bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Janus Face of Religion: On the Religious Factor in "New Wars"
Authors: Schäfer Heinrich 
Published: November 2004

AbstractEvery religion can be a base for respect and for violence. This is how the Bosnian peace activist Cvijeta Novacovic puts it. The Janus face of religion becomes especially visible when religion and politics mingle closely. This is the case in many of the so called "new wars," as for example in Bosnia, Kashmir, Sri Lanka, and other places. The present article focuses on how religion works within conflictive environments to mobilize people and to re-structure their identities. First, we will examine the special dynamics of new wars in order to focus the problem. Then, religion will be framed as a specific strategy of identity politics. On this basis we can analyze some ways by which religious logics operate in conflictive settings — for violence or for respect. The Bosnian war will serve as an example in most parts of the article.
Ham-Wasserman Lecture
Authors: Higgs Douglas R. 
Published: November 2004

Abstract
Over the past fifty years, many advances in our understanding of the general principles controlling gene expression during hematopoiesis have come from studying the synthesis of hemoglobin. Discovering how the α and β globin genes are normally regulated and documenting the effects of inherited mutations which cause thalassemia have played a major role in establishing our current understanding of how genes are switched on or off in hematopoietic cells. Previously, nearly all mutations causing thalassemia have been found in or around the globin loci, but rare inherited and acquired trans-acting mutations are being found with increasing frequency. Such mutations have demonstrated new mechanisms underlying human genetic disease. Furthermore, they are revealing new pathways in the regulation of globin gene expression which, in turn, may eventually open up new avenues for improving the management of patients with common types of thalassemia.
Hodgkin’s Lymphoma: Evolving Concepts with Implications for Practice
Authors: Meyer Ralph M. , Ambinder Richard F. , Stroobants Sigrid 
Published: November 2004

Abstract
Hodgkin’s lymphoma is a unique neoplasm of B lymphocytes. Recent data provide new understandings of the pathogenesis and options for staging and therapy of the disease. Three specific topics are addressed in this chapter.
In Section I, Dr. Richard Ambinder reviews implications of the relationship of Epstein-Barr virus (EBV) and Hodgkin’s lymphoma. This relation includes varying geographic epidemiologic associations, including varying associations with the clinical syndrome of infectious mononucleosis. There are plausible mechanisms, including processes initiated by viral proteins, by which EBV might lead to tumorigenesis. These mechanisms include promotion of genetic instability and alteration of normal processes of apoptosis. In addition to an epidemiologic association and potential role in pathogenesis, viral antigens may pose theoretical targets for anti-cancer therapies, including vaccination.
In Section II, Dr. Sigrid Stroobants describes the potential role of positron emission tomographic (PET) scanning. By assessing differences in the metabolic activities of cancer cells, PET scanning may be superior to computerized tomographic scanning, which is limited to showing structural anatomical abnormalities. In patients with Hodgkin’s and non-Hodgkin’s lymphoma, PET scanning has been tested as an initial staging tool, to assess the rate of therapeutic response from a prognostic perspective, and to differentiate residual tumor from fibrotic masses in patients who have completed therapy. Particularly in assessing the nature of a residual mass seen with other post-therapeutic imaging modalities, PET scanning may provide unique information; very high negative predictive values have been reported. However, before this technology can be recommended for incorporation into standard management, properly conducted prospective trials are required to better evaluate the clinical utility of PET with respect to eventual patient outcomes.
In Section III, Dr. Ralph Meyer reviews current data regarding the management of patients with limited-stage Hodgkin’s lymphoma. Over the past decade, standard treatment has evolved to consist of combined-modality therapy that includes an abbreviated course of chemotherapy and involved-field radiation. As this therapy continues to include radiation therapy, patients will remain at risk of long-term toxicities that include the development of second cancers and cardiovascular events. These “late-effects” now account for more deaths than those attributed to progressive Hodgkin’s lymphoma. Comparative data testing the role of chemotherapy alone are now available and demonstrate that omission of radiation therapy results in small but statistically significant reduction in disease control, but no detectable differences in overall survival. Further follow-up will clarify whether chemotherapy alone is the preferred treatment option; at present patients should be informed of the trade-offs involved in choosing between this option and combined modality therapy.
Myelodysplastic Syndromes
Authors: List Alan F. , Vardiman James , Issa Jean-Pierre J. , DeWitte Theo M. 
Published: November 2004

