bluuebunny/crossref_metadata_2025_split huggingface dataset:
Uterine Rupture - Experience of 30 Cases at Faridpur Medical College Hospital
Authors: Mahbuba Dr , Alam Irin Parveen 
Published: January 2013

Rupture uterus is a rare and often catastrophic condition. It is associated with a high incidence of fetal and maternal mortality and morbidity. Our objective in this study is to determine incidence, etiology, trend, management, maternal and fetal outcome of uterine rupture in Faridpur Medical College Hospital. This is a prospective cross-sectional study of patients with ruptured uterus from the period of January 2011 to December 2011 admitted at Faridpur Medical College Hospital. All the cases of ruptured uterus who were either admitted with uterine rupture or who developed it in hospital were included in the study. Patients having ruptured uterus due to congenital anomaly were excluded from the study. Patients were initially assessed in labour ward, relevant sociodemographic data, previous antenatal and surgical history recorded. Ways of management, maternal and fetal outcome were taken for analysis. There were 30 cases of ruptured uterus out of total 3606 deliveries (including 1809 caesarian sections) over a one year time period, with a prevalence of 0.83%. The most common age group was 21-30 years. A majority of patients 16(53.3%) were cases of unscarred uterus presenting with rupture; the common cause of rupture in scarred uterus was injudicious use of oxytocin (13,43.33%). Proper antenatal care, appropriate counseling of patients with history of previous caesarian section for hospital delivery, training of skilled birth attendant can reduce mortality and morbidity due to rupture uterus. DOI: http://dx.doi.org/10.3329/fmcj.v7i2.13504 Faridpur Med. Coll. J. 2012;7(2):79-81
Hyperinfection with Strongyloides stercoralis in an Immunosuppressed Patient
Authors: Masud Hasan , Sarker Md Khalequzzaman , Rana Mushtaque Ahmad , Ahmed Dewan Saifuddin , Islam MM Shahin Ul , Raihan ASMA 
Published: January 2013

Strongyloides stercoralis is a common intestinal parasite in tropics and subtropics. In Bangladesh, prevalence is likely to be high due to poor sanitation. Clinical presentations are frequently nonspecific. However, in immunosuppressed individuals, infection becomes overwhelming and may disseminate and results in high rates of mortality. Unless a high index of suspicion, this readily treatable disease may be missed. Here we report a case of hyperinfection with Strongyloides stercoralis in a patient who was on corticosteroid treatment. A 45 years old male was admitted in Gastroenterology department of Bangabandhu Sheikh Mujib Medical University (BSMMU) with the complaints of abdominal pain, vomiting and diarrhea for 2 weeks. He was on prednisolone 60 mg with omeprazole 40 mg daily for 4 weeks for his eyelid drooping prior to the development of abdominal symptoms. Physical examination revealed a severely malnourished, moderately anemic patient with muscle wasting, angular stomatitis, desquamated skins of feet and hands. Abdominal examination revealed generalized tenderness with moderate ascites. Investigations revealed Hb-7.4 gm/dl with normal WBC count (eosinophil-11% before steroid therapy), S.albumin-19gm/l with prolonged prothrombin time and hypokalemia. USG of abdomen revealed moderate ascites. Endoscopy of upper GIT showed congestion and multiple erosions in the stomach and also in the duodenum. Biopsy from the duodenum revealed adult Strongyloides stercoralis on the surface, larva and ova in the duodenal crypts. The patient was treated with 10 days of oral ivermectin along with blood transfusion, correction of nutritional status and electrolyte imbalance. Patient was discharged home after a total of 20 days of hospitalization DOI: http://dx.doi.org/10.3329/fmcj.v7i2.13526 Faridpur Med. Coll. J. 2012;7(2):98-101
Pressions budgétaires à l'hôpital : une étude qualitative du concept de « RAPM » auprès de praticiens hospitaliers
Authors: Georgescu Irène , Naro Gérald 
Published: January 2013

