bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hospitalization Subsequent to Diagnosis in Young Patients With Diabetes in Chicago, Illinois
Authors: Estrada Carmela L. , Danielson Kirstie K. , Drum Melinda L. , Lipton Rebecca B. 
Published: August 2009

OBJECTIVES: Rehospitalization after a diabetes diagnosis in youth signals the failure of outpatient management. We examined risk factors for rehospitalization among young patients with diabetes.
PATIENTS AND METHODS: We queried 535 participants diagnosed before 18 years of age from the Chicago Childhood Diabetes Registry. Demographic, social, and clinical data were used in logistic models of diabetes-related rehospitalization, as well as, among those rehospitalized, frequent (≥ once per 2 years' duration) versus infrequent rehospitalization rates.
RESULTS: Mean (range) duration was 5.1 years (0.1–19.2 years). The sample was 55% non-Hispanic black, 11% non-Hispanic white, 26% Hispanic, and 7% other/mixed race; 86% had presumed type 1 diabetes; and 47% were underinsured. Overall, 46% reported rehospitalization for diabetes. In multivariable logistic regression, ever being rehospitalized was significantly associated with diabetes duration (per year, odds ratio [OR]: 1.26; P &lt; .01), female gender (OR: 1.67; P = .01), underinsurance (versus private insurance; OR: 1.79; P &lt; .01), presumed phenotype (non–type 1 diabetes versus type 1; OR: 0.32; P &lt; .01), and diagnosis at a community hospital (versus tertiary care facility; OR: 1.96; P &lt; .01) and tended to be higher for those of nonwhite race (OR: 1.94; P = .07). Among those rehospitalized, multivariable associations with frequent rehospitalization were presumed phenotype (non–type 1 diabetes versus type 1; OR: 2.74; P = .04), head of household not working (versus employed; OR: 1.88; P = .02), and younger age at questionnaire (per year; OR: 0.94; P = .01).
CONCLUSIONS: Rehospitalization is common in young patients with diabetes, especially for those with limited resources, indicating the need for improved outpatient services. Comprehensive initial education and support available to young patients with diabetes diagnosed at tertiary care facilities and their families may have lasting protective effects.
The incidence class and the hierarchy of orbits
Authors: Fehér László , Patakfalvi Zsolt 
Published: August 2009

Abstract
R. Rimányi defined the incidence class of two singularities η and ζ as [η]|ζ, the restriction of the Thom polynomial of η to ζ. He conjectured that (under mild conditions) [η]|ζ ≠ 0 ⇔ ζ ⊂ $$
\bar \eta
$$. Generalizing this notion we define the incidence class of two orbits η and ζ of a representation. We give a sufficient condition (positivity) for ζ to have the property that [η]|ζ ≠ 0 ⇔ ζ ⊂ $$
\bar \eta
$$ for any other orbit η. We show that for many interesting cases, e.g. the quiver representations of Dynkin type positivity holds for all orbits. In other words in these cases the incidence classes completely determine the hierarchy of the orbits. We also study the case of singularities where positivity doesn’t hold for all orbits.
Periodic harmonic functions on lattices and points count in positive characteristic
Authors: Zaidenberg Mikhail 
Published: August 2009

Abstract
This survey deals with pluri-periodic harmonic functions on lattices with values in a field of positive characteristic. We mention, as a motivation, the game “Lights Out” following the work of Sutner [20], Goldwasser- Klostermeyer-Ware [5], Barua-Ramakrishnan-Sarkar [2, 19], Hunzikel-Machiavello-Park [12] e.a.; see also [22, 23] for a more detailed account. Our approach uses harmonic analysis and algebraic geometry over a field of positive characteristic.
Rehabilitation of Stroke Patients - Effects of Early Intervention of Physical Therapy on Functional Outcome
Authors: Nessa Jebun , Khaleque Md Abdul , Begum Shahanaz , Ahmed AH Hamid , Islam Shafiqul , Afsan Md 
Published: August 2009

