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Search Results: 1 - 10 of 138930 matches for " K. Malone "
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Ring chromosome 18 abnormality in acute myelogenous leukemia: the clinical dilemma
Shanthi Sivendran, Stephen Gruenstein, Adriana K Malone, Vesna Najfeld
Journal of Hematology & Oncology , 2010, DOI: 10.1186/1756-8722-3-25
Abstract: Prognostic features in AML are strongly influenced by genetic changes in leukemic cells[2]. Currently, based on cytogenetic findings and mutational status of some genes, patients are stratified into favorable, intermediate, and unfavorable risk categories[2]. These categories are key determinants for attainment of complete remission and overall survival[2]. Recent updated evidence-and expert opinion-based recommendations for the diagnosis and management of AML have provided further categorizations of AML based on pretreatment chromosomal abnormalities[3]. However, there are rare, recurrent, cytogenetic abnormalities in AML that have not been classified. This is primarily due to the small number of reported patients, whose risk category and response to treatment is not well known. Ring chromosomes are rare cytogenetic abnormalities that occur in less than 10% of hematopoietic malignancies but have been reported in up to 70% of mesenchymal tumors[1]. They vary in size, shape, and number. Only two patients were reported with AML and a ring chromosome 18 abnormality[4,5]. In this report we describe a patient with M5 AML with a ring 18 abnormality and discuss the etiology, clinical features, classification, and the clinical dilemma related to treatment of ring chromosome aberrations in AML.A 36 year old man presented with a one month history of nausea, loss of appetite, diarrhea, night sweats, and a twelve pound weight loss. He had no significant past medical history and, despite his work in construction, denied any previous chemical or radiation exposure. Peripheral blood revealed anemia (Hb 8.2 g/dL), thrombocytopenia (38 × 103/uL) and a white cell count of 2.6 × 103/uL. A bone marrow biopsy demonstrated a markedly hypercellular marrow (90-100% cellularity) with increased mature and immature granulocytes and atypical megakaryoctyes. The bone marrow aspirate contained myeloblasts, monoblasts, and promonocytes accounting for 36% of the cellularity. Significant dysplasia
Diet of three large pelagic fishes associated with drifting fish aggregating devices (DFADs) in the western equatorial Indian Ocean
Malone, M. A.,Buck, K. M.,Moreno, G.,Sancho, G.
Animal Biodiversity and Conservation , 2011,
Abstract: Several species of fish, aggregate around DFADs in marine tropical waters. We captured three predatory species: yellow fin tuna (Thunnus albacares), wahoo (Acanthocybium solandri) and dolphinfish (Coryphaena hippurus) from aggregations under DFADs in the Western Indian Ocean to characterize their diet and determine whether they fed on other DFAD associated organisms. Yellowfin tuna did not feed on DFAD–associated prey, while wahoo and dolphinfish did exploit resources aggregated by the DFADs, though they predominantly fed on other non–associated organisms. Opportunistic feeding on surface swarming stomatopod crustaceans was observed in yellowfin tuna and dolphinfish associated with FADs, but was not observed in wahoo.
Diabetic Cardiovascular Risk and Carnitine Deficiency
—Carnitine Deficiency in Clinical Diabetes Mellitus
 [PDF]

John I. Malone, Michael A. Malone, Anthony D. Morrison
Journal of Diabetes Mellitus (JDM) , 2014, DOI: 10.4236/jdm.2014.43029
Abstract:

Background: Type 1 diabetes mellitus increases the risk of coronary heart disease. The Pittsburgh IDDM morbidity and mortality study reported greater than 10 fold coronary heart disease mortality compared with US national data [1]. Adults with diabetes have heart disease death rates 2 to 4 times higher than adults without diabetes [2]. Diabetic cardiomyopathy explains much of this survival difference and carnitine deficiency is a cause of cardiomyopathy. Research Design and Methods: Adult subjects (40) with type 1 diabetes mellitus were seen for a routine annual visit having no clinical complaints. Fasting serum samples were collected for annual chemistries and the measurement of carnitine. Results: The mean total (40.8 ± 8.8) [40 - 80 nmol/ml] and free (32.9 ± 7.9) [30 - 60 nmol/ml] carnitine levels for this group included 43% low total and 28% low free carnitine. The mean esterified/free (E/F) carnitine ratio (0.25 ± 0.09) for this group was elevated indicating carnitine insufficiency. Conclusions: Fatty acids are the primary energy source for diabetic heart muscle, and carnitine is essential for intracellular fatty acid transport and ATP production. Therefore, mild carnitine deficiency can compromise fatty acid energy production in a failing heart. Carnitine deficiency in subjects at high risk for cardiovascular failure is a possible unrecognized reason for the 4 fold increased death rate in patients with type 1 diabetes. Supplementation with oral carnitine could reduce that increased risk of heart failure, in patients with type 1 diabetes. Intravenous carnitine may be life saving when managing acute cardiac failure in patients with diabetes mellitus. Normal carnitine levels in patients with type

Isometries of Products of Path-Connected Locally Uniquely Geodesic Metric Spaces with the Sup Metric are Reducible
William Malone
Mathematics , 2009,
Abstract: Let $M_i$ and $N_i$ be path-connected locally uniquely geodesic metric spaces that are not points and $f:\prod_{i=1}^m M_i\to \prod_{i=1}^n N_i$ be an isometry where $\prod_{i=1}^n N_i$ and $\prod_{i=1}^m M_i$ are given the sup metric. Then $m=n$ and after reindexing $M_i$ is isometric to $N_i$ for all $i$. Moreover $f$ is a composition of an isometry that reindexes the factor spaces and an isometry that is a product of isometries $f_i:M_i\to N_i$.
