bluuebunny/crossref_metadata_2025_split huggingface dataset:
Physical and clinicopathologic findings in foals derived by use of somatic cell nuclear transfer: 14 cases (2004–2008)
Authors: Johnson Aime K. , Clark-Price Stuart C. , Choi Young-Ho , Hartman David L. , Hinrichs Katrin 
Published: May 2010

Abstract
Objective—To describe the health status of foals derived by use of somatic cell nuclear transfer (NT) at a university laboratory.
Design—Retrospective case series.
Animals—14 live-born NT-derived foals.
Procedures—Medical records from 2004 through 2008 were evaluated to identify all pregnancies resulting in live-born NT-derived foals. Information obtained included gestation length, birth weight, foaling complications, gross abnormalities of the fetal membranes, appearance of the umbilicus, mentation of the foal, limb deformities, and any other abnormalities detected in the neonatal period. Clinicopathologic data were also evaluated when available. Records of 4 recipient mares during gestation were included.
Results—Six foals were clinically normal for all evaluated variables. The most common abnormalities detected in the remaining 8 foals included maladjustment, enlarged umbilical remnant, and angular deformity of the forelimbs. Two foals died within 7 days after parturition; in the remaining foals, these conditions all resolved with medical or surgical management. Large offspring syndrome and gross abnormalities of the fetal membranes were not detected. The 12 surviving foals remained healthy.
Conclusions and Clinical Relevance—Associated problems of calves resulting from use of NT have been reported, but there are few data on the outcome of foals resulting from adult somatic cell NT in horses. Although this population of foals had a lower perinatal mortality rate than has been reported for NT-derived calves, some NT-derived foals required aggressive supportive care. Birth of foals derived from NT should take place at a center equipped to handle critical care of neonates.
The relative motion of membranes
Authors: Roberts Mark 
Published: May 2010

AbstractThe relative classical motion of membranes is governed by the equation (w β cα c r βa)a = R δγβα r gb x δa p aγ, where w is the hessian. This is a generalization of the geodesic deviation equation and can be derived from the lagrangian p · ṙ. Quantum mechanically the picture is less clear. Some quantizations of the classical equations are attempted so that the question as to whether the Universe started with a quantum fluctuation can be addressed.
Preexisting Comorbid Psychiatric Conditions and Mortality in Nonsurgical Intensive Care Patients
Authors: Abrams Thad E. , Vaughan-Sarrazin Mary , Rosenthal Gary E. 
Published: May 2010

Purpose To examine the effects of preexisting comorbid psychiatric conditions on mortality in a large cohort of patients admitted to a nonsurgical intensive care unit.
Methods This retrospective cohort study involved 66 672 consecutive eligible nonsurgical patients admitted to intensive care units in 129 Veterans Health Administration hospitals during 2005 and 2006. Preexisting comorbid psychiatric conditions were identified by using diagnoses from outpatient encounters in the prior year for depression, anxiety, psychosis, bipolar disorders, and posttraumatic stress disorder. Generalized estimating equations were used to adjust the risks of inhospital and 30-day mortality for demographics, comorbid medical conditions, markers of severity, and abnormal findings on laboratory tests at admission.
Results Comorbid psychiatric conditions were identified in 28% (n = 18 698) of patients. Patients with preexisting comorbid psychiatric conditions had lower (P &lt; .001) unadjusted inhospital mortality (7.3% vs 8.7%) and 30-day mortality (10.0% vs 12.8%) than did patients without such conditions. After demographics, comorbid medical conditions, and severity were adjusted for, risk of in-hospital mortality among patients with comorbid psychiatric conditions was somewhat higher (odds ratio, 1.07, 95% confidence interval, 1.01–1.14; P = .02), although differences in 30-day mortality (odds ratio, 1.01, 95% confidence interval, 0.94–1.08; P = .70) were no longer significant.
Conclusion Preexisting comorbid psychiatric conditions are common among intensive care patients, but after comorbid medical conditions and severity were adjusted for, preexisting comorbid psychiatric conditions were not associated with a higher risk of 30-day mortality in a large national cohort of veterans.
Erbb2 DNA Vaccine Combined with Regulatory T Cell Deletion Enhances Antibody Response and Reveals Latent Low-Avidity T Cells: Potential and Limits of Its Therapeutic Efficacy
Authors: Rolla Simona , Ria Francesco , Occhipinti Sergio , Di Sante Gabriele , Iezzi Manuela , Spadaro Michela , Nicolò Chiara , Ambrosino Elena , Merighi Irene Fiore , Musiani Piero , Forni Guido , Cavallo Federica 
Published: May 2010

