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Search Results: 1 - 10 of 229540 matches for " Deborah C. Smith "
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Rainbows, Time Zones, and Other Mind-Dependent Objects: Making Sense of the Relevant Notions of “Mind-Dependence” in the Debate between Metaphysical Realists and Antirealists  [PDF]
Deborah C. Smith
Open Journal of Philosophy (OJPP) , 2012, DOI: 10.4236/ojpp.2012.21006
Abstract: In a recent article, Sam Page distinguishes four kinds of mind-(in)dependence: ontological, causal, structural, and individuative. He argues that, despite the fact that the metaphysical realism/antirealism debate has been frequently characterized as a debate between those who accept and those who deny that the world is causally and/or structurally dependent on minds, many antirealists are primarily interested in defending the claim that the world is individuatively mind-dependent. In this article, I critically examine these differing senses of “mind-dependence” highlighting ways in which they remain ambiguous and identifying various entailment relations between them. I argue that there is reason to believe that ontological dependence, structural dependence, and the only sort of individuative dependence that is relevant to the metaphysical debate are coextensive notions. As such, any argument that succeeds in establishing that it is incoherent to suppose that everything is ontologically and/or structurally dependent thereby establishes the incoherence of metaphysical antirealism.
Defining the expression of marker genes in equine mesenchymal stromal cells
Deborah J Guest, Jennifer C Ousey, Matthew RW Smith
Stem Cells and Cloning: Advances and Applications , 2008, DOI: http://dx.doi.org/10.2147/SCCAA.S3824
Abstract: ing the expression of marker genes in equine mesenchymal stromal cells Original Research (5181) Total Article Views Authors: Deborah J Guest, Jennifer C Ousey, Matthew RW Smith Published Date November 2008 Volume 2008:1 Pages 1 - 9 DOI: http://dx.doi.org/10.2147/SCCAA.S3824 Deborah J Guest1, Jennifer C Ousey1, Matthew RW Smith2 1Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, CB8 7UU; 2Reynolds House Referrals, Greenwood Ellis and Partners, 166 High Street, Newmarket, Suffolk, CB8 9WS, UK Abstract: Mesenchymal stromal (MS) cells have been derived from multiple sources in the horse including bone marrow, adipose tissue and umbilical cord blood. To date these cells have been investigated for their differentiation potential and are currently being used to treat damage to horse musculoskeletal tissues. However, no work has been done in horse MS cells to examine the expression profile of proteins and cell surface antigens that are expressed in human MS cells. The identification of such profiles in the horse will allow the comparison of putative MS cells isolated from different laboratories and different tissues. At present it is difficult to ascertain whether equivalent cells are being used in different reports. Here, we report on the expression of a range of markers used to define human MS cells. Using immunocytochemistry we show that horse MS cells homogenously express collagens, alkaline phosphatase activity, CD44, CD90 and CD29. In contrast, CD14, CD79α and the embryonic stem cell markers Oct-4, SSEA (stage specific embryonic antigen) -1, -3, -4, TRA (tumor rejection antigen) -1–60 and -1–81 are not expressed. The MS cells also express MHC class I antigens but do not express class II antigens, although they are inducible by treatment with interferon gamma (IFN-γ).
