The University of Oklahoma Health science Center is the health science branch of the University of Oklahoma. Located in Oklahoma City, it serves as the primary place of instruction for many of Oklahoma's health professions. It is one of only four health centers in the United States with seven professional colleges.The nineteen buildings that make up the OUHSC campus occupies a fifteen block area in Oklahoma City near the Oklahoma State Capitol. Surrounding these buildings are an additional twenty health-related buildings some of which are owned by the University of Oklahoma. The Health science Center is the core of a wider complex known as the Oklahoma Health Center. The major clinical facilities on campus are part of OU Medicine and include the OU Medical Center hospital complex, The Children's Hospital, OU Physicians and OU Children's Physicians clinics, Harold Hamm Diabetes Center and the Peggy and Charles Stephenson Oklahoma Cancer Center. Also part of the major clinical facilities is the Oklahoma City VA Medical Center. Wikipedia.
Biosense Webster Israel Ltd. and The University of Oklahoma Health Sciences Center | Date: 2017-01-18
A method, consisting of ablating tissue for a time period, measuring a contact force applied during the time period, and measuring a power used during the time period. The method further includes ceasing ablating the tissue when a desired size of a lesion produced in the tissue, as estimated using an integral over the time period of a product of the contact force raised to a first non-unity exponent and the power raised to a second non-unity exponent, is reached.
News Article | May 25, 2017
DUARTE, CA--(Marketwired - May 25, 2017) - Prolacta Bioscience®, the pioneer in human milk-based neonatal nutritional products for premature infants, announced today that it passed the halfway point in a clinical trial evaluating the effect of adding Prolact CR®, a caloric fortifier made from 100 percent human milk cream, to an exclusive human milk-based diet (EHMD)1 for very low birth weight (VLBW) premature infants. The study is evaluating the length of stay and incidence of bronchopulmonary dysplasia (BPD) and has enrolled 127 of the 210 participants weighing between 500 and 1,250g (1 lb 1 oz to 2 lbs 12 oz). The randomized controlled study is evaluating whether adding the human milk cream-based caloric fortifier can decrease the length of hospital stay and reduce BPD, a form of debilitating chronic lung disease not uncommon in VLBW babies. The milk cream caloric fortifier is added as a supplement to an EHMD, which includes the use of 100 percent human milk-based fortifier Prolact+ H2MF®, and is the recommended diet for VLBW infants. "Due to the increased energy and macronutrient requirements of VLBW infants in general, and those with BPD in particular, unfortified human milk does not meet their nutritional needs," said Amy Hair, M.D., lead investigator, Assistant Professor of Pediatrics at Baylor College of Medicine, and the Director of Neonatal Nutrition at Texas Children's Hospital. "VLBW infants require 20 to 40 percent more calories than their age-matched counterparts. These infants also are at higher risk for postnatal growth failure due to disruptions in their feeding regimens. An earlier randomized clinical trial looking at growth suggested that Prolact CR® reduced the incidence and severity of BPD in the group receiving additional nutrients provided from fat." The study, "A Randomized Trial of the Use of Human Milk Cream to Decrease Length of Stay in Extremely Premature Infants," is currently being conducted at Akron Children's Hospital at Boardman, Boardman, Ohio (Linda Cooper, M.D.); Innsbruck Medical University, Innsbruck, Austria (Ursula Kiechl-Kohlendorfer, M.D.); Michigan State University-Sparrow Hospital, Lansing, Mich. (Padmani Karna, M.D.); University of Texas Health Science Center at San Antonio, San Antonio, Texas (Cynthia Blanco, M.D.); Winnie Palmer Hospital for Women & Babies, Orlando, Fla. (Jose Perez, M.D.); Wasatch Neonatal LC, Orem, Utah (Dale Gerstmann, M.D.); St. Joseph's Women's Hospital, Tampa, Fla. (Jenelle Ferry, M.D.); St. John Medical Center, Tulsa, Okla. (Craig Anderson, D.O.); Cook Children's Medical Center, Fort Worth, Texas (David Riley, M.D.); St. Louis Children's Hospital, St. Louis, Mo. (Stephanie Attarian, M.D.); The University of Oklahoma Health Sciences Center, Oklahoma City, Okla. (Andrea Willeitner, M.D.); and Texas Tech University Health Sciences Center El Paso, El Paso, Texas (Lewis Rubin, M.D.). "This clinical trial is the result of secondary findings that were observed in an earlier trial, and underscores the need for continued study of the unique properties in human milk," said Scott Elster, CEO of Prolacta. "We look forward to seeing how Prolact CR® affects lengths of stay and BPD with the hope of uncovering new therapeutic benefits for this fragile patient population." This new clinical trial seeks to verify observations on length of stay and BPD with the use of Prolact CR® from a prior multi-center, randomized trial ("Premature Infants 