bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hôpital : le temps de travail sous tension. Une comparaison Belgique, Italie, France, Grande-Bretagne, Pays-Bas et Suède
Authors: Baret Christophe 
Published: October 2010

Hospital : el tiempo de trabajo bajo tensión.
Una comparación entre Bélgica, Italia, Francia,
Inglaterra, Holanda y Suecia
Esta investigación sobre las nuevas formas de empleo y de gestión del tiempo de trabajo en el sector de la salud fue realizada en seis países de la Unión Europea. En el piano teórico, el enfoque adoptado se inspira del análisis societal y trata de identificar las principales relaciones sociales que inter-actuan con el fenómeno estudiado. Cuatro categorías de relaciones sociales han sido identificadas a priori y confïrmadas por la investigación : el espacio socio-económico, el espacio organizacional, el espacio reglamentario y el espacio doméstico. Desde el punto de vista empírico, la investigación se basa en un método de estudio de casos, realizando en cada país el estudio detenido de un hospital, particularmente en los servicios de ortopedia y obstetricia. Las observaciones realizadas dan resultados contrastados. Effectivamente, si las prácticas de gestión del empleo y del tiempo de trabajo son muy diferentes de un país a otro, tal como por ejemplo lo muestra la diferencia en las tasas de tiempo de empleo parcial, hay evoluciones comunes en los seis países, sobre todo en la intensificación de la carga de trabajo del personal sanitario debida al triple efecto de una limitación de los efectivos por razones económicas, de una demanda social creciente de mejoría en la calidad de los tratamientos y de la carencia de mano de obra.
Aux origines de l'Inserm : André Chevallier et l'Institut national d'hygiène
Authors: Picard Jean-François 
Published: October 2010

Before Inserm : André Chevallier and The Institut national d'hygiène
It was in 1941, under the Vichy government that the INH, later to become the Inserm, the first ongoing government organization was created for research in medicine and public health in France. One can presume that an authoritarian regime is more capable of establishing a health policy than a parliamentary democracy which is more sensitive to the protection of the individual and minorities, but it is also necessary to recognize the importance of American aid to France during WWII and in particular that of the International Health division of the Rockefeller Foundation. The first general manager of INH was Pr André Chevallier, a physician specialized in physiology of nutrition and vitamines in Marseille. From 1942 to 1946, the date when Chevallier resigned from the management of the INH in Paris for political reasons — too much collaborations not with the Germans but with the Americans! — , he placed the most emphasis on questions of prenatal care and pediatrics in response to the problems of food and vitamines shortages. Another sections of the INH was in charge of social diseases, such as tuberculosis, syphilis or cancer. In spite it had most difficulty in doing its work in epidemiology because of the tradition of corporatism and the silent resistance of French practitioners to social medicine, to the great satisfaction of the French Ministry of Health, the INH could publish the conclusions of its first survey before the war ended.
Soins palliatifs : la recherche de l'« entre-deux » (Commentaire)
Authors: Lebeer Guy 
Published: October 2010

The invisible work of home palliative care support teams
Medical care of the dying patient is shaped by a specific model, the palliative care model. Born 30 years ago in Great Britain, this model has spread in the health care System across western countries. In France, its spread is mainly supported by small specialised teams gatthering physicians, nurses, psychologists, social workers who afford consultance, training, support to health care workers and lay carers. This paper presents a research based on monographs of three home palliative care support teams. This text emphasises the invisible work relying on a typology of activities, their context and objectives.
La lutte contre le sida en Thaïlande : de la logique de santé publique à la logique industrielle
Authors: Guennif Samira , Mfuka Claude 
Published: October 2010

Aids struggle in Thailand: from public health policy logic to industrial policylogic
Thailand' s efforts to slow the AIDS epinvestissements directs etrangers-mic are successful thanks to a preventive policy. Now, the issue is to ensure access for people with palliative cares and antiretroviral treatments. To provinvestissements directs etrangers low-cost treatments, Thailand can mobilize national generic industry. However, the recent modifications of the intellectual propriety rights do not urge local firms to produce generics. Finally, public health policy is unable to mobilize the industrial policy in order to improve affordability of treatments to infected people.
Notch Ligand Delta-Like 4 Regulates Development and Pathogenesis of Allergic Airway Responses by Modulating IL-2 Production and Th2 Immunity
Authors: Jang Sihyug , Schaller Matthew , Berlin Aaron A. , Lukacs Nicholas W. 
Published: October 2010

