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Search Results: 1 - 10 of 467628 matches for " Deborah A Johnson "
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The monosaccharide transporter gene family in land plants is ancient and shows differential subfamily expression and expansion across lineages
Deborah A Johnson, Jeffrey P Hill, Michael A Thomas
BMC Evolutionary Biology , 2006, DOI: 10.1186/1471-2148-6-64
Abstract: Here, we utilize expressed sequence tag (EST) data to study gene duplication and expression patterns in the monosaccharide transporter (MST) gene family across the land plants. In Arabidopsis, there are 53 MST genes that form seven distinct subfamilies. We created profile hidden Markov models of each subfamily and searched EST databases representing diverse land plant lineages to address the following questions: 1) Are homologs of each Arabidopsis subfamily present in the earliest land plants? 2) Do expression patterns among subfamilies and individual genes within subfamilies differ across lineages? 3) Has gene duplication within each lineage resulted in lineage-specific expansion patterns? We also looked for correlations between relative EST database representation in Arabidopsis and similarity to orthologs in early lineages.Homologs of all seven MST subfamilies were present in land plants at least 400 million years ago. Subfamily expression levels vary across lineages with greater relative expression of the STP, ERD6-like, INT and PLT subfamilies in the vascular plants. In the large EST databases of the moss, gymnosperm, monocot and eudicot lineages, EST contig construction reveals that MST subfamilies have experienced lineage-specific expansions. Large subfamily expansions appear to be due to multiple gene duplications arising from single ancestral genes. In Arabidopsis, one or a few genes within most subfamilies have much higher EST database representation than others. Most highly represented (broadly expressed) genes in Arabidopsis have best match orthologs in early divergent lineages.The seven subfamilies of the Arabidopsis MST gene family are ancient in land plants and show differential subfamily expression and lineage-specific subfamily expansions. Patterns of gene expression in Arabidopsis and correlation of highly represented genes with best match homologs in early lineages suggests that broadly expressed genes are often highly conserved, and that most gen
OTC analgesics and drug interactions: clinical implications
Fendrick A Mark,Pan Deborah E,Johnson Grace E
Osteopathic Medicine and Primary Care , 2008, DOI: 10.1186/1750-4732-2-2
Abstract: The risk of drug interactions with concurrent use of multiple medications is a clinically relevant issue. Many patients are unaware that over-the-counter (OTC) analgesics can cause potentially serious adverse effects when used in combination with other common medications such as anticoagulants, corticosteroids, or antihypertensive agents. Of particular significance is the increased risk of upper abdominal gastrointestinal adverse events in patients who take traditional nonsteroidal anti-inflammatory drugs (NSAIDs). This risk is dose dependent and further increased in patients who take more than one NSAID or use NSAIDs in combination with certain other medications. Some NSAIDs may also mitigate the antiplatelet benefits of aspirin and may increase blood pressure in patients with hypertension. Clinicians should be aware of potential drug interactions with OTC analgesics when prescribing new medications. Additionally, patients should be properly counseled on the appropriate and safe use of OTC analgesics.
Novel Case of Metastatic Testicular Immature Teratoma Invading the Duodenum
Timothy V. Johnson, Adeboye O. Osunkoya, Keith Delman, Deborah A. BaumgartenViraj A. Master
The Open Surgical Oncology Journal , 2009, DOI: 10.2174/1876504100901010016]
Abstract: We present the first report of an immature teratoma arising from a germ cell testicular cancer invading the duodenum. While other seminomatous and non-seminomatous germ cell tumors are known to metastasize to the duodenum, this is the first such case involving an immature teratoma directly invading the duodenum from a metastatic retroperitoneal mass.