750-1,250g Birth Weight Supplemented with a Novel Human Milk-Derived Cream are Discharged Sooner," published in Breastfeeding Medicine in 2016). This analysis found that infants who received Prolact CR® were discharged, on average, 12 days earlier than those who did not receive the cream supplement. In the initial trial, infants who developed BPD may have derived an even greater benefit, a finding which prompted this new study. About Prolacta Bioscience Prolacta Bioscience, Inc. is a privately-held life sciences company dedicated to Advancing the Science of Human Milk®. The company pioneered the development of human milk-based neonatal nutritional products to meet the needs of critically ill, premature infants in the neonatal intensive care unit (NICU). Prolacta leads the industry in the quality and safety of nutritional products made from donor breast milk, and operates the first and only pharmaceutical-grade manufacturing facility for the processing of human milk. 1 An EHMD is when 100% percent of the protein, fat and carbohydrates in an infant's intake are derived solely from human milk.
Hay D.L.,University of Auckland |
Pioszak A.A.,The University of Oklahoma Health Sciences Center
Annual Review of Pharmacology and Toxicology | Year: 2016
It is now recognized that G protein-coupled receptors (GPCRs), once considered largely independent functional units, have a far more diverse molecular architecture. Receptor activity-modifying proteins (RAMPs) provide an important example of proteins that interact with GPCRs to modify their function. RAMPs are able to act as pharmacological switches and chaperones, and they can regulate signaling and/or trafficking in a receptor-dependent manner. This review covers recent discoveries in the RAMP field and summarizes the known GPCR partners and functions of RAMPs. We also discuss the first peptide-bound structures of RAMP-GPCR complexes, which give insight into the molecular mechanisms that enable RAMPs to alter the pharmacology and signaling of GPCRs. Copyright © 2016 by Annual Reviews. All rights reserved.
Lovallo W.R.,The University of Oklahoma Health Sciences Center
Biological Psychology | Year: 2011
Studies of cardiovascular disease risk have explored the idea that exaggerated physiological responses to stress may signal increased risk of cardiovascular disease. We describe a neurophysiological model of brain structures and peripheral structures that may contribute to exaggerated reactivity. Level I in this model includes the limbic system and its interactions with the prefrontal cortex that determine stress appraisals and coping responses. Level II addresses the hypothalamus and brainstem that contribute outputs to the body and which also includes brainstem nuclei that feed back to Level I to modulate its functioning. Level III includes the peripheral tissues themselves. We then suggest that stress reactivity ranging from very low to very high has a normative midrange of intensity and present evidence that negative health outcomes may be associated with both exaggerated and diminished stress reactivity since both tendencies imply a loss of homeostatic regulation. In particular, dysregulation at Levels I and II in our heuristic model signify altered motivational function and an attendant alteration in outflow to the periphery and poor behavioral homeostasis. In consequence, poor affective and behavioral regulation would be expected to contribute to poor health behaviors therefore additionally impairing health. In conclusion, diminished as well as exaggerated physiological reactivity should be seen as nonoptimal functioning that can contribute to poor health outcomes. This conceptualization places physical health into the context of behavioral and physiological processes that contribute to homeostasis. © 2010.
McEver R.P.,The University of Oklahoma Health Sciences Center |
Zhu C.,Georgia Institute of Technology
Annual Review of Cell and Developmental Biology | Year: 2010
Rolling adhesion on vascular surfaces is the first step in recruiting circulating leukocytes, hematopoietic progenitors, or platelets to specific organs or to sites of infection or injury. Rolling requires the rapid yet balanced formation and dissociation of adhesive bonds in the challenging environment of blood flow. This review explores how structurally distinct adhesion receptors interact through mechanically regulated kinetics with their ligands to meet these challenges. Remarkably, increasing force applied to adhesive bonds first prolongs their lifetimes (catch bonds) and then shortens their lifetimes (slip bonds). Catch bonds mediate the counterintuitive phenomenon of flow-enhanced rolling adhesion. Force-regulated disruptions of receptor interdomain or intradomain interactions remote from the ligand-binding surface generate catch bonds. Adhesion receptor dimerization, clustering in membrane domains, and interactions with the cytoskeleton modulate the forces applied to bonds. Both inside-out and outside-in cell signals regulate these processes. Copyright © 2010 by Annual Reviews. All rights reserved.