AbstractActivation of the canonical Notch pathways has been implicated in Th cell differentiation, but the role of specific Notch ligands in Th2-mediated allergic airway responses has not been completely elucidated. In this study, we show that delta-like ligand 4 (Dll4) was upregulated on dendritic cells in response to cockroach allergen. Blocking Dll4 in vivo during either the primary or secondary response enhanced allergen-induced pathogenic consequences including airway hyperresponsiveness and mucus production via increased Th2 cytokines. In vitro assays demonstrated that Dll4 regulates IL-2 in T cells from established Th2 responses as well as during primary stimulation. Notably, Dll4 blockade during the primary, but not the secondary, response increased IL-2 levels in lung and lymph node of allergic mice. The in vivo neutralization of Dll4 was associated with increased expansion and decreased apoptosis during the primary allergen sensitization. Moreover, Dll4-mediated Notch activation of T cells during primary stimulation in vitro increased apoptosis during the contraction/resting phase of the response, which could be rescued by exogenous IL-2. Consistent with the role for Dll4-mediated IL-2 regulation in overall T cell function, the frequency of IL-4–producing cells was also significantly altered by Dll4 both in vivo and in vitro. These data demonstrate a regulatory role of Dll4 both in initial Th2 differentiation and in Th2 cytokine production in established allergic responses.
Polyinosinic-Polycytidylic Acid Treatment of Friend Retrovirus-Infected Mice Improves Functional Properties of Virus-Specific T Cells and Prevents Virus-Induced Disease
Authors: Gibbert Kathrin , Dietze Kirsten K. , Zelinskyy Gennadiy , Lang Karl S. , Barchet Winfried , Kirschning Carsten J. , Dittmer Ulf 
Published: October 2010

Abstract
The induction of type I IFN is the most immediate host response to viral infections. Type I IFN has a direct antiviral activity mediated by antiviral enzymes, but it also modulates the function of cells of the adaptive immune system. Many viruses can suppress type I IFN production, and in retroviral infections, the initial type I IFN is weak. Thus, one strategy of immunotherapy in viral infection is the exogenous induction of type I IFN during acute viral infection by TLR ligands. Along these lines, the TLR3/MDA5 ligand polyinosinic-polycytidylic acid [poly(I:C)] has already been used to treat viral infections. However, the immunological mechanisms underlying this successful therapy have not been defined until now. In this study, the Friend retrovirus (FV) mouse model was used to investigate the mode of action of poly(I:C) in antiretroviral immunotherapy. Postexposure, poly(I:C) treatment of FV-infected mice resulted in a significant reduction in viral loads and protection from virus-induced leukemia. This effect was IFN dependent because type I IFN receptor-deficient mice could not be protected by poly(I:C). The poly(I:C)-induced IFN response resulted in the expression of antiviral enzymes, which suppressed FV replication. Also, the virus-specific T cell response was augmented. Interestingly, it did not enhance the number of virus-specific CD4+ and CD8+ T cells, but rather the functional properties of these cells, such as cytokine production and cytotoxic activity. The results demonstrate a direct antiviral and immunomodulatory effect of poly(I:C) and, therefore, suggests its potential for clinical treatment of retroviral infections.
Dysregulation of Inflammatory Responses by Chronic Circadian Disruption
Authors: Castanon-Cervantes Oscar , Wu Mingwei , Ehlen J. Christopher , Paul Ketema , Gamble Karen L. , Johnson Russell L. , Besing Rachel C. , Menaker Michael , Gewirtz Andrew T. , Davidson Alec J. 
Published: October 2010