AbstractThe development of new therapeutic strategies for myelodysplastic syndromes (MDS) has gained new momentum fueled by improved characterization of the disease’s natural history and biology and by the recent US Food and Drug Administration (FDA) approval of the first agent with an indication for MDS. By integrating morphologic and cytogenetic features with greater discriminatory power, the World Health Organization (WHO) has refined the classification of these stem cell malignancies and enhanced its prognostic utility. Recognition that the malignant phenotype, which characterizes MDS, may arise from mechanistically diverse biological processes has raised new awareness that treatment strategies must be tailored to the pathobiology of the disease. Therapeutics targeting chromatin structure, angiogenesis and the microenvironment that nurtures the MDS phenotype have demonstrated remarkable activity and offer an opportunity to alter the natural history of the disease. This chapter provides an overview of recent developments in the characterization of MDS from the microscope to the laboratory and the translation of these findings into promising therapeutics.In Section I, Dr. James Vardiman reviews the cytogenetic abnormalities that characterize MDS, their clinical and pathologic significance, and the application of the WHO classification. In Section II, Dr. Alan List reviews treatment goals driven by prognostic variables and biological features of the disease that have led to promising small molecule, selective therapeutics. In Section III, Dr. Jean-Pierre Issa provides an overview of epigenetic events regulating gene expression, which may be exploited therapeutically by chromatin remodeling agents. In Section IV, Dr. Theo DeWitte discusses new developments in hematopoietic stem cell transplantation, including reduced-intensity and myeloablative approaches.
Thrombophilia and New Anticoagulant Drugs
Authors: Weitz Jeffrey I. , Middeldorp Saskia , Geerts William , Heit John A. 
Published: November 2004

Abstract
Venous thromboembolism, which includes deep vein thrombosis and pulmonary embolism, is the result of an imbalance among procoagulant, anticoagulant and profibrinolytic processes. This imbalance reflects a complex interplay between genetic and environmental or acquired risk factors. Genetic thrombophilic defects influence the risk of a first episode of thrombosis. How these defects influence the risk of recurrence in patients whose first episode of venous thromboembolism was unprovoked is less certain. Thus, when anticoagulants are stopped, patients with unprovoked venous thromboembolism have a risk of recurrence of at least 7% to 10% per year, even in the absence of an underlying thrombophilic defect. Consequently, there is a trend toward longer durations of anticoagulation therapy for these patients, which is problematic given the limitation of existing anticoagulants. This chapter provides an overview of the thrombophilic defects and how they influence the risk of venous thromboembolism. The chapter also details advances in anticoagulant therapy, focusing on new inhibitors of factor Xa and thrombin.
In Section I, Dr. Saskia Middeldorp describes the various thrombophilic defects and reviews their relative importance in the pathogenesis of a first episode of venous thromboembolism. She then discusses the influence of these defects on the risk of recurrent thrombotic events in patients with unprovoked venous thromboembolism and in those whose thrombosis occurred in association with a known risk factor, such as surgery.
In Section II, Dr. William Geerts reviews the pharmacology of new parenteral and oral factor Xa inhibitors and describes the results of the Phase II and III clinical trials with these agents. He then provides perspective on the potential advantages and drawbacks of these drugs for the prevention and treatment of venous thromboembolism.
In Section III, Dr. John Heit focuses on direct thrombin inhibitors. He discusses their mechanism of action and compares and contrasts their pharmacological profiles prior to describing the results of Phase II and III clinical trials. Dr. Heit then provides perspective on the potential advantages and limitations of these drugs relative to existing anticoagulants.
Transfusion Medicine
Authors: Goodnough Lawrence T. , Hewitt Patricia E. , Silliman Christopher C. 
Published: November 2004

