bluuebunny/crossref_metadata_2025_split huggingface dataset:
Translating religion and development: Emerging perspectives from critical ethnographies of faith-based organizations
Authors: Bolotta Giuseppe , Scheer Catherine , Feener R. Michael 
Published: October 2019

Since the turn of the twenty-first century, there has been a remarkable surge of interest among both policy makers and academics on religion and its engagements with development. Within this context, ‘religious non-governmental organizations (RNGOs)’ or ‘faith-based organizations’ (FBOs) have garnered considerable attention. Early attempts to understand FBOs often took the form of typological mapping exercises, the cumulative effect of which has been the construction of a field of ‘RNGOs’ that can be analysed as distinct from—and possibly put into the service of—the work of purportedly secular development actors. However, such typologies imply problematic distinctions between over-determined imaginations of separate spheres of ‘religion’ and ‘development’. In this article, we innovatively extend the potential of ethnographic approaches highlighting aspects of ‘brokerage’ and ‘translation’ to FBOs and identify new, productive tensions of convergent analysis. These, we argue, provide original possibilities of comparison and meta-analysis to explore contemporary entanglements of religion and development. This article was written as part of a broader research project on Religion and NGOs in Asia. We are grateful to the Henry R. Luce Initiative on Religion in International Affairs at the Henry Luce Foundation for their generous support of this research. We would also like to thank Philip Fountain and other members of the National University of Singapore’s Asia Research Institute for stimulating conversations that have informed our thinking in this article, and the anonymous reviewers for PIDS who have helped us to improve on earlier drafts.
Mean muscle attenuation correlates with severe acute pancreatitis unlike visceral adipose tissue and subcutaneous adipose tissue
Authors: Sternby Hanna , Mahle Mariella , Linder Nicolas , Erichson-Kirst Laureen , Verdonk Robert C , Dimova Alexandra , Ignatavicius Povilas , Ilzarbe Lucas , Koiva Peeter , Penttilä Anne , Regnér Sara , Bollen Thomas L , Brill Richard , Stangl Franz , Wohlgemuth Walter A , Singh Vijay , Busse Harald , Michl Patrick , Beer Sebastian , Rosendahl Jonas 
Published: October 2019

BackgroundAcute pancreatitis (AP) is a frequent disorder with considerable morbidity and mortality. Obesity has previously been reported to influence disease severity.ObjectiveThe aim of this study was to investigate the association of adipose and muscle parameters with the severity grade of AP.MethodsIn total 454 patients were recruited. The first contrast‐enhanced computed tomography of each patient was reviewed for adipose and muscle tissue parameters at L3 level. Associations with disease severity were analysed through logistic regression analysis. The predictive capacity of the parameters was investigated using receiver operating characteristic (ROC) curves.ResultsNo distinct variation was found between the AP severity groups in either adipose tissue parameters (visceral adipose tissue and subcutaneous adipose tissue) or visceral muscle ratio. However, muscle mass and mean muscle attenuation differed significantly with p‐values of 0.037 and 0.003 respectively. In multivariate analysis, low muscle attenuation was associated with severe AP with an odds ratio of 4.09 (95% confidence intervals: 1.61–10.36, p‐value 0.003). No body parameter presented sufficient predictive capability in ROC‐curve analysis.ConclusionsOur results demonstrate that a low muscle attenuation level is associated with an increased risk of severe AP. Future prospective studies will help identify the underlying mechanisms and characterise the influence of body composition parameters on AP.
Multiple Myeloma: New Insights and Therapeutic Approaches
Authors: Anderson Kenneth C. , Kyle Robert A. , Dalton William S. , Landowski Terry , Shain Kenneth , Jove Richard , Hazlehurst Lori , Berenson James 
Published: October 2019

