bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long-Term Shoulder Function after Type I and II Acromioclavicular Joint Disruption
Authors: Mikek Martin 
Published: June 2008

Background Acromioclavicular joint separations are very common lesions, with the majority falling into Rockwood classification type I and II. It is generally agreed that conservative treatment of these injuries leads to good functional results, although there are some studies that suggest these injuries are associated with a high incidence of persistent symptoms. Hypothesis Type I and II acromioclavicular joint disruption significantly impairs long-term shoulder function. Study Design Case series; Level of evidence, 4. Methods The shoulder function of 23 patients who were treated for type I or II acromioclavicular joint disruption was evaluated at a mean of 10.2 years after injury. The objective and subjective measures of the injured shoulder were assessed using Constant, University of California-Los Angeles Shoulder Scale, and Simple Shoulder Test scores and were compared with results of the uninjured shoulder. Results At an average follow-up of 10.2 years, 12 of 23 patients (52%) reported at least occasional acromioclavicular joint symptoms. The average Constant score for the injured shoulder was 70.5 and 86.8 for the uninjured shoulder ( P < .001). The average University of California-Los Angeles Shoulder Scale score for the injured shoulder was 24.1 and 29.2 for the uninjured shoulder ( P < .001). The average Simple Shoulder Test value for the injured shoulder was 9.7 and 10.9 for the uninjured shoulder ( P < .002). The extent of acromioclavicular joint disruption and acromioclavicular joint width did not have any statistically significant influence on the shoulder functional scores. Conclusion Type I and II acromioclavicular joint disruptions impair long-term shoulder function in about half of patients 10 years after injury.
Essai Conceptualisation de l'intervention éducative en santé publique
Authors: Descarpentries Jacqueline 
Published: June 2008

La fonction sociale de l'éducation pour la santé génère un questionnement propre qui est par nature différent de ceux soulevés par les interventions de protection telles que la vaccination obligatoire et les dépistages de masses. L'éducation pour la santé ne se présente plus uniquement sous la forme d'une intervention éducative justifiée par les évidences épidémiologiques pour la gestion des risques-au nom du principe de précaution-; mais elle se veut aussi participer à la hiérarchie implicite des valeurs de la société contemporaine. A la fois lieu de la normalisation et de la rationalisation de la vie, mais aussi lieu de la responsabilité citoyenne véhiculant des valeurs telles l'autonomie, la liberté individuelle, le libre arbitre, elle participe aujourd'hui à la laïcisation des corps, et aux compétences psychosociales et demain au développement durable de la santé publique. L'éducation pour la santé implique une connaissance des enjeux propres à la fonction sociale de l'éducation contingente à la santé publique qui sont insensiblement mais profondément liés à une archéologie des savoirs et des pouvoirs: des épistémologies des sciences de la vie et du vivant, des concepts et des méthodes qui ont naturalisé l'objet santé. Cette archéologie assigne à l'éducation une fonction sociale à la fois de biologisation de la vie, mais aussi de durabilité du développement humain en hésitant entre nature et culture. Par une approche réflexive et critique, nos travaux de recherches participent à une élucidation des modes d'intervention éducatifs en santé publique, où le travail éducatif est entendu comme une modalité d'intervention dans les mandats de la santé publique. Il permet d'identifier une réalité sociale et historique étroitement liée aux traditions, aux conditions nationales, mondiales, économiques, politiques et culturelles des Etats dans lesquelles il s'est développé pour penser les conditions d'une éducation pour la santé tout au long de la vie. Nous élaborons une posture de recherche autour de la conceptualisation de l'intervention éducative en santé publique à partir de l'étude de différentes dimensions psychopédagogique, didactique, organisationnelle et sociale. (Promot Educ 2008; Supp(1): 14-16)
Promotion de la santé au Luxembourg
Authors: Wagener Yolande 
Published: June 2008

