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Search Results: 1 - 10 of 407937 matches for " Francine M. Scott "
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A Tissue Culture Model of Murine Gammaherpesvirus Replication Reveals Roles for the Viral Cyclin in Both Virus Replication and Egress from Infected Cells
Francine M. Scott, Samuel H. Speck
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0093871
Abstract: Passage through the eukaryotic cell cycle is regulated by the activity of cyclins and their cyclin-dependent kinase partners. Rhadinoviruses, such as Kaposi’s sarcoma-associated herpesvirus (KSHV) and murine gammaherpesvirus 68 (MHV68), encode a viral homologue of mammalian D-type cyclins. In MHV68, the interaction of the viral cyclin with its CDK partners is important for acute replication in the lungs following low dose inoculation. Attempts to further study this requirement in vitro have been limited by the lack of available tissue culture models that mimic the growth defect observed in vivo. It is hypothesized that analysis of virus replication in a cell line that displays properties of primary airway epithelium, such as the ability to polarize, might provide a suitable environment to characterize the role of the v-cyclin in virus replication. We report here MHV68 replication in the rat lung cell line RL-65, a non-transformed polarizable epithelial cell line. These analyses reveal a role for the v-cyclin in both virus replication, as well as virus egress from infected cells. As observed for acute replication in vivo, efficient replication in RL-65 cells requires CDK binding. However, we show that the KSHV v-cyclin (K-cyclin), which utilizes different CDK partners (CDK4 and CDK6) than the MHV68 v-cyclin (CDK2 and CDC2), can partially rescue the replication defect observed with a v-cyclin null mutant – both in vitro and in vivo. Finally, we show that MHV68 is shed from both the apical and basolateral surfaces of polarized RL-65 cells. In summary, the RL-65 cell line provides an attractive in vitro model that mimics critical aspects of MHV68 replication in the lungs.
Increased Ndfip1 in the Substantia Nigra of Parkinsonian Brains Is Associated with Elevated Iron Levels
Jason Howitt, Amanda M. Gysbers, Scott Ayton, Francine Carew-Jones, Ulrich Putz, David I. Finkelstein, Glenda M. Halliday, Seong-Seng Tan
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0087119
Abstract: Iron misregulation is a central component in the neuropathology of Parkinson's disease. The iron transport protein DMT1 is known to be increased in Parkinson's brains linking functional transport mechanisms with iron accumulation. The regulation of DMT1 is therefore critical to the management of iron uptake in the disease setting. We previously identified post-translational control of DMT1 levels through a ubiquitin-mediated pathway led by Ndfip1, an adaptor for Nedd4 family of E3 ligases. Here we show that loss of Ndfip1 from mouse dopaminergic neurons resulted in misregulation of DMT1 levels and increased susceptibility to iron induced death. We report that in human Parkinson's brains increased iron concentrations in the substantia nigra are associated with upregulated levels of Ndfip1 in dopaminergic neurons containing α-synuclein deposits. Additionally, Ndfip1 was also found to be misexpressed in astrocytes, a cell type normally devoid of this protein. We suggest that in Parkinson's disease, increased iron levels are associated with increased Ndfip1 expression for the regulation of DMT1, including abnormal Ndfip1 activation in non-neuronal cell types such as astrocytes.
Effect of Sample Matrix on Radial and Axial Profiles of Ion Abundance in Inductively Coupled Plasma Mass Spectrometry  [PDF]
Clarisse Mariet, Francine Carrot, Mélanie Moskura
American Journal of Analytical Chemistry (AJAC) , 2011, DOI: 10.4236/ajac.2011.27085
Abstract: In inductively coupled plasma mass spectrometry (ICP-MS) analysis, only a few options are available to deal with non-spectroscopic interferences. Considering that diluting the sample is impractical for traces analysis, other alternatives must be employed. Traditionally, the method of standard additions is used to correct the matrix effect but it is a time consuming method. Others methods involves separation techniques. Another way to overcome matrix interferences is to understand the mechanism involved and adjust plasma viewing conditions to reduce or eliminate the effect. In this study, the effect of various concomitant elements in ICP-MS was assessed by measuring the distribution of selected singly charged analyte ions (Al, V, Cr, Mn, Ni, Co, Cu, Zn, As, In, Ba, La, Ce, Pb), doubly charged ions (La, Ce, Ba and Pb) and oxides ions (BaO) in the presence of concomitant elements spanning a mass range from 23 (Na) to 133 (Cs) u.m.a. and different ionization energies. Concomitant elements are alkali metals, alkaline earth metals and Si. Analyte ion suppression was observed while moving the ICP across and away from the sampling interface with or without a single concomitant element. Matrix effect measures were realised, firstly, to highlight the relation between the signal extinction of an analyte and the masse of the concomitant element, and secondly to highlight the relation between the removal of the analyte signal and the first ionization energy of the element of matrix. A dependence upon both the mass of the matrix element and the mass of the analyte was observed. The suppression seems increased with increasing matrix element mass and decreased with increasing analyte mass. The effect of the mass of the matrix element was the more significant of the two factors. If space-charge effects were found to be significant for matrix elements of much lower mass, it seems diffusion also played an active part for heavier matrix elements. Finally, some evidence was found for a shift in ion-atom equilibrium for dications and for energy demand regarding oxides.