Abstract
In the vein-to-vein flow of blood from donor to patient, the role of the transfusion medicine specialist has become increasingly centered at the bedside. Three clinically centered issues in blood safety and in blood conservation are presented in this chapter.
In Section I, Dr. Patricia Hewitt presents the epidemiologic and clinical evidence regarding new variant Creutzfeldt-Jakob disease (nvCJD) in the UK and its relevance to transfusion medicine. Lessons learned from the responses by the National Blood Service to this crisis are discussed, particularly in the context of recent evidence of a case of vCJD transmission by blood transfusion and a second case of apparent transmission of abnormal prion protein without development of clinical illness.
In Section II, Dr. Christopher Silliman and his colleagues summarize recent knowledge gained regarding transfusion-related acute lung injury (TRALI), which is now the leading cause of transfusion-related mortality. Two different etiologies have been proposed: a single antibody-medicated event, involving anti-HLA Class I and Class II, or anti-granulocyte antibodies; and a two-event model, which includes the clinical condition of the patient resulting in pulmonary endothelial activation and neutrophil sequestration. The second event is the transfusion of a biologic response modifier (lipids or antibodies) in the blood component that activates primed neutrophils. Prevention, clinical treatment, and proposed definition of TRALI are discussed.
In Section III, Dr. Lawrence Goodnough and colleagues present a transfusion medicine service approach to the utilization of recombinant factor VIIa (rFVIIa) in non-approved clinical settings. rFVIIa has a potential role as a hemostatic intervention in a variety of clinical settings, yet few clinical trials have been completed to date to guide indications for its use. The policies presented here are those in place at the authors’ medical center, and will undergo periodic review and revision as relevant new information and data are generated.
Immune-Mediated Hemolytic Anemia
Authors: Rosse Wendell F. , Hillmen Peter , Schreiber Alan D. 
Published: November 2004

AbstractHemolytic anemia due to immune function is one of the major causes of acquired hemolytic anemia. In recent years, as more is known about the immune system, these entities have become better understood and their treatment improved. In this section, we will discuss three areas in which this progress has been apparent.In Section I, Dr. Peter Hillmen outlines the recent findings in the pathogenesis of paroxysmal nocturnal hemoglobinuria (PNH), relating the biochemical defect (the lack of glycosylphosphatidylinositol [GPI]-linked proteins on the cell surface) to the clinical manifestations, particularly hemolysis (and its effects) and thrombosis. He discusses the pathogenesis of the disorder in the face of marrow dysfunction insofar as it is known. His major emphasis is on innovative therapies that are designed to decrease the effectiveness of complement activation, since the lack of cellular modulation of this system is the primary cause of the pathology of the disease. He recounts his considerable experience with a humanized monoclonal antibody against C5, which has a remarkable effect in controlling the manifestations of the disease. Other means of controlling the action of complement include replacing the missing modulatory proteins on the cell surface; these studies are not as developed as the former agent.In Section II, Dr. Alan Schreiber describes the biochemistry, genetics, and function of the Fcγ receptors and their role in the pathobiology of autoimmune hemolytic anemia and idiopathic thrombocytopenic purpura due to IgG antibodies. He outlines the complex varieties of these molecules, showing how they vary in genetic origin and in function. These variations can be related to three-dimensional topography, which is known in some detail. Liganding IgG results in the transduction of a signal through the tyrosine-based activation motif and Syk signaling. The role of these receptors in the pathogenesis of hematological diseases due to IgG antibodies is outlined and the potential of therapy of these diseases by regulation of these receptors is discussed.In Section III, Dr. Wendell Rosse discusses the forms of autoimmune hemolytic anemia characterized by antibodies that react preferentially in the cold–cold agglutinin disease and paroxysmal cold hemoglobinuria (PCH). The former is due to IgM antibodies with a common but particular structure that reacts primarily with carbohydrate or carbohydrate-containing antigens, an interaction that is diminished at body temperature. PCH is a less common but probably underdiagnosed illness due to an IgG antibody reacting with a carbohydrate antigen; improved techniques for the diagnosis of PCH are described. Therapy for the two disorders differs somewhat because of the differences in isotype of the antibody. Since the hemolysis in both is primarily due to complement activation, the potential role of its control, as by the monoclonal antibody described by Dr. Hillmen, is discussed.
Acute Myeloid Leukemia
Authors: Stone Richard M. , O'Donnell Margaret R. , Sekeres Mikkael A. 
Published: November 2004