Context: Early initiation of rehabilitation procedures in stroke patients can enable greater return of neurological functions and prevents complication, thereby improves long term outcome and quality of life. Functional Independence measure (FIM) score is one of the commonest scale used to measure outcome. Study design: Prospective type of study. Place of study: Dept. of Physical Medicine and Rehabilitation, BSMMU. Method: 48 acute onset first episode stroke patients were assessed Rehabilitation procedures started immediately after attending the Dept. According to a comprehensive rehabilitation plan physical therapy, speech therapy, occupational therapy was given and continued for 8 weeks, with proper education to the patient and the attendant. Result: Outcome was measured and the result showed significant improvements (p value <0.001) in early treatment group of patients. Key words: Stroke, FIM, Outcome. doi: 10.3329/bja.v7i1.3028 Bangladesh Journal of Anatomy January 2009, Vol. 7 No. 1 pp. 62-67
Testing of the OMERACT 8 Draft Validation Criteria for a Soluble Biomarker Reflecting Structural Damage in Rheumatoid Arthritis: A Systematic Literature Search on 5 Candidate Biomarkers
Authors: SYVERSEN SILJE W. , LANDEWE ROBERT , van der HEIJDE DÉSIRÉE , BATHON JOAN M. , BOERS MAARTEN , BYKERK VIVIAN P. , FITZGERALD OLIVER , GLADMAN DAFNA D. , GARNERO PATRICK , GEUSENS PIET , EL-GABALAWY HANI , INMAN ROBERT D. , KRAUS VIRGINIA , KVIEN TORE K. , MEASE PHILIP J. , ØSTERGAARD MIKKEL , RITCHLIN CHRISTOPHER J. , TAK PAUL-PETER , TAYLOR WILLIAM J. , MAKSYMOWYCH WALTER P. 
Published: August 2009

Objective.To test the OMERACT 8 draft validation criteria for soluble biomarkers by assessing the strength of literature evidence in support of 5 candidate biomarkers.Methods.A systematic literature search was conducted on the 5 soluble biomarkers RANKL, osteoprotegerin (OPG), matrix metalloprotease (MMP-3), urine C-telopeptide of types I and II collagen (U-CTX-I and U CTX-II), focusing on the 14 OMERACT 8 criteria. Two electronic voting exercises were conducted to address: (1) strength of evidence for each biomarker as reflecting structural damage according to each individual criterion and the importance of each individual criterion; (2) overall strength of evidence in support of each of the 5 candidate biomarkers as reflecting structural damage endpoints in rheumatoid arthritis (RA) and identification of omissions to the criteria set.Results.The search identified 111 articles. The strength of evidence in support of these biomarkers reflecting structural damage was low for all biomarkers and was rated highest for U-CTX-II [score of 6.5 (numerical rating scale 0–10)]. The lowest scores for retention of specific criteria in the draft set went to criteria that refer to the importance of animal studies, correlations with other biomarkers reflecting damage, and an understanding of the metabolism of the biomarker.Conclusion.Evidence in support of any of the 5 tested biomarkers (MMP-3, CTX-I, CTX-II, OPG, RANKL) was inadequate to allow their substitution for radiographic endpoints in RA. Three of the criteria in the draft criteria set might not be required, but few omissions were identified.
Reappraisal of OMERACT 8 Draft Validation Criteria for a Soluble Biomarker Reflecting Structural Damage Endpoints in Rheumatoid Arthritis, Psoriatic Arthritis, and Spondyloarthritis: The OMERACT 9 v2 Criteria
Authors: MAKSYMOWYCH WALTER P. , LANDEWÉ ROBERT , TAK PAUL-PETER , RITCHLIN CHRISTOPHER J. , ØSTERGAARD MIKKEL , MEASE PHILIP J. , EL-GABALAWY HANI , GARNERO PATRICK , GLADMAN DAFNA D. , FITZGERALD OLIVER , ALETAHA DANIEL , BYKERK VIVIEN P. , BATHON JOAN M. , SYVERSEN SILJE W. , BOERS MAARTEN , GEUSENS PIET , INMAN ROBERT D. , KRAUS VIRGINIA B. , KVIEN TORE K. , TAYLOR WILLIAM J. , WELLS GEORGE A. , van der HEIJDE DÉSIRÉE 
Published: August 2009