Résumé En se basant sur le courant « Reliance on Accounting Performance Measures » (RAPM) cet article a pour objectif de proposer une réflexion sur les effets du contrôle des résultats introduit à l’hôpital public. Ce travail exploratoire, réalisé à partir de 31 entretiens semi-directifs, tente de comprendre la problématique du RAPM ainsi que ses effets sur les attitudes et les comportements des professionnels du secteur hospitalier public. Les résultats révèlent l’existence d’une pression budgétaire qui s’accompagne de conflits de rôle, des résistances et une tendance à la manipulation de données. En soulignant le caractère réducteur des précédents travaux menés dans le champ du RAPM, l’étude propose d’intégrer dans la compréhension du phénomène, les dimensions organisationnelles et institutionnelles de l’hôpital.
Les dimensions de la performance des cabinets d'audit légal – Le point de vue des auditeurs
Authors: Causse Geneviève , Vu Viet Ha Tran 
Published: January 2013

Résumé La présente recherche étudie les dimensions de la performance des cabinets d’audit, dans leur mission d’audit légal des comptes, telles que perçues par les auditeurs eux-mêmes. L’outil d’analyse de la performance se présente sous la forme d’un tableau de bord stratégique intégré. La construction de l’échelle de mesure suit la démarche préconisée par Churchill (1979). L’étude met en évidence les dimensions de la performance des cabinets d’audit retenues par les auditeurs français. Les résultats de l’étude font apparaître que parmi les axes d’analyse – Finance, Client, Processus, Capital humain – les dimensions de la performance retenues ont toutes trait aux trois derniers axes. Aucune des dimensions de l’axe Finance n’est validée. Un autre apport de l’étude est le lien établi entre la vision de la performance et la classification des cabinets. Une analyse typologique a permis de répartir les cabinets en quatre groupes : les réputés, les normatifs, les adaptatifs et les passifs.
La conscience dominante. Rapports sociaux de race et subjectivation
Authors: Cervulle Maxime 
Published: January 2013

Résumé À partir des travaux britanniques et états-uniens conduits depuis la fin des années 1980 autour de la construction sociale et historique des identités blanches et de leur articulation avec le racisme systémique, cet article propose d’ouvrir quelques pistes de réflexions théoriques relatives à ce que le concept de ‘blanchité’ permet de penser. Il s’agit, en particulier, de saisir les formes et modalités de la conscience des dominants, afin de détisser les trames de subjectivation raciales qui, malgré la contestation scientifique des théories racialistes, semblent perdurer, ainsi que de considérer le racisme en tant que « champ d’action positive », c’est-à-dire générant des sujets. L’enjeu est donc d’appréhender les pratiques de soi par lesquelles se constitue un sujet blanc, afin de saisir les formes de consentement tacite à la domination que manifestent ceux et celles qui en seraient les bénéficiaires.
La langue, l'éducateur et la psychose
Authors: Lego Gaëlle 
Published: January 2013

Résumé L’avancée du libéralisme et de la technoscience produit quelque chose d’inédit dans le lien social aujourd’hui. Des nouveaux termes émergent, plus en vogue avec les signifiants de cette nouvelle modernité : l’homme devient une machine à réparer à l’infini, niant ainsi la castration. La catégorie de l’impossible ne fait plus point de butée, et l’être entend satisfaire ses besoins au travers d’une accumulation d’objets-gadgets. Pourtant, la pratique éducative, la civilisation se soutiennent d’une soustraction de jouissance et d’un rapport à l’altérité. Nous verrons, à partir d’une vignette clinique, comment le « travail à plusieurs » en institution permet de soutenir un acte orienté par une éthique.
Lettre aux acteurs
Authors: Maier Anna 
Published: January 2013

Résumé Cet article est celui d’une jeune étudiante qui a travaillé dans un ehpad lors de deux remplacements d’été. Elle parle avec une grande tendresse des vieux et proteste avec vigueur contre la manière dont ils sont traités par manque de personnel, de temps, de réflexion d’équipe. Elle parle des « enjeux humains quotidiens de la structure » et dénonce la façon dont le système y répond au moyen de protocoles, en « stérilisant le langage ».
La parentalité à l'épreuve de la responsabilisation juridique
Authors: Haudiquet Agathe , Roekens Nathalie 
Published: January 2013