This review discusses the evolution of novel diagnostic and treatment strategies for multiple myeloma based upon increased understanding of basic disease pathogenesis. Although myeloma has remained an incurable illness to date, these new developments will derive treatments to improve outcome and achieve eventual cure.In Section I, Dr. Kyle reviews the results of current therapy for multiple myeloma, including high dose therapy and stem cell transplantation which have proven to achieve improved response rates, event-free, and overall survival. Supportive therapy, such as erythropoietin to treat disease-related anemia, and methods of prophylaxis against infection, which both lessen toxicities of treatment and improve quality of life for patients, are also addressed.In Section II, Dr. Dalton with Drs. Landowski, Shain, Jove and Hazlehurst discusses mechanisms of drug resistance in myeloma, with emphasis on novel treatment approaches to prevent development of drug resistance and to overcome drug resistance. Laboratory studies delineating mechanisms whereby myeloma cells resist drug-induced apoptosis provide the framework for related treatment protocols for patients with refractory disease.In Section III, Dr. Berenson reviews the management of complications in bone, which occur in the majority of patients with myeloma and are the major cause of decreased quality of life. New insights into the mediators of bone resorption and new bone formation in the marrow milieu have already derived effective bisphosphonate therapy. These drugs not only reduce bone complications and related pain, thereby improving quality of life, but also may have intrinsic anti-tumor activity by virtue of inducing tumor cell adherence to marrow, reducing interleukin-6 secretion, inducing tumor cell apoptosis, or inhibiting angiogenesis.In the last section, Dr. Anderson explores the potential for future therapies which offer great promise to improve patient outcomes. First, drugs which alter the marrow microenvironment include thalidomide and its derivative immunomodulatory drugs, which act directly on tumor cells to induce apoptosis or G1 growth arrest, alter tumor cell adhesion to marrow stroma, inhibit angiogenesis, and trigger a cellular anti-tumor response. The proteasome inhibitors both act directly on tumor cells and also inhibit the transcription factor NFκB-dependent upregulation of IL-6 secretion triggered by tumor cell adhesion. Second, delineation of both growth and apoptotic pathways has derived novel treatment strategies. Third, the preclinical basis and early clinical trial results using vaccination and adoptive immunotherapy to harness autoimmune and alloimmune anti-myeloma responses are presented. This review sets the stage for an evolving new biologically based treatment paradigm in myeloma targeting both the tumor and its microenvironment to improve outcome and achieve eventual cure.
New Views of Sickle Cell Disease Pathophysiology and Treatment
Authors: Rosse Wendell F. , Narla Mohandas , Petz Lawrence D. , Steinberg Martin H. 
Published: October 2019

AbstractThis review addresses several areas of concern in the care of patients with sickle cell disease. In Sections I and II, the fundamental pathogenetic mechanisms of sickle cell disease and their clinical consequences are discussed. Dr. Narla presents the evidence for abnormal cell adhesiveness by SS cells and Dr. Rosse examines the role of the increased whole blood viscosity. In Section III, Dr. Petz reviews common and uncommon alloimmune consequences of transfusion in sickle cell disease and discusses the diagnosis and management of sickle cell patients with hyperhemolysis after transfusion. In Section IV, Dr. Steinberg gives an update on the use of hydroxyurea in the treatment of sickle cell disease, including the SC and S-β thalassemia variants.
Status of Cytomegalovirus Prevention and Treatment in 2000
Authors: Zaia John A. , Sissons J.G. Patrick , Riddell Stanley , Diamond Don J. , Wills M.R. , Carmichael A.J. , Weekes M.P. , Gandhi M. , La Rosa C. , Villacres M. , Lacey S. , Markel S. , Sun J. 
Published: October 2019

