bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessing the effects of varied temperature and pH on the growth and sclerotial formation of Rhizoctonia solani Kuhn, isolated from paddy field: a case study.
Authors: Dutta Sambit , Das Souvik , Sarkar Abhijit , Tarafdar Jayanta , Chowdhury Ashim 
Published: April 2014

Rhizoctonia solani Kuhn, is one of the most important pathogen of rice causing the sheath blight disease which accounts for heavy crop losses in all the major rice growing areas of the world, including tropical Asia. The proliferation of this soil borne pathogen depends on many abiotic factors. The two most common factors associated with the growth and spread of the pathogen is pH and temperature which has been studied in the present study. Both pH and temperature had significant effect on the growth of the fungal mycelial and sclerotial formation. A non-linear regression model for growth of the fungal mycelia revealed that growth occurred best at pH 6.0 and temperature 30°C for all treatments studied. No growth was observed below 15°C. In agricultural fields sclerotia, forms the means for the spread of the pathogen causing secondary disease incidence as well as survival of the pathogen in harsher conditions. Sclerotia formed between the temperatures of 20°C and 30°C, with an optimum at 30°C and pH 6.0. DOI: http://dx.doi.org/10.3126/ijls.v8i2.10226 International Journal of Life Sciences Vol.8(2): 2014; 4-9
Microalgae Cultivation in Different pH, Temperature and Media for Lipid Production
Authors: Jayaramareddy Dakshayini , Krishnappa Ravikumar , Thimmappa Girisha Sirangala 
Published: April 2014

Lipids produced by microalgal biomass can be grouped into nonpolar lipids and polar lipids, which can be easily converted into biofuels. Microalgal samples were collected from three different ponds of Bangalore and cultured in the laboratory to find the effect of different pH, temperature and media on the production of biomass and lipids. Among these, pH-9, temperature -25°C and Beneck’s media was most suitable for production of biomass (35.80 g/L) and lipids from the isolated microalgae Chlorella sp. compare to Chladospora sp. (13.33 g/L). Chlorella sp. Showed 0.32 (OD) at pH-9, 0.43 (OD) at temperature-25°C and 2.94 (OD) in Beneck’s media. Our result revealed that nutrient supply along with measured variables affects the production of biomass and lipids in different microalgae.DOI: http://dx.doi.org/10.3126/ijls.v8i2.10227 International Journal of Life Sciences Vol.8(2): 2014; 13-17
Concilier priorité de santé et liberté réelle : l'action du “care” capacitant
Authors: Léonard Christian 
Published: April 2014

Les critiques formulées à l’égard de l’État-providence prennent la forme de privatisations, essentiellement implicites, notamment dans le domaine des soins de santé. Les priorités qui sont alors fixées, tout aussi implicitement, imposent une charge croissante à un patient « financièrement responsabilisé ». Nous montrons que le “care” est de nature à libérer l’individu, à le responsabiliser réellement afin qu’il devienne acteur de sa santé. Une responsabilité individuelle qui se déploie vers une responsabilité collective nécessaire à la refondation de la solidarité.
L'avis du bien-portant doit-il plus compter que celui du malade pour décider de la distribution des soins de santé ? Un examen par les théories de la justice sociale
Authors: Tovar Élisabeth 
Published: April 2014

La dimension sanitaire de la vie en société pose d’épineuses difficultés aux théories de la justice sociale. A-sanitaires par nature, ces théories proposent des critères d’équité décrivant la juste répartition des ressources de la société entre des personnes égales en dignité mais inégales en dotations naturelles et en positions sociales. Dans cet article, deux questions sont discutées, à la lumière, notamment, des travaux menés en éthique empirique : l’incorporation de la santé dans l’étalon de mesure de la justice dans la société et la légitimité des malades à énoncer les critères d’équité.
La “méthode de l'Arucah” pour élaborer des priorités de santé : un exemple de démocratie de terrain
Authors: Bréchat Pierre-Henri , Batifoulier Philippe , Jeunet Odile , Magnin-Feysot Christian 
Published: April 2014

