bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analysis of Magnetic Resonance Images of Disk Positions and Deformities in 1,265 Patients with Temporomandibular Disorder
Authors: Choi Yong-Suk , Asaumi Jun-ichi , Hisatomi Miki , Unetsubo Teruhisa , Yanagi Yoshinobu , Matsuzaki Hidenobu , Konouchi Hironobu , Hwang Eui-Hwan , Lee Sang-Rae 
Published: March 2009

Objectives
To compare MRI manifestations according to gender and age and to identify correlations between clinical manifestations and MRI findings in patients with temporomandibular disorder (TMD) as based on a large series.

Materials and Methods
Fat suppressed oblique sagittal images of the open and closed mouth were acquired, and MRI scanning parameters were applied.

Results
The patients consisted of 946 females (average, 36.6 years old), and 319 males (average, 34.3 years old). In all TMD patients, 945 had symptoms in the unilateral temporomandibular joint (TMJ) and 320 in the bilateral TMJ. There were significant differences in the distribution of disk positions based on age, regardless of gender, in the unilaterally and bilaterally symptomatic groups; however, the results were not significant in the asymptomatic group. There were significant differences with respect to the distribution of disk positions between males and females in asymptomatic group and in the unilaterally symptomatic group, although the bilaterally symptomatic group did not show significant differences in this regard. As regards the disk positions in the joints of the three groups (asymptomatic group, unilaterally and bilaterally symptomatic groups), there were significant interactive effects of disk positions, regardless of gender. There were statistically significant age-related differences in disk deformities in all symptom groups, regardless of gender, except for in the group of males lacking symptoms in either joint. As regards disk deformities among the three groups studies here, there were significant interactive effects for disk positions, regardless of gender.
Zinc Project: Subsea Maintenance and Remedial Action Approach for the Subsea Control System
Authors: Stair M.A. , Clark G.A. , Schmidt R.J. 
Published: March 2009

Abstract
Zinc is a 10 slot subsea production template and manifold installed in awater depth of 1460 feet in the Exxon Mississippi Canyon Block 354 Field in theGulf of Mexico. Zinc, which is located approximately 50 miles south of GrandIsle, produces through three flowlines to the Exxon Alabaster Platform locatedin Mississippi Block 397 approximately 6 miles to the west of Zinc. AnElectrohydraulic Multiplexed Control System provides for control and monitoringof the Zinc subsea and platform equipment.
This paper describes Exxon's maintenance and remedial action approach forthe Zinc Subsea Control System. A companion overview paper describes theequipment resulting from this approach.

Introduction
Subsea equipment reliability/availability is a critical factor in keepingsubsea wells on production, and thus in maximizing a subsea project's economicreturn. Equipment availability is dictated by the combination of (a) theequipment's inherent reliability, (b) the levels of redundancy provided, (c)the capability to perform routine equipment inspection, performance evaluation, and maintenance, and (d) the timeliness that repairs can be effected whenrequired. The challenge for the Zinc Project Team in providing for maintenanceand repair capabilities was to achieve a proper balance of these factors, thusbalancing the project's initial investment and operating costs.
Zinc has a planned production life of 20 years. To be assured of achievingthis production life, considerable maintenance capabilities have beenincorporated into the Zinc equipment. The most extreme of these capabilities isretrieval and reinstallation of the Zinc Subsea Production Manifold, whichcontains all manifold piping and valves, the Subsea Control System equipment, and the hydraulic distribution network. This is done independently of theSubsea Template; however, to do so will require that all wells be killed andsuitably plugged and the X-mas Trees removed.
Retrieving and reinstalling the Subsea Manifold for repair will be verycostly and not without risk to the wells and equipment. To minimize the chancesof having to undertake this operation due to control system failure, the ZincElectrohydraulic Multiplex Subsea Control System equipment has incorporatedsubstantial redundancy and maintenance provisions as the clearly preferredmeans of repair.
Recent Developments in the Towing of Very Long Pipeline Bundles Using the CDTM Method
Authors: Dercksen Albertus , Taconis Taco 
Published: March 2009

Abstract
Fully integrated pipeline bundles are built and tested onshore. The bundlesare towed to the field using the Controlled Depth Towing Method (CDTM). Recently this method was used to tow a very long bundle (6.7 km) to the Piperfield in the British sector of the North Sea.
Time domain simulations were carried out to predict the bundle behaviour indifferent situations. A discussion of the numerical model will be presented. Several parts of the bundle configuration were model tested and full scalemonitoring was performed during the tow at sea. Bundle tow in still water andsurvival sea states is discussed as well as the impacts of failure modes on thebundle behaviour.

