bluuebunny/crossref_metadata_2025_split huggingface dataset:
Health-related job loss: findings from a community-based survey
Authors: Solomon Christine , Poole Jason , Palmer Keith T , Coggon David 
Published: November 2006

Aims:To explore the frequency, nature, determinants and outcome of health-related job loss (HRJL) in men sampled from the general population of three rural areas.Methods:Data on lifetime occupational history, including any HRJL, were obtained as part of a postal survey of men aged 24–70 years in three rural areas of England and Wales. Incidence rates were calculated for first health-related loss of a job that had been held for ⩾1 year. Associations with risk factors were examined by Poisson regression, and by application of conditional logistic regression in a nested case–control study.Results:HRJL was reported by 1408 (13%) of the 10 559 men who had held long-term jobs. The incidence rose steeply with age for cardiorespiratory and neurological disorders, but for accidents and poisoning the trend was, if anything, in the reverse direction. An increase in incidence over time was most marked for musculoskeletal disorders and mental illness, and much less prominent for cardiorespiratory and neurological disease. In comparison with other occupations, the risk was lower in agricultural workers (odds ratio (OR) 0.6, 95% CI 0.5 to 0.8), and higher in policemen (OR 2.4, 95% CI 1.6 to 3.7) and teachers (OR 2.0, 95% CI 1.5 to 2.7), this differential being even greater for HRJL caused by mental illness. Risk was also increased in employees relative to the self-employed (OR 2.0, 95% CI 1.7 to 2.3). Shift work was associated with a higher incidence of job loss caused by mental illness (OR 1.5, 95%CI 1.1–2.2), and heavy lifting with HRJL caused by musculoskeletal disorders (OR 2.6, 95% CI 2.0 to 3.5). After HRJL, 61% of subjects had subsequently obtained further long-term employment, usually within 1 year.Conclusions:In the population studied, HRJL has become increasingly common, especially in relation to musculoskeletal disorders and mental illness. In addition to being associated with ergonomic stresses in the workplace, it may be importantly influenced by cultural and economic factors. Future research should focus on the minority of workers who leave a job for health reasons and do not rapidly return to further work.
Gamma Glutamyl Transferase and Metabolic Syndrome, Cardiovascular Disease, and Mortality Risk
Authors: Lee Douglas S. , Evans Jane C. , Robins Sander J. , Wilson Peter W. , Albano Irene , Fox Caroline S. , Wang Thomas J. , Benjamin Emelia J. , D’Agostino Ralph B. , Vasan Ramachandran S. 
Published: November 2006

Objective—To determine whether serum γ-glutamyl transferase (GGT) predicts cardiovascular disease (CVD) morbidity and mortality, accounting for temporal changes in known CVD risk factors and C-reactive protein (CRP).Methods and Results—In 3451 Framingham Study participants (mean age 44 years, 52% women) we examined the relations of GGT with CVD risk factors, and prospectively determined the risk of new-onset metabolic syndrome, incident CVD, and death. GGT was positively associated with body mass index, blood pressure, LDL cholesterol, triglycerides, and blood glucose in cross-sectional analysis (P<0.005). On follow-up (mean 19 years), 968 participants developed metabolic syndrome, 535 developed incident CVD, and 362 died. The risk of metabolic syndrome increased with higher GGT (multivariable-adjusted hazard ratio [HR] per SD increment log-GGT, 1.26 [95%CI; 1.18 to 1.35]). Adjusting for established CVD risk factors (as time-dependent covariates updated quadriennially) and baseline CRP, a 1-SD increase in log-GGT conferred a 13% increase in CVD risk (P=0.007) and 26% increased risk of death (P<0.001). Individuals in the highest GGT quartile experienced a 67% increase in CVD incidence (multivariable-adjusted HR 1.67, 95%CI; 1.25 to 2.22).Conclusion—An increase in serum GGT predicts onset of metabolic syndrome, incident CVD, and death suggesting that GGT is a marker of metabolic and cardiovascular risk.
Establishment of a High Sensitivity Plasma Assay for Human Pentraxin3 as a Marker for Unstable Angina Pectoris
Authors: Inoue Kenji , Sugiyama Akira , Reid Patrick C. , Ito Yukio , Miyauchi Katsumi , Mukai Sei , Sagara Mina , Miyamoto Kyoko , Satoh Hirokazu , Kohno Isao , Kurata Takeshi , Ota Hiroshi , Mantovani Alberto , Hamakubo Takao , Daida Hiroyuki , Kodama Tatsuhiko 
Published: November 2006