Cunningham M.W.,The University of Oklahoma Health Sciences Center
Current Opinion in Rheumatology | Year: 2012
Purpose of review: To give an overview of the current hypotheses of the pathogenesis of rheumatic fever and group A streptococcal autoimmune sequelae of the heart valve and brain. Recent findings: Human monoclonal antibodies (mAbs) derived from rheumatic heart disease have provided evidence for crossreactive autoantibodies that target the dominant group A streptococcal epitope of the group A carbohydrate, N-acetyl-beta-D-glucosamine (GlcNAc), and heart valve endothelium, laminin and laminar basement membrane. T cells in peripheral blood and in rheumatic heart valves revealed the presence of T cells crossreactive with streptococcal M protein and cardiac myosin. For initiation of disease, evidence suggests a two-hit hypothesis for antibody attack on the valve endothelium with subsequent extravasation of T cells through activated endothelium into the valve to form granulomatous lesions and Aschoff bodies. Autoantibodies against the group A streptococcal carbohydrate epitope GlcNAc and cardiac myosin and its peptides appear during progression of rheumatic heart disease. However, autoantibodies against collagen that are not crossreactive may form because of the release of collagen from damaged valve or to responses to collagen bound in vitro by certain serotypes of streptococci. In Sydenham chorea, human mAbs derived from disease target the group A carbohydrate epitope GlcNAc and gangliosides and dopamine receptors found on the surface of neuronal cells in the brain. Human mAbs and autoantibodies in Sydenham chorea were found to signal neuronal cells and activate calcium calmodulin-dependent protein kinase II (CaMKII) in neuronal cells and recognize the intracellular protein biomarker tubulin. Summary: To summarize, pathogenic mechanisms of crossreactive autoantibodies which target the valve in rheumatic heart disease and the neuronal cell in Sydenham chorea share a common streptococcal epitope GlcNAc and target intracellular biomarkers of disease including cardiac myosin in the myocardium and tubulin, a protein abundant in the brain. However, intracellular antigens are not believed to be the basis for disease. The theme of molecular mimicry in streptococcal autoimmune sequelae is the recognition of targeted intracellular biomarker antigens such as cardiac myosin and brain tubulin, while targeting extracellular membrane antigens such as laminin on the valve surface endothelium or lysoganglioside and dopamine receptors in the brain. Antibody binding to these cell surface antigens may lead to valve damage in rheumatic heart disease or neuropsychiatric behaviors and involuntary movements in Sydenham chorea. © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Esmon C.T.,The University of Oklahoma Health Sciences Center
Thrombosis and Haemostasis | Year: 2014
Great advances have been made in recent years in understanding the haemostatic system and the molecular and cellular basis of thrombus formation. Although directly targeting factor Xa or thrombin (factor IIa) for effective anticoagulation is now well established, evidence has emerged suggesting that factor Xa and thrombin are involved in other physiological and pathophysiological cellular processes, including inflammation. These non-haemostatic activities of factor Xa and thrombin are predominantly mediated via the activation of proteinaseactivated receptors. Studies have indicated a potential role of coagulation proteins (including factor Xa and thrombin) in the progression of disease conditions such as atherothrombosis. Preclinical studies have provided evidence for the effects of direct factor Xa or direct thrombin inhibition beyond anticoagulation, including anti-inflammatory activities and atherosclerotic plaque stabilisation. In this article, the non-haemostatic activities of factor Xa and thrombin and the effects of direct inhibition of these coagulation factors on these activities are summarised. In addition, the potential roles of factor Xa and thrombin in atherosclerosis and atherothrombosis are explored and the cardiovascular profiles of rivaroxaban, apixaban and dabigatran etexilate observed in phase III clinical studies are discussed. © Schattauer 2014.