Résumé Avec l’avènement de l’individualisme juridique, on a assisté à celui de la responsabilisation juridique, chacun étant responsable du respect de ses droits. La responsabilité existe depuis que le système juridique est né, mais on constate que son champ continue de s’élargir au fil du temps, sans épargner la sphère familiale. Le droit français n’a cessé de responsabiliser les acteurs de la sphère familiale, y compris l’enfant, leur conférant un ensemble de droits et de devoirs, constituant autant de prétextes à une responsabilisation juridique galopante et symptomatique d’une société reposant sur un système juridique individualiste. Ainsi, la famille (et à travers elle la parentalité) en tant qu’institution, unité, se trouve être « malmenée ». Cela est dû au fait que les relations juridiques qui unissent les membres d’une famille créent des droits et des obligations réciproques, le droit de l’un s’affirmant à travers l’obligation de l’autre, allant parfois jusqu’à générer des situations paradoxales.
Peripheral Blood NK Cells from Breast Cancer Patients Are Tumor-Induced Composite Subsets
Authors: Mamessier Emilie , Pradel Lydie C. , Thibult Marie-Laure , Drevet Charlotte , Zouine Atika , Jacquemier Jocelyne , Houvenaeghel Gilles , Bertucci François , Birnbaum Daniel , Olive Daniel 
Published: January 2013

AbstractHuman NK lymphocytes are involved in antitumor immunity. The therapeutic potential of this population against cancers has stimulated their study and led to the discovery of several NK cell subsets, each of which is endowed with different immunoregulatory functions. We have previously reported that NK cell functions are profoundly altered in advanced breast cancer patients. In this study, we show that these tumor-mediated alterations also variably affect NK cell subsets. We found that in addition to the known human CD56dimCD16+, CD56brightCD16−, and CD56−CD16+ NK cell subsets, two additional subsets, namely the CD56brightCD16+ and CD56dimCD16− subsets, were increased in the peripheral blood of patients with advanced invasive breast cancers. These subsets corresponded to the main two subsets found at the tumor site. The extensive phenotype of these subsets revealed an “à la carte” pattern of expression for the various NK receptors, functional molecules, adhesion molecules, and chemokine receptors, depending on the subset. We next compared these subsets to known NK cell populations endowed with specific phenotypic characteristics, but also with functional properties. Our data show that advanced breast cancer patients have an increased proportion of more immature and noncytotoxic NK cell subsets in their peripheral blood, which might account for at least part of the low cytotoxic functions observed in these patients. They reveal a major heterogeneity and plasticity of the NK cell compartment, which are both tightly linked to the microenvironment. The identification of NK cell subsets endowed with particular functional capabilities might help monitor residual antitumor NK cell-mediated responses in breast cancer patients.
Kidins220/ARMS Associates with B-Raf and the TCR, Promoting Sustained Erk Signaling in T Cells
Authors: Deswal Sumit , Meyer Anja , Fiala Gina J. , Eisenhardt Anja E. , Schmitt Lisa C. , Salek Mogjiborahman , Brummer Tilman , Acuto Oreste , Schamel Wolfgang W. A. 
Published: January 2013