Abstract
Rat (r)Erbb2 transgenic BALB-neuT mice genetically predestined to develop multiple invasive carcinomas allow an assessment of the potential of a vaccine against the stages of cancer progression. Because of rErbb2 expression in the thymus and its overexpression in the mammary gland, CD8+ T cell clones reacting at high avidity with dominant rErbb2 epitopes are deleted in these mice. In BALB-neuT mice with diffuse and invasive in situ lesions and almost palpable carcinomas, a temporary regulatory T cells depletion combined with anti-rErbb2 vaccine markedly enhanced the anti-rErbb2 Ab response and allowed the expansion of latent pools of low-avidity CD8+ T cells bearing TCRs repertoire reacting with the rErbb2 dominant peptide. This combination of a higher Ab response and activation of a low-avidity cytotoxic response persistently blocked tumor progression at stages in which the vaccine alone was ineffective. However, when diffuse and invasive microscopic cancers become almost palpable, this combination was no longer able to secure a significant extension of mice survival.
Identification and Characterization of a Lupus Suppressor 129 Locus on Chromosome 3
Authors: Carlucci Francesco , Fossati-Jimack Liliane , Dumitriu Ingrid E. , Heidari Yasin , Walport Mark J. , Szajna Marta , Baruah Paramita , Garden Oliver A. , Cook H. Terence , Botto Marina 
Published: May 2010

Abstract
The 129-derived Sle16 is a susceptibility locus for systemic autoimmunity when present on the C57BL/6 (B6) background. Genetic analysis of a (129×B6)F2 cross identified a region from the B6 chromosome 3 (Sle18) with positive linkage to antinuclear Abs. In this study, we have generated a B6 congenic strain harboring the 129 allele of Sle18 and intercrossed this line with the lupus-prone B6.129-Sle16 strain. The presence of the 129-Sle18 allele in the B6.129-Sle16Sle18 double congenic mice suppressed the development of Sle16-mediated autoantibody production and ameliorated the renal pathology. The 129-Sle18 locus rectified the B cell abnormalities detected in the B6.129-Sle16 mice, such as the reduction in the percentage of marginal zone B and B1a cells and the increased number of germinal centers. The B6.129-Sle16Sle18 spleens still displayed an increased percentage of activated T and B cells. However, in the B6.129-Sle16Sle18 strain the percentage of naive T cells was equivalent to that in B6.129-Sle18 and B6 mice and these cells showed a reduced proliferative response to anti-CD3 stimulation compared with B6.129-Sle16 T cells. There was a significant increase in the percentage of CD4+FoxP3+regulatory T cells in all congenic strains. These cells had normal regulatory function when tested in vitro. Thus, 129-Sle18 represents a novel, non-MHC lupus-suppressor locus probably operating as a functional modifier of B cells that, in combination with other factors, leads to lupus resistance. Further characterization of this locus will help to uncover the immune mechanism(s) conferring protection against lupus.
Maintenance of Immune Tolerance to a Neo-Self Acetylcholine Receptor Antigen with Aging: Implications for Late-Onset Autoimmunity
Authors: Stacy Sue , Williams Earlanda L. , Standifer Nathan E. , Pasquali Amanda , Krolick Keith A. , Infante Anthony J. , Kraig Ellen 
Published: May 2010

