bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gender Differences in Lower Extremity Landing Mechanics Caused by Neuromuscular Fatigue
Authors: Kernozek Thomas W. , Torry Michael R. , Iwasaki Mark 
Published: November 2007

Background Neuromuscular fatigue has been suggested as an extrinsic factor in the mechanism of noncontact anterior cruciate ligament injury in both genders. Purpose To determine and describe the lower extremity kinematic and kinetic differences caused by neuromuscular fatigue during drop landings and compare changes between age- and skill-matched male and female athletes. Methods Inverse dynamic solutions estimated lower extremity flexion-extension and varus-valgus kinematics and kinetics for 14 female and 16 male athletes performing a single-legged 50-cm drop landing. Subjects performed landings prefatigue and postfatigue with fatigue induced via a parallel squat exercise (60% of 1 repetition maximum) until failure. A mixed-model, repeated-measures analysis of variance (fatigue * gender) was performed on select kinematic and kinetic variables. Results Neuromuscular fatigue caused men and women to land with more hip flexion (main effect fatigue, P = .012; main effect gender, P = .001). Men exhibited greater peak knee flexion angles postfatigue; women did not alter knee flexion (fatigue * gender, P =.028). Men exhibited larger peak knee varus angles irrespective of fatigue (main effect gender, P = .039; main effect fatigue, P = .127; fatigue * gender, P = .153); women demonstrated larger peak valgus angles overall (main effects gender, P = .009). There were no changes with fatigue (main effect fatigue, P = .127) or a different response due to fatigue with gender (fatigue * gender, P = .091). Women exhibited greater knee anterior shear force postfatigue (fatigue * gender, P = .010). Men and women exhibited lower knee extension moments (main effect fatigue, P = .000; main effect gender, P = .927; fatigue * gender, P = .309) and abduction moments (main effect fatigue, P = .014; main effect gender, P = .670; fatigue * gender, P = .191). Conclusion Neuromuscular fatigue caused significant alterations in women that may be indicative of the noncontact anterior cruciate ligament injury mechanisms. Clinical Relevance Current noncontact anterior cruciate ligament prevention programs should incorporate a fatigue component to help minimize the deleterious effects of neuromuscular fatigue on landing mechanics.
Anterior Translation at the Glenohumeral Joint
Authors: Stapleton Claire H. , Herrington Lee , George Keith 
Published: November 2007

Background Lesions to the axillary artery are reported in overhead athletes. One speculated cause is repeated transient compression by the humeral head due to excessive laxity at the glenohumeral joint. Hypotheses (1) Anterior translation of the glenohumeral joint alters axillary artery diameter and blood flow characteristics, and (2) individuals demonstrating inducible axillary artery compression with the arm in an overhead position (as indicated by diameter and blood flow characteristics) will demonstrate greater magnitudes of anterior translation. Study Design Descriptive laboratory study. Methods After receiving ethical approval and screening for problematic conditions/injuries, 26 subjects were tested (10 men and 16 women; mean age [standard deviation], 25 years [4]). Axillary artery diameter and peak systolic velocity were measured with B-mode and Doppler ultrasound before, during, and after glenohumeral anterior translation at 90° of abduction, 60° of external rotation, and 30° of horizontal flexion, and at baseline and a simulated overhead throwing position (120° of abduction, 90° of external rotation, and 30° of horizontal extension). The magnitude of anterior translation was captured with B-mode ultrasound using a posterior transverse approach. Results Application of the glide resulted in a significant (F2,21 = 9.965, P = .001) reduction in axillary artery diameter and a significant increase in peak systolic velocity (F2,21 = 5.286, P = .014). Subjects demonstrating clinically significant levels of axillary artery compression (>50% reduction in vessel diameter with the arm in the overhead throwing position) exhibited significantly (t = −2.260, P = .040) greater ranges of anterior translation at the glenohumeral joint than the 9 subjects who exhibited <10% reduction in arterial diameter. Conclusions This investigation provides the first empirical support for the clinical opinion that glenohumeral anterior translation could be a mechanism for inducible axillary artery compression. Clinical Relevance The response of axillary artery hemodynamics in normal, healthy individuals is the first step in the process of determining whether the finding of inducible axillary artery compression in overhead athletes with arterial pathology is related to glenohumeral translation.
The J-Bone Graft for Anatomical Glenoid Reconstruction in Recurrent Posttraumatic Anterior Shoulder Dislocation
Authors: Auffarth Alexander , Schauer Josef , Matis Nicholas , Kofier Barbara , Hitzl Wolfgang , Resch Herbert 
Published: November 2007