Introduction
Fully integrated pipeline bundles are built and tested at the productionsite. After completion the bundle is launched and towed to the field. Often itwill be necessary to cross other pipelines located on the tow route from theproduction site.
To achieve clearance with these other pipelines it is essential to perform asafe tow. To this extent a dynamic analysis of the tow is carried out.
The importance of having reliable numerical methods to predict the dynamicbehaviour of towed pipeline bundles is given by the fact that it is extremelydifficult to carry out model tests on these systems due to their immenselengths.
The numerical model presented in this paper is based on a lumped massapproach, allowing flexibility with respect to modelling of differentconfigurations. Model tests were carried out to gather information aboutessential items of the tow. Full scale monitoring was carried out to validatethe numerical model for future projects.
In principle CDTM involves the transportation of a pipeline bundle suspendedbetween two tugs, the Leading Tug (LT) and the Trailing Tug (TT), Figure 1. Tomaintain control during tow, the bundle is designed and constructed withinspecific tolerances with respect to its submerged weight.
Transcriptional Modulation of the Immune Response by Peroxisome Proliferator-Activated Receptor-α Agonists in Autoimmune Disease
Authors: Gocke Anne R. , Hussain Rehana Z. , Yang Yuhong , Peng Haiyan , Weiner Jeffrey , Ben Li-Hong , Drew Paul D. , Stuve Olaf , Lovett-Racke Amy E. , Racke Michael K. 
Published: March 2009

Abstract
Peroxisome proliferator-activated receptor-α (PPARα) agonists have been shown to have a therapeutic benefit in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis (MS). In this study, we investigated the mechanism by which the PPARα agonist gemfibrozil induces immune deviation and protects mice from EAE. We demonstrated that treatment with gemfibrozil increases expression of the Th2 transcription factor GATA-3 and decreases expression of the Th1 transcription factor T-bet in vitro and directly ex vivo. These changes correlated with an increase in nuclear PPARα expression. Moreover, the protective effects of PPARα agonists in EAE were shown to be partially dependent on IL-4 and to occur in a receptor-dependent manner. PPARα was demonstrated, for the first time, to regulate the IL-4 and IL-5 genes and to bind the IL-4 promoter in the presence of steroid receptor coactivator-1, indicating that PPARα can directly transactivate the IL-4 gene. Finally, therapeutic administration of PPARα agonists ameliorated clinically established EAE, suggesting that PPARα agonists may provide a treatment option for immune-mediated inflammatory diseases.
Functional Killer Ig-Like Receptors on Human Memory CD4+ T Cells Specific for Cytomegalovirus
Authors: van Bergen Jeroen , Kooy-Winkelaar Engelina M. C. , van Dongen Henrike , van Gaalen Floris A. , Thompson Allan , Huizinga Tom W. J. , Feltkamp Mariet C. W. , Toes René E. M. , Koning Frits 
Published: March 2009

Abstract
Although very few CD4+ T cells express killer Ig receptors (KIR), a large proportion of CD4+ T cells with a late memory phenotype, characterized by the absence of CD28, does express KIR. Here, we show that KIR expression on CD4+ T cells is also associated with memory T cell function, by showing that the frequency of CMV-specific cells is higher in CD4+KIR+ than CD4+KIR− T cells. In addition, engagement of an inhibitory KIR inhibited the CMV-specific proliferation of these CD4+KIR+ memory T cells, but had no detectable effect on cytokine production. Our data reveal that, in marked contrast with CD8+ T cells, the activity of a subset of CMV-specific CD4+ T cells is modulated by HLA class I-specific KIR. Thus, the CMV-induced down-regulation of HLA class I may in fact enhance memory CMV-specific CD4+ T cell responses restricted by HLA class II.
TLR2/MyD88-Dependent and -Independent Activation of Mast Cell IgE Responses by the Skin Commensal Yeast Malassezia sympodialis
Authors: Selander Christine , Engblom Camilla , Nilsson Gunnar , Scheynius Annika , Andersson Carolina Lunderius 
Published: March 2009