La “méthode de l’Arucah” permet à la société civile de s’approprier la question des priorités de santé, de leur identification à leur hiérarchisation. C’est une méthode de sondage des priorités par les citoyens eux-mêmes et donc un exemple de démocratie de terrain qui, de plus, permet de faire des priorités de santé basées sur des valeurs sociétales partagées et des préférences morales. Cette méthode comporte cinq étapes successives et complémentaires : 1) une méthode d’enquête statistique, complétée par 2) une méthode délibérative ou argumentative, 3) une étape de compréhension des paradoxes que les résultats peuvent soulever, suivie par 4) un débat public qui permet à la société civile de trouver des compromis avec les représentants de l’État et de l’assurance maladie, ainsi 5) qu’une évaluation. Ces travaux peuvent être utiles au ministère en charge de la santé et à l’agence régionale de santé pour identifier ou valider des priorités et définir des actions. Ils peuvent également être utilisés dans le cadre de l’expérimentation d’une allocation de financements issue d’une enveloppe régionale contrainte.
The Number of Responding CD4 T Cells and the Dose of Antigen Conjointly Determine the Th1/Th2 Phenotype by Modulating B7/CD28 Interactions
Authors: Rudulier Christopher D. , McKinstry K. Kai , Al-Yassin Ghassan A. , Kroeger David R. , Bretscher Peter A. 
Published: April 2014

Abstract
Our previous in vivo studies show that both the amount of Ag and the number of available naive CD4 T cells affect the Th1/Th2 phenotype of the effector CD4 T cells generated. We examined how the number of OVA-specific CD4 TCR transgenic T cells affects the Th1/Th2 phenotype of anti-SRBC CD4 T cells generated in vivo upon immunization with different amounts of OVA-SRBC. Our observations show that a greater number of Ag-dependent CD4 T cell interactions are required to generate Th2 than Th1 cells. We established an in vitro system that recapitulates our main in vivo findings to more readily analyze the underlying mechanism. The in vitro generation of Th2 cells depends, as in vivo, upon both the number of responding CD4 T cells and the amount of Ag. We demonstrate, using agonostic/antagonistic Abs to various costimulatory molecules or their receptors, that the greater number of CD4 T cell interactions, required to generate Th2 over Th1 cells, does not involve CD40, OX40, or ICOS costimulation, but does involve B7/CD28 interactions. A comparison of the level of expression of B7 molecules by APC and CD4 T cells, under different conditions resulting in the substantial generation of Th1 and Th2 cells, leads us to propose that the critical CD28/B7 interactions, required to generate Th2 cells, may directly occur between CD4 T cells engaged with the same B cell acting as an APC.
Soluble HLA-I/Peptide Monomers Mediate Antigen-Specific CD8 T Cell Activation through Passive Peptide Exchange with Cell-Bound HLA-I Molecules
Authors: Allard Mathilde , Oger Romain , Benlalam Houssem , Florenceau Laetitia , Echasserieau Klara , Bernardeau Karine , Labarrière Nathalie , Lang François , Gervois Nadine 
Published: April 2014

Abstract
Accumulating evidence that serum levels of soluble class I HLA molecules (sHLA-I) can, under various pathological conditions, correlate with disease stage and/or patient survival, has stimulated interest in defining whether sHLA-I can exert immunological functions. However, despite a mounting number of publications suggesting the ability of sHLA-I to affect immune effectors in vitro, the precise underlying mechanism still remains controversial. In this article, we address potential functions of both classical and nonclassical sHLA-I, using soluble recombinant HLA-I/peptide monomers, and clearly demonstrate their ability to trigger Ag-specific activation of CD8 T cells in vitro. Furthermore, we provide strong evidence that this behavior results from the passive transfer of peptides from monomers to T cell–bound HLA-I molecules, allowing for fratricide representation and activation. Hence, we proposed a unifying model of T cell activation by HLA-I/peptide monomers, reappraising the potential involvement of sHLA-I molecules in the immune response.
Cutting Edge: A Soluble Form of CTLA-4 in Patients with Autoimmune Thyroid Disease
Authors: Oaks Martin K. , Hallett Karen M. 
Published: April 2014

Abstract
We have recently identified a novel transcript of the CTLA-4 gene that may represent a native soluble form of CTLA-4 (sCTLA-4). To determine whether sCTLA-4 was expressed in humans, we applied a sensitive enzyme immunoassay on serum from patients with autoimmune thyroid disease (ATD). Eleven of 20 patients with ATD had circulating levels of sCTLA-4 ranging from 28 to 78 ng/ml, whereas only 1 of 30 apparently healthy volunteers had a level greater than 4 ng/ml. sCTLA-4 immunoreactivity was inhibited by its binding to B7.1, suggesting that sCTLA-4 is a functional receptor. Immunoprecipitation analysis of serum from patients with ATD revealed a polypeptide consistent with the predicted size of sCTLA-4. We conclude that a native soluble form of CTLA-4 is derived from an alternate transcript of the CTLA-4 gene, and its level in plasma is elevated among a population of patients with ATD.
Perinatal Deletion of B Cells Expressing Surface Ig Molecules That Lack V(D)J-Encoded Determinants in the Bursa of Fabricius Is Not Due to Intrafollicular Competition
Authors: Sayegh Camil E. , Ratcliffe Michael J. H. 
Published: April 2014

