bluuebunny/crossref_metadata_2025_split huggingface dataset:
Motion(Less)in Limine
Authors: Scofield Giles 
Published: January 2007

“When the two come into conflict, democracy takes priority to philosophy.”Richard Rorty“There are some people who use philosophy to lead people astray.”St. AugustineAs any seasoned litigator knows, occasionally one interposes an evidentiary objection not simply for the sake of preventing this or that from occurring in court, but also for the purpose of alerting a court to and educating it about the likelihood that it will have to rule on what may prove to be a substantial evidentiary dispute. Instead of waiting until a trial has begun and somebody else’s expert witness is ready, willing, able and - most of all - present to testify, it can be useful to file a motionin limine, a pre-trial motion that seeks to bar or set limits to an expert’s testimony.
Dangerous Times for Medicaid
Authors: Jacobi John V. 
Published: January 2007

These are indeed dangerous times. In the name of “cost-effectiveness,” we cut back health benefits to the poor, who are more likely to be sick than the nonpoor. We miss our chance to heal. In the setting, we’re told, of “scarce resources,” we imperil the health care safety net. In the name of expedience, we miss our chance to be humane and compassionate.’Medicaid is again - still - the subject of reform discussions in Washington and in state capitals. The program has been subject to varying, sometimes conflicting pressures since its inception. Its primary purpose has been serving the health care needs of the poor and disabled. It was structured, however, to appeal to (or at least to not alienate) private health care providers. In addition, its mix of state and federal funding and control was intended to draw in the states as partners.
The Confidentiality and Privacy Implications of Functional Magnetic Resonance Imaging
Authors: Tovino Stacey A. 
Published: January 2007

Advances in science and technology frequently raise new ethical, legal, and social issues, and developments in neuroscience and neuroimaging technology are no exception. Within the field of neuroethics, leading scientists, ethicists, and humanists are exploring the implications of efforts to image, study, treat, and enhance the human brain.This article focuses on one aspect of neuroethics: the confidentiality and privacy implications of advances in functional magnetic resonance imaging (“fMRI”). Following a brief orientation to fMRI and an overview of some of its current and proposed uses, this article highlights key confidentiality and privacy issues raised by fMRI in the contexts of health care, research, employment, insurance, criminal justice, litigation, and cognitive privacy.
Dietary Supplements: Reports Reviewed by Tia Powell and Barbara A. Noah
Authors: Powell Tia , Noah Barbara A. 
Published: January 2007

The Institute of Medicine’s 2005 publication,Dietary Supplements: A Framework for Evaluating Safety, is authoritative and thorough, and thus representative of other reports by the Institute of Medicine (IOM). What makes this report particularly interesting, however, is the rich political subtext that exists in the interstices of the report, popping up here and there in brief comments and barely suppressed yelps of exasperation. To understand this context, it is useful to reflect for a moment on the special nature of the IOM and its relationship to government.IOM is part of the National Academy of Sciences, and is a private, non-governmental organization that does not receive direct federal funding for its work. Rather, IOM studies are often funded by contract with governmental entities that request reports on particular topics. As a case in point, the dietary supplement study was requested and paid for by the FDA.
Eccentric Loading, Shock-Wave Treatment, or a Wait- and-See Policy for Tendinopathy of the Main Body of Tendo Achillis
Authors: Rompe Jan D. , Nafe Bernhard , Furia John P. , Maffulli Nicola 
Published: January 2007

Background Few randomized controlled trials compare different methods of management in chronic tendinopathy of the main body of tendo Achillis. Purpose To compare the effectiveness of 3 management strategies—group 1, eccentric loading; group 2, repetitive low-energy shock-wave therapy (SWT); and group 3, wait and see—in patients with chronic tendinopathy of the main body of tendo Achillis. Study Design Randomized controlled trial; Level of evidence, 1. Methods Seventy-five patients with a chronic recalcitrant (>6 months) noninsertional Achilles tendinopathy were enrolled in a randomized controlled study. All patients had received unsuccessful management for >3 months, including at least (1) peritendinous local injections, (2) nonsteroidal anti-inflammatory drugs, and (3) physiotherapy. A computerized random-number generator was used to draw up an allocation schedule. Analysis was on intention-to-treat basis. Results At 4 months from baseline, the Victorian Institute of Sport Assessment (VISA)-A score increased in all groups, from 51 to 76 points in group 1 (eccentric loading), from 50 to 70 points in group 2 (repetitive low-energy SWT), and from 48 to 55 points in group 3 (wait and see). Pain rating decreased in all groups, from 7 to 4 points in group 1, from 7 to 4 points in group 2, and from 8 to 6 points in group 3. Fifteen of 25 patients in group 1 (60%), 13 of 25 patients in group 2 (52%), and 6 of 25 patients in Group 3 (24%) reported a Likert scale of 1 or 2 points (“completely recovered” or “much improved”). For all outcome measures, groups 1 and 2 did not differ significantly. For all outcome measures, groups 1 and 2 showed significantly better results than group 3. Conclusion At 4-month follow-up, eccentric loading and low-energy SWT showed comparable results. The wait- and-see strategy was ineffective for the management of chronic recalcitrant tendinopathy of the main body of the Achilles tendon.
Efficacy of Continuous Intra-articular Bupivacaine Infusion for Postoperative Analgesia after Anterior Cruciate Ligament Reconstruction
Authors: Parker Richard D. , Streem Kathleen , Schmitz Leah , Group Marguerite , Martineau Paul A. 
Published: January 2007