Abstract
Atopic eczema (AE) is a chronic inflammatory skin disease. Approximately 50% of adult AE patients have allergen-specific IgE reactivity to the skin commensal yeast Malassezia spp. Due to the ruptured skin barrier in AE, it is likely that Malassezia can come into contact with mast cells, which are known to be involved in AE. We therefore hypothesized that Malassezia spp. can activate mast cells. Bone marrow-derived mast cells (BMMCs) were generated from wild type, TLR2, TLR4, and MyD88 gene-deleted mice and cocultured with Malassezia sympodialis extract. We recorded that M. sympodialis induced release of cysteinyl leukotrienes in a dose-dependent manner in nonsensitized and IgE-anti-trinitrophenyl-sensitized BMMCs, respectively, with three times higher levels in the latter type of cells. IgE-sensitized BMMCs also responded by degranulation as assessed by release of β-hexosaminidase, increased MCP-1 production through a MyD88-independent pathway, and activated phosphorylation of the MAPK ERK1/2. Furthermore, M. sympodialis enhanced the degranulation of IgE receptor cross-linked wild-type BMMCs and altered the IL-6 release dose-dependently. This degranulation was independent of TLR2, TLR4, and MyD88, whereas the IL-6 production was dependent on the TLR2/MyD88 pathway and MAPK signaling. In conclusion, M. sympodialis extract can activate nonsensitized and IgE-sensitized mast cells to release inflammatory mediators, to enhance the IgE-mediated degranulation of mast cells, and to modulate MAPK activation and by signaling through the TLR2/MyD88 pathway to modify the IL-6 production of IgE receptor cross-linked mast cells. Collectively, these findings indicate that M. sympodialis can activate mast cells and might thus exacerbate the inflammatory response in AE.
Autophagy Is Essential for Mitochondrial Clearance in Mature T Lymphocytes
Authors: Pua Heather H. , Guo Jian , Komatsu Masaaki , He You-Wen 
Published: March 2009

Abstract
Macroautophagy plays an important role in the regulation of cell survival, metabolism, and the lysosomal degradation of cytoplasmic material. In the immune system, autophagy contributes to the clearance of intracellular pathogens, MHCII cross-presentation of endogenous Ags, as well as cell survival. We and others have demonstrated that autophagy occurs in T lymphocytes and contributes to the regulation of their cellular function, including survival and proliferation. Here we show that the essential autophagy gene Atg7 is required in a cell-intrinsic manner for the survival of mature primary T lymphocytes. We also find that mitochondrial content is developmentally regulated in T but not in B cells, with exit from the thymus marking a transition from high mitochondrial content in thymocytes to lower mitochondrial content in mature T cells. Macroautophagy has been proposed to play an important role in the clearance of intracellular organelles, and autophagy-deficient mature T cells fail to reduce their mitochondrial content in vivo. Consistent with alterations in mitochondrial content, autophagy-deficient T cells have increased reactive oxygen species production as well as an imbalance in pro- and antiapoptotic protein expression. With much recent interest in the possibility of autophagy-dependent developmentally programmed clearance of organelles in lens epithelial cells and erythrocytes, our data demonstrate that autophagy may have a physiologically significant role in the clearance of superfluous mitochondria in T lymphocytes as part of normal T cell homeostasis.
CD4-Positive T Lymphocytes Provide a Neuroimmunological Link in the Control of Adult Hippocampal Neurogenesis
Authors: Wolf Susanne A. , Steiner Barbara , Akpinarli Akgul , Kammertoens Thomas , Nassenstein Christina , Braun Armin , Blankenstein Thomas , Kempermann Gerd 
Published: March 2009