La mise en œuvre de la promotion de la santé et de l'éducation pour la santé ne sont pas identiques d'un pays à l'autre. Les problèmes identifiés, les priorités d'intervention, les dispositifs en place, les « coutumes » de démarches et de stratégie, les possibilités infra-structurelles, organisationnelles, matérielles et professionnelles, l'organisation des services de santé, l'histoire et le développement de la santé publique, les systèmes de santé et de sécurité sociale, la culture de communication et de partenariat, la volonté politique, la demande publique… figurent parmi les facteurs qui influencent les initiatives établies dans les pays. Certains pays ont commencé le processus par des actions au niveau national, (législation, organe national de coordination), d'autres à des niveaux régionaux ou même locaux, certains ont développé des programmes globaux, d'autres ont favorisé de promouvoir la santé dans certains « settings » précis ( p.ex: écoles, hôpitaux) Dans cet exposé, nous essayons de rendre compte de la promotion de la santé et de l'éducation pour la santé au Luxembourg: développement, aspects positifs et négatifs, domaines d'intervention, facilités et limites, domaines de réflexion et de recherche, états des lieux et futur. (Promot Educ 2008; Supp(1): 22-25)
La place de la promotion de la santé et de l'éducation pour la santé dans le système de santé français
Authors: Fayard Annick , Marchand Annie-Claude 
Published: June 2008

Le système de santé français reste très centré sur le curatif. La santé publique y occupe désormais une place plus importante mais son développement s'effectue prioritairement dans le champ des urgences sanitaires. Cependant, la prévention et l'éducation pour la santé prennent progressivement place dans le système depuis les années 1990. Le Conseil des Ministres entérine en 2001 un programme national d'éducation pour la santé (PNEPS) et, dans son sillage une circulaire ministérielle préconise l'élaboration de schémas régionaux d'éducation pour la santé (SREPS). Le législateur crée en 2002 l'Institut National de Prévention et d'Education pour la Santé (INPES). Enfin, la nouvelle loi de santé publique prévoit en 2004 la mise en place dans chaque région d'un plan régional de santé publique (PRSP). Ce plan doit comporter, outre les programmes et actions pluriannuels thématiques, un programme de santé scolaire et d'éducation pour la santé. Conformément à ses missions, l'INPES soutient le renforcement de la recherche et le développement des pôles de compétences en éducation pour la santé, ces plates formes de ressources et de services en éducation et promotion de la santé prévues par les SREPS. Mais ces initiatives restent modestes et isolées au regard des besoins de ce champ d'intervention. L'articulation de la recherche avec la formation et les pratiques des intervenants reste un défi. Jusqu'alors, les recherches ont porté essentiellement sur les facteurs explicatifs et rarement sur les modalités d'intervention ou sur l'efficacité des actions. De plus, la formation initiale dans ce domaine reste insuffisamment développée et les contenus des programmes de formation sont très disparates et faiblement articulés à la recherche. L'absence d'une politique globale sur ces questions constitue un frein au développement de ce secteur d'intervention. (Promot Educ 2008; Supp(1): 31-34)
Le développement de la recherche-action européenne en promotion de la santé mentale : Pourquoi ? Comment ?
Authors: Fond-Harmant Laurence 
Published: June 2008

En matière de recherche en promotion de la santé mentale, les chercheurs et experts européens expriment le manque d'outils spécifiques d'analyse, évalués, validés et les limites des actions d'intervention au regard des priorités. Ils proposent le développement de recherches sans exclusive disciplinaire (neurologie, sciences sociales, psychiatrie…). L'article présente 4 axes prioritaires pour contribuer à produire des hypothèses, des modèles, des méthodes de mesures et d'évaluation et des connaissances nouvelles. 1- Créer les fondements d'une discipline de recherche à part entière, « Promotion de la santé mentale » faisant cruellement défaut dans le paysage scientifique. Les travaux porteront sur la définition de la santé mentale et sur son articulation à la psychiatrie. Ils auront pour objectif de définir des problématiques adaptés au contexte social et politique européen en proposant des outils conceptuels et des méthodes. 2- Analyser les problèmes de santé mentale en s'appuyant sur les meilleures connaissances disponibles notamment par: • la définition précise des pathologies, l'estimation de leur fréquence et leur retentissement (en terme de mortalité, d'incapacité, de prise en charge, de traitement…) dans la population générale, • l'identification des principaux déterminants associés à leur survenue ou à l'importance de leur impact et en particulier ceux dont la survenance peut être modifiée par des politiques de santé publique, • l'identification des stratégies « efficaces » en promotion de la santé mentale. 3- Développer un regard international sur la question de la santé mentale et des inégalités sociales en Europe. Cet angle d'attaque ouvre le champs à des approches comparatives entre pays. Ces travaux analyseront les implications politiques et devront faire ressortir les changements et les évolutions possibles. 4- Articuler la formation à la recherche. Des travaux de recherche-action expérimentale doivent soutenir les professionnels non psychiatres qui doivent s'adapter à des conditions pour lesquelles ils ne sont pas préparés dans leur cursus initiaux de formation. (Promot Educ 2008; Supp(1): 64-70)
Targeting MEK/MAPK signal transduction module potentiates ATO-induced apoptosis in multiple myeloma cells through multiple signaling pathways
Authors: Lunghi Paolo , Giuliani Nicola , Mazzera Laura , Lombardi Guerino , Ricca Micaela , Corradi Attilio , Cantoni Anna Maria , Salvatore Luigi , Riccioni Roberta , Costanzo Antonio , Testa Ugo , Levrero Massimo , Rizzoli Vittorio , Bonati Antonio 
Published: June 2008

