bluuebunny/crossref_metadata_2025_split huggingface dataset:
Folksonomy, Tagging and Taxonomy for Effective Learning. Perspectives of Learning 2.0 in the XXI century
Authors: Cannata Cosimo 
Published: June 2009

This paper reflects upon the issues posed by students' extensive use of collaborative internet tools, or social web (Web 2.0). Internet-based cooperative activities are usually underrated by academic and offical school practice, though students dedicate most of their time to the web. Moreover, the paper attempts to consider the innovative collaborative practices of Web 2.0, of social bookmarking ("Tagging") as part of future teaching standards, and what are the perspectives in the near future.
Finally, the aims of the paper are to understand the interactions between students' real life and learning and to explore possible, reliable, criteria for assessment of students' activities through Web 2.0.
Tuberculosis Is Associated with a Down-Modulatory Lung Immune Response That Impairs Th1-Type Immunity
Authors: Almeida Alexandre S. , Lago Patrícia M. , Boechat Neio , Huard Richard C. , Lazzarini Luiz C. O. , Santos Adalberto R. , Nociari Marcelo , Zhu Hongxia , Perez-Sweeney Beatriz M. , Bang Heejung , Ni Quanhong , Huang Jie , Gibson Andrea L. , Flores Vera C. , Pecanha Lorena R. , Kritski Afrânio L. , Lapa e Silva José R. , Ho John L. 
Published: June 2009

AbstractImmune mediators associated with human tuberculosis (TB) remain poorly defined. This study quantified levels of lung immune mediator gene expression at the time of diagnosis and during anti-TB treatment using cells obtained by induced sputum. Upon comparison to patients with other infectious lung diseases and volunteers, active pulmonary TB cases expressed significantly higher levels of mediators that counteract Th1-type and innate immunity. Despite the concomitant heightened levels of Th1-type mediators, immune activation may be rendered ineffectual by high levels of intracellular (SOCS and IRAK-M) and extracellular (IL-10 and TGF-βRII, IL-1Rn, and IDO) immune suppressive mediators. These modulators are a direct response to Mycobacterium tuberculosis as, by day 30 of anti-TB treatment, many suppressive factors declined to that of controls whereas most Th1-type and innate immune mediators rose above pretreatment levels. Challenge of human immune cells with M. tuberculosis in vitro up-regulated these immune modulators as well. The observed low levels of NO synthase-2 produced by alveolar macrophages at TB diagnosis, along with the heightened amounts of suppressive mediators, support the conclusion that M. tuberculosis actively promotes down-modulatory mediators to counteract Th1-type and innate immunity as an immunopathological strategy. Our data highlight the potential application of immune mediators as surrogate markers for TB diagnosis or treatment response.
Lack of MyD88 Protects the Immunodeficient Host Against Fatal Lung Inflammation Triggered by the Opportunistic Bacteria Burkholderia cenocepacia
Authors: Ventura Grasiella M. de C. , Balloy Viviane , Ramphal Reuben , Khun Huot , Huerre Michel , Ryffel Bernhard , Plotkowski Maria-Cristina M. , Chignard Michel , Si-Tahar Mustapha 
Published: June 2009

Abstract
Burkholderia cenocepacia is an opportunistic pathogen of major concern for cystic fibrosis patients as well as immunocompromised cancer patients and transplant recipients. The mechanisms by which B. cenocepacia triggers a rapid health deterioration of the susceptible host have yet to be characterized. TLR and their key signaling intermediate MyD88 play a central role in the detection of microbial molecular patterns and in the initiation of an effective immune response. We performed a study to better understand the role of TLR-MyD88 signaling in B. cenocepacia-induced pathogenesis in the immunocompromised host, using an experimental murine model. The time-course of several dynamic parameters, including animal survival, bacterial load, and secretion of critical inflammatory mediators, was compared in infected and immunosuppressed wild-type and MyD88−/− mice. Notably, when compared with wild-type mice, infected MyD88−/− animals displayed significantly reduced levels of inflammatory mediators (including KC, TNF-α, IL-6, MIP-2, and G-CSF) in blood and lung airspaces. Moreover, despite a higher transient bacterial load in the lungs, immunosuppressed mice deficient in MyD88 had an unexpected survival advantage. Finally, we showed that this B. cenocepacia-induced life-threatening infection of wild-type mice involved the proinflammatory cytokine TNF-α and could be prevented by corticosteroids. Altogether, our findings demonstrate that a MyD88-dependent pathway can critically contribute to a detrimental host inflammatory response that leads to fatal pneumonia.
IL-1R Signaling within the Central Nervous System Regulates CXCL12 Expression at the Blood-Brain Barrier and Disease Severity during Experimental Autoimmune Encephalomyelitis
Authors: McCandless Erin E. , Budde Matthew , Lees Jason R. , Dorsey Denise , Lyng Eric , Klein Robyn S. 
Published: June 2009