Allogeneic Splenocyte Transfer and Lipopolysaccharide Inhalations Induce Differential T Cell Expansion and Lung Injury: A Novel Model of Pulmonary Graft-versus-Host Disease
Tereza Martinu, Christine V. Kinnier, Jesse Sun, Francine L. Kelly, Margaret E. Nelson, Stavros Garantziotis, W. Michael Foster, Scott M. Palmer
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0097951
Abstract: Background Pulmonary GVHD (pGVHD) is an important complication of hematopoietic cell transplant (HCT) and is thought to be a consequence of the HCT conditioning regimen, allogeneic donor cells, and posttransplant lung exposures. We have previously demonstrated that serial inhaled lipopolysaccharide (LPS) exposures potentiate the development of pGVHD after murine allogeneic HCT. In the current study we hypothesized that allogeneic lymphocytes and environmental exposures alone, in the absence of a pre-conditioning regimen, would cause features of pGVHD and would lead to a different T cell expansion pattern compared to syngeneic cells. Methods Recipient Rag1?/? mice received a transfer of allogeneic (Allo) or syngeneic (Syn) spleen cells. After 1 week of immune reconstitution, mice received 5 daily inhaled LPS exposures and were sacrificed 72 hours after the last LPS exposure. Lung physiology, histology, and protein levels in bronchoalveolar lavage (BAL) were assessed. Lung cells were analyzed by flow cytometry. Results Both Allo and Syn mice that undergo LPS exposures (AlloLPS and SynLPS) have prominent lymphocytic inflammation in their lungs, resembling pGVHD pathology, not seen in LPS-unexposed or non-transplanted controls. Compared to SynLPS, however, AlloLPS have significantly increased levels of BAL protein and enhancement of airway hyperreactivity, consistent with more severe lung injury. This injury in AlloLPS mice is associated with an increase in CD8 T cells and effector CD4 T cells, as well as a decrease in regulatory to effector CD4 T cell ratio. Additionally, cytokine analysis is consistent with a preferential Th1 differentiation and upregulation of pulmonary CCL5 and granzyme B. Conclusions Allogeneic lymphocyte transfer into lymphocyte-deficient mice, followed by LPS exposures, causes features of pGVHD and lung injury in the absence of a pre-conditioning HCT regimen. This lung disease associated with an expansion of allogeneic effector T cells provides a novel model to dissect mechanisms of pGVHD independent of conditioning.
Peroxisome Proliferator-Activated Receptor δ: A Target with a Broad Therapeutic Potential for Drug Discovery
Francine M. Gregoire
PPAR Research , 2008, DOI: 10.1155/2008/736362
Abstract:
Knowledge translation approaches to implement guidelines? Plan, assess, tailor, and learn
Ducharme Francine M
Allergy, Asthma & Clinical Immunology , 2010, DOI: 10.1186/1710-1492-6-s4-a7
Abstract:
Induction of the GABA Cell Phenotype: An In Vitro Model for Studying Neurodevelopmental Disorders
Sivan Subburaju, Francine M. Benes
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0033352
Abstract: Recent studies of the hippocampus have suggested that a network of genes is associated with the regulation of the GAD67 (GAD1) expression and may play a role in γ-amino butyric acid (GABA) dysfunction in schizophrenia (SZ) and bipolar disorder (BD). To obtain a more detailed understanding of how GAD67 regulation may result in GABAergic dysfunction, we have developed an in vitro model in which GABA cells are differentiated from the hippocampal precursor cell line, HiB5. Growth factors, such as PDGF, and BDNF, regulate the GABA phenotype by inducing the expression of GAD67 and stimulating the growth of cellular processes, many with growth cones that form appositions with the cell bodies and processes of other GAD67-positive cells. These changes are associated with increased expression of acetylated tubulin, microtubule-associated protein 2 (MAP2) and the post-synaptic density protein 95 (PSD95). The addition of BDNF, together with PDGF, increases the levels of mRNA and protein for GAD67, as well as the high affinity GABA uptake protein, GAT1. These changes are associated with increased concentrations of GABA in the cytoplasm of “differentiated” HiB5 neurons. In the presence of Ca2+ and K+, newly synthesized GABA is released extracellularly. When the HiB5 cells appear to be fully differentiated, they also express GAD65, parvalbumin and calbindin, and GluR subtypes as well as HDAC1, DAXX, PAX5, Runx2, associated with GAD67 regulation. Overall, these results suggest that the HiB5 cells can differentiate into functionally mature GABA neurons in the presence of gene products that are associated with GAD67 regulation in the adult hippocampus.