Background The increasing trend toward outpatient surgery has stimulated the development of techniques focused on decreasing perioperative and postoperative pain. Pain control infusion pumps are gaining in popularity in orthopaedic procedures to control postoperative pain. Hypothesis Continuous infusion of bupivacaine via a catheter placed intra-articular into the knee after anterior cruciate ligament reconstruction using ipsilateral autograft quadrupled semitendinosus will decrease postoperative pain scores and narcotic and NSAID consumption. Study Design Randomized controlled trial; Level of evidence, 1. Methods: Three randomized study groups of 21 subjects were evaluated group I, 0.25% bupivacaine infused intra-articular at 4 mL/hour for 72 hours (study); Group II, 0.9% saline infused intra-articular at 4 mL/hr for 72 hours (placebo); Group III, no intra-articular infusion catheter (control). Each subject received general anesthesia and preemptive intra-articular anesthesia. Visual analog scale pain scores and analgesic use were compiled for the 96-hour study period. Results With the exception of significantly higher total narcotic usage in the control group compared with the study group only for the time period of 48 to 72 hours, there were no other statistically significant differences between each of the study groups with respect to pain and narcotic and NSAID use for the entire study period. Conclusion The continuous infusion of intra-articular bupivacaine via pain control infusion pumps after anterior cruciate ligament reconstruction using ipsilateral autograft quadrupled semitendinosus cannot be supported when postoperative visual analog scale pain scores and analgesic use are the rationale for justification.
Quadriceps Inhibition Induced by an Experimental Knee Joint Effusion Affects Knee Joint Mechanics during a Single-Legged Drop Landing
Authors: Palmieri-Smith Riann M. , Kreinbrink Jennifer , Ashton-Miller James A. , Wojtys Edward M. 
Published: January 2007

Background Arthrogenic quadriceps muscle inhibition accompanies knee joint effusion and impedes rehabilitation after knee joint injury. Hypothesis We hypothesized that an experimentally induced knee joint effusion would cause arthrogenic quadriceps muscle inhibition and lead to increased ground reaction forces, as well as sagittal plane knee angles and moments, during a single-legged drop landing. Study Design Controlled laboratory study. Methods Nine subjects (4 women and 5 men) underwent 4 conditions (no effusion, lidocaine injection, “low” effusion [30 mL], and “high” effusion [60 mL]) and then performed a single-legged drop landing. Lower extremity muscle activity, peak sagittal plane knee flexion angles, net sagittal plane knee moments, and peak ground reaction forces were measured. Results Vastus medialis and lateralis activity were decreased during the low and high effusion conditions (P < .05). However, increases in peak ground reaction forces and decreases in peak knee flexion angle and net knee extension moments occurred only during the high effusion condition (P < .05). Conclusions Knee joint effusion induced quadriceps inhibition and altered knee joint mechanics during a landing task. Subjects landed with larger ground reaction forces and in greater knee extension, thereby suggesting that more force will be transferred to the knee joint and its passive restraints when quadriceps inhibition is present. Clinical Relevance Knee joint effusion results in arthrogenic quadriceps muscle inhibition, increasing loading about the knee that may potentially increase the risk of future knee joint trauma or degeneration.
Revision of Failed Arthroscopic Bankart Repairs
Authors: Sisto Domenick J. 
Published: January 2007