Defining the expression of marker genes in equine mesenchymal stromal cells
Deborah J Guest,Jennifer C Ousey,Matthew RW Smith
Stem Cells and Cloning: Advances and Applications , 2008,
Abstract: Deborah J Guest1, Jennifer C Ousey1, Matthew RW Smith21Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, CB8 7UU; 2Reynolds House Referrals, Greenwood Ellis and Partners, 166 High Street, Newmarket, Suffolk, CB8 9WS, UKAbstract: Mesenchymal stromal (MS) cells have been derived from multiple sources in the horse including bone marrow, adipose tissue and umbilical cord blood. To date these cells have been investigated for their differentiation potential and are currently being used to treat damage to horse musculoskeletal tissues. However, no work has been done in horse MS cells to examine the expression profile of proteins and cell surface antigens that are expressed in human MS cells. The identification of such profiles in the horse will allow the comparison of putative MS cells isolated from different laboratories and different tissues. At present it is difficult to ascertain whether equivalent cells are being used in different reports. Here, we report on the expression of a range of markers used to define human MS cells. Using immunocytochemistry we show that horse MS cells homogenously express collagens, alkaline phosphatase activity, CD44, CD90 and CD29. In contrast, CD14, CD79α and the embryonic stem cell markers Oct-4, SSEA (stage specific embryonic antigen) -1, -3, -4, TRA (tumor rejection antigen) -1–60 and -1–81 are not expressed. The MS cells also express MHC class I antigens but do not express class II antigens, although they are inducible by treatment with interferon gamma (IFN-γ).Keywords: mesenchymal stem cells, equine, gene expression
Hybridization in Parasites: Consequences for Adaptive Evolution, Pathogenesis, and Public Health in a Changing World
Kayla C. King?,Rike B. Stelkens?,Joanne P. Webster?,Deborah F. Smith,Michael A. Brockhurst
PLOS Pathogens , 2015, DOI: 10.1371/journal.ppat.1005098
Abstract:
Functional Analysis of Leishmania Cyclopropane Fatty Acid Synthetase
Samuel O. Oyola, Krystal J. Evans, Terry K. Smith, Barbara A. Smith, James D. Hilley, Jeremy C. Mottram, Paul M. Kaye, Deborah F. Smith
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0051300
Abstract: The single gene encoding cyclopropane fatty acid synthetase (CFAS) is present in Leishmania infantum, L. mexicana and L. braziliensis but absent from L. major, a causative agent of cutaneous leishmaniasis. In L. infantum, usually causative agent of visceral leishmaniasis, the CFAS gene is transcribed in both insect (extracellular) and host (intracellular) stages of the parasite life cycle. Tagged CFAS protein is stably detected in intracellular L. infantum but only during the early log phase of extracellular growth, when it shows partial localisation to the endoplasmic reticulum. Lipid analyses of L. infantum wild type, CFAS null and complemented parasites detect a low abundance CFAS-dependent C19Δ fatty acid, characteristic of a cyclopropanated species, in wild type and add-back cells. Sub-cellular fractionation studies locate the C19Δ fatty acid to both ER and plasma membrane-enriched fractions. This fatty acid is not detectable in wild type L. major, although expression of the L. infantum CFAS gene in L. major generates cyclopropanated fatty acids, indicating that the substrate for this modification is present in L. major, despite the absence of the modifying enzyme. Loss of the L. infantum CFAS gene does not affect extracellular parasite growth, phagocytosis or early survival in macrophages. However, while endocytosis is also unaffected in the extracellular CFAS nulls, membrane transporter activity is defective and the null parasites are more resistant to oxidative stress. Following infection in vivo, L. infantum CFAS nulls exhibit lower parasite burdens in both the liver and spleen of susceptible hosts but it has not been possible to complement this phenotype, suggesting that loss of C19Δ fatty acid may lead to irreversible changes in cell physiology that cannot be rescued by re-expression. Aberrant cyclopropanation in L. major decreases parasite virulence but does not influence parasite tissue tropism.