AbstractCircadian rhythms modulate nearly every mammalian physiological process. Chronic disruption of circadian timing in shift work or during chronic jet lag in animal models leads to a higher risk of several pathologies. Many of these conditions in both shift workers and experimental models share the common risk factor of inflammation. In this study, we show that experimentally induced circadian disruption altered innate immune responses. Endotoxemic shock induced by LPS was magnified, leading to hypothermia and death after four consecutive weekly 6-h phase advances of the light/dark schedule, with 89% mortality compared with 21% in unshifted control mice. This may be due to a heightened release of proinflammatory cytokines in response to LPS treatment in shifted animals. Isolated peritoneal macrophages harvested from shifted mice exhibited a similarly heightened response to LPS in vitro, indicating that these cells are a target for jet lag. Sleep deprivation and stress are known to alter immune function and are potential mediators of the effects we describe. However, polysomnographic recording in mice exposed to the shifting schedule revealed no sleep loss, and stress measures were not altered in shifted mice. In contrast, we observed altered or abolished rhythms in the expression of clock genes in the central clock, liver, thymus, and peritoneal macrophages in mice after chronic jet lag. We conclude that circadian disruption, but not sleep loss or stress, are associated with jet lag-related dysregulation of the innate immune system. Such immune changes might be a common mechanism for the myriad negative health effects of shift work.
An Intrinsic Mechanism Predisposes Foxp3-Expressing Regulatory T Cells to Th2 Conversion In Vivo
Authors: Wang Yunqi , Souabni Abdallah , Flavell Richard A. , Wan Yisong Y. 
Published: October 2010

Abstract
Naturally occurring regulatory T (nTreg) cells express Foxp3 and were originally discovered as immune suppressors critical for self-tolerance and immune homeostasis. Through yet-to-be-defined mechanisms, nTreg cells were recently shown to convert into proinflammatory cells. Particularly, attenuation of Foxp3 expression led to Th2 conversion of nTreg cells in vivo. In this paper, we demonstrated an nTreg-specific mechanism controlling their Th2 conversion. We found that wild-type nTreg cells expressing reduced levels of Foxp3 but not those expressing no Foxp3 produced the Th2 cytokine IL-4. Intriguingly, IL-4 production by converted nTreg cells is required for Th2 differentiation of coexisting naive CD4 T cells in vivo, suggesting that Th2 conversion of nTreg cells might be critical for directing Th2 immune responses. Th2 conversion of nTreg cells was not due to their inability to become Th1 cells, because IFN-γ was produced by Foxp3-low–expressing cells when IL-4/STAT-6 signaling was abrogated. Surprisingly, however, unlike naive CD4 T cells whose IL-4 production is dependent on STAT-6, Foxp3-low–expressing cells generated IL-4 independent of STAT-6, indicating an intrinsic mechanism that favors nTreg-to-Th2 differentiation. Indeed, compared with naive CD4 T cells, nTreg expressed elevated levels of GATA-3 independent of STAT-6. And GATA-3 was required for nTreg-to-Th2 conversion. Foxp3 may account for this GATA-3 upregulation in nTreg cells, because ectopic expression of Foxp3 preferentially promoted GATA-3 but not T-bet expression. Thus, we have identified an intrinsic mechanism that imposes a Th2/Th1 imbalance and predisposes Foxp3-expressing cells to IL-4 production independent of STAT-6 signaling.
PTPα Activates Lyn and Fyn and Suppresses Hck to Negatively Regulate FcεRI-Dependent Mast Cell Activation and Allergic Responses
Authors: Samayawardhena Lionel A. , Pallen Catherine J. 
Published: October 2010

AbstractMast cell activation via FcεRI involves activation of the Src family kinases (SFKs) Lyn, Fyn, and Hck that positively or, in the case of Lyn, negatively regulate cellular responses. Little is known of upstream activators of these SFKs in FcεRI-dependent signaling. We investigated the role of receptor protein tyrosine phosphatase (PTP)α, a well-known activator of SFKs in diverse signaling systems, FcεRI-mediated mast cell activation, and IgE-dependent allergic responses in mice. PTPα−/− bone marrow-derived mast cells hyperdegranulate and exhibit increased cytokine and cysteinyl leukotriene secretion, and PTPα−/− mice display enhanced IgE-dependent anaphylaxis. At or proximal to FcεRI, PTPα−/− cells have reduced IgE-dependent activation of Lyn and Fyn, as well as reduced FcεRI and SHIP phosphorylation. In contrast, Hck and Syk activation is enhanced. Syk hyperactivation correlated with its increased phosphorylation at positive regulatory sites and defective phosphorylation at a negative regulatory site. Distal to FcεRI, we observed increased activation of PI3K and MAPK pathways. These findings demonstrate that PTPα activates the FcεRI-coupled kinases Lyn and Fyn and suppresses Hck activity. Furthermore, the findings indicate that hyperactivation of PTPα−/− mast cells and enhanced IgE-dependent allergic responses of PTPα−/− mice are due to the ablated function of PTPα as a critical regulator of Lyn negative signaling.
Slit2 Regulates Attractive Eosinophil and Repulsive Neutrophil Chemotaxis through Differential srGAP1 Expression during Lung Inflammation
Authors: Ye Bu-Qing , Geng Zhen H. , Ma Li , Geng Jian-Guo 
Published: October 2010