Objectives.A draft set of criteria for the validation of soluble biomarkers reflecting damage endpoints was proposed at OMERACT 8. At OMERACT 9 we aimed to scrutinize the necessity for each of these criteria according to the objectives of the working group.Methods.The OMERACT 8 draft criteria and the principle objectives of the validation process were clarified at a meeting of the working group in London, December 2007. A new framework was proposed after the following steps were conducted: (A) A systematic review of the literature focusing on the draft criteria and a preselected group of biomarkers (MMP3, CTX-II, RANKL, OPG, CTX-I) followed by a Delphi consensus exercise addressing the importance of individual criteria and identification of omissions in the draft set. (B) Formal debate as well as group discussion centered on the key arguments for inclusion/exclusion of specific criteria. (C) Onsite interactive electronic voting on the importance of specific criteria. The framework was presented and discussed at OMERACT 9 in both breakout and plenary sessions followed by a vote on its acceptance.Results.The objectives of rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis biomarkers in relation to their predictive validity for damage endpoints was clarified and supported by OMERACT 9 participants. The OMERACT 8 draft validation criteria were reformulated into an essential category focused on criteria addressing the OMERACT Filter elements of discrimination (incorporating truth) and feasibility, and a desirable but nonessential category of other criteria addressing truth. This revised draft set was endorsed by participants at OMERACT 9.Conclusion.A revised set of validation criteria has been drafted by consensus at OMERACT 9 that focuses on the performance characteristics of biomarker assays, the importance of addressing potential confounders, and the essential requirement for clinical validation studies.
Reducing Invasiveness, Duration, and Cost of Magnetic Resonance Imaging in Rheumatoid Arthritis by Omitting Intravenous Contrast Injection — Does It Change the Assessment of Inflammatory and Destructive Joint Changes by the OMERACT RAMRIS?
Authors: ØSTERGAARD MIKKEL , CONAGHAN PHILIP G. , O’CONNOR PHILIP , SZKUDLAREK MARCIN , KLARLUND METTE , EMERY PAUL , PETERFY CHARLES , GENANT HARRY , McQUEEN FIONA M. , BIRD PAUL , LASSERE MARISSA , EJBJERG BO 
Published: August 2009

Objective.Gadolinium (Gd)-enhanced magnetic resonance imaging (MRI) provides highly sensitive assessment of inflammatory and destructive changes in rheumatoid arthritis (RA) joints, but intravenous (IV) Gd injection prolongs examination time and increases cost, invasiveness, and patient discomfort. We explored to what extent RA joint pathologies in wrists and metacarpophalangeal (MCP) joints can be reliably assessed by unenhanced MRI images compared with Gd-enhanced MRI as the reference method.Methods.MRI data sets from 2 RA substudies were scored according to preliminary OMERACT RA MRI scoring system (RAMRIS): Substudy A included 1.0 T/1.5 T MR images from 40 RA patients, which were scored twice by 2 experienced readers. Substudy B included 0.2 T dedicated extremity MRI (E-MRI) images from 55 patients, scored twice by one experienced reader. The first reading included only unenhanced images, whereas complete image sets were available for the second reading.Results.Gd contrast injection appeared unimportant to MRI scores of bone erosions and bone edema in RA wrist and MCP joints. However, when post-Gd MRI was considered the standard reference, MRI without Gd provided only moderate to high agreement concerning assessment of synovitis, and omitting the post-Gd acquisitions increased the interreader variation on synovitis scores. Low-field (0.2 T) E-MRI in these exercises provided a lower sensitivity of unenhanced imaging for synovitis than MRI using higher-field strengths.Conclusion.Omitting IV contrast injection did not change scores of bone erosions and bone edema, but decreased the reliability of synovitis scores. However, this disadvantage may for some purposes be outweighed by the possibility to assess more joints and/or greater feasibility.
The C-Type Lectin-Like Receptor CLEC-1, Expressed by Myeloid Cells and Endothelial Cells, Is Up-Regulated by Immunoregulatory Mediators and Moderates T Cell Activation
Authors: Thebault Pamela , Lhermite Natacha , Tilly Gaëlle , Le Texier Laëtitia , Quillard Thibaut , Heslan Michele , Anegon Ignacio , Soulillou Jean-Paul , Brouard Sophie , Charreau Beatrice , Cuturi Maria-Cristina , Chiffoleau Elise 
Published: August 2009

Abstract
C-type lectin receptors have recently been described as playing crucial roles in immunity and homeostasis since these proteins are able to recognize pathogens as well as self-Ags. We identified the C-type lectin-like receptor-1, CLEC-1, as being overexpressed in a model of rat allograft tolerance. We previously described in this model the expression of numerous cytoprotective molecules by graft endothelial cells and their interplay with regulatory CD4+CD25+ T cells. In this study, we demonstrate that CLEC-1 is expressed by myeloid cells and specifically by endothelial cells in tolerated allografts and that CLEC-1 expression can be induced in endothelial cells by alloantigen-specific regulatory CD4+CD25+ T cells. Analysis of CLEC-1 expression in naive rats demonstrates that CLEC-1 is highly expressed by myeloid cells and at a lower level by endothelial cells, and that its expression is down-regulated by inflammatory stimuli but increased by the immunoregulators IL-10 or TGFβ. Interestingly, we demonstrate in vitro that inhibition of CLEC-1 expression in rat dendritic cells increases the subsequent differentiation of allogeneic Th17 T cells and decreases the regulatory Foxp3+ T cell pool. Additionally, in chronically rejected allograft, the decreased expression of CLEC-1 is associated with a higher production of IL-17. Taken together, our data suggest that CLEC-1, expressed by myeloid cells and endothelial cells, is enhanced by regulatory mediators and moderates Th17 differentiation. Therefore, CLEC-1 may represent a new therapeutic agent to modulate the immune response in transplantation, autoimmunity, or cancer settings.
Impaired Lung Dendritic Cell Migration and T Cell Stimulation Induced by Immunostimulatory Oligonucleotides Contribute to Reduced Allergic Airway Inflammation
Authors: Constabel Hannelore , Stankov Metodi V. , Hartwig Christina , Tschernig Thomas , Behrens Georg M. N. 
Published: August 2009