Case-Control Study of Fetal Microchimerism and Breast Cancer
Vijayakrishna K. Gadi, Kathleen E. Malone, Katherine A. Guthrie, Peggy L. Porter, J. Lee Nelson
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0001706
Abstract: Background Prior pregnancy is known to protect against development of breast cancer. Recent studies have demonstrated that pregnancy has the capacity to establish small numbers of immunologically active fetal-derived cells in the mother, a phenomenon known as fetal microchimerism (FMc). We asked whether presence of FMc, routinely acquired during pregnancy, is a protective factor for breast cancer. Methodology/Principal Findings DNA extracts from peripheral blood specimens were obtained from a population-based case-control study of risk factors for breast cancer in women 21 to 45 years old. Specimens were tested with quantitative PCR for presence and concentrations of male DNA presumed to derive from prior pregnancies with a male fetus. Odds ratios (OR) and 95% confidence intervals (CI) were estimated with consideration of multiple established reproductive and environmental risk factors for breast cancer. FMc results were generated on 99 parous women, 54 with primary invasive breast cancer and 45 general population controls. FMc prevalence was 56% (25/45) and 26% (14/54) in controls and cases, respectively. Women harboring FMc were less likely to have had breast cancer (OR = 0.29, 95% CI 0.11–0.83; p = 0.02, adjusting for age, number of children, birth of a son, history of miscarriage, and total DNA tested). In addition, FMc concentrations were higher in controls versus cases (p = 0.01). Median concentrations were 2 (0–78) and 0 (0–374) fetal genomes/106 maternal genomes in controls and cases, respectively. Conclusions Results suggest that the enigma of why some parous women are not afforded protection from breast cancer by pregnancy might in part be explained by differences in FMc. Mechanistic studies of FMc-derived protection against breast cancer are warranted.
Diet as prophylaxis and treatment for venous thromboembolism?
David K Cundiff, Paul S Agutter, P Malone, John C Pezzullo
Theoretical Biology and Medical Modelling , 2010, DOI: 10.1186/1742-4682-7-31
Abstract: The literature concerning dietary influences on VTE incidence was reviewed. Hypotheses concerning the etiology of VTE were critiqued in relationship to the rationale for dietary versus anticoagulant approaches to prophylaxis and treatment.Epidemiological evidence suggests that a diet with ample fruits and vegetables and little meat may substantially reduce the risk of VTE; vegetarian, vegan, or Mediterranean diets favorably affect serum markers of hemostasis and inflammation. The valve cusp hypoxia hypothesis of DVT/VTE etiology is consistent with the development of VTE being affected directly or indirectly by diet. However, it is less consistent with the rationale of using anticoagulants as VTE prophylaxis. For both prophylaxis and treatment of VTE, we propose RCTs comparing standard anticoagulation with low VTE risk diets, and we discuss the statistical considerations for an example of such a trial.Because of (a) the risks of biochemical anticoagulation as anti-VTE prophylaxis or treatment, (b) the lack of placebo-controlled efficacy data supporting anticoagulant treatment of VTE, (c) dramatically reduced hospital-acquired FPE incidence in surgical patients without anticoagulant prophylaxis from 1980 - 2010 relative to the 1960s and 1970s, and (d) evidence that VTE incidence and outcomes may be influenced by diet, randomized controlled non-inferiority clinical trials are proposed to compare standard anticoagulant treatment with potentially low VTE risk diets. We call upon the U. S. National Institutes of Health and the U.K. National Institute for Health and Clinical Excellence to design and fund those trials.The consensus view that DVT and VTE are hematological disorders arose shortly after the Second World War and had become the new orthodoxy by the early 1960s. It still dominates research and practice in the field. Essentially, this consensus added 'hypercoagulability' to the 'stasis' and 'vessel wall injury' thesis of Hunterian pathophysiology, generating a set
Cetuximab in Refractory Skin Cancer Treatment
Sini J Kalapurakal, James Malone, K. Thomas Robbins, Lucinda Buescher, John Godwin, Krishna Rao
Journal of Cancer , 2012,
Abstract: Objectives: Non-melanoma skin cancer is the most common malignancy in US, with an annual incidence of in excess of 1.5 million cases. In the majority of cases, locoregional treatment is curative and systemic therapy is not indicated. Platinum-based chemotherapy regimens have been used most commonly in refractory cases. The use of cetuximab, a monoclonal antibody targeting epidermal growth factor receptor [EGFR], has been reported for skin cancer treatment. This current study evaluated eight cases of locally advanced and refractory basal cell or squamous cell cancers which were treated with cetuximab. Methods: This is a retrospective study on eight patients who had received cetuximab for treatment of cutaneous carcinoma since 2007 at Southern Illinois University School of Medicine (SIU-SOM) Medical Oncology clinic. Results: Three of the four patients with basal cell carcinoma and two of the four patients with squamous cell carcinoma maintained remission on treatment.. The main side effect was acneiform rash which required termination of treatment for one patient and dose reduction in another. Conclusion: The study indicates that cetuximab may have a beneficial role for patients with non-melanoma cutaneous carcinomas that are refractory to standard therapy.