Abstract
Age-related changes in immune regulation are likely to account for the age-associated increase in serum autoantibody levels and in certain autoimmune disorders, such as myasthenia gravis (MG). To demonstrate directly a loss of immune tolerance in older individuals, responses to the acetylcholine receptor, the autoantigen in MG, were assessed in transgenic mice expressing the Torpedo californica acetylcholine receptor (TAChR) α-chain as a neo-self Ag. T cells from young transgenic mice had been shown to be tolerant to p146–162, the TAChR α-chain peptide that dominated young nontransgenic T cell responses in vitro. The immunodominance of p146–162 was not lost with age; fine specificity was preserved. Moreover, T cell tolerance to p146–162, as well as to other epitopes of the TAChR α-chain extracellular domain, was maintained in old transgenic mice. Even multiple TAChR immunizations coupled with the MG-enhancing cytokine, IL-12, did not break tolerance. In addition, T cells exhibiting CD4 upregulation, an early activation marker, were reduced in frequency equivalently in old and young transgenic animals, suggesting that immune regulation in this model was not impacted by aging. Moreover, B cell tolerance was also maintained with age. The persistence of immune tolerance was accompanied by an increase in the proportion of T regulatory cells; it is speculated that this may compensate for deficiencies in central tolerance that occur owing to thymic involution. In summary, our study reveals, for the first time, that some immune tolerance mechanisms do survive aging; this suggests that certain late-onset autoimmune disorders may be induced by a specific insult that disrupts immune homeostasis.
Treatment of Autoimmune Arthritis Using RNA Interference-Modulated Dendritic Cells
Authors: Zheng Xiufen , Suzuki Motohiko , Ichim Thomas E. , Zhang Xusheng , Sun Hongtao , Zhu Fei , Shunnar Aminah , Garcia Bertha , Inman Robert D. , Min Weiping 
Published: May 2010

AbstractDendritic cells (DCs) have a dual ability to either stimulate or suppress immunity, which is primarily associated with the expression of costimulatory molecules. Ag-loaded DCs have shown encouraging clinical results for treating cancer and infectious diseases; however, the use of these cells as a means of suppressing immune responses is only recently being explored. Here, we describe the induction of RNA interference through administering short interfering RNA (siRNA) as a means of specifically generating tolerogenic DCs. Knockdown of CD40, CD80, and CD86, prior to loading DCs with the arthritogenic Ag collagen II, led to a population of cells that could effectively suppress onset of collagen-induced arthritis. Maximum benefits were observed when all three genes were concurrently silenced. Disease suppression was associated with inhibition of collagen II-specific Ab production and suppression of T cell recall responses. Downregulation of IL-2, IFN-γ, TNF-α, and IL-17 and increased FoxP3+ cells with regulatory activity were observed in collagen-induced arthritis mice treated with siRNA-transfected DCs. Collectively, these data support the use of ex vivo gene manipulation in DCs using siRNA to generate tailor-made tolerogenic vaccines for treating autoimmunity.
Scaffolding Adaptor Protein Gab1 Is Required for TLR3/4- and RIG-I–Mediated Production of Proinflammatory Cytokines and Type I IFN in Macrophages
Authors: Zheng Yuejuan , An Huazhang , Yao Ming , Hou Jin , Yu Yizhi , Feng Gensheng , Cao Xuetao 
Published: May 2010