AbstractCytomegalovirus (CMV) infection continues to be a problem in selected populations following hematopoietic stem cell transplantation (SCT). Although there have been no new antiviral agents for management of this infection in recent years, the methods for using the existing agents have improved with newer assays for detection of virus. In addition, our understanding of immunity to CMV has undergone considerable expansion. This paper will address these new aspects relating to CMV infection in the setting of SCT.In Section I Dr. Zaia reviews the pathogenesis of CMV and the current epidemiology of CMV disease following marrow or blood allo-SCT with emphasis on late-onset disease. The current lab tests available for preemptive management are summarized including the role for conventional shell vial cultures, and a comparison of the CMV antigenemia assay with the new nucleic acid-based assays, including the hybrid capture assay, the NASBA assay, and “real-time” PCR assays. Use of antiviral agents with these tests in the preemptive management of CMV infection is discussed.Ultimately, what is necessary is restoration of adequate CMV immunity, and that requires understanding the basics of the CMV-specific immune response. In Section II, Dr. Sissons traces the evolution of the CTL response from primary infection into memory and reviews recent advances in the understanding of cytotoxic T cell based immunity to CMV, based on the use of T cell clonotypic analysis and markers of T cell memory and activation, with conventional CTL functional assays.In Section III Dr. Riddell presents approaches to correction of the problem of CMV pathogenesis, namely direct restoration of the CMV-specific cellular immune deficiency. Attempts at passive therapies will be reviewed with the focus on current problems and approaches to these problems.In Section IV, Dr. Diamond presents work on the identification of multiple HLA-allele specific cytotoxic T cell epitopes specific for CMV-pp65 and - pp150. Specific epitopes are recognized by CMV-seropositive individuals including healthy donors, SCT recipients, and AIDS patients, indicating their potential usefulness as vaccines. One of these epitopes is recognized by most individuals who express the HLA A*0201 Class I allele. Pre-clinical evaluation in HLA2.1 transgenic mice of vaccine structures utilizing this epitope, and alternative delivery systems are described. Possible methods for vaccination of donor and/or recipient of a SCT as well as their limitations, utilizing synthetic or viral vaccines, are discusseed.
Transfusion Medicine: New Clinical Applications of Cellular Immunotherapy
Authors: Brenner Malcolm , Rossig Claudia , Sili Uluhan , Young James W. , Goulmy Els 
Published: October 2019

AbstractThere is now clear clinical evidence that adoptive cellular immunotherapy can eradicate hematologic malignancy and cure otherwise lethal viral infections. With this knowledge comes the challenge of improving the effectiveness and safety of the approach and of simplifying the methodologies required whilst still meeting appropriate federal regulatory guidelines. This review provides an overview of the current status of cellular immunotherapies and addresses how they may be implemented and the future directions they are likely to take.In Section I, Dr. Brenner with Drs. Rossig and Sili reviews the clinical experience to date with adoptive transfer of viral antigen-specific T cells for the successful treatment of Epstein-Barr virus-associated malignancies as well as viral infectious diseases. Genetic modification of the T cell receptor of the infused cells to potentiate such T cells as well as modifications to improve safety of the infusions are described.In Section II, Dr. Young describes the hematopoietic lineages of human dendritic cells and some of their immunotherapeutic applications. The critical importance of dendritic cells to T cell immunity and the capacity to generate dendritic cells in large numbers has spawned enormous interest in the use of these specialized leukocytes to manipulate cellular immunity. Successful cytokine-driven differentiation of dendritic cells reveal two types, myeloid- and plasmacytoid or lymphoid-related dendritic cells. The effects of maturation on phenotype and function of the dendritic cells and their use as immune adjuvants in dendritic cell vaccines to elicit antitumor and antiviral immunity are reviewed.In Section III, Professor Goulmy illustrates some current and future approaches towards tumor-specific cellular therapy of hematopoietic malignancy. Minor histocompatibility antigen (mHag) disparities between HLA-matched bone marrow donor and recipient can induce allo-responses that may participate in post bone marrow transplantation (BMT) graft-versus-leukemia (GVL) reactivities. A lack of such allo-reactivity may result in relapse of leukemia after BMT. In these patients, adoptive immunotherapy with cytotoxic T cells (CTLs) specific for hematopoietic system-restricted mHags may be used as an extension of current efforts using immunotherapy with donor lymphocyte infusions. Adoptive immunotherapy with CTLs specific for the hematopoietic system-restricted mHags, however, offers the prospect of greater and more predictable effectiveness in the absence of graft-versus-host disease.
Clinical Consequences of New Insights in the Pathophysiology of Disorders of Iron and Heme Metabolism
Authors: Brittenham Gary M. , Weiss Günter , Brissot Pierre , Lainé Fabrice , Guillygomarc'h Anne , Guyader Dominique , Moirand Romain , Deugnier Yves 
Published: October 2019