Objective—Plasma pentraxin 3 (PTX3) levels are increased in patients with acute myocardial infarction, yet its involvement in unstable angina pectoris (UAP) remains unclear. To critically evaluate the role of PTX3 in UAP, a sensitive and precise measurement of PTX3 concentration is needed.Methods and Results—We established a high sensitive plasma ELISA assay system for the detection of PTX3 using monoclonal antibodies. The lower limit of detection of our ELISA was 0.1 ng/mL, sensitivity far greater than the current commercially available kit. Plasma samples were obtained from 162 consecutive patients treated for hypertension, hyperlipidemia, diabetes mellitus, or cardiovascular disease at a physician’s office. PTX3 was not associated with any known coronary risk factors. Additionally, we collected plasma samples from 252 consecutive subjects admitted to a university hospital for coronary artery assessment by coronary angiography. PTX3 was significantly increased in patients in whom coronary intervention was performed. We further analyzed the plasma level of PTX3 in 52 patients with effort angina (EAP) and 16 patients with UAP. Compared with the control group, PTX3 were significantly higher in the UAP group.Conclusions—The levels of plasma PTX3 were increased in patients with arterial inflammation, especially UAP. This PTX3 detection system will be useful for the prediction of UAP.
Can Pulse Oximetry or a Bedside Swallowing Assessment Be Used to Detect Aspiration After Stroke?
Authors: Ramsey Deborah J. C. , Smithard David G. , Kalra Lalit 
Published: November 2006

Background and Purpose—Desaturation during swallowing may help to identify aspiration in stroke patients. This study investigated pulse oximetry, bedside swallowing assessment (BSA), and videofluoroscopy as tests for detecting aspiration after stroke.Methods—Swallowing was assessed in 189 stroke patients (mean±SD age, 70.9±12.3 years) within 5 days of symptom onset with a modified BSA (water replaced by radio-opaque contrast agent, followed by chest radiography to detect aspiration). Simultaneous pulse oximetry recorded the greatest desaturation from baseline for 10 minutes from modified BSA onset. Videofluoroscopy was undertaken in 54 (28%) patients.Results—Modified BSA showed a safe swallow in 98 (51.9%), unsafe swallow in 85 (45.0%), and silent aspiration in 6 (3.2%) patients. During swallowing, desaturation by >2% occurred in 27 (27.6%) and by >5% in 3 (3.1%) of the 98 safe-swallow patients on modified BSA. Of the 85 unsafe-swallow patients, only 28 (32.9%) desaturated by >2% and 6 (7.1%) by >5%. Desaturation did not occur in any of the 6 silent aspirators. With the modified BSA to detect aspiration, sensitivity and specificity, respectively, were 0.31 and 0.72 for desaturation >2% and 0.07 and 0.97 for desaturation >5%. By videofluoroscopy, sensitivity and specificity for detecting aspiration were 0.47 and 0.72 for modified BSA, 0.33 and 0.62 for desaturation >2%, and 0.13 and 0.95 for desaturation >5%. Combining a failed modified BSA with desaturation >2% or >5% did not significantly improve predictive values.Conclusions—Modified BSA and pulse oximetry during swallowing, whether alone or in combination, showed inadequate sensitivity, specificity, and predictive values for detection of aspiration compared with videofluoroscopy in stroke patients.
Academic Discourses on School–Based Teacher Collaboration: Revisiting the Arguments
Authors: Lavié José Manuel 
Published: November 2006

Purpose: After decades arguing the necessity of transforming schools into collaborative workplaces, teacher collaboration has been taken up by various discursive logics offering different viewpoints of the concept. This article reviews some of these discourses and looks at their main arguments, pointing to the contradictions and tensions between them and highlighting the contested and cooptive nature of teacher collaboration. Proposed Conceptual Argument: This article differentiates provisionally between five discourses on teacher collaboration: Cultural discourses describe teacher collaboration as being embedded in cultural forms that blur the boundaries between personal and professional and stimulate interdependency and collective responsibility. School effectiveness and improvement discourses depict teacher collaboration as a product of cultural management led by the school's principal. School–as–community discourses embed teacher collaboration in a vision of schools as communities, where contractual models of relationships are transcended in pursuit of more inclusive environments. Restructuring discourses elaborate the idea of a “new professional” capable of getting involved in collaborative practices within an ever–learning organization. Finally, critical discourses articulate an approach that integrates democratic practices, community participation, and shared reflection on teaching as a social and political praxis. Implications: Although valuable lessons can be learned by considering these discourses as providing a complementary grasp, they also advance differing arguments as to the purposes of teacher collaboration, the differentiated way in which it is approached, and the position of conflict in collaborative processes. As value–embedded frameworks, discourses orientate the practice of collaboration toward substantially different projects of school change resulting in conservative or transformative practices.
RNAi-mediated silencing of TEL/AML1 reveals a heat-shock protein– and survivin-dependent mechanism for survival
Authors: Diakos Christofer , Krapf Gerd , Gerner Christopher , Inthal Andrea , Lemberger Christof , Ban Jozef , Dohnal Alexander M. , Panzer-Grümayer E. Renate 
Published: November 2006

