2n+1 is just the number of ways that 0 can be represented as a sum of integers between–n and n (with no repetitions). By adapting an argument of van Lint (in which he answered a question of Erdős), a simple explicit formula for the asymptotic behavior of the sequence {an} is given. Finally, we describe the order structure of the K0-groups of an important class of Furstenberg crossed products, obtaining their complete Elliott invariant using classification results of H. Lin and N. C. Phillips.
Curvature of K-contact Semi-Riemannian Manifolds
Authors: Perrone Domenico 
Published: May 2013

Abstract.In this paper we characterize K-contact semi-Riemannian manifolds and Sasakian semi- Riemannian manifolds in terms of curvature. Moreover, we show that any conformally flat K-contact semi-Riemannian manifold is Sasakian and of constant sectional curvature κ = ɛ, where ɛ = ± denotes the causal character of the Reeb vector field. Finally, we give some results about the curvature of a K-contact Lorentzian manifold.
An Occupational Therapy Intervention Service to Hostels for Homeless People: An Overview
Authors: Parmenter Vanessa , Fieldhouse Jon , Barham Ruth 
Published: May 2013

This evaluation of an Occupational Therapy Intervention Service within homeless persons' hostels in Bristol, England, highlights the efficacy of occupational therapy with this service user group and reflects on the practicalities of delivering such a service in an inter-agency context. Occupational therapy engaged homeless individuals with complex needs who were often defended against change in their own lives. Over 7 months an Occupational Therapy Intervention Service provided an individual service for 16 residents and made a further 542 contacts through group work. The creation of psychosocial microenvironments within hostels allowed individuals to experience themselves differently and contemplate the possibility of change. The importance of collaborative working between occupational therapists and hostel staff is examined in the light of the psychologically informed environments agenda.
Programa nacional de crédito da agricultura familiar e impactos nas economias locais no estado do Paraná
Authors: Antunes Rodrigo Lopes , Camara Marcia Regina Gabardo , Nascimento Sidnei Pereira do , Sereia Vanderlei José , Anhesini João Amilcar Rodrigues 
Published: May 2013

O objetivo deste artigo é analisar o impacto do programa nacional de crédito para a agricultura familiar (PRONAF) na economia de 60 municípios paranaenses que contrataram crédito entre 2000 e 2005. A evolução do crédito rural mostra que a partir da década de 1990, há expansão dos contratos e dos recursos; sua intensificação ocorre após 1999, quando introduz a diferenciação entre os agricultores familiares. A agricultura familiar tem grande importância para a economia paranaense, respondendo por 45% da produção das principais culturas e 65% dos animais. O estudo é empírico, de natureza econométrica, de corte transversal, tem por finalidade verificar o efeito dos recursos do PRONAF sobre as dimensões sociais, tributária e produtiva do Estado. Conclui-se que há relações estatisticamente significativas entre o PRONAF e as variáveis selecionadas para análise e que após 13 anos de sua institucionalização, continua cumprindo o objetivo de promover o desenvolvimento da agricultura familiar.
La franco-américanité de Louis Dantin vue à travers son amitié littéraire avec Marine Leland
Authors: Godbout Patricia 
Published: May 2013

Cet article met en relief l’importance de l’amitié littéraire entre Louis Dantin et Marine Leland, professeure de français du Smith College, au Massachusetts. Leland fait la connaissance de Dantin à Boston au début de la décennie 1940, c’est-à-dire vers la fin de la vie de Dantin. La découverte de l’oeuvre critique et poétique de cet écrivain par Leland sera très importante. Cette amitié littéraire est l’occasion d’examiner notamment ici le rapport qu’a entretenu Louis Dantin avec la « franco-américanie ».
Le Lascaux Mont-Royal de Normand de Bellefeuille et la honte du passé québécois
Authors: Laforest Daniel 
Published: May 2013

Cet article examine un motif central de l’oeuvre de Normand de Bellefeuille — le temps immémorial de la caverne de Lascaux — afin de montrer comment celui-ci contribue à une conception originale de la situation de l’écrivain québécois dans l’histoire sociale des cinquante dernières années. Le temps d’avant ayant été occupé par la misère historique indépassable des aïeux, comment interroger d’où l’on vient avec l’écriture sans produire une relativité qui aurait pour effet d’enterrer définitivement ceux-ci ? Comment accepter, au-delà du soupçon et des architectures théoriques du formalisme, que l’on est soi-même pétri d’histoire ?
Growth hormone receptor (GHR) gene polymorphism and prader–willi syndrome
Authors: Butler Merlin G. , Roberts Jennifer , Hayes Jena , Tan Xiaoyu , Manzardo Ann M. 
Published: May 2013

AbstractPrader–Willi syndrome (PWS) is a genomic imprinting disorder due to loss of paternally expressed genes in the 15q11–q13 region and characterized by hypotonia, a poor suck, failure to thrive, hypogonadism/hypogenitalism, growth hormone deficiency, learning, and behavioral problems and hyperphagia leading to early childhood obesity. Growth hormone acts as a ligand for the growth hormone receptor (GHR) coded by a gene polymorphic for an exon‐3 deletion (d3) seen in about 50% of Caucasians and associated with an increased response to growth hormone (GH) therapy. We examined 69 individuals with PWS (average age ± SD = 20.1 ± 12.8 year). The GHR allele distribution in our PWS subjects was similar to reported data in the literature with no gender or PWS genetic subtype differences. A negative correlation was found with age for height standard deviational scores and a positive correlation with age for weight and BMI for non‐GH treated PWS subjects. Adjusting for effects of age and gender, individuals with PWS and the d3/d3 allele showed a significant increase in BMI compared with those having the full length (fl) allele. In addition, 12 infants and children with PWS were examined when growth and GH data were available before and during GH treatment. A significant increase in growth rate (1.7 times) was noted in the presence of the d3 allele (fl/fl = 0.87 cm/month; fl/d3 or d3/d3 = 1.5 cm/month; P < 0.05). The presence of the d3 allele and its impact on growth and medical care of individuals with PWS while on GH therapy should be further investigated. © 2013 Wiley Periodicals, Inc.
In vivo metabolism study of bergenin in rats by HPLC‐QTOF mass spectrometry
Authors: Song Haojing , Wang Jin , Zhang Rui , Liu Xiaoyan , Yuan Guiyan , Wei Chunmin , Zhao Wenjing , Li Rong , Wang Benjie , Guo Ruichen 
Published: May 2013

ABSTRACTBergenin is the major component of Ardisia creanta sims and Rodgersia sambucifolia hemsl with many biological activities. Although bergenin has been used to treat human diseases in China for man years, there is no report regarding its metabolism. This is the first report to separate and identify the metabolites of bergenin in vivo. In the study, HPLC/Q‐TOF‐MS/MS was used to investigate the metabolites of bergenin in vivo by analyzing the rat body fluid and feces samples. Three metabolites of bergenin were finally identified by the TIC chromatograms, and the structures were also confirmed by their MS2 spectra. Copyright © 2013 John Wiley & Sons, Ltd.