Abstract
Multiple sclerosis (MS) is an autoimmune disease of the CNS characterized by disruption of the blood-brain barrier (BBB). This breach in CNS immune privilege allows undeterred trafficking of myelin-specific lymphocytes into the CNS where they induce demyelination. Although the mechanism of BBB compromise is not known, the chemokine CXCL12 has been implicated as a molecular component of the BBB whose pattern of expression is specifically altered during MS and which correlates with disease severity. The inflammatory cytokine IL-1β has recently been shown to contribute not only to BBB permeability but also to the development of IL-17-driven autoimmune responses. Using experimental autoimmune encephalomyelitis, the rodent model of MS, we demonstrate that IL-1β mediates pathologic relocation of CXCL12 during the induction phase of the disease, before the development of BBB disruption. We also show that CD4, CD8, and, surprisingly γδ T cells are all sources of IL-1β. In addition, γδ T cells are also targets of this cytokine, contributing to IL-1β-mediated production of IL-17. Finally, we show that the level of CNS IL-1R determines the clinical severity of experimental autoimmune encephalomyelitis. These data suggest that T cell-derived IL-1β contributes to loss of immune privilege during CNS autoimmunity via pathologic alteration in the expression of CXCL12 at the BBB.
Aryl Hydrocarbon Receptor Activation Inhibits In Vitro Differentiation of Human Monocytes and Langerhans Dendritic Cells
Authors: Platzer Barbara , Richter Susanne , Kneidinger Doris , Waltenberger Darina , Woisetschläger Maximilian , Strobl Herbert 
Published: June 2009

AbstractThe transcription factor aryl hydrocarbon receptor (AhR) represents a promising therapeutic target in allergy and autoimmunity. AhR signaling induced by the newly described ligand VAF347 inhibits allergic lung inflammation as well as suppresses pancreatic islet allograft rejection. These effects are likely mediated via alterations in dendritic cell (DC) function. Moreover, VAF347 induces tolerogenic DCs. Langerhans cells (LCs) are immediate targets of exogenous AhR ligands at epithelial surfaces; how they respond to AhR ligands remained undefined. We studied AhR expression and function in human LCs and myelopoietic cell subsets using a lineage differentiation and gene transduction model of human CD34+ hematopoietic progenitors. We found that AhR is highly regulated during myeloid subset differentiation. LCs expressed highest AhR levels followed by monocytes. Conversely, neutrophil granulocytes lacked AhR expression. AhR ligands including VAF347 arrested the differentiation of monocytes and LCs at an early precursor cell stage, whereas progenitor cell expansion or granulopoiesis remained unimpaired. AhR expression was coregulated with the transcription factor PU.1 during myeloid subset differentiation. VAF347 inhibited PU.1 induction during initial monocytic differentiation, and ectopic PU.1 restored monocyte and LC generation in the presence of this compound. AhR ligands failed to interfere with cytokine receptor signaling during LC differentiation and failed to impair LC activation/maturation. VAF347-mediated antiproliferative effect on precursors undergoing LC lineage differentiation occurred in a clinically applicable serum-free culture model and was not accompanied by apoptosis induction. In conclusion, AhR agonist signaling interferes with transcriptional processes leading to monocyte/DC lineage commitment of human myeloid progenitor cells.
Coexpression of IL-18 Strongly Attenuates IL-12-Induced Systemic Toxicity through a Rapid Induction of IL-10 without Affecting its Antitumor Capacity
Authors: Rodriguez-Galan Maria Cecilia , Reynolds Della , Correa Silvia G. , Iribarren Pablo , Watanabe Morihiro , Young Howard A. 
Published: June 2009