Abstract
CpG-containing oligonucleotides (CpG) have been shown to reduce key features of allergic airway inflammation in mouse models. Given the inhibitory effects of CpG treatment on Ag presentation of subsequently encountered Ags via MHC class I and II molecules by dendritic cells (DC), we hypothesized that intranasal CpG treatment would lead to reduced Ag-specific T cell stimulation in the lung-draining lymph nodes, thereby reducing the inflammatory response in sensitized mice. Intranasal CpG administration led to phenotypic maturation of lung and mediastinal lymph node DC as determined by expression of MHC class II, CD80, and CD86. This was accompanied by a significant reduction in the proliferation of adoptively transferred Ag-specific CD4+ and CD8+ T cells in mediastinal lymph nodes, when CpG was given before inhalative OVA challenges. DC obtained from mediastinal lymph nodes of CpG-treated mice before OVA inhalation led to reduced T cell stimulation via MHC class I and II molecules. In addition, CpG diminished airway eosinophilia and pulmonary infiltration after sensitization or following adoptive transfer of Ag-specific Th2 cells. These results were explained by reduced CCL21 expression and inhibition of lung DC migration following CpG administration, which could be restored by transfer of bone marrow-derived DC, because CpG had no major impact on the constitutive MHC class II Ag presentation of protein-derived Ag by lung tissue-derived DC. We conclude that CpG treatment can effectively impair the DC-mediated Ag transport from the lungs to the lymph nodes, resulting in reduced T cell activation and blunted airway inflammation.
The Gli3 Transcription Factor Expressed in the Thymus Stroma Controls Thymocyte Negative Selection Via Hedgehog-Dependent and -Independent Mechanisms
Authors: Hager-Theodorides Ariadne L. , Furmanski Anna L. , Ross Susan E. , Outram Susan V. , Rowbotham Nicola J. , Crompton Tessa 
Published: August 2009

AbstractThe Hedgehog (Hh) responsive transcription factor Gli3 is required for efficient thymocyte development in the fetus. In this study we show that Gli3, not detected in adult thymocytes, is expressed in the murine fetal and adult thymus stroma. PCR array analysis revealed Cxcl9, Rbp1, and Nos2 as novel target genes of Gli3. We show that Gli3 positively regulates the expression of these genes, most likely by suppressing an intermediate repressor. Deletion of autoreactive thymocytes depends on their interactions with the thymus stroma. Repression of the proapoptotic gene Nos2 in Gli3 mutants coincides with reduced apoptosis of double positive thymocytes undergoing negative selection in vitro and in vivo, and the production of autoreactive thymocytes. Taken together these data indicate that Gli3 controls thymocyte apoptosis and negative selection possibly via the regulation of Nos2. Defective Gli3 expression in the thymus stroma also resulted in decreased CD5 expression on mature thymocytes and inappropriate production of MHC class I-selected CD4+ cells, both consistent with reduced TCR signal strength. Overall our data indicate that Gli3 expressed in the thymus stroma regulates negative selection and TCR signal strength via Hh-dependent and -independent mechanisms, with implications for autoimmunity.
Jagged1 on Dendritic Cells and Notch on CD4+ T Cells Initiate Lung Allergic Responsiveness by Inducing IL-4 Production
Authors: Okamoto Masakazu , Matsuda Hiroyuki , Joetham Anthony , Lucas Joseph J. , Domenico Joanne , Yasutomo Koji , Takeda Katsuyuki , Gelfand Erwin W. 
Published: August 2009