Maf1 Is a Novel Target of PTEN and PI3K Signaling That Negatively Regulates Oncogenesis and Lipid Metabolism
Beth M. Palian equal contributor,Aarti D. Rohira equal contributor,Sandra A. S. Johnson equal contributor,Lina He,Ni Zheng,Louis Dubeau,Bangyan L. Stiles,Deborah L. Johnson
PLOS Genetics , 2014, DOI: doi/10.1371/journal.pgen.1004789
Abstract: Maf1 was initially identified as a transcriptional repressor of RNA pol III-transcribed genes, yet little is known about its other potential target genes or its biological function. Here, we show that Maf1 is a key downstream target of PTEN that drives both its tumor suppressor and metabolic functions. Maf1 expression is diminished with loss of PTEN in both mouse models and human cancers. Consistent with its role as a tumor suppressor, Maf1 reduces anchorage-independent growth and tumor formation in mice. PTEN-mediated changes in Maf1 expression are mediated by PTEN acting on PI3K/AKT/FoxO1 signaling, revealing a new pathway that regulates RNA pol III-dependent genes. This regulatory event is biologically relevant as diet-induced PI3K activation reduces Maf1 expression in mouse liver. We further identify lipogenic enzymes as a new class of Maf1-regulated genes whereby Maf1 occupancy at the FASN promoter opposes SREBP1c-mediated transcription activation. Consistent with these findings, Maf1 inhibits intracellular lipid accumulation and increasing Maf1 expression in mouse liver abrogates diet-mediated induction of lipogenic enzymes and triglycerides. Together, these results establish a new biological role for Maf1 as a downstream effector of PTEN/PI3K signaling and reveal that Maf1 is a key element by which this pathway co-regulates lipid metabolism and oncogenesis.
Transcriptome analysis of embryo maturation in maize
Keat Thomas Teoh, Deborah Vicuna Requesens, Shivakumar P Devaiah, Daniel Johnson, Xiuzhen Huang, John A Howard, Elizabeth E Hood
BMC Plant Biology , 2013, DOI: 10.1186/1471-2229-13-19
Abstract: We undertook a transcriptomic analysis of normal maturing embryos at 15, 21 and 27 days after pollination (DAP), of one elite maize germplasm line that was utilized in crosses to transgenic plants. More than 19,000 genes were analyzed by this method and the challenge was to select subsets of genes that are vitally important to embryo development and maturation for the initial analysis. We describe the changes in expression for genes relating to primary metabolic pathways, DNA synthesis, late embryogenesis proteins and embryo storage proteins, shown through transcriptome analysis and confirmed levels of transcription for some genes in the transcriptome using qRT-PCR.Numerous genes involved in embryo maturation have been identified, many of which show changes in expression level during the progression from 15 to 27 DAP. An expected array of genes involved in primary metabolism was identified. Moreover, more than 30% of transcripts represented un-annotated genes, leaving many functions to be discovered. Of particular interest are the storage protein genes, globulin-1, globulin-2 and an unidentified cupin family gene. When expressing foreign proteins in maize, the globulin-1 promoter is most often used, but this cupin family gene has much higher expression and may be a better candidate for foreign gene expression in maize embryos. Results such as these allow identification of candidate genes and promoters that may not otherwise be available for use. mRNA seq data archived in NCBI SRA; Accession number: ACC=SRA060791 subid=108584.