Abstract
The TEL/AML1 fusion gene results from the most frequent t(12;21)(p13;q22) translocation in childhood acute lymphoblastic leukemia (ALL). Its contribution to transformation is largely unknown, in particular with respect to survival and apoptosis. We therefore silenced TEL/AML1 expression in leukemic REH cells by RNA inhibition, which eventually led to programmed cell death. Microarray and 2D gel electrophoresis data demonstrated a differential regulation of heat-shock proteins (HSPs), among them HSP90, as well as of its client, survivin. Consistent with these findings, ectopic expression of TEL/AML1 in Ba/F3 cells increased protein levels of HSP90 and survivin and conferred resistance to apoptotic stimuli. Our data suggest that TEL/AML1 not only contributes to leukemogenesis by affecting an antiapoptotic network but also seems to be indispensable for maintaining the malignant phenotype. The functional relationship between TEL/AML1, HSP90, and survivin provides the rational for targeted therapy, be it the fusion gene or the latter 2 proteins.
Gfi1b:green fluorescent protein knock-in mice reveal a dynamic expression pattern of Gfi1b during hematopoiesis that is largely complementary to Gfi1
Authors: Vassen Lothar , Okayama Taro , Möröy Tarik 
Published: November 2006

Abstract
Gfi1b and Gfi1 are 37- and 55-kDa transcriptional repressors that share common features such as a 20-amino acid (aa) N-terminal SNAG domain, a nonconserved intermediary domain, and 6 highly conserved C-terminal zinc fingers. Both gene loci are under autoregulatory and cross-regulatory feedback control. We have generated a reporter mouse strain by inserting the cDNA for green fluorescent protein (GFP) into the Gfi1b gene locus which allowed us to follow Gfi1b expression during hematopoiesis and lymphopoiesis by measuring green fluorescence. We found highly dynamic expression patterns of Gfi1b in erythroid cells, megakaryocytes, and their progenitor cells (MEPS) where Gfi1 is not detected. Vice versa, Gfi1b could not be found in granulocytes, activated macrophages, or their granulomonocytic precursors (GMPs) or in mature naive or activated lymphocytes where Gfi1 is expressed, suggesting a complementary regulation of both loci during hematopoiesis. However, Gfi1b was found to be up-regulated in early stages of B-cell and in a subset of early T-cell development, where Gfi1 is also present, suggesting that cross-regulation of both loci exists but is cell-type specific.
In vivo dynamics of regulatory T-cell trafficking and survival predict effective strategies to control graft-versus-host disease following allogeneic transplantation
Authors: Nguyen Vu H. , Zeiser Robert , daSilva Daniel L. , Chang Daisy S. , Beilhack Andreas , Contag Christopher H. , Negrin Robert S. 
Published: November 2006

AbstractCD4+CD25+ regulatory T cells (Tregs) suppress immune responses to alloantigens. The in vivo circulation and tissue localization of Tregs during an adaptive immune response remain unclear. We noninvasively tracked luciferase-expressing Tregs over time in an allogeneic bone marrow transplant model and demonstrated colocalization with effector T cells and initial expansion in secondary lymphoid organs before migration into inflamed tissues. Inflammation induced by irradiation and the allogeneic setting provided crucial stimuli for early Treg expansion and migration, leading to parallel reduction of effector T-cell proliferation in lymphoid organs and peripheral tissues. Treg transplants conferred long-term protection from systemic inflammatory challenge consistent with Treg in vivo survival. Suppression occurred during multiple phases of inflammation, but is optimal in the initial phase, providing protection from graft-versus-host disease while maintaining the graft-versus-tumor effect even at physiologic doses of Tregs due to their in vivo expansion, hence overcoming a major barrier to potential clinical applications of Tregs given their rarity.
Infiltrating neutrophils induce allospecific CTL in response to immunization with apoptotic cells via MCP-1 production
Authors: Shiratsuchi Yoshiko , Iyoda Takuya , Tanimoto Naoko , Kegai Daisuke , Nagata Kisaburo , Kobayashi Yoshiro 
Published: November 2006