Abstract
Jagged1, a Notch ligand, and Notch have been implicated in Th2 differentiation, but their role in initiating IL-4 production and Th2 differentiation in vivo and the development of allergic airway responses has not been defined. In this study, we show that Jagged1 is up-regulated on bone marrow-derived dendritic cells (BMDCs) pulsed with allergen and that the transfer of these BMDCs before allergen challenge induces airway hyperresponsiveness (AHR) and eosinophilic airway inflammation. Treatment of CD4+ T cells with a γ-secretase inhibitor (GSI), which inhibits Notch signaling, resulted in decreased cytokine production when the cells were cocultured with allergen-pulsed, Jagged1-expressing BMDCs and, after the transfer of allergen-pulsed BMDCs, IL-4-deficient (IL-4−/−) recipients of GSI-treated naive CD4+ T cells developed lower levels of AHR, reduced numbers of eosinophils, and lower Th2 cytokine levels when challenged with allergen. In vivo treatment of wild-type mice with Jagged1-Fc enhanced AHR and airway inflammation, whereas the transfer of BMDC transfected with Jagged1 small interfering RNA (siRNA) cells into WT or IL-4−/− mice before transfer of CD4+ T cells resulted in decreased AHR, inflammation, and Th2 cytokines, indicating the critical role for Jagged1 expression on APCs. These data identify the essential role of the interactions between Notch on CD4+ T cells and Jagged1 on APCs in the initiation of IL-4 production and Th2 differentiation for the development of AHR and allergic airway inflammation.
γ-Aminobutyric Acid Transporter 1 Negatively Regulates T Cell Activation and Survival through Protein Kinase C-Dependent Signaling Pathways
Authors: Wang Ying , Luo Qingqiong , Xu Yan , Feng Dechun , Fei Jian , Cheng Qi , Xu Lingyun 
Published: August 2009

Abstract
γ-aminobutyric acid transporter 1 (GAT-1), as the major regulator in maintaining a γ-aminobutyric acid reservoir in the CNS, plays negative roles in experimental autoimmune encephalomyelitis pathogenesis. Our previous study has revealed that, besides its wide expression in the CNS, GAT-1 expression can be induced on activated T cells triggered by Ag. However, the function of GAT-1 in T cell activation is unclear. In this study, we show that GAT-1 deficiency induces more vigorous cell cycle entry and less cell apoptosis in T cells, thus leading to enhanced cell proliferation. GAT-1 deficiency promotes T cell division and survival by down-regulating cyclin dependent kinase inhibitor p27kip1, differentially regulating the pro- and anti-apoptotic proteins Bcl-2, Bcl-xl, and Bad and activating transcription factor NF-κB through induction of translocation and phosphorylation of protein kinase C (PKC) θ. In addition, our data reveal that GAT-1 expression on T cells is modulated by PKC activation. Taken together, the data show that GAT-1 negatively regulates T cell activation and survival through PKC-dependent signaling pathways.
Genetic Complementation Results in Augmented Autoantibody Responses to Lupus-Associated Antigens
Authors: Sim Davis L. , Bagavant Harini , Scindia Yogesh M. , Ge Yan , Gaskin Felicia , Fu Shu Man , Deshmukh Umesh S. 
Published: August 2009

Abstract
Lupus-prone female New Zealand Mixed (NZM)2328 mice develop high titers of anti-nuclear and anti-dsDNA autoantibodies. Despite high expression of type I IFNs, these mice do not develop autoantibodies to the small nuclear ribonucleoprotein (snRNP) complex. Thus, additional genetic factors must regulate the generation of anti-snRNP autoantibodies. In contrast, despite much lower expression of type 1 IFNs, the diabetes-prone NOD mice spontaneously make anti-snRNP autoantibodies, albeit at a low incidence. To determine whether combination of high type I IFN response of NZM mice with appropriate susceptibility genes of NOD mice would result in anti-snRNP Ab response, cohorts of (NZM2328 × NOD)F1 mice were generated and characterized for development of autoimmunity. In comparison with parental strains, the PBMCs from F1 mice showed intermediate expression of type I IFN-responsive genes and augmented expression of IL-6 transcripts. TLR7 expression was similar in all strains. The F1 mice had very high incidence and titer of anti-snRNP autoantibodies, anti-nuclear Abs, and anti-dsDNA autoantibodies. The levels of anti-snRNP autoantibody correlated with the expression levels of type I IFN-responsive genes. None of the F1 mice developed diabetes, and only female mice developed severe renal disease. Our data demonstrate that only in presence of appropriate susceptibility genes, anti-snRNP autoantibodies are induced and type I IFNs amplify this response. A synergy between IL-6 and type I IFNs might be critical for amplifying overall autoantibody responses in systemic lupus erythematosus. In NZM/NOD F1 mouse, genetic complementation between NZM and NOD genes leads to expression of phenotypes similar to those seen in certain lupus patients.