MMP1 bimodal expression and differential response to inflammatory mediators is linked to promoter polymorphisms
Muna Affara, Benjamin J Dunmore, Deborah A Sanders, Nicola Johnson, Cristin G Print, D Charnock-Jones
BMC Genomics , 2011, DOI: 10.1186/1471-2164-12-43
Abstract: In this study, we used a novel but straightforward method based on agglomerative hierarchical clustering to identify bimodally expressed transcripts in human umbilical vein endothelial cell (HUVEC) microarray data from 15 individuals. We found that MMP1 mRNA abundance was bimodally distributed in un-treated HUVECs and showed a bimodal response to inflammatory mediator treatment. RT-PCR and MMP1 activity assays confirmed the bimodal regulation and DNA sequencing of 69 individuals identified an MMP1 gene promoter polymorphism that segregated precisely with the MMP1 bimodal expression. Chromatin immunoprecipation (ChIP) experiments indicated that the transcription factors (TFs) ETS1, ETS2 and GATA3, bind to the MMP1 promoter in the region of this polymorphism and may contribute to the bimodal expression.We describe a simple method to identify putative bimodally expressed RNAs from transcriptome data that is effective yet easy for non-statisticans to understand and use. This method identified bimodal endothelial cell expression of MMP1, which appears to be biologically significant with implications for inflammatory disease. (271 Words)Numerous strategies have been used in an attempt to sift through the vast amounts of data produced from microarray expression studies [1-4]. There has been much interest given to the identification of bimodally expressed mRNA transcripts, particularly in the context of cancer, where two distinct populations of patients can be defined by differing levels of a set of specific transcripts. These make excellent candidate biomarkers and often tend to show good correlation between transcript and protein abundance [5]. To this end, statistical approaches using mixture-model based clustering combined with either Akaike information criterion (AIC) or the Bayesian informatics criterion (BIC) have frequently been applied [6-9]. One method based on systematic classification of gene expression profiles has been applied to over 2,000 microarray samples
Recruitment activities for a nationwide, population-based, group-randomized trial: the VA MI-Plus study
Ellen Funkhouser, Deborah A Levine, Joe K Gerald, Thomas K Houston, Nancy K Johnson, Jeroan J Allison, Catarina I Kiefe
Implementation Science , 2011, DOI: 10.1186/1748-5908-6-105
Abstract: With a recruitment goal of 200 eligible community-based outpatient clinics, parent VHA facilities (medical centers) were recruited because they oversee their affiliated clinics and the research conducted there. Eligible facilities had at least four VHA-owned and -operated primary care clinics, an affiliated Institutional Review Board (IRB), and no ongoing, potentially overlapping, quality-improvement study. Between December 2003 and December 2005, in two consecutive phases, we used initial and then intensified recruitment strategies.Overall, 48 of 66 (73%) eligible facilities were recruited. Of the 219 clinics and 957 clinicians associated with the 48 facilities, 168 (78%) clinics and 401 (42%) clinicians participated. The median time from initial facility contact to clinic enrollment was 222 days, which decreased by over one-third from the first to the second recruitment phase (medians: 323 and 195 days, respectively; p < .001), when more structured recruitment with physician recruiters was implemented and a dedicated IRB manager was added to the coordinating center staff.Large group-randomized trials benefit from having dedicated physician investigators and IRB personnel involved in recruitment. A large-scale, nationally representative, group-randomized trial of community-based clinics is feasible within the VHA or a similar national healthcare system.Implementation research is the scientific study of methods to promote the rapid uptake of research findings and, hence, improve the health of individuals and populations [1]. Group-randomized trials (GRTs) are an increasingly important tool for implementation research. Typically, individuals (e.g., clinicians) are clustered within subunits (e.g., clinics) that may be further clustered within higher-level units (e.g., facilities or health systems). Accordingly, the unit of randomization and the intervention target may be different (e.g., clinics and clinicians, respectively). Unlike the traditional randomized clinical
Pretest probability assessment derived from attribute matching
Jeffrey A Kline, Charles L Johnson, Charles V Pollack, Deborah B Diercks, Judd E Hollander, Craig D Newgard, J Lee Garvey
BMC Medical Informatics and Decision Making , 2005, DOI: 10.1186/1472-6947-5-26