Abstract
We demonstrate that blockade of the MEK/ERK signaling module, using the small-molecule inhibitors PD184352 or PD325901 (PD), strikingly enhances arsenic trioxide (ATO)–induced cytotoxicity in human myeloma cell lines (HMCLs) and in tumor cells from patients with multiple myeloma (MM) through a caspase-dependent mechanism. In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction. In HMCLs carrying a nonfunctional p53, cotreatment with PD strikingly elevates the (DR4 + DR5)/(DcR1 + DcR2) tumor necrosis factor (TNF)–related apoptosis-inducing ligand (TRAIL) receptors ratio and caspase-8 activation of ATO-treated cells. In MM cells, irrespective of p53 status, the combined PD/ATO treatment increases the level of the proapoptotic protein Bim (PD-mediated) and decreases antiapoptotic protein Mcl-1 (ATO-mediated). Moreover, Bim physically interacts with both DR4 and DR5 TRAIL receptors in PD/ATO-treated cells, and loss of Bim interferes with the activation of both extrinsic and intrinsic apoptotic pathways in response to PD/ATO. Finally, PD/ATO treatment induces tumor regression, prolongs survival, and is well tolerated in vivo in a human plasmacytoma xenograft model. These preclinical studies provide the framework for testing PD325901 and ATO combination therapy in clinical trials aimed to improve patient outcome in MM.
A review of transfusion practice before, during, and after hematopoietic progenitor cell transplantation
Authors: Gajewski James L. , Johnson Viviana V. , Sandler S. Gerald , Sayegh Antoine , Klumpp Thomas R. 
Published: June 2008

AbstractThe increased use of hematopoietic progenitor cell (HPC) transplantation has implications and consequences for transfusion services: not only in hospitals where HPC transplantations are performed, but also in hospitals that do not perform HPC transplantations but manage patients before or after transplantation. Candidates for HPC transplantation have specific and specialized transfusion requirements before, during, and after transplantation that are necessary to avert the adverse consequences of alloimmunization to human leukocyte antigens, immunohematologic consequences of ABO-mismatched transplantations, or immunosuppression. Decisions concerning blood transfusions during any of these times may compromise the outcome of an otherwise successful transplantation. Years after an HPC transplantation, and even during clinical remission, recipients may continue to be immunosuppressed and may have critically important, special transfusion requirements. Without a thorough understanding of these special requirements, provision of compatible blood components may be delayed and often urgent transfusion needs prohibit appropriate consultation with the patient's transplantation specialist. To optimize the relevance of issues and communication between clinical hematologists, transplantation physicians, and transfusion medicine physicians, the data and opinions presented in this review are organized by sequence of patient presentation, namely, before, during, and after transplantation.
Requirement of TLR2-mediated signaling for the induction of IL-15 gene expression in human monocytic cells by HSV-1
Authors: Ahmad Rasheed , El Bassam Souad , Cordeiro Paulo , Menezes José 
Published: June 2008

AbstractExposure of human monocytic cells to herpes simplex virus type 1 (HSV-1) results in immediate up-regulation of interleukin (IL)–15 gene expression. However, the receptor involved in this induction is not known. Here, we provide evidence that this induction depends on TLR2-mediated signaling pathway. Through the use of small interfering RNAs (siRNAs), we demonstrate that HSV-1–induced up-regulation of IL-15 gene expression in monocytic THP1 cells requires the presence of the adaptors MyD88, IRAK1, and TRAF6. Interestingly, TIRAP/Mal, an adaptor molecule specifically recruited to TLR2 and TLR4, was also required for maximal up-regulation of IL-15. This response was completely abrogated by anti-TLR2, but not anti-TLR4, blocking mAbs in both primary monocytes and THP1 cells. Furthermore, THP1 cells rendered defective in TLR2 expression by disrupting the expression of Sp1, a major transcription factor involved in TLR2 promoter activity, were unable to up-regulate IL-15 gene expression in response to HSV-1. In addition, HSV-1–induced NF-κB activation was significantly reduced after neutralization of TLR2 and the adaptor proteins. Altogether, these results unequivocally show that HSV-1 induces TLR2-dependent activation of IL-15 gene expression, which requires the recruitment of both MyD88 and TIRAP/Mal and the activation of IRAK1 and TRAF6 leading to NF-κB translocation to the nucleus.
MHC class I–specific inhibitory receptors and their ligands structure diverse human NK-cell repertoires toward a balance of missing self-response
Authors: Yawata Makoto , Yawata Nobuyo , Draghi Monia , Partheniou Fotini , Little Ann-Margaret , Parham Peter 
Published: June 2008