Abstract
IL-12 is an excellent candidate for the treatment of cancer due to its ability to drive strong antitumor responses. Recombinant IL-12 protein is currently used in cancer patients; however, systemic expression of rIL-12 presents disadvantages including cost and dose limitation due to its toxicity. In this study, we used hydrodynamic shear of cDNA as a tool to achieve systemic expression of IL-12. We found that sustained but toxic levels of serum IL-12 could be generated in 6- to 7-wk-old B6 mice after a single injection of the cDNA. Unexpectedly, we observed that when IL-12 cDNA is coinjected with IL-18 cDNA, IL-12 antitumor activity was maintained, but there was a significant attenuation of IL-12 toxicity, as evidenced by a greater survival index and a diminution of liver enzymes (ALT and AST). Interestingly, after IL-12 plus IL-18 cDNA administration, more rapid and higher IL-10 levels were observed than after IL-12 cDNA treatment alone. To understand the mechanism of protection, we coinjected IL-12 plus IL-10 cDNAs and observed an increase in survival that correlated with diminished serum levels of the inflammatory cytokines TNF-α and IFN-γ. Confirming the protective role of early IL-10 expression, we observed a significant decrease in survival in IL-10 knockout mice or IL-10R-blocked B6 mice after IL-12 plus IL-18 treatment. Thus, our data demonstrate that the high and early IL-10 expression induced after IL-12 plus IL-18 cDNA treatment is critical to rapidly attenuate IL-12 toxicity without affecting its antitumor capacity. These data could highly contribute to the design of more efficient/less toxic protocols for the treatment of cancer.
Increased Antigen Cross-Presentation but Impaired Cross-Priming after Activation of Peroxisome Proliferator-Activated Receptor γ Is Mediated by Up-Regulation of B7H1
Authors: Klotz Luisa , Hucke Stephanie , Thimm Dominik , Classen Sabine , Gaarz Andrea , Schultze Joachim , Edenhofer Frank , Kurts Christian , Klockgether Thomas , Limmer Andreas , Knolle Percy , Burgdorf Sven 
Published: June 2009

Abstract
Dendritic cells are able to take up exogenous Ags and present Ag-derived peptides on MHC class I molecules, a process termed cross-presentation. The mannose receptor (MR), an endocytic receptor expressed on a variety of APCs, has been demonstrated to target soluble Ags exclusively toward cross-presentation. In this study, we investigated the role of the murine nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ), a ligand-activated transcription factor with immunomodulatory properties, in MR-mediated endocytosis and cross-presentation of the model Ag OVA. We could demonstrate both in vitro and in vivo that activation of PPARγ resulted in increased MR expression, which in consequence led to enhanced MR-mediated endocytosis and elevated cross-presentation of soluble OVA. Concomitantly, activation of PPARγ in dendritic cells induced up-regulation of the coinhibitory molecule B7H1, which, despite enhanced cross-presentation, caused an impaired activation of naive OVA-specific CD8+ T cells and the induction of T cell tolerance. These data provide a mechanistic basis for the immunomodulatory action of PPARγ which might open new possibilities in the development of therapeutic approaches aimed at the control of excessive immune responses, e.g., in T cell-mediated autoimmunity.
The Expression and Function of the NKRP1 Receptor Family in C57BL/6 Mice
Authors: Aust Jonathan G. , Gays Frances , Mickiewicz Katarzyna M. , Buchanan Ella , Brooks Colin G. 
Published: June 2009

Abstract
NKRP1 receptors were discovered more than 20 years ago, but due to a lack of appropriate reagents, our understanding of them has remained limited. Using a novel panel of mAbs that specifically recognize mouse NKRP1A, D, and F molecules, we report here that NKRP1D expression is limited to a subpopulation of NK cells, but in contrast to Ly49 receptors appears to be expressed in a normal codominant manner. NKRP1D− and NKRP1D+ NK cells are functionally distinct, NKRP1D+ cells showing reduced expression of various Ly49 receptors, elevated expression of CD94/NKG2 receptors, and higher IFN-γ secretion and cytotoxicity than NKRP1D− cells. Furthermore, NKRP1D+ NK cells were unable to kill transfected cells expressing high levels of Clr-b molecules, but readily killed MHC class-I-deficient blast cells that express only low levels of Clr-b. NKRP1A and NKRP1F were expressed at low levels on all splenic and bone marrow NK cells, but mAb-induced cross-linking of NKRP1A and NKRP1F caused no significant enhancement or inhibition of NK cell cytotoxicity and no detectable production of IFN-γ. NKRP1A, D, and F expression could not be detected on NKT cells, all of which express NKRP1C, and although some activated T cells expressed NKRP1C and perhaps low levels of NKRP1A, no significant expression of NKRP1D or F could be detected. NKRP1 molecules expressed on NK cells or transfectants were down-regulated by cross-linking with mAbs or cell surface ligands, and using this phenomenon as a functional assay for NKRP1-ligand interaction revealed that NKRP1F can recognize CLR-x.
Conservation of Structural and Functional Features in a Primordial CD80/86 Molecule from Rainbow Trout (Oncorhynchus mykiss), a Primitive Teleost Fish
Authors: Zhang Yong-An , Hikima Jun-ichi , Li Jun , LaPatra Scott E. , Luo Yan-Ping , Sunyer J. Oriol 
Published: June 2009