Abstract
During embryonic development, the avian bursa of Fabricius selects B cell precursors that have undergone productive V(D)J recombination for expansion in oligoclonal follicles. During this expansion, Ig diversity is generated by gene conversion. We have used retroviral gene transfer in vivo to introduce surface Ig molecules that lack V(D)J-encoded determinants into B cell precursors. This truncated μ heavy chain supports both B cell expansion within embryo bursal lymphoid follicles and gene conversion. We show that individual follicles can be colonized exclusively by cells expressing the truncated μ chain and lacking endogenous surface IgM, ruling out a requirement for V(D)J-encoded determinants in the establishment of bursal lymphoid follicles. In striking contrast to their normal development in the embryo, bursal cells expressing the truncated μ-chain exhibit reduced rates of cell division and increased levels of apoptosis after hatching. The level of apoptosis in individual follicles reflects the proportion of cells within the follicle that express the truncated μ-chain. In particular, high levels of apoptosis are associated with follicles containing exclusively cells expressing the truncated μ receptor. Thus, apoptotic elimination of such cells is not due to competition within the follicle by cells expressing endogenous surface IgM receptors. This provides the first direct demonstration that the regulation of B cell development in the avian bursa after hatching differs fundamentally from that seen in the embryo. The requirement for intact IgM expression when the bursa is exposed to exogenous Ag implicates a role for Ag in avian B cell development after hatching.
Sequential Cleavage by Metallopeptidases and Proteasomes Is Involved in Processing HIV-1 ENV Epitope for Endogenous MHC Class I Antigen Presentation
Authors: López Daniel , Gil-Torregrosa Beatriz C. , Bergmann Cornelia , Del Val Margarita 
Published: April 2014

AbstractAntigenic peptides derived from viral proteins by multiple proteolytic cleavages are bound by MHC class I molecules and recognized by CTL. Processing predominantly takes place in the cytosol of infected cells by the action of proteasomes. To identify other proteases involved in the endogenous generation of viral epitopes, specifically those derived from proteins routed to the secretory pathway, we investigated presentation of the HIV-1 ENV 10-mer epitope 318RGPGRAFVTI327 (p18) to specific CTL in the presence of diverse protease inhibitors. Both metalloproteinase and proteasome inhibitors decreased CTL recognition of the p18 epitope expressed from either native gp160 or from a chimera based on the hepatitis B virus secretory core protein as carrier protein. Processing of this epitope from both native ENV and the hepatitis B virus secretory core chimeric protein appeared to proceed by a TAP-dependent pathway that involved sequential cleavage by proteasomes and metallo-endopeptidases; however, other protease activities could replace the function of the lactacystin-sensitive proteasomes. By contrast, in a second TAP-independent pathway we detected no contribution of metallopeptidases for processing the ENV epitope from the chimeric protein. These results show that, in the classical TAP-dependent MHC class I pathway, endogenous Ag processing of viral proteins to yield the p18 10-mer epitope requires metallo-endopeptidases in addition to proteasomes.
Systemic Immune Deviation in the Brain That Does Not Depend on the Integrity of the Blood-Brain Barrier
Authors: Wenkel Hartmut , Streilein J. Wayne , Young Michael J. 
Published: April 2014

AbstractOVA injected into the brain of normal mice evoked a deviant immune response (brain-associated immune deviation (BRAID)) that was deficient in OVA-specific delayed-type hypersensitivity. This response was not dependent on an intact blood-brain barrier since BRAID was induced even when OVA was injected into a newly created lesion site with extensive BBB leakage. However, newly activated microglia at the injection site 2 days after ablation of the striatum correlated with the loss of BRAID. At day 4 after trauma, when activated microglia were only visible further away from the injection site, BRAID was again able to be induced. In contrast to immune deviation elicited via the eye, an intact spleen was not required for BRAID, nor was BRAID adoptively transferable with spleen cells. In contrast i.v. injection of cervical lymph node cells harvested 8 days after OVA injection into the striatum was able to transfer BRAID into naive animals. Together, these data indicate that immune privilege in the brain is actively maintained and is mediated by an immune deviation mechanism that differs from eye-derived immune deviation and arises even when the BBB is compromised.
Human Vascular Endothelial Cells Stimulate Memory But Not Naive CD8+ T Cells to Differentiate into CTL Retaining an Early Activation Phenotype
Authors: Dengler Thomas J. , Pober Jordan S. 
Published: April 2014