Background The results following open revision surgery following a failed arthroscopic Bankart procedure are not well documented. Purpose To evaluate the results of patients with a failed arthroscopic Bankart repair treated with a traditional, open Bankart repair. Study Design Case series; Level of evidence, 4. Methods Thirty patients (28 male and 2 female) who had a mean age of 24 years (range 15-36) at the time of operation were evaluated. The mean interval from the time of the operation to the final follow-up was 46 months (range 24-55). The rating systems of Rowe and the University of California at Los Angeles (UCLA) were recorded preoperatively and at the time of the final evaluation. Results After open repair, mean modified Rowe scores improved from 25 preoperatively to 84.2 points. The results were excellent in 2 (6.7%), good in 24 (80%), and fair in 4 (13.3%); there were no poor results. The UCLA shoulder score improved from a mean of 17 points preoperatively to 29 points (P = .001 for all comparisons). Twenty-six patients (87%) did not have an anchor placement inferior to the 4-o'clock position for a right shoulder or the 8-o'clock position for the left shoulder after the index arthroscopic repair. There were no rotator interval closures performed at the index arthroscopic Bankart repair, and 10 patients (33%) required an interval closure at the open revision procedure. Twenty-five patients (83%) immobilized the operated arm in a sling for less than 2 weeks following the index arthroscopic repair. Conclusion Patients with failed arthroscopic Bankart repairs can be successfully treated with a revision, open Bankart repair. Inadequate postoperative immobilization, large rotator intervals, and improper anchor placement are possible risk factors that may increase the incidence of failure of an arthroscopic Bankart repair.
Growth factor independence-1 (Gfi-1) plays a role in mediating specific granule deficiency (SGD) in a patient lacking a gene-inactivating mutation in the C/EBPϵ gene
Authors: Khanna-Gupta Arati , Sun Hong , Zibello Theresa , Lee Han Myung , Dahl Richard , Boxer Laurence A. , Berliner Nancy 
Published: January 2007

Abstract
Neutrophil-specific granule deficiency (SGD) is a rare congenital disorder marked by recurrent bacterial infections. Neutrophils from SGD patients lack secondary and tertiary granules and their content proteins and lack normal neutrophil functions. Gene-inactivating mutations in the C/EBPϵ gene have been identified in 2 SGD patients. Our studies on a third SGD patient revealed a heterozygous mutation in the C/EBPϵ gene. However, we demonstrate elevated levels of C/EBPϵ and PU.1 proteins in the patient's peripheral blood neutrophils. The expression of the transcription factor growth factor independence-1 (Gfi-1), however, was found to be markedly reduced in our SGD patient despite the absence of an obvious mutation in this gene. This may explain the elevated levels of both C/EBPϵ and PU.1, which are targets of Gfi-1 transcriptional repression. We have generated a growth factor–dependent EML cell line from the bone marrow of Gfi-1+/− and Gfi-1+/+ mice as a model for Gfi-1–deficient SGD, and demonstrate that lower levels of Gfi-1 expression in the Gfi-1+/− EML cells is associated with reduced levels of secondary granule protein (SGP) gene expression. Furthermore, we demonstrate a positive role for Gfi-1 in SGP expression, in that Gfi-1 binds to and up-regulates the promoter of neutrophil collagenase (an SGP gene), in cooperation with wild-type but not with mutant C/EBPϵ. We hypothesize that decreased Gfi-1 levels in our SGD patient, together with the mutant C/EBPϵ, block SGP expression, thereby contributing to the underlying etiology of the disease in our patient.
Proplatelet formation is regulated by the Rho/ROCK pathway
Authors: Chang Yunhua , Auradé Frédéric , Larbret Frédéric , Zhang Yanyan , Le Couedic Jean-Pierre , Momeux Laurence , Larghero Jerôme , Bertoglio Jacques , Louache Fawzia , Cramer Elisabeth , Vainchenker William , Debili Najet 
Published: January 2007