Background Posttraumatic shoulder dislocations with glenoid rim fractures show high rates of dislocation recurrence. For glenoid rim defects exceeding a certain size, several investigators recommend bone grafting. Few reports on anatomical glenoid reconstruction addressing this problem are published. Hypothesis Anatomical glenoid reconstruction by the J-bone graft creates permanent joint stability without a clinically relevant loss of motion. Study Design Case series; Level of evidence, 4. Methods Forty-seven shoulders with glenoid rim fractures after recurrent anterior dislocation were stabilized by a J-bone graft. For clinical outcome, motion and strength compared with the uninjured shoulder, as well as sports activity, were recorded. The Rowe score and the Constant-Murley score were used for scoring. In cases of follow-up exceeding 6 years, computed tomography scans were obtained and compared to preoperative radiographs. Results The mean Rowe score was 94.3 for the affected shoulder and 96.8 for the uninjured side. The Constant score reached 93.5 and 95 points, respectively. Loss of external rotation was 4.36° in adduction and 3.19° at 90° of abduction. The computed tomography evaluation included 24 shoulders at a mean follow-up of 106.2 months. There were no recurrences of instability and 1 traumatic graft fracture. Of the 19 patients in whom arthropathy was present at follow-up, 11 had arthrosis before surgery. Conclusion The J-bone graft is capable of creating a stable shoulder joint without causing extensive loss of motion on the long term in patients with traumatic glenoid rim fractures after shoulder dislocation. In some patients, mild to moderate arthropathy develops despite anatomical glenoid reconstruction.
Politics as the Church's Business: William Temple's Christianity and Social Order Revisited
Authors: Brown Malcolm 
Published: November 2007

ABSTRACTChristianity and Social Order was a creature of its time and, although influential over several decades, is challenged by today's plurality and globalization. Nevertheless, the ascendancy of Radical and Neo-Orthodoxy repeats imbalances of the Christendom Group which Temple was concerned to counter. Temple's greatest weakness for today is his failure to appreciate the trend towards profound social plurality, and its challenge to his strong idea of nationhood. However, today's global economy suggests that plurality must be held in tension with other aspects of the dominant market model. Temple's work reinforces important critiques of market economics, including scepticism about the alleged impossibility of moral agreement. This in turn suggests that total abandonment of Temple's Middle Axiom approach may be premature. A better-developed theology of correctives would reflect classic Christian vocabulary, cohere with Temple's approach, and offer a route toward the revitalization of the Anglican tradition of public theology.
Grace and Nation: Coleridge's On the Constitution of Church and State
Authors: Gregory Alan 
Published: November 2007

ABSTRACTUnderstanding Coleridge's classic work On the Constitution of Church and State requires paying close attention to the system of distinctions and relations he sets up between the state, the ‘national church’, and the ‘Christian church’. The intelligibility of these relations depends finally on Coleridge's Trinitarianism, his doctrine of ‘divine ideas’, and the subtle analogy he draws between the Church of England as both an ‘established’ church of the nation and as a Christian church and the distinction and union of divinity and humanity in Christ. Church and State opens up, in these ‘saving’ distinctions and connections, important considerations for the integrity and role of the Christian church within a religiously plural national life.
The Genetic Basis of Myeloproliferative Disorders
Authors: Skoda Radek 
Published: November 2007