This review examines the clinical consequences for the practicing hematologist of remarkable new insights into the pathophysiology of disorders of iron and heme metabolism. The familiar proteins of iron transport and storage—transferrin, transferrin receptor, and ferritin—have recently been joined by a host of newly identified proteins that play critical roles in the molecular management of iron homeostasis. These include the iron-regulatory proteins (IRP-1 and -2), HFE (the product of the HFE gene that is mutated in most patients with hereditary hemochromatosis), the divalent metal transporter (DMT1), transferrin receptor 2, ceruloplasmin, hephaestin, the “Stimulator of Fe Transport” (SFT), frataxin, ferroportin 1 and others. The growing appreciation of the roles of these newly identified proteins has fundamental implications for the clinical understanding and laboratory evaluation of iron metabolism and its alterations with iron deficiency, iron overload, infection, and inflammation.In Section I, Dr. Brittenham summarizes current concepts of body and cellular iron supply and storage and reviews new means of evaluating the full range of body iron stores including genetic testing for mutations in the HFE gene, measurement of serum ferritin iron, transferrin receptor, reticulocyte hemoglobin content and measurement of tissue iron by computed tomography, magnetic resonance imaging and magnetic susceptometry using superconducting quantum interference device (SQUID) instrumentation.In Section II, Dr. Weiss discusses the improved understanding of the molecular mechanisms underlying alterations in iron metabolism due to chronic inflammatory disorders. The anemia of chronic disorders remains the most common form of anemia found in hospitalized patients. The network of interactions that link iron metabolism with cellular immune effector functions involving pro- and anti-inflammatory cytokines, acute phase proteins and oxidative stress is described, with an emphasis on the implications for clinical practice.In Section III, Dr. Brissot and colleagues discuss how the diagnosis and management of hereditary hemochromatosis has changed following the identification of the gene, HFE, that is mutated in most patients with hereditary hemochromatosis, and the subsequent development of a genotypic test. The current understanding of the molecular effects of HFE mutations, the usefulness of genotypic and phenotypic approaches to screening and diagnosis and recommendations for management are summarized.
Clinical Consequences of New Insights in the Pathophysiology of Disorders of Iron and Heme Metabolism
Authors: Brittenham Gary M. , Weiss Günter , Brissot Pierre , Lainé Fabrice , Guillygomarc'h Anne , Guyader Dominique , Moirand Romain , Deugnier Yves 
Published: October 2019

AbstractThis review examines the clinical consequences for the practicing hematologist of remarkable new insights into the pathophysiology of disorders of iron and heme metabolism. The familiar proteins of iron transport and storage—transferrin, transferrin receptor, and ferritin—have recently been joined by a host of newly identified proteins that play critical roles in the molecular management of iron homeostasis. These include the iron-regulatory proteins (IRP-1 and -2), HFE (the product of the HFE gene that is mutated in most patients with hereditary hemochromatosis), the divalent metal transporter (DMT1), transferrin receptor 2, ceruloplasmin, hephaestin, the “Stimulator of Fe Transport” (SFT), frataxin, ferroportin 1 and others. The growing appreciation of the roles of these newly identified proteins has fundamental implications for the clinical understanding and laboratory evaluation of iron metabolism and its alterations with iron deficiency, iron overload, infection, and inflammation.In Section I, Dr. Brittenham summarizes current concepts of body and cellular iron supply and storage and reviews new means of evaluating the full range of body iron stores including genetic testing for mutations in the HFE gene, measurement of serum ferritin iron, transferrin receptor, reticulocyte hemoglobin content and measurement of tissue iron by computed tomography, magnetic resonance imaging and magnetic susceptometry using superconducting quantum interference device (SQUID) instrumentation.In Section II, Dr. Weiss discusses the improved understanding of the molecular mechanisms underlying alterations in iron metabolism due to chronic inflammatory disorders. The anemia of chronic disorders remains the most common form of anemia found in hospitalized patients. The network of interactions that link iron metabolism with cellular immune effector functions involving pro- and anti-inflammatory cytokines, acute phase proteins and oxidative stress is described, with an emphasis on the implications for clinical practice.In Section III, Dr. Brissot and colleagues discuss how the diagnosis and management of hereditary hemochromatosis has changed following the identification of the gene, HFE, that is mutated in most patients with hereditary hemochromatosis, and the subsequent development of a genotypic test. The current understanding of the molecular effects of HFE mutations, the usefulness of genotypic and phenotypic approaches to screening and diagnosis and recommendations for management are summarized.
Hematology Grants Workshop—2000
Authors: Todd Robert F. , Miller Donald M. , Silverstein Roy L. 
Published: October 2019