Predation by Argyrodes (Theridiidae) on Solitary and Communal Spiders
Deborah Smith Trail
Psyche , 1980, DOI: 10.1155/1980/74071
Abstract:
Comparative Expression Profiling of Leishmania: Modulation in Gene Expression between Species and in Different Host Genetic Backgrounds
Daniel P. Depledge,Krystal J. Evans,Alasdair C. Ivens,Naveed Aziz,Asher Maroof,Paul M. Kaye,Deborah F. Smith
PLOS Neglected Tropical Diseases , 2009, DOI: 10.1371/journal.pntd.0000476
Abstract: Background Genome sequencing of Leishmania species that give rise to a range of disease phenotypes in the host has revealed highly conserved gene content and synteny across the genus. Only a small number of genes are differentially distributed between the three species sequenced to date, L. major, L. infantum and L. braziliensis. It is not yet known how many of these genes are expressed in the disease-promoting intracellular amastigotes of these species or whether genes conserved between the species are differentially expressed in the host. Methods/Principal Findings We have used customised oligonucleotide microarrays to confirm that all of the differentially distributed genes identified by genome comparisons are expressed in intracellular amastigotes, with only a few of these subject to regulation at the RNA level. In the first large-scale study of gene expression in L. braziliensis, we show that only ~9% of the genes analysed are regulated in their RNA expression during the L. braziliensis life cycle, a figure consistent with that observed in other Leishmania species. Comparing amastigote gene expression profiles between species confirms the proposal that Leishmania transcriptomes undergo little regulation but also identifies conserved genes that are regulated differently between species in the host. We have also investigated whether host immune competence influences parasite gene expression, by comparing RNA expression profiles in L. major amastigotes derived from either wild-type (BALB/c) or immunologically compromised (Rag2?/? γc?/?) mice. While parasite dissemination from the site of infection is enhanced in the Rag2?/? γc?/? genetic background, parasite RNA expression profiles are unperturbed. Conclusion/Significance These findings support the hypothesis that Leishmania amastigotes are pre-adapted for intracellular survival and undergo little dynamic modulation of gene expression at the RNA level. Species-specific parasite factors contributing to virulence and pathogenicity in the host may be limited to the products of a small number of differentially distributed genes or the differential regulation of conserved genes, either of which are subject to translational and/or post-translational controls.
The Use of Regenerative Medicine in the Management of Invasive Bladder Cancer
Matthew E. Hyndman,Deborah Kaye,Nicholas C. Field,Keith A. Lawson,Norm D. Smith,Gary D. Steinberg,Mark P. Schoenberg,Trinity J. Bivalacqua
Advances in Urology , 2012, DOI: 10.1155/2012/653652
Abstract: Muscle invasive and recurrent nonmuscle invasive bladder cancers have been traditionally treated with a radical cystectomy and urinary diversion. The urinary diversion is generally accomplished through the creation of an incontinent ileal conduit, continent catheterizable reservoir, or orthotopic neobladder utilizing small or large intestine. While radical extirpation of the bladder is often successful from an oncological perspective, there is a significant morbidity associated with enteric interposition within the genitourinary tract. Therefore, there is a great opportunity to decrease the morbidity of the surgical management of bladder cancer through utilization of novel technologies for creating a urinary diversion without the use of intestine. Clinical trials using neourinary conduits (NUC) seeded with autologous smooth muscle cells are currently in progress and may represent a significant surgical advance, potentially eliminating the complications associated with the use of gastrointestinal segments in the urinary reconstruction, simplifying the surgical procedure, and greatly facilitating recovery from cystectomy. 1. Introduction An estimated 73,510 people in the United States will be diagnosed with bladder cancer resulting in approximately 14,880 deaths in 2012 [1]. It is the fifth most common cancer in the United States and is responsible for 3% of all cancer deaths. Bladder cancer is 3-4 times more prevalent amongst males than females. White males and females are more likely to be diagnosed with and die from bladder cancer than African American males and females. Disease incidence peaks in the 8th decade of life [2–4]. The percentage of patients with invasive cancer also increases with age. The incidence of invasive bladder cancer in men greater than 70 years old is 3.5% compared to 0.41% amongst 40–59-year-old males [2]. Bladder cancer is hypothesized to occur because of a variety of factors, including carcinogen exposure, radiation, chemotherapy, infection, inflammation, nutrition, genetics, and geography. However, the polygenetic basis of bladder cancer is linked to various genetic mutations. Thelen and Schaeuble were the first authors to describe a familial occurrence of bladder cancer; however, a familial syndrome has not been described [5]. An extensive number of genes have been hypothesized to play a role in bladder cancer etiology and prognosis, including chromosome 9 deletions, RAS gene mutations, P53, and Rb [6, 7]. Some of these mutations are common in many types of bladder cancer, while others are more specific to nonmuscle invasive