Abstract
In mammals, interaction of CD28 with CD80 or CD86 molecules provides costimulatory signals for T cell activation that leads to increased IL-2 gene and protein expression by activated T cells. Thus far, CD80 and CD86 have been cloned and functionally characterized only in mammals and birds. To shed light into the evolution of CD80 and CD86, we have cloned and functionally characterized a rainbow trout (rt) molecule (rtCD80/86) that shows the highest degree of sequence conservation and phylogenetic relationship with CD80 and CD86 molecules. Moreover, its genomic organization was almost identical to that of human CD86. Rainbow trout possess one membrane-bound and two soluble CD80/86 transcripts, all of which are derived from the same rtCD80/86 gene. The membrane-bound form exhibited its highest degree of expression in lymphoid tissues, particularly on B cells. Incubation of trout leukocytes with LPS and bacteria leads to up-regulation of rtCD80/86 gene expression. Importantly, we show that trout and other teleost fish contain a single CD80/86 gene, thus suggesting that this gene may represent the ancestor from which CD80 and CD86 arose by gene duplication in more evolved species. To gain further insights into the function of rtCD80/86, we have identified and cloned trout IL-2 and have shown that recombinantly produced trout CD80/86 up-regulates the expression of IL-2 in trout blood leukocytes. Significantly, this finding indicates that the capacity to modulate IL-2 expression is a primordial function that has been conserved both in fish and mammalian CD80/CD86 molecules throughout 350 million years of evolution.
The Call for Raising Standards: Promising Responses
Authors: Alvoid Lee 
Published: June 2009

What is the status of ambitious national recommendations designed to develop the talent of our brightest students? Have states, districts, and individual schools taken action? Are we much further along as a nation in raising the expectation level for gifted and talented students? As a former middle and high school principal, I have pictures of specific students in mind when I contemplate these answers. There has been progress, but not nearly enough has been accomplished.
Young Leaders: Growing through Mentoring
Authors: Manning Sandra 
Published: June 2009

“Hey, you got it!” Caitlyn exclaimed as Leisha identified the letter B on a flash card. Caitlyn is a 2nd-grade student in a gifted and talented program. Leisha is a kindergarten student. Both girls are part of a cross-age mentoring experience that Caitlyn's teacher implemented with the help of a kindergarten teacher in the same school. Motivated by a graduate course in gifted education, Caitlyn's teacher decided to include a leadership skill component in the general education classroom for her gifted and talented students. She designed and initiated across-age mentoring program in which gifted students were paired with at-risk kindergarten students for weekly tutoring and mentoring meetings.
Evaluating the First Year Experience: Students' Knowledge, Attitudes, and Behaviors
Authors: Schrader P. G. , Brown Scott W. 
Published: June 2009

First Year Experience (FYE) programs have been implemented in universities and colleges to address the emergent needs of matriculating students. It is well documented that many students are not prepared for the rigors of postsecondary education and FYE programs are designed to supplement the necessary academic and life skills. These academic and life skills range from knowing the location of the library to seeking out appropriate personnel when personal issues arise. Evaluating programs developed to address such a wide range of knowledge and skills is an obvious challenge, especially when each FYE is customized for each corresponding university or college. In the case of one FYE program at a large university, evaluation of student Knowledge, Attitudes, and Behaviors (KAB) provided a conceptual model to examine the program as a whole. This particular study revealed the following about the FYE program: The KAB approach is pragmatic and efficient. FYE programs are capable of increasing knowledge, which is a principle objective of the courses. The FYE program impacted attitudes associated with academic and life skills. Males and females participate and respond to the FYE differently. For example, females reported significantly higher attitudes than males. The study of FYE Programs overall is highly complex. Further longitudinal studies focusing on retention and attrition are needed.
Nanostructured Bulk Silicon as an Effective Thermoelectric Material
Authors: Bux Sabah K. , Blair Richard G. , Gogna Pawan K. , Lee Hohyun , Chen Gang , Dresselhaus Mildred S. , Kaner Richard B. , Fleurial Jean‐Pierre 
Published: June 2009