Abstract: Eight clinical variables (attributes) were chosen by classification and regression tree analysis of a prospectively collected reference database of 14,796 emergency department (ED) patients evaluated for possible ACS. For attribute matching, a computer program identifies patients within the database who have the exact profile defined by clinician input of the eight attributes. The novel method was compared with the LRE for ability to produce PTP estimation <2% in a validation set of 8,120 patients evaluated for possible ACS and did not have ST segment elevation on ECG. 1,061 patients were excluded prior to validation analysis because of ST-segment elevation (713), missing data (77) or being lost to follow-up (271).In the validation set, attribute matching produced 267 unique PTP estimates [median PTP value 6%, 1st–3rd quartile 1–10%] compared with the LRE, which produced 96 unique PTP estimates [median 24%, 1st–3rd quartile 10–30%]. The areas under the receiver operating characteristic curves were 0.74 (95% CI 0.65 to 0.82) for the attribute matching curve and 0.68 (95% CI 0.62 to 0.77) for LRE.The attribute matching system categorized 1,670 (24%, 95% CI = 23–25%) patients as having a PTP < 2.0%; 28 developed ACS (1.7% 95% CI = 1.1–2.4%). The LRE categorized 244 (4%, 95% CI = 3–4%) with PTP < 2.0%; four developed ACS (1.6%, 95% CI = 0.4–4.1%).Attribute matching estimated a very low PTP for ACS in a significantly larger proportion of ED patients compared with a validated LRE.Despite its importance, pretest probability assessment remains a relatively imprecise and inferential process, sometimes referred to as the "doctor's best guess" [1,2]. Previous authors have broadly defined pretest probability as the clinician's estimate of the probability of disease from the patient's words, physical findings, risk factors, and exposures, rendered prior to knowledge of objective test results [3,4]. Presently, the most widely recognized quantitative method of determining pretest
ISG20L1 is a p53 family target gene that modulates genotoxic stress-induced autophagy
Kathryn G Eby, Jennifer M Rosenbluth, Deborah J Mays, Clayton B Marshall, Christopher E Barton, Seema Sinha, Kimberly N Johnson, Luojia Tang, Jennifer A Pietenpol
Molecular Cancer , 2010, DOI: 10.1186/1476-4598-9-95
Abstract: We identified a p53 target gene, ISG20L1, and show that transcription of the gene can be regulated by all three p53 family members (p53, p63, and p73). We generated an antibody to ISG20L1 and found that it localizes to the nucleolar and perinucleolar regions of the nucleus and its protein levels increase in a p53- and p73-dependent manner after various forms of genotoxic stress. When ectopically expressed in epithelial cancer-derived cell lines, ISG20L1 expression decreased clonogenic survival without a concomitant elevation in apoptosis and this effect was partially rescued in cells that were ATG5 deficient. Knockdown of ISG20L1 did not alter 5-FU induced apoptosis as assessed by PARP and caspase-3 cleavage, sub-G1 content, and DNA laddering. Thus, we investigated the role of ISG20L1 in autophagy, a process commonly associated with type II cell death, and found that ISG20L1 knockdown decreased levels of autophagic vacuoles and LC3-II after genotoxic stress as assessed by electron microscopy, biochemical, and immunohistochemical measurements of LC3-II.Our identification of ISG20L1 as a p53 family target and discovery that modulation of this target can regulate autophagic processes further strengthens the connection between p53 signaling and autophagy. Given the keen interest in targeting autophagy as an anticancer therapeutic approach in tumor cells that are defective in apoptosis, investigation of genes and signaling pathways involved in cell death associated with autophagy is critical.Recently, several studies have shown that p53 can regulate autophagy in both a transcriptionally-dependent and -independent manner [1]. Autophagy is commonly studied as a mechanism to maintain metabolic homeostasis in cells undergoing starvation [2]. During starvation, cells form double membrane autophagosomes that engulf cellular contents for degradation and these vesicles then recycle the basic metabolic components for consumption [3]. Although originally thought to be primarily in
Set up to Fail: Inadequate Educational Support for Orphans in Central Kenya  [PDF]
Ginger A. Johnson
Advances in Anthropology (AA) , 2011, DOI: 10.4236/aa.2011.11001
Abstract: In response to Kenya's goal of free and universal primary education for every child by 2015, this paper describes a few of the obstacles that one of the most visible periphery populations in Kenya, orphaned children, face in attempting to reach this objective. The most frequently cited barriers of children and their caretakers to consistent school attendance included: inability to pay school fees, lack of a school uniform, difficulty in providing assis- tance to orphaned children, presence of disease/illness in the family and disruption of education due to political violence. Conducted in a Kikuyu community in the Kinangop District of Central Kenya following the 2007/2008 presidential election riots, this study utilized multiple regression, logistic regression and MANOVA statistical tests to determine if families caring for orphaned children of primary school age differed significantly from families with no orphans in the home. Discriminant function and Mahalanobis testing further revealed differ- ences in types of households, with the presence of orphans in the home (particularly AIDS orphans) significantly increasing the amount of school fees owed per family. Qualitative data obtained from semi-structured interviews with families and open-ended interviews with their primary school aged children contextualized study results and inform policy recommendations.
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