AbstractEndothelial cell (EC)-selective alloreactive CTL may mediate alloimmune vascular injury. In the present study, EC-selective CTL were generated in cocultures of purified human CD8+ T cells with allogeneic EC and were compared with conventional CTL against corresponding B lymphoblastoid cells (BLC). EC caused activation and expansion of memory but not naive CD8+ T cells, which differentiated into EC-selective CTL that retained high surface expression of CD69, CD25, and CD62L and displayed low intracellular perforin content. In contrast, BLC-stimulated CTL could be generated from naive or memory CD8+ T cells and showed a more mature phenotype (low CD69, CD25, and CD62L with higher levels of perforin). The expansion of alloreactive T cells by EC stimulation was 5- to 20-fold less effective than in corresponding BLC-stimulated cultures, accounting for a reduction in the assayable cytotoxicity of individual microcultures. In these IL-2-supplemented cocultures, no effect on CTL generation or phenotype was observed by mAb blocking of costimulation provided by LFA-3, ICAM-1, or CD40, by addition of comitogenic anti-CD28 mAb, or by preactivation of EC with CD40 ligand. Cyclosporine inhibited CTL expansion and cytotoxicity similarly in both EC- and BLC-stimulated cultures but did not affect the phenotype of those CTL that did emerge. This study extends the characterization of endothelium as an immunoregulatory cell type distinct from conventional APC and may explain why graft rejection within the arterial intima, an anatomic compartment in which EC may be the primary type of APC, is separable from rejection in the graft parenchyma.
Absence of IFN-γ or IL-12 Has Different Effects on Experimental Myasthenia Gravis in C57BL/6 Mice
Authors: Karachunski Peter I. , Ostlie Norma S. , Monfardini Cristina , Conti-Fine Bianca M. 
Published: April 2014

AbstractImmunization with acetylcholine receptor (AChR) causes experimental myasthenia gravis (EMG). Th1 cells facilitate EMG development. IFN-γ and IL-12 induce Th1 responses: we investigated whether these cytokines are necessary for EMG development. We immunized wild-type (WT) C57BL/6 mice and IFN-γ and IL-12 knockout mutants (IFN-γ−/−, IL-12−/−) with Torpedo AChR (TAChR). WT and IFN-γ−/− mice developed EMG with similar frequency, IL-12−/−mice were resistant to EMG. All strains synthesized anti-AChR Ab that were not IgM or IgE. WT mice had anti-AChR IgG1, IgG2b, and IgG2c, IFN-γ−/− mice had significantly less IgG2c, and IL-12−/− mice less IgG2b and IgG2c. All mice had IgG bound to muscle synapses, but only WT and IFN-γ−/− mice had complement; WT mice had both IgG2b and IgG2c, IFN-γ−/− only IgG2b, and IL-12−/− neither IgG2b nor IgG2c. CD4+ cells from all AChR-immunized mice proliferated in response to AChR and recognized similar epitopes. After stimulation with TAChR, CD4+ cells from IFN-γ−/− mice secreted less IL-2 and similar amounts of IL-4 and IL-10 as WT mice. CD4+ cells from IL-12−/− mice secreted less IFN-γ, but more IL-4 and IL-10 than WT mice, suggesting that they developed a stronger Th2 response to TAChR. The EMG resistance of IL-12−/− mice is likely due to both reduction of anti-TAChR Ab that bind complement and sensitization of modulatory Th2 cells. The reduced Th1 function of IFN-γ−/− mice does not suffice to reduce all complement-fixing IgG subclasses, perhaps because as in WT mice a protective Th2 response is missing.
Tolerance to Cardiac Allografts Via Local and Systemic Mechanisms After Adenovirus-Mediated CTLA4Ig Expression
Authors: Guillot Cécile , Mathieu Patrick , Coathalem Hélène , Le Mauff Brigitte , Castro Maria G. , Tesson Laurent , Usal Claire , Laumonier Thomas , Brouard Sophie , Soulillou Jean-Paul , Lowenstein Pedro R. , Cuturi Maria Cristina , Anegon Ignacio 
Published: April 2014