Abstract
Directional migration of leukocytes is an essential step in leukocyte trafficking during inflammatory responses. However, the molecular mechanisms governing directional chemotaxis of leukocytes remain poorly understood. The Slit family of guidance cues has been implicated for inhibition of leuocyte migration. We report that Clara cells in the bronchial epithelium secreted Slit2, whereas eosinophils and neutrophils expressed its cell-surface receptor, Robo1. Compared to neutrophils, eosinophils exhibited a significantly lower level of Slit-Robo GTPase-activating protein 1 (srGAP1), leading to activation of Cdc42, recruitment of PI3K to Robo1, enhancment of eotaxin-induced eosinophil chemotaxis, and exaggeration of allergic airway inflammation. Notably, OVA sensitization elicited a Slit2 gradient at so-called bronchus–alveoli axis, with a higher level of Slit2 in the bronchial epithelium and a lower level in the alveolar tissue. Aerosol administration of rSlit2 accelerated eosinophil infiltration, whereas i.v. administered Slit2 reduced eosinophil deposition. In contrast, Slit2 inactivated Cdc42 and suppressed stromal cell-derived factor-1α–induced chemotaxis of neutrophils for inhibiting endotoxin-induced lung inflammation, which were reversed by blockade of srGAP1 binding to Robo1. These results indicate that the newly identified Slit2 gradient at the bronchus–alveoli axis induces attractive PI3K signaling in eosinophils and repulsive srGAP1 signaling in neutrophils through differential srGAP1 expression during lung inflammation.
PRDM1/Blimp-1 Controls Effector Cytokine Production in Human NK Cells
Authors: Smith Matthew A. , Maurin Michelle , Cho Hyun Il , Becknell Brian , Freud Aharon G. , Yu Jianhua , Wei Sheng , Djeu Julie , Celis Esteban , Caligiuri Michael A. , Wright Kenneth L. 
Published: October 2010

Abstract
NK cells are major effectors of the innate immune response through cytolysis and bridge to the adaptive immune response through cytokine release. The mediators of activation are well studied; however, little is known about the mechanisms that restrain activation. In this report, we demonstrate that the transcriptional repressor PRDM1 (also known as Blimp-1 or PRDI-BF1) is a critical negative regulator of NK function. Three distinct PRDM1 isoforms are selectively induced in the CD56dim NK population in response to activation. PRDM1 coordinately suppresses the release of IFN-γ, TNF-α, and TNF-β through direct binding to multiple conserved regulatory regions. Ablation of PRDM1 expression leads to enhanced production of IFN-γ and TNF-α but does not alter cytotoxicity, whereas overexpression blocks cytokine production. PRDM1 response elements are defined at the IFNG and TNF loci. Collectively, these data demonstrate a key role for PRDM1 in the negative regulation of NK activation and position PRDM1 as a common regulator of the adaptive and innate immune response.
Hydroxylase Inhibition Abrogates TNF-α–Induced Intestinal Epithelial Damage by Hypoxia-Inducible Factor-1–Dependent Repression of FADD
Authors: Hindryckx Pieter , De Vos Martine , Jacques Peggy , Ferdinande Liesbeth , Peeters Harald , Olievier Kim , Bogaert Sara , Brinkman Brigitta , Vandenabeele Peter , Elewaut Dirk , Laukens Debby 
Published: October 2010