AbstractThermoelectric power sources have consistently demonstrated their extraordinary reliability and longevity for deep space missions and small unattended terrestrial systems. However, more efficient bulk materials and practical devices are required to improve existing technology and expand into large‐scale waste heat recovery applications. Research has long focused on complex compounds that best combine the electrical properties of degenerate semiconductors with the low thermal conductivity of glassy materials. Recently it has been found that nanostructuring is an effective method to decouple electrical and thermal transport parameters. Dramatic reductions in the lattice thermal conductivity are achieved by nanostructuring bulk silicon with limited degradation in its electron mobility, leading to an unprecedented increase by a factor of 3.5 in its performance over that of the parent single‐crystal material. This makes nanostructured bulk (nano‐bulk) Si an effective high temperature thermoelectric material that performs at about 70% the level of state‐of‐the‐art Si0.8Ge0.2 but without the need for expensive and rare Ge.
Characterization, Cathodoluminescence, and Field‐Emission Properties of Morphology‐Tunable CdS Micro/Nanostructures
Authors: Zhai Tianyou , Fang Xiaosheng , Bando Yoshio , Dierre Benjamin , Liu Baodan , Zeng Haibo , Xu Xijin , Huang Yang , Yuan Xiaoli , Sekiguchi Takashi , Golberg Dmitri 
Published: June 2009

AbstractHigh‐quality, uniform one‐dimensional CdS micro/nanostructures with different morphologies—microrods, sub‐microwires and nanotips—are fabricated through an easy and effective thermal evaporation process. Their structural, cathodoluminescence and field‐emission properties are systematically investigated. Microrods and nanotips exhibit sharp near‐band‐edge emission and broad deep‐level emission, whereas sub‐microwires show only the deep‐level emission. A significant decrease in a deep‐level/near‐band‐edge intensity ratio is observed along a tapered nanotip towards a smaller diameter part. This behavior is understood by consideration of defect concentrations in the nanotips, as analyzed with high‐resolution transmission electron microscopy. Field‐emission measurements show that the nanotips possess the best field‐emission characteristics among all 1D CdS nanostructures reported to date, with a relatively low turn‐on field of 5.28 V µm−1 and the highest field‐enhancement factor of 4 819. The field‐enhancement factor, turn‐on and threshold fields are discussed related to structure morphology and vacuum gap variations under emission.
Preparation, Structure, and Electrochemical Properties of Reduced Graphene Sheet Films
Authors: Tang Longhua , Wang Ying , Li Yueming , Feng Hongbing , Lu Jin , Li Jinghong 
Published: June 2009

AbstractThis paper describes the preparation, characterization, and electrochemical properties of reduced graphene sheet films (rGSFs), investigating especially their electrochemical behavior for several redox systems and electrocatalytic properties towards oxygen and some small molecules. The reduced graphene sheets (rGSs) are produced in high yield by a soft chemistry route involving graphite oxidation, ultrasonic exfoliation, and chemical reduction. Transmission electron microscopy (TEM), X‐ray diffraction (XRD), scanning electron microscopy (SEM), X‐ray photoelectron spectroscopy (XPS) and Raman spectroscopy clearly demonstrate that graphene was successfully synthesized and modified at the surface of a glassy carbon electrode. Several redox species, such as Ru(NH3)63+/2+, Fe(CN)63−/4−, Fe3+/2+ and dopamine, are used to probe the electrochemical properties of these graphene films by using the cyclic voltammetry method. The rGSFs demonstrate fast electron‐transfer (ET) kinetics and possess excellent electrocatalytic activity toward oxygen reduction and certain biomolecules. In our opinion, this microstructural and electrochemical information can serve as an important benchmark for graphene‐based electrode performances.