AbstractThe activation kinetics of MAPK Erk are critical for T cell development and activation. In particular, sustained Erk signaling is required for T cell activation and effector functions, such as IL-2 production. Although Raf-1 triggers transient Erk activation, B-Raf is implicated in sustained Erk signaling after TCR stimulation. In this study, we show that B-Raf is dephosphorylated on its inhibitory serine 365 upon TCR triggering. However, it is unknown how B-Raf activation is coupled to the TCR. Using mass spectrometry, we identified protein kinase D–interacting substrate of 220 kDa (Kidins220)/ankyrin repeat-rich membrane spanning protein, mammalian target of rapamycin, Rictor, Dock2, and GM130 as novel B-Raf interaction partners. We focused on Kidins220, a protein that has been studied in neuronal cells and found that it associated with the pre-TCR, αβTCR, and γδTCR. Upon prolonged TCR stimulation, the Kidins220–TCR interaction was reduced, as demonstrated by immunoprecipitation and proximity ligation assays. We show that Kidins220 is required for TCR-induced sustained, but not transient, Erk activation. Consequently, induction of the immediate early gene products and transcription factors c-Fos and Erg-1 was blocked, and upregulation of the activation markers CD69, IL-2, and IFN-γ was reduced. Further, Kidins220 was required for optimal calcium signaling. In conclusion, we describe Kidins220 as a novel TCR-interacting protein that couples B-Raf to the TCR. Kidins220 is mandatory for sustained Erk signaling; thus, it is crucial for TCR-mediated T cell activation.
Computational Identification of Antigen-Binding Antibody Fragments
Authors: Burkovitz Anat , Leiderman Olga , Sela-Culang Inbal , Byk Gerardo , Ofran Yanay 
Published: January 2013

AbstractDetermining which parts of the Ab are essential for Ag recognition and binding is crucial for understanding B cell–mediated immunity. Identification of fragments of Abs that maintain specificity to the Ag will also allow for the development of improved Ab-based therapy and diagnostics. In this article, we show that structural analysis of Ab–Ag complexes reveals which fragments of the Ab may bind the Ag on their own. In particular, it is possible to predict whether a given CDR is likely to bind the Ag as a peptide by analyzing the energetic contribution of each CDR to Ag binding and by assessing to what extent the interaction between that CDR and the Ag depends on other CDRs. To demonstrate this, we analyzed five Ab–Ag complexes and predicted for each of them which of the CDRs may bind the Ag on its own as a peptide. We then show that these predictions are in agreement with our experimental analysis and with previously published experimental results. These findings promote our understanding of the modular nature of Ab–Ag interactions and lay the foundation for the rational design of active CDR-derived peptides.
Keratinocyte Overexpression of IL-17C Promotes Psoriasiform Skin Inflammation
Authors: Johnston Andrew , Fritz Yi , Dawes Sean M. , Diaconu Doina , Al-Attar Paul M. , Guzman Andrew M. , Chen Cynthia S. , Fu Wen , Gudjonsson Johann E. , McCormick Thomas S. , Ward Nicole L. 
Published: January 2013

Abstract
IL-17C is a functionally distinct member of the IL-17 family that binds IL-17 receptor E/A to promote innate defense in epithelial cells and regulate Th17 cell differentiation. We demonstrate that IL-17C (not IL-17A) is the most abundant IL-17 isoform in lesional psoriasis skin (1058 versus 8 pg/ml; p &lt; 0.006) and localizes to keratinocytes (KCs), endothelial cells (ECs), and leukocytes. ECs stimulated with IL-17C produce increased TNF-α and KCs stimulated with IL-17C/TNF-α produce similar inflammatory gene response patterns as those elicited by IL-17A/TNF-α, including increases in IL-17C, TNF-α, IL-8, IL-1α/β, IL-1F5, IL-1F9, IL-6, IL-19, CCL20, S100A7/A8/A9, DEFB4, lipocalin 2, and peptidase inhibitor 3 (p &lt; 0.05), indicating a positive proinflammatory feedback loop between the epidermis and ECs. Psoriasis patients treated with etanercept rapidly decrease cutaneous IL-17C levels, suggesting IL-17C/TNF-α–mediated inflammatory signaling is critical for psoriasis pathogenesis. Mice genetically engineered to overexpress IL-17C in KCs develop well-demarcated areas of erythematous, flakey involved skin adjacent to areas of normal-appearing uninvolved skin despite increased IL-17C expression in both areas (p &lt; 0.05). Uninvolved skin displays increased angiogenesis and elevated S100A8/A9 expression (p &lt; 0.05) but no epidermal hyperplasia, whereas involved skin exhibits robust epidermal hyperplasia, increased angiogenesis and leukocyte infiltration, and upregulated TNF-α, IL-1α/β, IL-17A/F, IL-23p19, vascular endothelial growth factor, IL-6, and CCL20 (p &lt; 0.05), suggesting that IL-17C, when coupled with other proinflammatory signals, initiates the development of psoriasiform dermatitis. This skin phenotype was significantly improved following 8 wk of TNF-α inhibition. These findings identify a role for IL-17C in skin inflammation and suggest a pathogenic function for the elevated IL-17C observed in lesional psoriasis skin.
Butyrophilin-like 2 Modulates B7 Costimulation To Induce Foxp3 Expression and Regulatory T Cell Development in Mature T Cells
Authors: Swanson Ryan M. , Gavin Marc A. , Escobar Sabine S. , Rottman James B. , Lipsky Brian P. , Dube Shishir , Li Li , Bigler Jeannette , Wolfson Martin , Arnett Heather A. , Viney Joanne L. 
Published: January 2013