Role of denileukin diftitox in the treatment of persistent or recurrent cutaneous T-cell lymphoma
Frederick Lansigan, Diane M Stearns, Francine Foss
Cancer Management and Research , 2010, DOI: http://dx.doi.org/10.2147/CMAR.S5009
Abstract: le of denileukin diftitox in the treatment of persistent or recurrent cutaneous T-cell lymphoma Review (3934) Total Article Views Authors: Frederick Lansigan, Diane M Stearns, Francine Foss Published Date February 2010 Volume 2010:2 Pages 53 - 59 DOI: http://dx.doi.org/10.2147/CMAR.S5009 Frederick Lansigan1, Diane M Stearns1, Francine Foss2 1Hematology/Oncology, Norris Cotton Cancer Center, Dartmouth Hitchcock Medical Center, Lebanon, NH, USA; 2Yale Comprehensive Cancer Center, Yale University School of Medicine, New Haven, CT, USA Abstract: Denileukin diftitox (Ontak ) is indicated for the treatment of patients with persistent or recurrent cutaneous T-cell lymphoma (CTCL), a rare lymphoproliferative disorder of the skin. Denileukin diftitox was the first fusion protein toxin approved for the treatment of a human disease. This fusion protein toxin combines the IL2 protein with diphtheria toxin, and targets the CD25 subunit of the IL2 receptor, resulting in the unique delivery of a cytocidal agent to CD-25 bearing T-cells. Historically, immunotherapy targeting malignant T-cells including monoclonal antibodies has been largely ineffective as cytocidal agents compared to immunotherapy directed against B-cells such as rituximab. This review will summarize the development of denileukin diftitox, its proposed mechanism of action, the pivotal clinical trials that led to its FDA approval, the improvements in quality of life, and the common toxicities experienced during the treatment of patients with CTCL. CTCL is often a chronic progressive lymphoma requiring the sequential use of treatments such as retinoids, traditional chemotherapy, or biological response modifiers. The incorporation of the immunotoxin denileukin diftitox into the sequential or combinatorial treatment of CTCL will also be addressed.
PPARS and Obesity
Francine M. Gregoire,Sander Kersten,Wallace Harrington
PPAR Research , 2007, DOI: 10.1155/2007/78475
Abstract:
Une solidarité en mouvement : figures de la militance féministe québécoise
Sandrine Ricci,Mélissa Blais,Francine Descarries
Amnis , 2008, DOI: 10.4000/amnis.563
Abstract: Notre article pose la question de l'engagement féministe dans le Québec du XXIe siècle. Il aborde la question du rapport au militantisme de praticiennes du mouvement des femmes québécois (MFQ), à la lumière de l’évolution tant dudit mouvement que des courants de pensée féministe qui le traversent. Plus particulièrement, il introduit la figure de la militante féministe professionnelle qui, selon notre hypothèse, représente une figure devenue centrale dans le paysage de la militance québécoise, suite à l’institutionnalisation du mouvement des femmes. Nous examinons la trajectoire militante de trois de ces praticiennes du MFQ, pour mettre en lumière les différents rapports à la militance que recouvre la figure de la militante féministe professionnelle et ce, en prenant en compte leur inscription dans la théorie féministe et dans la continuité sociohistorique. Nuestro artículo estudia el compromiso político de las feministas en el Quebec del siglo XXI. Analiza la relación que existe entre las trabajadoras del movimiento quebequense de mujeres (MFQ) y la militancia, a la luz de la evolución de dicho movimiento y de las corrientes de pensamiento en torno a las cuales se estructura. Más concretamente, introduce la figura de la militante feminista profesional , la cual, según nuestra hipótesis, representa una figura central en el paisaje del militantismo quebequense, en particular a raíz de la institucionalización del movimiento de mujeres. Examinamos la trayectoria militante de tres trabajadoras del MFQ, con el objetivo de subrayar las diversas relaciones que la figura de la militante feminista profesional mantiene con el militantismo, tomando en cuenta su inscripción en la teoría feminista y en la continuidad socio-histórica. This article examines the question of feminist commitment in 21st century Quebec. It looks at the ways workers in the Quebec women's movement (MFQ) relate to activism in light of the evolution of the movement over time and of the conceptual frameworks that cross it. More specifically, it introduces the figure of the "professional feminist activist" which now represents a key figure in the landscape of Quebec activism following the institutionalization of the women's movement. We are focusing on the activist path of three of these MFQ actors to highlight the various relationships to activism that the figure of the professional feminist activist comprises, taking into account their inclusion in the social and historical continuity as well as in feminist theory.
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