Abstract
RIG-I–like helicases and TLRs are critical sensors in the induction of type I IFN and proinflammatory cytokines to initiate innate immunity against invading pathogens. However, the mechanisms for the full activation of TLR and RIG-I–triggered innate response remain to be fully investigated. Grb2-associated binder 1 (Gab1), a member of scaffolding/adaptor proteins, can mediate signal transduction from many receptors, however, whether and how Gab1 is required for TLR and RIG-I–triggered innate responses remain unknown. In this study, we demonstrated that Gab1 significantly enhances TLR4-, TLR3-, and RIG-I–triggered IL-6, IL-1β, and IFN-α/β production in macrophages. Gab1 knockdown in primary macrophages or Gab1 deficiency in mouse embryonic fibroblasts significantly suppresses TLR3/4- and RIG-I–triggered production of IL-6, IL-1β, and IFN-α/β. Consistently, Gab1 deficiency impairs vesicular stomatitis virus (VSV) infection-induced IFN-α/β production. In addition to promoting both MyD88- and TLR/IL-1 receptor domain-containing adaptor protein inducing IFN-β–dependent MAPKs and NF-κB activation, Gab1 enhances PI3K/Akt activation by directly binding p85 in TLR signaling and VSV infection. Accordingly, Gab1 inhibits VSV replication and VSV infection-induced cell damage by inducing type I IFNs and IFN-inducible gene expression via PI3K/Akt pathway. Therefore, Gab1 is needed for full activation of TLR3/4- and RIG-I–triggered innate responses by promoting activation of PI3K/Akt, MAPKs, and NF-κB pathways.
Acute Serum Amyloid A Induces Migration, Angiogenesis, and Inflammation in Synovial Cells In Vitro and in a Human Rheumatoid Arthritis/SCID Mouse Chimera Model
Authors: Connolly Mary , Marrelli Alessandra , Blades Mark , McCormick Jennifer , Maderna Paola , Godson Catherine , Mullan Ronan , FitzGerald Oliver , Bresnihan Barry , Pitzalis Costantino , Veale Douglas J. , Fearon Ursula 
Published: May 2010

Abstract
Serum amyloid A (A-SAA), an acute-phase protein with cytokine-like properties, is expressed at sites of inflammation. This study investigated the effects of A-SAA on chemokine-regulated migration and angiogenesis using rheumatoid arthritis (RA) cells and whole-tissue explants in vitro, ex vivo, and in vivo. A-SAA levels were measured by real-time PCR and ELISA. IL-8 and MCP-1 expression was examined in RA synovial fibroblasts, human microvascular endothelial cells, and RA synovial explants by ELISA. Neutrophil transendothelial cell migration, cell adhesion, invasion, and migration were examined using transwell leukocyte/monocyte migration assays, invasion assays, and adhesion assays with or without anti–MCP-1/anti–IL-8. NF-κB was examined using a specific inhibitor and Western blotting. An RA synovial/SCID mouse chimera model was used to examine the effects of A-SAA on cell migration, proliferation, and angiogenesis in vivo. High expression of A-SAA was demonstrated in RA patients (p &lt; 0.05). A-SAA induced chemokine expression in a time- and dose-dependent manner (p &lt; 0.05). Blockade with anti-scavenger receptor class B member 1 and lipoxin A4 (A-SAA receptors) significantly reduced chemokine expression in RA synovial tissue explants (p &lt; 0.05). A-SAA induced cell invasion, neutrophil–transendothelial cell migration, monocyte migration, and adhesion (all p &lt; 0.05), effects that were blocked by anti–IL-8 or anti–MCP-1. A-SAA–induced chemokine expression was mediated through NF-κB in RA explants (p &lt; 0.05). Finally, in the RA synovial/SCID mouse chimera model, we demonstrated for the first time in vivo that A-SAA directly induces monocyte migration from the murine circulation into RA synovial grafts, synovial cell proliferation, and angiogenesis (p &lt; 0.05). A-SAA promotes cell migrational mechanisms and angiogenesis critical to RA pathogenesis.
Identification of a Novel Human MD-2 Splice Variant That Negatively Regulates Lipopolysaccharide-Induced TLR4 Signaling
Authors: Gray Pearl , Michelsen Kathrin S. , Sirois Cherilyn M. , Lowe Emily , Shimada Kenichi , Crother Timothy R. , Chen Shuang , Brikos Constantinos , Bulut Yonca , Latz Eicke , Underhill David , Arditi Moshe 
Published: May 2010