AbstractPlatelets are released by megakaryocytes (MKs) via cytoplasmic extensions called proplatelets, which require profound changes in the microtubule and actin organization. Here, we provide evidence that the Rho/ROCK pathway, a well-known regulator of actin cytoskeleton, acts as a negative regulator of proplatelet formation (PPF). Rho is expressed at a high level during the entire MK differentiation including human CD34+ cells. Thrombopoietin stimulates its activity but at a higher extent in immature than in mature MKs. Overexpression of a dominant-negative or a spontaneously active RhoA leads to an increase or a decrease in PPF indicating that Rho activation inhibits PPF. This inhibitory effect is mediated through the main Rho effector, Rho kinase (ROCK), the inhibition of which also increases PPF. Furthermore, inhibition of Rho or ROCK in MKs leads to a decrease in myosin light chain 2 (MLC2) phosphorylation, which is required for myosin contractility. Interestingly, inhibition of the MLC kinase also decreases MLC2 phosphorylation while increasing PPF. Taken together, our results suggest that MLC2 phosphorylation is regulated by both ROCK and MLC kinase and plays an important role in platelet biogenesis by controlling PPF and fragmentation.
A randomized, placebo-controlled trial of oral beclomethasone dipropionate as a prednisone-sparing therapy for gastrointestinal graft-versus-host disease
Authors: Hockenbery David M. , Cruickshank Scott , Rodell Timothy C. , Gooley Ted , Schuening Friedrich , Rowley Scott , David Donald , Brunvand Mark , Berryman Brian , Abhyankar Sunil , Bouvier Michelle , McDonald George B. ,   for the orBec GVHD Study Group
Published: January 2007

AbstractWe tested the hypothesis that oral beclomethasone dipropionate (BDP) would control gastrointestinal graft-versus-host disease (GVHD) in patients with anorexia, vomiting, and diarrhea. Patients were randomized to prednisone for 10 days and either oral BDP 8 mg/d (n = 62) or placebo (n = 67) tablets for 50 days. At study day 10, prednisone was rapidly tapered while continuing study drug. On an intent-to-treat basis, the risk of GVHD-treatment failure was reduced for the BDP group at study day 50 (hazard ratio [HR] 0.63, 95% confidence interval [CI] 0.35-1.13) and at 30 days follow-up (HR 0.55, 95% CI 0.32-0.93). Among patients eligible for prednisone taper at study day 10, the risk of GVHD-treatment failure was significantly reduced at both study days 50 and 80 (HR 0.39 and 0.38, respectively). By day 200 after transplantation, 5 patients randomized to BDP had died compared with 16 deaths on placebo, a 67% reduction in the hazard of mortality (HR 0.33, P = .03). In 47 recipients of unrelated and HLA-mismatched stem cells, mortality at transplantation day 200 was reduced by 91% in the BDP group compared with placebo (HR 0.09, P = .02). The survival benefit was durable to 1 year after randomization. Oral BDP prevents relapses of gastrointestinal GVHD following tapering of prednisone; survival is statistically significantly better among patients receiving BDP.
Prolonged shear stress and KLF2 suppress constitutive proinflammatory transcription through inhibition of ATF2
Authors: Fledderus Joost O. , van Thienen Johannes V. , Boon Reinier A. , Dekker Rob J. , Rohlena Jakub , Volger Oscar L. , Bijnens Ann-Pascale J. J. , Daemen Mat J. A. P. , Kuiper Johan , van Berkel Theo J. C. , Pannekoek Hans , Horrevoets Anton J. G. 
Published: January 2007

AbstractAbsence of shear stress due to disturbed blood flow at arterial bifurcations and curvatures leads to endothelial dysfunction and proinflammatory gene expression, ultimately resulting in atherogenesis. KLF2 has recently been implicated as a transcription factor involved in mediating the anti-inflammatory effects of flow. We investigated the effect of shear on basal and TNF-α–induced genomewide expression profiles of human umbilical vein endothelial cells (HUVECs). Cluster analysis confirmed that shear stress induces expression of protective genes including KLF2, eNOS, and thrombomodulin, whereas basal expression of TNF-α–responsive genes was moderately decreased. Promoter analysis of these genes showed enrichment of binding sites for ATF transcription factors, whereas TNF-α–induced gene expression was mostly NF-κB dependent. Furthermore, human endothelial cells overlying atherosclerotic plaques had increased amounts of phosphorylated nuclear ATF2 compared with endothelium at unaffected sites. In HUVECs, a dramatic reduction of nuclear binding activity of ATF2 was observed under shear and appeared to be KLF2 dependent. Reduction of ATF2 with siRNA potently suppressed basal proinflammatory gene expression under no-flow conditions. In conclusion, we demonstrate that shear stress and KLF2 inhibit nuclear activity of ATF2, providing a potential mechanism by which endothelial cells exposed to laminar flow are protected from basal proinflammatory, atherogenic gene expression.
Antiendothelial cell antibodies mediate enhanced leukocyte adhesion to cytokine-activated endothelial cells through a novel mechanism requiring cooperation between FcγRIIa and CXCR1/2
Authors: Florey Oliver J. , Johns Michael , Esho Olubukola O. , Mason Justin C. , Haskard Dorian O. 
Published: January 2007