AbstractAdvances in our understanding of the pathophysiology of acute myeloid leukemia (AML) have not yet led to major improvements in disease-free and overall survival of adults with this disease. Only about one-third of those between ages 18–60 who are diagnosed with AML can be cured; disease-free survival is rare and current therapy devastating in older adults. In this chapter, challenges in the management of the adult with AML are discussed, including ongoing questions concerning the optimal choice of induction and postremission therapy such as the rationale for and role of allogeneic and autologous stem cell transplantation in a variety of settings, the special considerations pertaining to the older patient, and the development of new, so-called targeted therapies.In Section I, Dr. Richard Stone reviews state-of the-art therapy in AML in the era of change from a morphological to a genetically based classification system. Questions being addressed in ongoing randomized cooperative group trials include anthracycline dose during induction, the efficacy of drug-resistance modulators, and the utility of pro-apoptotic agents such as the anti-bcl-2 antisense oligonucloetide. Developmental therapeutics in AML include drug resistance modulation, anti-angiogenic strategies, immunotherapy, and signal transduction-active agents, particularly the farnesyl transferase inhibitors as well as those molecules that inhibit the FLT3 tyrosine kinase, activated via mutation in 30% of patients.In Section II Dr. Margaret O’Donnell discusses the role of stem cell transplantation in AML. Several advances including expanded donor pools, the movement toward peripheral blood stem cell collection, newer immunosuppressive drugs and antifungals, and particularly the advent of nonmyeloablative transplant have made the allogeneic option more viable. The subset-specific role for high-dose chemotherapy with autologous stem cell support and/or for allogeneic transplant in AML patients in first remission is outlined. Although preconceived notions about the role of transplant abound, the clinical data supporting a risk-adapted approach are covered. Finally, guidance concerning the use of nonmyeloablative or reduced-intensity allogeneic transplantation is provided.In Section III Dr. Mikkael Sekeres reviews the approach to the older patient with AML. Unique biological and therapeutic considerations make AML in this age group a vastly different disease than that in younger adults. The outcome data, including the role of specific anthracylines, hematopoietic growth factors, and drug-resistance modulators, are summarized. Communicating with older adults with AML and their families regarding selection of the optimal treatment strategy, often a stark choice between induction chemotherapy and palliative care, is covered.
Hereditary risk factors for the development of gastric cancer in younger patients
Authors: Yaghoobi Mohammad , Rakhshani Naser , Sadr Farhad , Bijarchi Raheleh , Joshaghani Yasamin , Mohammadkhani Ashraf , Attari Arezou , Akbari Mohammad Reza , Hormazdi Mahshid , Malekzadeh Reza 
Published: November 2004

Abstract
Background
It is believed that the development of gastric cancer (GC) before the age of 50 has a hereditary basis. Blood group A and history of gastric cancer in first-degree relatives have been shown to be risk factors for GC.

Methods
In this case-control study, we enrolled patients with GC who were diagnosed before the age of 50. Patients who were diagnosed as having GC were selected. A total of 534 cases were found; of these, 44 diagnosed before the age of 50 were included in the case group. For the control group, 22 males and 22 females were randomly selected from the remaining subjects, who had diagnoses of GC after the age of 50. All the surviving patients and family members of the dead patients were interviewed about the history of cancer in the family and the age at which other family members developed cancer. The blood group of each subject was also obtained.

Results
forty-four cases under 50 years old (mean age: 36.2 years) and forty-four controls (mean age: 67.1 years) were enrolled in the study. At the time of the study, 59.1% of the study group and 50% of the control group were alive (P value = NS). In the study group, 68.1%, 13.6%, 13.6% and 4.5% had blood groups O, A, B and AB, respectively. In the control group the corresponding figures were 27.7%, 63.6%, 6.8% and 4.5%. First or second-degree relatives with cancer, including gastric (the most frequent), breast, lung, gynecological and hematological malignancies, were noted in 54.5% of the cases and 11.4% of the controls (p < 0.01). Family histories of cancer were accepted as valid provided that they were based on valid medical documents.