Abstract
Myeloid differentiation factor 2 (MD-2) is a secreted gp that assembles with TLR4 to form a functional signaling receptor for bacterial LPS. In this study, we have identified a novel alternatively spliced isoform of human MD-2, termed MD-2 short (MD-2s), which lacks the region encoded by exon 2 of the MD-2 gene. Similar to MD-2, MD-2s is glycosylated and secreted. MD-2s also interacted with LPS and TLR4, but failed to mediate LPS-induced NF-κB activation and IL-8 production. We show that MD-2s is upregulated upon IFN-γ, IL-6, and TLR4 stimulation and negatively regulates LPS-mediated TLR4 signaling. Furthermore, MD-2s competitively inhibited binding of MD-2 to TLR4. Our study pinpoints a mechanism that may be used to regulate TLR4 activation at the onset of signaling and identifies MD-2s as a potential therapeutic candidate to treat human diseases characterized by an overly exuberant or chronic immune response to LPS.
Resolution of Inflammation in Murine Autoimmune Arthritis Is Disrupted by Cyclooxygenase-2 Inhibition and Restored by Prostaglandin E2-Mediated Lipoxin A4 Production
Authors: Chan Marion Man-Ying , Moore Andrea Rossi 
Published: May 2010

Abstract
Acute inflammation follows defined phases of induction, inflammation and resolution, and resolution occurs by an active process that requires cyclooxygenase-2 (COX-2) activity. This study aims to address whether this paradigm extends to recognized model of chronic inflammation. We demonstrated that murine collagen-induced arthritis follows a similar sequential course. Interestingly, COX-2 and its metabolite, the presumably proinflammatory PGE2, are present in the joints during resolution, and blocking COX-2 activity and PGE2 production within this period perpetuated, instead of attenuated, inflammation. Repletion with PGE2 analogs restored homeostasis, and this function is mediated by the proresolving lipoxygenase metabolite, lipoxin A4, a potent stop signal. Thus, the study provided in vivo evidence for a natural, endogenous link between the cyclooxygenase–lipoxygenase pathways and showed that PGE2 serves as a feedback inhibitor essential for limiting chronic inflammation in autoimmune arthritis. These findings may explain the enigma regarding why COX-2 inhibitors are palliative rather than curative in humans, because blocking resolution may mitigate the benefit of preventing induction.
Monocyte Trafficking to Hepatic Sites of Bacterial Infection Is Chemokine Independent and Directed by Focal Intercellular Adhesion Molecule-1 Expression
Authors: Shi Chao , Velázquez Peter , Hohl Tobias M. , Leiner Ingrid , Dustin Michael L. , Pamer Eric G. 
Published: May 2010

Abstract
Recruitment of CCR2+Ly6Chigh monocytes to sites of infection is essential for efficient clearance of microbial pathogens. Although CCR2-mediated signals promote monocyte emigration from bone marrow, the contribution of CCR2 to later stages of monocyte recruitment remains unresolved. In this article, we show that CCR2 deficiency markedly worsens hepatic Listeria monocytogenes infection because Ly6Chigh monocytes are retained in the bone marrow. Intravenously transferred, CCR2-deficient Ly6Chigh monocytes traffic normally to hepatic foci of infection and contribute to bacterial clearance. Pertussis toxin treatment of adoptively transferred monocytes does not impair their intrahepatic trafficking, suggesting that chemokine signaling, once CCR2+Ly6Chigh monocytes emigrate from the bone marrow, is not required for monocyte localization to sites of bacterial infection in the liver. Expression of ICAM-1 is induced in close proximity to foci of bacterial infection in the liver, including on CD31+ endothelial cells, and blockade of CD11b and CD44 diminishes monocyte localization to these hepatic foci. Our studies demonstrated that Ly6Chigh monocyte recruitment from the bloodstream to the L. monocytogenes-infected liver does not require chemokine receptor-mediated signals but instead is principally dependent on integrin- and extracellular matrix-mediated monocyte adhesion.
Do personality characteristics and beliefs predict intra‐group bullying between prisoners?
Authors: Turner Polly , Ireland Jane L. 
Published: April 2010