Abstract
Naive T cell activation involves at least two signals from an APC, one through the TCR via interaction with peptide–MHC complexes and a second through ligation of CD28 with B7 ligands. Following activation, T cells upregulate a host of other membrane-bound costimulatory molecules that can either promote or inhibit further T cell maturation and proliferation. In some cases, it is necessary to attenuate T cell activation to prevent deleterious inflammation, and inhibitory members of the B7/butyrophilin family of ligands have evolved to balance the strong stimuli the activating B7 ligands confer. Human genetic association and in vitro studies have implicated one such ligand, BTNL2, in controlling inflammation at mucosal surfaces. In this study, we show that recombinant mouse BTNL2 modifies B7/CD28 signaling to promote expression of Foxp3, a transcription factor necessary for regulatory T cell (Treg) development and function. BTNL2 blocks Akt-mediated inactivation of Foxo1, a transcription factor necessary for Foxp3 expression. Immunophenotyping and gene profiling reveal that BTNL2-induced Treg share many properties with natural Treg, and in vivo they suppress enteritis induced by mouse effector T cells. These findings describe a mechanism by which environmental Ag-specific Tregs may be induced by APC expressing specific modulators of costimulatory signals.
Antitumor Effect of Paclitaxel Is Mediated by Inhibition of Myeloid-Derived Suppressor Cells and Chronic Inflammation in the Spontaneous Melanoma Model
Authors: Sevko Alexandra , Michels Tillmann , Vrohlings Melissa , Umansky Ludmila , Beckhove Philipp , Kato Masashi , Shurin Galina V. , Shurin Michael R. , Umansky Viktor 
Published: January 2013

AbstractThe antitumor effects of paclitaxel are generally attributed to the suppression of microtubule dynamics resulting in defects in cell division. New data demonstrated that in ultralow noncytotoxic concentrations, paclitaxel modulated in immune cells in vitro the activity of small Rho GTPases, the key regulators of intracellular actin dynamics. However, the immunomodulatory properties of paclitaxel in vivo have not been evaluated. In this study, using the ret transgenic murine melanoma model, which mimics human cutaneous melanoma, we tested effects of ultralow noncytotoxic dose paclitaxel on functions of myeloid-derived suppressor cells (MDSCs), chronic inflammatory mediators, and T cell activities in the tumor microenvironment in vivo. Administration of paclitaxel significantly decreased accumulation and immunosuppressive activities of tumor-infiltrating MDSCs without alterations of the bone marrow hematopoiesis. This was associated with the inhibition of p38 MAPK activity, TNF-α and production, and S100A9 expression in MDSCs. The production of mediators of chronic inflammation in the tumor milieu also was diminished. Importantly, reduced tumor burden and increased animal survival upon paclitaxel application was mediated by the restoration of CD8 T cell effector functions. We suggest that the ability of paclitaxel in a noncytotoxic dose to block the immunosuppressive potential of MDSCs in vivo represents a new therapeutic strategy to downregulate immunosuppression and chronic inflammation in the tumor microenvironment for enhancing the efficacy of concomitant anticancer therapies.
Porcine γδ T Lymphocytes Can Be Categorized into Two Functionally and Developmentally Distinct Subsets according to Expression of CD2 and Level of TCR
Authors: Stepanova Katerina , Sinkora Marek 
Published: January 2013