Chernausek S.D.,The University of Oklahoma Health Sciences Center
Journal of Clinical Endocrinology and Metabolism | Year: 2012
Intrauterine growth restriction (IUGR) is prevalent worldwide and affects children and adults in multiple ways. These include predisposition to type 2 diabetes mellitus, the metabolic syndrome, cardiovascular disease, persistent reduction in stature, and possibly changes in the pattern of puberty. A review of recent literature confirms that the metabolic effects of being born small for gestational age are evident in the very young, persist with age, and are amplified by adiposity. Furthermore, the pattern of growth in the first few years of life has a significant bearing on a person's later health, with those that show increasing weight gain being at the greatest risk for future metabolic dysfunction. Treatment with exogenous human GH is used to improve height in children who remain short after being small for gestational age at birth, but the response of individuals remains variable and difficult to predict. The mechanisms involved in the metabolic programming of IUGR children are just beginning to be explored. It appears that IUGR leads to widespread changes in DNA methylation and that specific "epigenetic signatures" for IUGR are likely to be found in various fetal tissues. The challenge is to link such alterations with modifications in gene expression and ultimately the metabolic abnormalities of adulthood, and it represents one of the frontiers for research in the field. Copyright © 2012 by The Endocrine Society.
Cunningham M.W.,The University of Oklahoma Health Sciences Center
International Reviews of Immunology | Year: 2014
The group A streptococcus, Streptococcus pyogenes, and its link to autoimmune sequelae, has acquired a new level of understanding. Studies support the hypothesis that molecular mimicry between the group A streptococcus and heart or brain are important in directing immune responses in rheumatic fever. Rheumatic carditis, Sydenham chorea and a new group of behavioral disorders called pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections are reviewed with consideration of autoantibody and T cell responses and the role of molecular mimicry between the heart, brain and group A streptococcus as well as how immune responses contribute to pathogenic mechanisms in disease. In rheumatic carditis, studies have investigated human monoclonal autoantibodies and T cell clones for their crossreactivity and their mechanisms leading to valve damage in rheumatic heart disease. Although studies of human and animal sera from group A streptococcal diseases or immunization models have been crucial in providing clues to molecular mimicry and its role in the pathogenesis of rheumatic fever, study of human monoclonal autoantibodies have provided important insights into how antibodies against the valve may activate the valve endothelium and lead to T cell infiltration. Passive transfer of anti-streptococcal T cell lines in a rat model of rheumatic carditis illustrates effects of CD4+ T cells on the valve. Although Sydenham chorea has been known as the neurological manifestation of rheumatic fever for decades, the combination of autoimmunity and behavior is a relatively new concept linking brain, behavior and neuropsychiatric disorders with streptococcal infections. In Sydenham chorea, human mAbs and their expression in transgenic mice have linked autoimmunity to central dopamine pathways as well as dopamine receptors and dopaminergic neurons in basal ganglia. Taken together, the studies reviewed provide a basis for understanding streptococcal sequelae and how immune responses against group A streptococci influence autoimmunity and inflammatory responses in the heart and brain. Copyright © 2014 Informa Healthcare USA, Inc.
George J.N.,The University of Oklahoma Health Sciences Center
Blood | Year: 2010
Thrombotic thrombocytopenic purpura (TTP) is the common name for adults with microangiopathic hemolytic anemia, thrombocytopenia, with or without neurologic or renal abnormalities, and without another etiology; children without renal failure are also described as TTP. The diagnosis of TTP is an indication for plasma exchange treatment, but beginning treatment requires sufficient confidence in the diagnosis to justify the risk of plasma exchange complications. Documentation of a severe deficiency of plasma ADAMTS13 activity, defined as less than 10% of normal, is not essential for the diagnosis of TTP. Some patients without severe ADAMTS13 deficiency may benefit from plasma exchange treatment; in addition, some patients with severe ADAMTS13 deficiency may subsequently be diagnosed with another cause for their clinical features. However, severe acquired ADAMTS13 deficiency does define a subgroup of patients who appear to benefit from treatment with corticosteroids and other immunosuppressive agents in addition to plasma exchange but who have a high risk for relapse. Approximately 80% of patients survive their acute episode, a survival rate that has not changed since the introduction of plasma exchange treatment. Although recovery may appear to be complete, many patients have persistent minor cognitive abnormalities. More effective as well as safer treatment for TTP is needed. © 2010 by The American Society of Hematology.