AbstractBlockade of the CD28/B7 T cell costimulatory pathway prolongs allograft survival and induces tolerance in some animal models. We analyzed the efficacy of a CTLA4Ig-expressing adenovirus in preventing cardiac allorejection in rats, the mechanisms underlying heart transplant acceptance, and whether the effects of CTLA4Ig were restricted to the graft microenvironment or were systemic. CTLA4Ig gene transfer into the myocardium allowed indefinite graft survival (&gt;100 days vs 9 ± 1 days for controls) in 90% of cases, whereas CTLA4Ig protein injected systemically only prolonged cardiac allograft survival (by up to 22 days). CTLA4Ig could be detected in the graft and in the serum for at least 1 year after gene transfer. CTLA4Ig gene transfer induced local intragraft immunomodulation at day 5 after transplantation, as shown by decreased expression of the IL-2R and MHC II Ags; decreased levels of mRNA encoding for IFN-γ, inducible NO synthase, and TGF-β; and inhibited proliferative responses of graft-infiltrating cells. Systemic immune responses were also down-modulated, as shown by the suppression of Ab production against donor alloantigens and cognate Ags, up to at least 120 days after gene transfer. Alloantigenic and mitogenic proliferative responses of graft-infiltrating cells and total splenocytes were inhibited and were not reversed by IL-2. In contrast, lymph node cells and T cells purified from splenocytes showed normal proliferation. Recipients of long-term grafts treated with adenovirus coding for CTLA4Ig showed organ and donor-specific tolerance. These data show that expression of CTLA4Ig was high and long lasting after adenovirus-mediated gene transfer. This expression resulted in down-modulation of responses against cognate Ags, efficient suppression of local and systemic allograft immune responses, and ultimate induction of donor-specific tolerance.
IL-10 Is Required for Prevention of Necrosis in the Small Intestine and Mortality in Both Genetically Resistant BALB/c and Susceptible C57BL/6 Mice Following Peroral Infection withToxoplasma gondii
Authors: Suzuki Yasuhiro , Sher Alan , Yap George , Park Daniel , Neyer Lauri Ellis , Liesenfeld Oliver , Fort Madeline , Kang Hoil , Gufwoli Edgar 
Published: April 2014

AbstractThe role for IL-10 in the immunopathogenesis of acute toxoplasmosis following peroral infection was examined in both genetically susceptible C57BL/6 and resistant BALB/c mice. C57BL/6-background IL-10-targeted mutant (IL-10−/−) mice all died in 2 wk after infection with 20 cysts of the ME49 strain, whereas only 20% of control mice succumbed. Histological studies revealed necrosis in the small and large intestines and livers of infected IL-10−/− mice. The necrosis in the small intestine was the most severe pathologic response and was not observed in control mice. Treatment of infected IL-10−/− mice with either anti-CD4 or anti-IFN-γ mAb prevented intestinal pathology and significantly prolonged time to death. Treatment of these animals with anti-IL-12 mAb also prevented the pathology. Significantly greater amounts of IFN-γ mRNA were detected in the lamina propria lymphocytes obtained from the small intestine of infected IL-10−/− mice than those from infected control mice. In common with C57BL/6-background IL-10−/− mice, BALB/c-background IL-10−/− mice all died developing intestinal pathology after infection. Control BALB/c mice all survived even after infection with 100 cysts and did not develop the intestinal lesions. Treatment with anti-IFN-γ mAb prevented the pathology and prolonged time to death of the infected IL-10−/− mice. These results strongly suggest that IL-10 plays a critical role in down-regulating IFN-γ production in the small intestine following sublethal peroral infection with Toxoplasma gondii and that this down-regulatory effect of IL-10 is required for prevention of development of IFN-γ-mediated intestinal pathology and mortality in both genetically resistant BALB/c and susceptible C57BL/6 mice.
Expression of IFN-Inducible T Cell α Chemoattractant by Human Endothelial Cells Is Cyclosporin A-Resistant and Promotes T Cell Adhesion: Implications for Cyclosporin A-Resistant Immune Inflammation
Authors: Mazanet Melissa M. , Neote Kuldeep , Hughes Christopher C. W. 
Published: April 2014

AbstractIFN-inducible T cell α chemoattractant (I-TAC) is a recently discovered member of the CXC chemokine family. It is a potent T cell chemoattractant expressed by IFN-γ-treated astrocytes, monocytes, keratinocytes, bronchial epithelial cells, and neutrophils. In this study, we show that I-TAC is also expressed by IFN-γ-treated endothelial cells (EC), both at the mRNA and protein levels. Induction of the I-TAC message is rapid and sustained over 24 h. TNF-α does not induce I-TAC mRNA alone, but does act synergistically with IFN-γ. Blocking Abs to I-TAC, or to its receptor, CXCR3, reduce T cell adhesion to EC monolayers demonstrating that the expressed protein is functional. Finally, the expression of I-TAC by EC is resistant to the immunosuppressive drug cyclosporin A, suggesting that I-TAC may contribute to the chronic immune inflammation characteristic of graft arteriosclerosis.