Abstract
Adult hippocampal neurogenesis occurs in an exceptional permissive microenvironment. Neuroimmunological mechanisms might be prominently involved in the endogenous homeostatic principles that control baseline levels of adult neurogenesis. We show in this study that this homeostasis is partially dependent on CD4-positive T lymphocytes. Systemic depletion of CD4-positive T lymphocytes led to significantly reduced hippocampal neurogenesis, impaired reversal learning in the Morris water maze, and decreased brain-derived neurotrophic factor expression in the brain. No such effect of CD8 or B cells was observed. Repopulation of RAG2−/− mice with CD4, but not with CD8 cells again increased precursor cell proliferation. The T cells in our experiments were non-CNS specific and rarely detectable in the healthy brain. Thus, we can exclude cell-cell contacts between immune and brain cells or lymphocyte infiltration into the CNS as a prerequisite for an effect of CD4-T cells on neurogenesis. We propose that systemic CD4-T cell activity is required for maintaining cellular plasticity in the adult hippocampus and represents an evolutionary relevant communication route for the brain to respond to environmental changes.
Human Benign Prostatic Hyperplasia Stromal Cells As Inducers and Targets of Chronic Immuno-Mediated Inflammation
Authors: Penna Giuseppe , Fibbi Benedetta , Amuchastegui Susana , Cossetti Chiara , Aquilano Francesca , Laverny Gilles , Gacci Mauro , Crescioli Clara , Maggi Mario , Adorini Luciano 
Published: March 2009

Abstract
Benign prostatic hyperplasia (BPH), a highly prevalent prostatic condition, could involve an inflammatory component in disease pathogenesis. In this study, we show that human stromal prostate cells obtained from BPH tissue can actively contribute to the inflammatory process by secreting proinflammatory cytokines as well as chemokines able to recruit lymphomonuclear cells and by acting as APCs. BPH cells express all of the TLRs and their ligation leads to the secretion of CXCL8/IL-8, CXCL10, and IL-6. In addition, BPH cells express costimulatory as well as class I and class II MHC molecules, which activate alloreactive CD4+ cells that in turn markedly up-regulate IL-12/IL-23p40 and IL-12p75 secretion by BPH cells. Alloreactive CD4+ cells activated by BPH cells secrete IFN-γ and IL-17. These cytokines up-regulate IL-6, IL-8, and CXCL10 production by BPH cells, creating a positive feedback loop that can amplify inflammation. IL-8 induces autocrine/paracrine proliferation of BPH cells, indicating also a growth-promoting activity of this chemokine in disease pathogenesis. These results show that human BPH cells represent nonprofessional APCs able to induce and sustain chronic inflammatory processes, supporting the relevance of inflammation in BPH pathogenesis.
CXCR4/CXCL12 Hyperexpression Plays a Pivotal Role in the Pathogenesis of Lupus
Authors: Wang Andrew , Fairhurst Anna-Marie , Tus Katalin , Subramanian Srividya , Liu Yang , Lin Fangming , Igarashi Peter , Zhou Xin J. , Batteux Frederic , Wong Donald , Wakeland Edward K. , Mohan Chandra 
Published: March 2009

AbstractAmong various surface molecules screened, CXCR4 was significantly up-regulated on monocytes, neutrophils, B cell subsets, and plasma cells in multiple murine models of lupus with active nephritis, including B6.Sle1Yaa, BXSB, and MRL.lpr. TLR-mediated signaling and inflammatory cytokines accounted in part for this increase. Increased CXCR4 expression was associated with functional consequences, including increased migration and enhanced B cell survival. Simultaneously, the ligand for CXCR4, CXCL12, was significantly up-regulated in the nephritic kidneys. Treatment with a peptide antagonist of CXCR4 prolonged survival and reduced serum autoantibodies, splenomegaly, intrarenal leukocyte trafficking, and end organ disease in a murine model of lupus. These findings underscore the pathogenic role of CXCR4/CXCL12 in lymphoproliferative lupus and lupus nephritis and highlight this axis as a promising therapeutic target in this disease.
Cutting Edge: A2B Adenosine Receptor Signaling Provides Potent Protection during Intestinal Ischemia/Reperfusion Injury
Authors: Hart Melanie L. , Jacobi Barbara , Schittenhelm Jens , Henn Martina , Eltzschig Holger K. 
Published: March 2009