AbstractVariegated expression of 6 inhibitory HLA class I–specific receptors on primary NK cells was studied using high-dimension flow cytometry in 58 humans to understand the structure and function of NK-cell repertoires. Sixty-four subsets expressing all possible receptor com-binations were present in each repertoire, and the frequency of receptor-null cells varied among the donors. Enhancement in missing-self response between NK subsets varied substantially where subset responses were defined by donor KIR/HLA allotypes, reflecting the differences in interaction between inhibitory receptors and their ligands. This contrasted to the enhancement conferred by NKG2A, which was constant and of intermediate strength. We infer a mechanism that modulates frequencies of the NK subsets displaying diverse levels of missing-self response, a system that reduces the presence of KIR-expressing subsets that display either too strong or too weak a response and effectively replaces them with NKG2A-expressing cells in the repertoire. Through this high-resolution analysis of inhibitory receptor expression, 5 types of NK-cell repertoire were defined by their content of NKG2A+/NKG2A− cells, frequency of receptor-null cells, and degree of KIR receptor coexpression. The analyses provide new perspective on how personalized human NK-cell repertoires are structured.
Type II (tositumomab) anti-CD20 monoclonal antibody out performs type I (rituximab-like) reagents in B-cell depletion regardless of complement activation
Authors: Beers Stephen A. , Chan Claude H. T. , James Sonya , French Ruth R. , Attfield Kathrine E. , Brennan Claire M. , Ahuja Anupama , Shlomchik Mark J. , Cragg Mark S. , Glennie Martin J. 
Published: June 2008

AbstractAnti-CD20 monoclonal antibodies (mAbs) are classified into type I (rituximab-like) or type II (tositumomab-like) based on their ability to redistribute CD20 molecules in the plasma membrane and activate various effector functions. To compare type I and II mAbs directly in vivo and maximize Fc effector function, we selected and engineered mAbs with the same mouse IgG2a isotype and assessed their B-cell depleting activity in human CD20 transgenic mice. Despite being the same isotype, having similar affinity, opsonizing activity for phagocytosis, and in vivo half-life, the type II mAb tositumomab (B1) provided substantially longer depletion of B cells from the peripheral blood compared with the type I mAb rituximab (Rit m2a), and 1F5. This difference was also evident within the secondary lymphoid organs, in particular, the spleen. Failure to engage complement did not explain the efficacy of the type II reagents because type I mAbs mutated in the Fc domain (K322A) to prevent C1q binding still did not display equivalent efficacy. These results give support for the use of type II CD20 mAbs in human B-cell diseases.
Isolation of bacteria-containing phagosomes by magnetic selection
Authors: Lönnbro Per , Nordenfelt Pontus , Tapper Hans 
Published: June 2008

AbstractBackgroundThere is a growing awareness of the importance of intracellular events in determining the outcome of infectious disease. To improve the understanding of such events, like phagosome maturation, we set out to develop a versatile technique for phagosome isolation that is rapid and widely applicable to different pathogens.ResultsWe developed two different protocols to isolate phagosomes containing dead or live bacteria modified with small magnetic particles, in conjunction with a synchronized phagocytosis protocol and nitrogen cavitation. For dead bacteria, we performed analysis of the phagosome samples by microscopy and immunoblot, and demonstrated the appearance of maturation markers on isolated phagosomes.ConclusionWe have presented detailed protocols for phagosome isolation, which can be adapted for use with different cell types and prey. The versatility and simplicity of the approach allow better control of phagosome isolation, the parameters of which are critical in studies of host-bacteria interaction and phagosome maturation.
Dumpy-30 family members as determinants of male fertility and interaction partners of metal-responsive transcription factor 1 (MTF-1) in Drosophila
Authors: Vardanyan Alla , Atanesyan Lilit , Egli Dieter , Raja Sunil Jayaramaiah , Steinmann-Zwicky Monica , Renkawitz-Pohl Renate , Georgiev Oleg , Schaffner Walter 
Published: June 2008