Interaction Picture Density Matrix Quantum Monte Carlo
Fionn D. Malone,N. S. Blunt,James J. Shepherd,D. K. K. Lee,J. S. Spencer,W. M. C. Foulkes
Physics , 2015, DOI: 10.1063/1.4927434
Abstract: The recently developed density matrix quantum Monte Carlo (DMQMC) algorithm stochastically samples the N -body thermal density matrix and hence provides access to exact properties of many-particle quantum systems at arbitrary temperatures. We demonstrate that moving to the interaction picture provides substantial benefits when applying DMQMC to interacting fermions. In this first study, we focus on a system of much recent interest: the uniform electron gas in the warm dense regime. The basis set incompleteness error at finite temperature is investigated and extrapolated via a simple Monte Carlo sampling procedure. Finally, we provide benchmark calculations for a four-electron system, comparing our results to previous work where possible.
Expression in Aneuploid Drosophila S2 Cells
Yu Zhang,John H. Malone,Sara K. Powell,Vipul Periwal,Eric Spana,David M. MacAlpine,Brian Oliver
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1000320
Abstract: Extensive departures from balanced gene dose in aneuploids are highly deleterious. However, we know very little about the relationship between gene copy number and expression in aneuploid cells. We determined copy number and transcript abundance (expression) genome-wide in Drosophila S2 cells by DNA-Seq and RNA-Seq. We found that S2 cells are aneuploid for >43 Mb of the genome, primarily in the range of one to five copies, and show a male genotype (~ two X chromosomes and four sets of autosomes, or 2X;4A). Both X chromosomes and autosomes showed expression dosage compensation. X chromosome expression was elevated in a fixed-fold manner regardless of actual gene dose. In engineering terms, the system “anticipates” the perturbation caused by X dose, rather than responding to an error caused by the perturbation. This feed-forward regulation resulted in precise dosage compensation only when X dose was half of the autosome dose. Insufficient compensation occurred at lower X chromosome dose and excessive expression occurred at higher doses. RNAi knockdown of the Male Specific Lethal complex abolished feed-forward regulation. Both autosome and X chromosome genes show Male Specific Lethal–independent compensation that fits a first order dose-response curve. Our data indicate that expression dosage compensation dampens the effect of altered DNA copy number genome-wide. For the X chromosome, compensation includes fixed and dose-dependent components.
Expression in Aneuploid Drosophila S2 Cells
Yu Zhang,John H. Malone,Sara K. Powell,Vipul Periwal,Eric Spana,David M. MacAlpine,Brian Oliver
PLOS Biology , 2010, DOI: 10.1371/journal.pbio.1000320
Abstract: Extensive departures from balanced gene dose in aneuploids are highly deleterious. However, we know very little about the relationship between gene copy number and expression in aneuploid cells. We determined copy number and transcript abundance (expression) genome-wide in Drosophila S2 cells by DNA-Seq and RNA-Seq. We found that S2 cells are aneuploid for >43 Mb of the genome, primarily in the range of one to five copies, and show a male genotype (~ two X chromosomes and four sets of autosomes, or 2X;4A). Both X chromosomes and autosomes showed expression dosage compensation. X chromosome expression was elevated in a fixed-fold manner regardless of actual gene dose. In engineering terms, the system “anticipates” the perturbation caused by X dose, rather than responding to an error caused by the perturbation. This feed-forward regulation resulted in precise dosage compensation only when X dose was half of the autosome dose. Insufficient compensation occurred at lower X chromosome dose and excessive expression occurred at higher doses. RNAi knockdown of the Male Specific Lethal complex abolished feed-forward regulation. Both autosome and X chromosome genes show Male Specific Lethal–independent compensation that fits a first order dose-response curve. Our data indicate that expression dosage compensation dampens the effect of altered DNA copy number genome-wide. For the X chromosome, compensation includes fixed and dose-dependent components.
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