AbstractAntiendothelial cell antibodies (AECAs) are commonly detectable in diseases associated with vascular injury, including systemic lupus erythematosus (SLE), systemic sclerosis, Takayasu arteritis, Wegener granulomatosis, Behçet syndrome, and transplant arteriosclerosis. Here, we explore the hypothesis that these antibodies might augment polymorphonuclear leukocyte (PMN) adhesion to endothelium in inflammation. Initially, we established that a mouse IgG mAb bound to endothelial cells (ECs) significantly increased PMN adhesion to cytokine-stimulated endothelium in an FcγRIIa-dependent manner. Neutralizing antibodies, and adenoviral transduction of resting ECs, demonstrated that the combination of E-selectin, CXCR1/2, and β2 integrins is both necessary and sufficient for this process. We observed an identical mechanism using AECA IgG isolated directly from patients with SLE. Assembled immune complexes also enhanced PMN adhesion to endothelium, but, in contrast to adhesion because of AECAs, this process did not require CXCR1/2, was not inhibited by pertussis toxin, and was FcγRIIIb rather than FcγRIIa dependent. These data are the first to demonstrate separate nonredundant FcγRIIa and FcγRIIIb-mediated mechanisms by which EC-bound monomeric IgG and assembled immune complexes amplify leukocyte adhesion under dynamic conditions. Furthermore, the observation that FcγRIIa and CXCR1/2 cooperate to enhance PMN recruitment in the presence of AECAs suggests a mechanism whereby AECAs may augment tissue injury during inflammatory responses.
Expansion of spleen myeloid suppressor cells represses NK cell cytotoxicity in tumor-bearing host
Authors: Liu Cunren , Yu Shaohua , Kappes John , Wang Jianhua , Grizzle William E. , Zinn Kurt R. , Zhang Huang-Ge 
Published: January 2007

Abstract
Tumor growth promotes the expansion of myeloid suppressor cells. An inverse correlation between natural killer (NK) cell activation and myeloid suppressor cell (MSC) expansion in tumor-bearing patients and mice prompted us to investigate the role of MSCs in controlling NK antitumor cytotocixity. After adoptive transfer to naive recipients, CD11b+Gr-1+ MSCs freshly isolated from spleens of tumor-bearing mice but not naive mice were able to inhibit NK cell cytotoxicity. An in vivo imaging analysis indicates that the removal of tumors resulted in a significant increased ability (P < .05) in NK cell cytotoxicity to eliminate injected YAC-1 cells from the lungs. Fluorescence-activated cell sorter (FACS) analysis of the composition of lung leukocytes further indicates that the removal of tumors also leads to the reduction of MSCs accumulated in the lung. These data suggest that MSCs suppress NK cell cytotoxicity. The inhibition of NK cell cytotoxicity is cell-cell contact dependent. Inhibition of perforin but not granzyme B production was responsible for MSC-mediated inhibition of NK cytotoxicity. Western blot analyses further suggests that MSCs suppress IL-2–mediated NK cell cytotoxicity by affecting the activity of Stat5.
Activation of MAP kinase p38 is critical for the cell-cycle–controlled suppressor function of regulatory T cells
Authors: Adler Henric S. , Kubsch Sebastian , Graulich Edith , Ludwig Stephan , Knop Juergen , Steinbrink Kerstin 
Published: January 2007

AbstractRegulatory T cells play an essential role in the control of self-tolerance and processes of adaptive immunity. Tolerogenic IL-10–modulated human dendritic cells (IL-10DCs) induce anergic T cells with strong suppressive properties (iTregs) that inhibit the activation of effector T cells. In this study, we evaluated the interaction between cell-cycle regulation and intracellular signaling in these iTregs. Analysis of signal transduction events revealed a down-regulation of the mitogen-activated protein kinases (MAPKs) Jun N-terminal kinase (JNK) and a nonactivation of extracellular-signal–regulated kinase (ERK) in contrast to a marked activation of p38 MAPK and the p38 effector MAPK-activated protein kinases 2/3 (MAPKAP2/3). The elevated activation of p38 is critical for the induction and maintenance of anergy controlled by an increased expression of the cell-cycle inhibitor p27Kip1. Moreover, blocking experiments with the specific inhibitor SB203580 demonstrated that the regulatory function of iTregs is associated with an enhanced p38 MAPK activity. In contrast to other Treg populations, the suppressor function of iTregs is independent of IL-10. In conclusion, our data indicate that a cross-talk of cell-cycle regulation and p38-dependent signal transduction is required for the suppressor function of iTregs.