AbstractFor many decades, myeloproliferative disorders (MPD) were largely neglected orphan diseases. The conceptual work of William Dameshek in 1951 provided the basis for understanding MPD as a continuum of related syndromes, possibly with a common pathogenetic cause. Recognition of the clonal origin of peripheral blood cells in MPD in 1976 and the ability to grow erythroid colonies in vitro in the absence of added growth factors in 1974 initiated the search for genetic alterations that might be responsible for myeloproliferation. Mutations in the genes for the erythropoietin receptor, thrombopoietin and the von Hippel–Lindau protein were found to cause familial syndromes resembling MPD, but despite their phenotypic similarities, none of these mutations were later found in patients with the sporadic form of MPD. The discovery of activating mutations in the Janus kinase 2 (JAK2) in most patients with MPD has fully transformed and energized the MPD field. Sensitive assays for detecting the JAK2-V617F mutation have become an essential part of the diagnostic work-up, and JAK2 now constitutes a prime target for developing specific inhibitors for the treatment of patients with MPD. Despite this progress, many questions remain unsolved, including how a single JAK2 mutation causes three different MPD phenotypes, what other genes might be involved in the pathogenesis, and what are the factors determining the progression to acute leukemia.
Novel Thrombopoietic Agents
Authors: Andemariam Biree , Psaila Bethan , Bussel James B. 
Published: November 2007

AbstractThrombocytopenia is a primary manifestation of immune thrombocytopenic purpura (ITP) and may occur as a result of hepatitis C, malignancy, and treatment with chemotherapy. There is a need for additional means to treat thrombocytopenia in these settings. Recombinant thrombopoietin-like agents became available after the cloning of thrombopoietin in 1994. In clinical trials, these agents showed some efficacy in chemotherapy-induced thrombocytopenia, but their use was ultimately discontinued due to the development of neutralizing antibodies that cross-reacted with endogenous thrombopoietin and caused thrombocytopenia in healthy blood donors and other recipients. Subsequently, “second-generation” thrombopoietic agents without homology to thrombopoietin were developed. In the past 5 years, these second-generation thrombopoeitic growth factors have undergone substantial clinical development and have demonstrated safety, tolerability and efficacy in subjects with ITP and hepatitis C–related thrombocytopenia. These completed studies, many of which are available only in abstract form, and other ongoing studies suggest that thrombopoietic agents will enhance the hematologist’s ability to manage these and other causes of thrombocytopenia.
TTP and ADAMTS13: When Is Testing Appropriate?
Authors: Mannucci Pier Mannuccio , Peyvandi Flora 
Published: November 2007

Abstract
The last 10 years witnessed the publication of many studies on the pathophysiology of thrombotic thrombocytopenic purpura (TTP), a life-threatening disease characterized by microangiopathic hemolytic anemia, thrombocytopenia and multiorgan failure. The most important finding was the identification of a novel metalloprotease, named ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin type 1 motives), that is involved in the regulation of the size of von Willebrand factor (VWF), a major modulator of platelet adhesion and aggregation in the microcirculation. Inherited or acquired deficiencies of ADAMTS13 impair VWF cleavage, leading in turn to the disseminated formation of platelet-rich thrombi in the micro-circulation and to symptoms of end-organ ischemia. By measuring ADAMTS13 in plasma, it has been clearly shown that patients with inherited TTP have severe ADAMTS13 deficiency. However, patients with acquired TTP present with clinical and laboratory heterogeneity, and there are unequivocal cases of acquired TTP with measurable plasma levels of ADAMTS13. This heterogeneity poses a challenge for understanding the pathogenesis of TTP and selecting appropriate therapies.
Management of Pregnant Women with Thrombophilia or a History of Venous Thromboembolism
Authors: Bates Shannon M. 
Published: November 2007