AbstractOur previous studies demonstrated that i.p. injection of late apoptotic P388 cells caused phagocytosis by macrophages and transient infiltration of neutrophils into the peritoneal cavity. As neutrophils are known to function as effectors as well as regulators in the immune response, we examined the roles of infiltrating neutrophils in alloantigen-specific CTL induction after immunization with late apoptotic P388 cells. The CTL induction and infiltration of CD8+ T cells into the peritoneal cavity were inhibited by depletion of neutrophils by anti-Gr-1 mAb or inhibition of neutrophil infiltration by anti-MIP-2 antibody, suggesting that neutrophils are involved in CD8+ T cell infiltration into the peritoneal cavity. It is known that MIP-1α, MIP-1β, and MCP-1 are capable of attracting CD8+ T cells and that they are produced by neutrophils. These chemokines were detected in the peritoneal cavity, and among them, MCP-1 production was reduced remarkably by suppression of neutrophil infiltration. Moreover, infiltration of CD8+ T cells into the peritoneal cavity as well as CTL activity was clearly reduced by administering anti-MCP-1 antibody i.p. Furthermore, the CTL induction and infiltration of CD8+ T cells in neutrophil-depleted mice were restored significantly by administering recombinant murine MCP-1 into the peritoneal cavity. These results indicate that MCP-1 appears to link infiltration of neutrophils with CTL induction.
The Orphan Receptor Tyrosine Kinase Ror2 Promotes Osteoblast Differentiation and Enhances ex Vivo Bone Formation
Authors: Liu Yan , Bhat Ramesh A. , Seestaller-Wehr Laura M. , Fukayama Shoichi , Mangine Annamarie , Moran Robert A. , Komm Barry S. , Bodine Peter V. N. , Billiard Julia 
Published: November 2006

AbstractRor2 is a receptor tyrosine kinase, the expression of which increases during differentiation of pluripotent stem cells to osteoblasts and then declines as cells progress to osteocytes. To test whether Ror2 plays a role in osteoblastogenesis, we investigated the effects of Ror2 overexpression and down-regulation on osteoblastic lineage commitment and differentiation. Expression of Ror2 in pluripotent human mesenchymal stem cells (hMSCs) by adenoviral infection caused formation of mineralized extracellular matrix, which is the ultimate phenotype of an osteogenic tissue. Concomitantly, Ror2 over-expression inhibited adipogenic differentiation of hMSCs as monitored by lipid formation. Ror2 shifted hMSC fate toward osteoblastogenesis by inducing osteogenic transcription factor osterix and suppressing adipogenic transcription factors CCAAT/enhancer-binding protein α and peroxisome proliferator activated receptor γ. Infection with Ror2 virus also strongly promoted matrix mineralization in committed osteoblast-like MC3T3-E1 cells. Expression of Ror2 in a human preosteocytic cell line by stable transfection also promoted further differentiation, as judged by inhibited alkaline phosphatase activity, potentiated osteocalcin secretion, and increased cellular apoptosis. In contrast, down-regulation of Ror2 expression by short hairpin RNA essentially abrogated dexamethasone-induced mineralization of hMSCs. Furthermore, down-regulation of Ror2 expression in fully differentiated SaOS-2 osteosarcoma cells inhibited alkaline phosphatase activity. We conclude that Ror2 initiates commitment of MSCs to osteoblastic lineage and promotes differentiation at early and late stages of osteoblastogenesis. Finally, using a mouse calvariae ex vivo organ culture model, we demonstrate that these effects of Ror2 result in increased bone formation, suggesting that it may also activate mature osteoblasts.
Xenotransplantation of Long-Term-Cultured Swine Bone Marrow-Derived Mesenchymal Stem Cells
Authors: Nakamura Yasuhiro , Wang Xiaohong , Xu Chengsu , Asakura Atsushi , Yoshiyama Minoru , From Arthur H.L. , Zhang Jianyi 
Published: November 2006