AbstractPorcine γδ T cells have two levels of TCRγδ expression. Whereas TCRγδmed cells are mostly CD2+CD8− and CD2+CD8+, TCRγδhi cells are highly enriched for CD2−CD8−. This distribution is independent of bacterial colonization and it is already established in the thymus prior to export of γδ cells to the periphery. Sorting and cultivation experiments revealed that CD2−CD8− γδ cells are unable to acquire CD2 and CD8, whereas CD2+ subsets can gain or loose CD8. There is also differential susceptibility for proliferation between CD2+ and CD2− γδ cells. Although CD2−CD8− almost do not proliferate, proliferation of CD2+CD8− and CD2+CD8+ is substantial. Population of CD2− γδ cells is also absent in CD1+ immature thymocytes. Additionally, subpopulations of CD2+ and CD2− γδ cells in the thymus differ in expression of auxiliary surface molecules such as CD25, CD45RA/RC, and MHC class II. Moreover, TCRγδhi cells can generate TCRγδmed cells but never the opposite. The only exception is the thymus, where a few TCRγδmed cells can be induced to TCRγδhi but only under IL-2 influence. The repertoire of TCRδ is polyclonal in all subsets, indicating that there is the same extent of diversification and equal capability of immune responses. Results collectively indicate that CD2 expression determines two lineages of γδ cells that differ in many aspects. Because CD2− γδ cells are missing in the blood of humans and mice but are obvious in other members of γδ-high species such as ruminants and birds, our findings support the idea that circulating CD2− γδ T cells are a specific lineage.
Prostaglandin E2 Potentiates Mesenchymal Stem Cell–Induced IL-10+IFN-γ+CD4+ Regulatory T Cells To Control Transplant Arteriosclerosis
Authors: Hsu Wan-Tseng , Lin Cheng-Hsin , Chiang Bor-Luen , Jui Hsiang-Yiang , Wu Kenneth Kun-Yu , Lee Chii-Ming 
Published: January 2013

Abstract
Mesenchymal stem cells (MSCs) are known for their immunomodulatory functions. We previously demonstrated that bone marrow–derived MSCs effectively control transplant arteriosclerosis (TA) by enhancing IL-10+ and IFN-γ+ cells. The objective of this study is to elucidate the mechanism by which MSCs induce IL-10+IFN-γ+CD4+ regulatory T type 1 (TR1)–like cells. In an MLR system using porcine PBMCs, MSC-induced IL-10+IFN-γ+CD4+ cells, which confer resistance to allogeneic proliferation in an IL-10–dependent manner, resemble TR1-like cells. Both cyclooxygenase-derived PGE2 and IDO help to induce TR1-like cells by MSCs. MSCs constitutively secrete PGE2, which is augmented in allogeneic reactions. However, TR1-like cells were deficient in PGE2 and 4-fold less potent than were MSCs in suppressing MLR. PGE2 mimetic supplements can enhance the immunosuppressive potency of TR1-like cells. In a porcine model of allogeneic femoral arterial transplantation, MSC-induced TR1-like cells combined with PGE2, but not either alone, significantly reduced TA at the end of 6 wk (percentage of luminal area stenosis: TR1-like cells + PGE2: 11 ± 10%; PGE2 alone: 93 ± 8.7%; TR1-like cells alone: 88 ± 2.4% versus untreated 94 ± 0.9%, p &lt; 0.001). These findings indicate that PGE2 helps MSC-induced IL-10+IFN-γ+CD4+ TR1-like cells inhibit TA. PGE2 combined with MSC-induced TR1-like cells represents a new approach for achieving immune tolerance.