AbstractThis study assesses how beliefs about aggression and personality can predict engagement in intra‐group bullying among prisoners. A sample of 213 adult male prisoners completed the DIPC‐SCALED (bullying behavior), the EXPAGG (beliefs toward aggression), and the IPIP (a five‐factor measure of personality). It was predicted that bullies would hold greater instrumental beliefs supporting the use of aggression than the other categories, with perpetrators reporting lower scores on agreeableness, conscientiousness, and openness to experience, and higher scores on neuroticism (i.e. low scores on emotional stability) than the remaining sample. Bullies and bully‐victims endorsed greater instrumental aggressive beliefs than the victim category. Only one perpetrator group, bullies were predicted by reduced levels of agreeableness and increased levels of neuroticism, whereas bully/victims were predicted by decreased levels of neuroticism. Limitations of this study and directions for future research are discussed. Aggr. Behav. 36:261–270, 2010. © 2010 Wiley‐Liss, Inc.
Ultrasound of the knee during voluntary quadriceps contraction: A technique for detecting otherwise occult effusions
Authors: Ike Robert W. , Somers Emily C. , Arnold Erin L. , Arnold William J. 
Published: April 2010

AbstractObjectiveTo describe 1) a technique that can detect synovial effusions not seen on static ultrasound (US) examination and 2) the characteristics of patients with knee osteoarthritis (OA) for whom this technique proved useful.MethodsFrom reviewed records of 76 patients with knee OA (112 knees) that we had seen for US‐guided injections over a defined period, we found 45 knees with no detectable effusion on static US, of which 18 (14 patients) showed fluid when scanned during voluntary quadriceps contraction. For all patients, we had recorded effusion features (physical examination, presence and size on US), and success of joint entry was determined by getting synovial fluid and/or seeing an air echo or inflow of injected material.ResultsThe 14 patients we studied were obese (mean ± SEM body mass index 32.7 ± 2.3 kg/m2; 3 morbidly obese), with moderate to severe OA by radiography in most (Kellgren/Lawrence class 3 or 4 in 10 of 14 knees for which radiographs were available). The suprapatellar synovial space seen by US was small (mean ± SEM depth 0.38 ± 0.04 cm). Arthrocentesis obtained 0.5–16 ml of synovial fluid (mean ± SEM 2.9 ± 0.6 ml), which correlated with the depth of effusion as seen on US with the quadriceps in maximum contraction (Spearman's ρ = 0.5597, P = 0.0157). In 4 knees where arthrocentesis failed to retrieve fluid, we observed at injection the inflow of material and a linear air echo.ConclusionUS of the knee during voluntary quadriceps contraction can find effusions not detectable on static US. Such effusions provide targets for accurate aspiration and injection that would not be appreciated with static US.
A catalytic CC bond‐forming reaction between aliphatic fluorohydrocarbons and arylsilanes
Authors: Lühmann Nicole , Panisch Robin , Müller Thomas 
Published: May 2010

AbstractCC coupling reactions between arylsilanes and alkylfluorides are efficiently catalyzed by disilyl cation 1. Primary as well as secondary alkylfluorides were quantitatively coupled with arylsilanes; however, in the case of tertiary fluorides, the hydrodefluorination reaction predominated. Primary alkylfluorides were found to give arenes with mostly rearranged alkyl substituents. In all cases subsequent Friedel–Crafts‐type chemistry occurred. Copyright © 2010 John Wiley & Sons, Ltd.