Abstract
Gastrointestinal ischemia/reperfusion (IR) injury significantly contributes to the morbidity and mortality of critical illness. In this study, we hypothesized a protective role for extracellular adenosine signaling in intestinal IR injury. Initial profiling studies of mucosal scrapings following murine IR demonstrated selective induction of the A2B adenosine receptor (A2BAR) transcript. Moreover, gene-targeted mice for the A2BAR showed more profound intestinal IR injury compared with controls. In contrast, A2AAR−/− mice exhibited no differences in intestinal injury compared with littermate controls. In addition, selective inhibition of the A2BAR resulted in enhanced intestinal inflammation and injury during IR. Furthermore, A2BAR agonist treatment (BAY 60-6583) protected from intestinal injury, inflammation, and permeability dysfunction in wild-type mice, whereas the therapeutic effects of BAY 60-6583 were abolished following targeted A2BAR gene deletion. Taken together, these studies demonstrate the A2BAR as a novel therapeutic target for protection during gastrointestinal IR injury.
Central Role of Tumor-Associated CD8+ T Effector/Memory Cells in Restoring Systemic Antitumor Immunity
Authors: Kilinc Mehmet O. , Gu Tao , Harden Jamie L. , Virtuoso Lauren P. , Egilmez Nejat K. 
Published: March 2009

Abstract
Sustained delivery of IL-12 and GM-CSF to tumors induces the activation of tumor-resident CD8+ T effector/memory cells (Tem) followed by cytotoxic CD8+ T effector cell expansion. To determine whether the secondary effectors expanded from tumor-associated Tem or were primed de novo, activation kinetics of tumor-draining lymph node (TDLN) CD8+ T cells were analyzed. Treatment promoted a 4-fold increase in the numbers of TDLN CD8+ T cells displaying a CD69+CCR5+CD62L− periphery-homing effector phenotype by day 4 posttherapy. Pulse labeling of tumor and TDLN T cells with BrdU confirmed that proliferation occurred exclusively within the draining lymph nodes between days 1 and 4 with subsequent migration of primed CD8+ T effectors to tumors on day 7. Day 4 CD8+ T effector cells preferentially homed to and lysed experimental, but not control, tumors, establishing tumor specificity. To determine whether the secondary CD8+ T effector cell response was dependent on activation of tumor-resident CD8+ Tem, mice that were selectively depleted of tumor-infiltrating CD8+ T cells were treated and monitored for T effector priming. In the absence of tumor-resident CD8+ Tem, T effector cell expansion was completely abrogated in the TDLN, revealing that restoration of CD8+ Tem function was critical to the induction of secondary T effectors. T cell priming failed to occur in IFN-γ or perforin knockout mice, demonstrating that the requirement for Tem activation was associated with induction of Tem cytotoxicity. These data confirm that intratumoral IL-12 plus GM-CSF induces de novo priming of tumor-specific CD8+ T effector cells in the TDLN and establish the critical role of preexisting intratumoral CD8+ Tem in driving this process.
Anti-CD25 Antibody-Mediated Depletion of Effector T Cell Populations Enhances Susceptibility of Mice to Acute but Not Chronic Toxoplasma gondii Infection
Authors: Couper Kevin N. , Lanthier Paula A. , Perona-Wright Georgia , Kummer Lawrence W. , Chen Wangxue , Smiley Stephen T. , Mohrs Markus , Johnson Lawrence L. 
Published: March 2009

Abstract
Natural regulatory T cells (Tregs) constitutively express the IL-2R α-chain (CD25) on their surface. Consequently, administration of anti-CD25 Abs is a commonly used technique to deplete Treg populations in vivo. However, activated effector T cells may also transiently express CD25, and are thus also potential targets for anti-CD25 Abs. In this study using Toxoplasma gondii as a model proinflammatory infection, we have examined the capacity of anti-CD25 Abs to target effector T cell populations during an inflammatory episode, to determine to what extent that this action may modulate the outcome of disease. Anti-CD25 Ab-treated C57BL/6 mice displayed significantly reduced CD4+ T cell IFN-γ production during acute T. gondii infection and exhibited reduced weight loss and liver pathology during early acute infection; aspects of infection previously associated with effector CD4+ T cell responses. In agreement, anti-CD25 Ab administration impaired parasite control and caused mice to succumb to infection during late acute/early chronic stages of infection with elevated tissue parasite burdens. In contrast, anti-CD25 Ab treatment of mice with established chronic infections did not markedly affect brain parasite burdens, suggesting that protective T cell populations do not express CD25 during chronic stages of T. gondii infection. In summary, we have demonstrated that anti-CD25 Abs may directly abrogate effector T cell responses during an inflammatory episode, highlighting important limitations of the use of anti-CD25 Ab administration to examine Treg function during inflammatory settings.