Abstract
Hydroxylase inhibitors stabilize hypoxia-inducible factor-1 (HIF-1), which has barrier-protective activity in the gut. Because the inflammatory cytokine TNF-α contributes to inflammatory bowel disease in part by compromising intestinal epithelial barrier integrity, hydroxylase inhibition may have beneficial effects in TNF-α–induced intestinal epithelial damage. The hydroxylase inhibitor dimethyloxalylglycin (DMOG) was tested in a murine model of TNF-α–driven chronic terminal ileitis. DMOG-treated mice experienced clinical benefit and showed clear attenuation of chronic intestinal inflammation compared with that of vehicle-treated littermates. Additional in vivo and in vitro experiments revealed that DMOG rapidly restored terminal ileal barrier function, at least in part through prevention of TNF-α–induced intestinal epithelial cell apoptosis. Subsequent transcriptional studies indicated that DMOG repressed Fas-associated death domain protein (FADD), a critical adaptor molecule in TNFR-1-mediated apoptosis, in an HIF-1α–dependent manner. Loss of this FADD repression by HIF-1α-targeting small interfering RNA significantly diminished the antiapoptotic action of DMOG. Additional molecular studies led to the discovery of a previously unappreciated HIF-1 binding site in the FADD promoter, which controls repression of FADD during hypoxia. As such, the results reported in this study allowed the identification of an innate mechanism that protects intestinal epithelial cells during (inflammatory) hypoxia, by direct modulation of death receptor signaling. Hydroxylase inhibition could represent a promising alternative treatment strategy for hypoxic inflammatory diseases, including inflammatory bowel disease.
Mechanical Ventilators in US Acute Care Hospitals
Authors: Rubinson Lewis , Vaughn Frances , Nelson Steve , Giordano Sam , Kallstrom Tom , Buckley Tim , Burney Tabinda , Hupert Nathaniel , Mutter Ryan , Handrigan Michael , Yeskey Kevin , Lurie Nicole , Branson Richard 
Published: October 2010

ABSTRACTObjective: The supply and distribution of mechanical ventilation capacity is of profound importance for planning for severe public health emergencies. However, the capability of US health systems to provide mechanical ventilation for children and adults remains poorly quantified. The objective of this study was to determine the quantity of adult and pediatric mechanical ventilators at US acute care hospitals.Methods: A total of 5752 US acute care hospitals included in the 2007 American Hospital Association database were surveyed. We measured the quantities of mechanical ventilators and their features.Results: Responding to the survey were 4305 (74.8%) hospitals, which accounted for 83.8% of US intensive care unit beds. Of the 52 118 full-feature mechanical ventilators owned by respondent hospitals, 24 204 (46.4%) are pediatric/neonatal capable. Accounting for nonrespondents, we estimate that there are 62 188 full-feature mechanical ventilators owned by US acute care hospitals. The median number of full-feature mechanical ventilators per 100 000 population for individual states is 19.7 (interquartile ratio 17.2–23.1), ranging from 11.9 to 77.6. The median number of pediatric-capable device full-feature mechanical ventilators per 100 000 population younger than 14 years old is 52.3 (interquartile ratio 43.1–63.9) and the range across states is 22.1 to 206.2. In addition, respondent hospitals reported owning 82 755 ventilators other than full-feature mechanical ventilators; we estimate that there are 98 738 devices other than full-feature ventilators at all of the US acute care hospitals.Conclusions: The number of mechanical ventilators per US population exceeds those reported by other developed countries, but there is wide variation across states in the population-adjusted supply. There are considerably more pediatric-capable ventilators than there are for adults only on a population-adjusted basis.(Disaster Med Public Health Preparedness. 2010;4:199-206)
Disaster Preparedness Among Families of Children With Special Health Care Needs
Authors: Baker Lisa R. , Baker Mark D. 
Published: October 2010

ABSTRACTFamilies with children with special health care needs may present a challenge for disaster responders. This study examined the level of personal disaster preparedness among this at-risk population in relation to the general population, and explores whether special health care needs or perception of disaster risk affects preparedness levels. A convenience sample of 145 families presenting to an urban tertiary care children's hospital was surveyed using a previously validated instrument to gather information on levels of preparedness and factors influencing preparedness. In spite of significant special health care needs and concern about disasters, families remain unprepared for a disaster event. Health care and psychosocial support workers are in a unique position to increase preparedness levels in this at-risk population.(Disaster Med Public Health Preparedness. 2010;4:240-245)