Linkage Disequilibrium in Wild Mice
Cathy C Laurie,Deborah A Nickerson,Amy D Anderson,Bruce S Weir,Robert J Livingston,Matthew D Dean,Kimberly L Smith,Eric E Schadt,Michael W Nachman
PLOS Genetics , 2007, DOI: 10.1371/journal.pgen.0030144
Abstract: Crosses between laboratory strains of mice provide a powerful way of detecting quantitative trait loci for complex traits related to human disease. Hundreds of these loci have been detected, but only a small number of the underlying causative genes have been identified. The main difficulty is the extensive linkage disequilibrium (LD) in intercross progeny and the slow process of fine-scale mapping by traditional methods. Recently, new approaches have been introduced, such as association studies with inbred lines and multigenerational crosses. These approaches are very useful for interval reduction, but generally do not provide single-gene resolution because of strong LD extending over one to several megabases. Here, we investigate the genetic structure of a natural population of mice in Arizona to determine its suitability for fine-scale LD mapping and association studies. There are three main findings: (1) Arizona mice have a high level of genetic variation, which includes a large fraction of the sequence variation present in classical strains of laboratory mice; (2) they show clear evidence of local inbreeding but appear to lack stable population structure across the study area; and (3) LD decays with distance at a rate similar to human populations, which is considerably more rapid than in laboratory populations of mice. Strong associations in Arizona mice are limited primarily to markers less than 100 kb apart, which provides the possibility of fine-scale association mapping at the level of one or a few genes. Although other considerations, such as sample size requirements and marker discovery, are serious issues in the implementation of association studies, the genetic variation and LD results indicate that wild mice could provide a useful tool for identifying genes that cause variation in complex traits.
Variation in LPA Is Associated with Lp(a) Levels in Three Populations from the Third National Health and Nutrition Examination Survey
Logan Dumitrescu,Kimberly Glenn,Kristin Brown-Gentry,Cynthia Shephard,Michelle Wong,Mark J. Rieder,Joshua D. Smith,Deborah A. Nickerson,Dana C. Crawford
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0016604
Abstract: The distribution of lipoprotein(a) [Lp(a)] levels can differ dramatically across diverse racial/ethnic populations. The extent to which genetic variation in LPA can explain these differences is not fully understood. To explore this, 19 LPA tagSNPs were genotyped in 7,159 participants from the Third National Health and Nutrition Examination Survey (NHANES III). NHANES III is a diverse population-based survey with DNA samples linked to hundreds of quantitative traits, including serum Lp(a). Tests of association between LPA variants and transformed Lp(a) levels were performed across the three different NHANES subpopulations (non-Hispanic whites, non-Hispanic blacks, and Mexican Americans). At a significance threshold of p<0.0001, 15 of the 19 SNPs tested were strongly associated with Lp(a) levels in at least one subpopulation, six in at least two subpopulations, and none in all three subpopulations. In non-Hispanic whites, three variants were associated with Lp(a) levels, including previously known rs6919246 (p = 1.18×10?30). Additionally, 12 and 6 variants had significant associations in non-Hispanic blacks and Mexican Americans, respectively. The additive effects of these associated alleles explained up to 11% of the variance observed for Lp(a) levels in the different racial/ethnic populations. The findings reported here replicate previous candidate gene and genome-wide association studies for Lp(a) levels in European-descent populations and extend these findings to other populations. While we demonstrate that LPA is an important contributor to Lp(a) levels regardless of race/ethnicity, the lack of generalization of associations across all subpopulations suggests that specific LPA variants may be contributing to the observed Lp(a) between-population variance.
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