Conclusions
It seems that the development of GC before the age of 50 is likely to be accompanied by familial susceptibility. Interestingly, our study showed a significant correlation between blood group O and the development of gastric cancer under the age of 50.
Multimodal pressure-flow method to assess dynamics of cerebral autoregulation in stroke and hypertension
Authors: Novak Vera , Yang Albert CC , Lepicovsky Lukas , Goldberger Ary L , Lipsitz Lewis A , Peng Chung-Kang 
Published: November 2004

Abstract
Background
This study evaluated the effects of stroke on regulation of cerebral blood flow in response to fluctuations in systemic blood pressure (BP). The autoregulatory dynamics are difficult to assess because of the nonstationarity and nonlinearity of the component signals.

Methods
We studied 15 normotensive, 20 hypertensive and 15 minor stroke subjects (48.0 ± 1.3 years). BP and blood flow velocities (BFV) from middle cerebral arteries (MCA) were measured during the Valsalva maneuver (VM) using transcranial Doppler ultrasound.

Results
A new technique, multimodal pressure-flow analysis (MMPF), was implemented to analyze these short, nonstationary signals. MMPF analysis decomposes complex BP and BFV signals into multiple empirical modes, representing their instantaneous frequency-amplitude modulation. The empirical mode corresponding to the VM BP profile was used to construct the continuous phase diagram and to identify the minimum and maximum values from the residual BP (BPR) and BFV (BFVR) signals. The BP-BFV phase shift was calculated as the difference between the phase corresponding to the BPR and BFVR minimum (maximum) values. BP-BFV phase shifts were significantly different between groups. In the normotensive group, the BFVR minimum and maximum preceded the BPR minimum and maximum, respectively, leading to large positive values of BP-BFV shifts.

Conclusion
In the stroke and hypertensive groups, the resulting BP-BFV phase shift was significantly smaller compared to the normotensive group. A standard autoregulation index did not differentiate the groups. The MMPF method enables evaluation of autoregulatory dynamics based on instantaneous BP-BFV phase analysis. Regulation of BP-BFV dynamics is altered with hypertension and after stroke, rendering blood flow dependent on blood pressure.
Influence of pericardial suction blood retransfusion on memory function and release of protein S100B
Authors: Svenmarker S , Engström K G , Karlsson T , Jansson E , Lindholm R , Åberg T 
Published: November 2004

Background: To study the influence of pericardial suction blood (PSB) on postoperative memory disturbances and release patterns of protein S100B during and after cardiopulmonary bypass (CPB). Methods: Sixty male patients admitted for coronary artery bypass surgery were prospectively randomized to receive PSB either by using conventional cardiotomy suction retransfusion or after cell-saver processing. Results: The concentration of S100B rose during the period of CPB from 0.065±0.004 to 0.24±0.001 mg/L (p<0.001). PSB contained 18.0±1.7 mg/L of S100B. Direct retransfusion from the cardiotomy reservoir made the systemic level increase to 1.42±0.19 mg/L compared to 0.25±0.02 mg/L using a cell-saver. Signs of postoperative memory dysfunction (> 1 SD) were discovered in one of three tests, but were unrelated to technique of retransfusion. No associations were found between serum concentrations of S100B and memory function. Conclusion: In this study, retransfusion of PSB during cardiac surgery appeared not to cause memory disturbances. PSB contained high concentrations of protein S100B making its use as a marker of cerebral injury unsuitable.
Treatment of recurrent posterior dislocation of the shoulder in cerebral palsy by injection with botulinum toxin A into the M. subscapularis
Authors: de Boer K S , Rozing P M , Arendzen J H 
Published: November 2004

Subjects: A 20-year-old woman, known to have cerebral palsy and a spastic hemiparesis, suffered from frequent (up to 20 times a day) and painful posterior dislocation of the affected shoulder. Interventions: For the last two years we have treated her with injections with botulinum toxin A (100 U Botox®) in the M. subscapularis. Results: Pain and dislocation rate have improved substantially.