This year the Hematology Grants Workshop, chaired by Dr. Robert Todd, includes a comprehensive listing of available NIH, VA, and non-federal grants applicable to fellows and junior faculty as well as to established investigators.
In Section II, Dr. Donald Miller discusses the essential principles of successful grant writing with a special emphasis on the young investigator. He highlights the best strategies to take and the common mistakes to avoid.
In Section III, Dr. Roy Silverstein outlines the structure of the current NIH Integrated Review Group (IRG) system and the study sections of the most relevance to hematology. He traces the path that a grant takes from review to funding including the way in which grants are reviewed at NIH Study Section Meetings and provides advice in the preparation of revised applications.
A Polycythemia Vera Update: Diagnosis, Pathobiology, and Treatment
Authors: Pearson Thomas C. , Messinezy Maria , Westwood Nigel , Green Anthony R. , Bench Anthony J. , Green Anthony R. , Huntly Brian J.P. , Nacheva Elizabeth P. , Barbui Tiziano , Finazzi Guido 
Published: October 2019

This review focuses on polycythemia vera (PV)—its diagnosis, cellular and genetic pathology, and management. In Section I, Dr. Pearson, with Drs. Messinezy and Westwood, reviews the diagnostic challenge of the investigation of patients with a raised hematocrit. The suggested approach divides patients on their red cell mass (RCM) results into those with absolute (raised RCM) and apparent (normal RCM) erythrocytosis. A standardized series of investigations is proposed for those with an absolute erythrocytosis to confirm the presence of a primary (PV) or secondary erythrocytosis, with abnormal and normal erythropoietic compartments respectively, leaving a heterogenous group, idiopathic erythrocytosis, where the cause cannot be established. Since there is no single diagnostic test for PV, its presence is confirmed following the use of updated diagnostic criteria and confirmatory marrow histology.In Section II, Dr. Green with Drs. Bench, Huntly, and Nacheva reviews the evidence from studies of X chromosome inactivation patterns that support the concept that PV results from clonal expansion of a transformed hemopoietic stem cell. Analyses of the pattern of erythroid and myeloid colony growth have demonstrated abnormal responses to several cytokines, raising the possibility of a defect in a signal transduction pathway shared by several growth factors. A number of cytogenetic and molecular approaches are now focused on defining the molecular lesion(s).In the last section, Dr. Barbui with Dr. Finazzi addresses the complications of PV, notably thrombosis, myelofibrosis and acute leukemia. Following an evaluation of published data, a management approach is proposed. All patients should undergo phlebotomy to keep the hematocrit (Hct) below 0.45, which may be all that is required in those at low thrombotic risk and with stable disease. In those at high thrombotic risk or with progressive thrombocytosis or splenomegaly, a myelosuppressive agent should be used. Hydroxyurea has a role at all ages, but 32P or busulfan may be used in the elderly. In younger patients, interferon-α or anagrelide should be considered. Low-dose aspirin should be used in those with thrombotic or ischemic complications.