Abstract
Pregnancy is associated with an increased risk of venous thromboembolism (VTE), and this condition remains an important cause of maternal morbidity and mortality. Approximately 50% of gestational VTE are associated with thrombophilia. Recent studies suggest that there is also a link between thrombophilia and pregnancy loss, as well as other gestational vascular complications. Although the most compelling data derive from women with antiphospholipid antibodies, the use of anticoagulation for prevention of these complications in women with heritable thrombophilia is becoming more frequent. This article reviews the management and prevention of VTE and other complications related to the heritable thrombophilias during pregnancy, an area that remains particularly challenging because of the potential for anticoagulant-related fetal as well as maternal complications and the paucity of good-quality data upon which to base clinical decisions.
Management of Thrombohemorrhagic Syndromes (THS) in Hematologic Malignancies
Authors: Falanga Anna , Rickles Frederick R. 
Published: November 2007

AbstractThe rate of venous thromboembolism (VTE) in patients with acute leukemia or lymphomas is comparable with that of other “high-risk” cancer types. Chemotherapy and anti-angiogenic drugs increase the thrombotic risk in patients with lymphomas, acute leukemias and multiple myeloma (MM). Patients with hematologic malignancies often present with a hypercoagulable state or chronic disseminated intravascular coagulation (DIC) in the absence of active thrombosis and/or bleeding. Malignant cell procoagulant properties, cytotoxic therapies, and concomitant infections are major determinants for clotting activation in hematologic malignancies. In acute leukemia, clinical manifestations range from localized venous or arterial thrombosis to a diffuse, life-threatening thrombohemorrhagic syndrome (THS). All-trans retinoic acid (ATRA) has greatly improved the management of acute promyelocytic leukemia (APL), but has not significantly changed the rate of early hemorrhagic deaths and may actually promote thrombosis. Randomized, controlled trials (RCTs) of different prophylactic regimens to prevent VTE or THS in hematologic malignancies are urgently needed, particularly in patients with lymphoma or MM during chemotherapy and in patients with APL. Anticoagulant therapy is a particular challenge in patients with hematologic malignancies, since these patients are at very high risk for hemorrhage. No guidelines are available for the prophylaxis or treatment of VTE; extrapolations can be made from existing guidelines for management of patients with other malignancies; prolonged periods of treatment-induced thrombocytopenia in patients with hematologic malignancies, however, require a more judicious application of standard anticoagulant approaches. Use of the newer anticoagulants will require careful assessment of hemorrhagic risk in this group of high-risk patients but may be justified under special circumstances.
Towards the Generation of Patient-Specific Pluripotent Stem Cells for Combined Gene and Cell Therapy of Hematologic Disorders
Authors: Daley George Q. 
Published: November 2007

AbstractHematopoietic stem cell transplantation (HSCT) has proven successful for the treatment of a host of genetic and malignant diseases of the blood, but immune barriers to allogeneic tissue transplantation have hindered wider application. Likewise, gene therapy now appears effective in the treatment of various forms of immune deficiency, and yet insertional mutagenesis from viral gene transfer has raised safety concerns. One strategy for addressing the limitations of both gene therapy and allogeneic transplantation entails the creation of pluripotent stem cells from a patient’s own somatic cells, thereby enabling precise in situ gene repair via homologous recombination in cultured cells, followed by autologous tissue transplantation. In murine model systems, the methods of somatic cell nuclear transfer, parthenogenesis, and direct somatic cell reprogramming with defined genetic factors have been used to generate pluripotent stem cells, and initial efforts at therapeutic gene repair and tissue transplantation suggest that the technology is feasible. Generating patient-specific autologous pluripotent stem cells provides an opportunity to combine gene therapy with autologous cell therapy to treat a host of human conditions. However, a number of technical hurdles must be overcome before therapies based on pluripotent human stem cells will appear in the clinic.
The Biology of the Germinal Center
Authors: Natkunam Yasodha 
Published: November 2007