Abstract
Swine-derived MSCs were efficiently isolated and extensively expanded using a low fetal serum content growth medium to which selected growth factors were added. After ≥96 cell population doublings (PDs), MSCs were devoid of cytogenetic abnormalities. In vitro chondrogenic and osteogenic differentiation capacity was preserved after 80 PDs. To test therapeutic efficacy, 1 × 106 80-PD MSCs were injected directly into the peri-infarct zone of hearts of immunodeficient (non-obese diabetic/severe combined immunodeficient) mice at the time of acute myocardial infarction. Engrafted MSCs survived in the infarcted hearts for at least 4 weeks. Echocardiography at 2 and 4 weeks postinfarction revealed a significant preservation of the left ventricular ejection fractions of infarct hearts receiving MSCs compared with infarct hearts receiving saline. Peri-infarct zone capillarity was better preserved in MSC-treated hearts than other infarct groups of hearts, but infarct size was comparable in all groups. Only rare engrafted MSCs expressed cardiac-specific or endothelial cell-specific markers. Hence, 80-PD MSCs retained the capacity to promote functional improvement in the infarcted heart despite minimal differentiation of MSCs into cardiomyocytes or endothelial cells. These data suggest that the beneficial effects of MSC transplantation most likely result from the trophic effects of MSC-released substances on native cardiac and vascular cells. The capacity to massively expand MSC lines without loss of therapeutic efficacy may prove to be useful in the clinical setting where “off the shelf” MSCs may be required for interventions in patients with acute coronary syndromes.
Identification of Common Pathways Mediating Differentiation of Bone Marrow- and Adipose Tissue-Derived Human Mesenchymal Stem Cells into Three Mesenchymal Lineages
Authors: Liu Tong Ming , Martina Monique , Hutmacher Dietmar W. , Hui James Hoi Po , Lee Eng Hin , Lim Bing 
Published: November 2006

Abstract
Mesenchymal stem cells derived from human bone marrow (hBMSCs) and human adipose tissue (hAMSCs) represent a useful source of progenitor cells for cell therapy and tissue engineering. However, it is not clear what the similarities and differences between them are. Like hBMSCs, hAMSCs can differentiate into osteogenic, adipogenic, and chondrogenic cells. Whether MSCs derived from different tissue sources represent fundamentally similar or different cell types is not clear. Given the possible different sources of MSCs for cell therapy, a comprehensive comparison of the different MSCs would be very useful. Here, we compared the transcriptome profile of hAMCS and hBMSCs during directed differentiation into bone, cartilage, and fat. Our data revealed considerable similarities between bone marrow-derived MSCs (BMSCs) and adipose tissue-derived MSCs (AMSCs). We uncovered an interesting bifurcation of pathways in both BMSCs and AMSCs, in which osteogenesis and adipogenesis appear to be linked in a differentiation branch separate from chondrogenesis. Our data suggest that although a set of common genes may be needed for early differentiation into all three lineages, a different set of signature genes is associated with maturation into fully differentiated cells. The recruitment of different late differentiation factors explains and supports our conclusion that BMSCs differentiate more efficiently into bone and cartilage, whereas AMSCs differentiate better into adipocytes. This study not only generated a rich database for continuing molecular characterization of various MSCs but also provided a rational basis for assessing qualities of MSCs from different sources for the purpose of cell-based therapy and tissue engineering.
Concise Review: Embryonic Stem Cells: A New Tool to Study Osteoblast and Osteoclast Differentiation
Authors: Duplomb Laurence , Dagouassat Maylis , Jourdon Philippe , Heymann Dominique 
Published: November 2006

AbstractBone remodeling involves synthesis of organic matrix by osteoblasts and bone resorption by osteoclasts. A tight collaboration between these two cell types is essential to maintain a physiological bone homeostasis. Thus, osteoblasts control bone-resorbing activities and are also involved in osteoclast differentiation. Any disturbance between these effectors leads to the development of skeletal abnormalities and/or bone diseases. In this context, the determination of key genes involved in bone cell differentiation is a new challenge to treat any skeletal disorders. Different models are used to study the differentiation process of these cells, but all of them use pre-engaged progenitor cells, allowing us to study only the latest stages of the differentiation. Embryonic stem (ES) cells come from the inner mass of the blastocyst prior its implantation to the uterine wall. Because of their capacity to differentiate into all germ layers, and so into all tissues of the body, ES cells represent the best model by which to study earliest stages of bone cell differentiation. Osteoblasts are generated by two methods, one including the generation of embryoid body, the other not. Mineralizing cells are obtained after 2 weeks of culture and express all the specific osteoblastic markers (alkaline phosphatase, type I collagen, osteocalcin, and others). Osteoclasts are generated from a single-cell suspension of ES cells seeded on a feeder monolayer, and bone-resorbing cells expressing osteoclastic markers such as tartrate-resistant alkaline phosphatase or receptor activator of nuclear factor κB are obtained within 11 days. The aim of this review is to present recent discoveries and advances in the differentiation of both osteoblasts and osteoclasts from ES cells.