Abstract

Background
Metal-responsive transcription factor 1 (MTF-1), which binds to metal response elements (MREs), plays a central role in transition metal detoxification and homeostasis. A Drosophila interactome analysis revealed two candidate dMTF-1 interactors, both of which are related to the small regulatory protein Dumpy-30 (Dpy-30) of the worm C. elegans. Dpy-30 is the founding member of a protein family involved in chromatin modifications, notably histone methylation. Mutants affect mating type in yeast and male mating in C. elegans.

Results
Constitutive expression of the stronger interactor, Dpy-30L1 (CG6444), in transgenic flies inhibits MTF-1 activity and results in elevated sensitivity to Cd(II) and Zn(II), an effect that could be rescued by co-overexpression of dMTF-1. Electrophoretic mobility shift assays (EMSA) suggest that Dpy-30L1 interferes with the binding of MTF-1 to its cognate MRE binding site. Dpy-30L1 is expressed in the larval brain, gonads, imaginal discs, salivary glands and in the brain, testes, ovaries and salivary glands of adult flies. Expression of the second interactor, Dpy-30L2 (CG11591), is restricted to larval male gonads, and to the testes of adult males. Consistent with these findings, dpy-30-like transcripts are also prominently expressed in mouse testes. Targeted gene disruption by homologous recombination revealed that dpy-30L1 knockout flies are viable and show no overt disruption of metal homeostasis. In contrast, the knockout of the male-specific dpy-30L2 gene results in male sterility, as does the double knockout of dpy-30L1 and dpy-30L2. A closer inspection showed that Dpy-30L2 is expressed in elongated spermatids but not in early or mature sperm. Mutant sperm had impaired motility and failed to accumulate in sperm storage organs of females.

Conclusion
Our studies help to elucidate the physiological roles of the Dumpy-30 proteins, which are conserved from yeast to humans and typically act in concert with other nuclear proteins to modify chromatin structure and gene expression. The results from these studies reveal an inhibitory effect of Dpy-30L1 on MTF-1 and an essential role for Dpy-30L2 in male fertility.
Association between PPARGC1A polymorphisms and the occurrence of nonalcoholic fatty liver disease (NAFLD)
Authors: Yoneda Masato , Hotta Kikuko , Nozaki Yuichi , Endo Hiroki , Uchiyama Takashi , Mawatari Hironori , Iida Hiroshi , Kato Shingo , Hosono Kunihiro , Fujita Koji , Yoneda Kyoko , Takahashi Hirokazu , Kirikoshi Hiroyuki , Kobayashi Noritoshi , Inamori Masahiko , Abe Yasunobu , Kubota Kensuke , Saito Satoru , Maeyama Shiro , Wada Koichiro , Nakajima Atsushi 
Published: June 2008

AbstractBackgroundGenetic factors as well as environmental factors are important in the development of NAFLD and in this study we investigated associations between polymorphisms of peroxisome proliferators-activated receptor γ coactivator 1α polymorphism (PPARGC1A) and NAFLD.AimsWe recruited 115 patients with biopsy-proven NAFLD, 65 with NASH and 50 with simple steatosis, and 441 healthy control subjects and investigated 15 SNPs ofPPARGC1A.ResultsSNP rs2290602 had the lowestpvalue in the dominant mode (p= 0.00095), and the odds ratio for NAFLD (95% CI) was 2.73 (1.48 – 5.06). rs2290602 was significantly associated with NAFLD even when the most conservative Bonferroni's correction was applied (p= 0.0143). The frequency of the T allele of rs2290602 was significantly higher in the NASH patients than in the control subjects (p= 0.00093, allele frequency mode), and its frequency in the NASH patients tended to be higher than in the simple steatosis patients (p= 0.09). The results of the real-time RT-PCR study showed that intrahepatic mRNA expression ofPPARGC1Awas lower in the TT group than in the GG or GT group at SNP rs2290602 (p = 0.0454).ConclusionThis is the first study to demonstrate a significant association between genetic variations inPPARGC1Aand NAFLD. This finding suggested thatPPARGC1Apolymorphism and lower expression ofPPARGC1AmRNA in the liver are an important genetic contribution to etiology of NAFLD.