Abstract
The immune system requires the production of high affinity antibodies of different subclasses to accomplish its many effector functions. Specific steps in B-cell ontogeny that occur within germinal centers of secondary lymphoid organs create much of the diversity in the immune system. This process also provides the raw material for the genesis of B-cell lymphomas as misdirection of the molecular machinery that regulate these steps can cause chromosomal translocations, prevent apoptosis and promote proliferation of abnormal clones. Many recent avenues of investigation have elucidated that the germinal center is a dynamic microenvironment where B-cells undergo repeated rounds of mutation and selection. Gene expression studies have further shown that malignancies derived from germinal center B-cells elaborate specific gene expression signatures that derive from neoplastic cells as well as elements of the host response such as T-cells and macrophages. This review will examine the current understanding of B-cell development in the germinal center and the key molecules involved in this process. Interactions between lymphoma cells and their cellular partners and models in the growth and development of follicular lymphoma will be presented.
Follicular NHL: From Antibodies and Vaccines to Graft-versus-Lymphoma Effects
Authors: Maloney David G. 
Published: November 2007

AbstractMonoclonal antibody therapy with rituximab in combination with standard chemotherapy has improved the survival of patients with advanced-stage follicular lymphoma (FL). A series of next-generation anti-CD20 antibodies may be less immunogenic and have even greater antitumor activity through augmented interactions with host effector mechanisms responsible for tumor cell kill. Additional approaches with patient-specific immunoglobulin idiotype vaccines; novel monoclonal antibodies binding to biologically active cell-surface antigen are also demonstrating early clinical activity. Antibodies targeting radioisotopes, toxins or drugs are also slowly entering clinical trials and practice. Last, allogeneic stem cell transplantation following reduced-intensity conditioning provides graft-versus-tumor immune responses that may be able to control FL and allow this risky but potentially curative treatment option to older patents or those with comorbidities.
Vaccine Therapy for B-Cell Lymphomas: Next-Generation Strategies
Authors: Neelapu Sattva S. , Kwak Larry W. 
Published: November 2007

AbstractActive immunotherapy is a promising approach for the treatment of lymphomas. Immunization with the clonal tumor immunoglobulin, idiotype, expressed on the surface of B-cell malignancies was associated with induction of tumor-specific cellular and humoral immunity, molecular remissions, and prolonged disease-free survival in early clinical trials. Idiotype vaccination was also demonstrated to induce tumor-specific T-cell immunity in the absence of B cells following treatment with rituximab-containing chemotherapy, suggesting that vaccines may be used in combination with rituximab. Three double-blind randomized phase 3 idiotype vaccine trials are currently ongoing to definitively determine the clinical benefit of idiotype vaccination in patients with lymphoma. Novel second-generation lymphoma vaccines are in development to streamline the production of patient-specific cancer vaccines and show encouraging results in preclinical and pilot clinical studies. To enhance the clinical efficacy of active immunotherapy, future clinical trials are likely to use a combination strategy with the lymphoma vaccine to stimulate an antitumor T-cell response and the simultaneous suppression of immune regulatory pathways to augment the induced T-cell response.
Engineering Antitumor Immunity by T-Cell Adoptive Immunotherapy
Authors: Riddell Stanley R. 
Published: November 2007

Abstract
The adoptive transfer of antigen-specific T cells has been used successfully to treat experimental tumors in animal models and viral infections in humans, but harnessing the exquisite specificity and potency of T cells to treat human malignancy has proven challenging. The efforts to use T cells to treat patients with cancer have often been informative in identifying limitations that must be overcome to improve therapeutic efficacy, and a clearer picture of the requirements for successful adoptive T-cell transfer is gradually emerging. Indolent and a subset of aggressive B-cell lymphomas in humans have been shown to be susceptible to eradication by T cells in clinical settings where highly immunogenic minor histocompatibility or viral antigens are presented by tumor cells. In this article, we will review how recent advances in our understanding of the properties of antigen-specific T cells that facilitate their long-term persistence in vivo and reversion to the memory pool after in vitro culture, combined with approaches to molecularly engineer T cells with receptors that target molecules expressed by B-cell lymphoma, are providing opportunities to broaden the application of T-cell therapy and improve its efficacy for this disease.