The University of Alabama at Birmingham is a public university in Birmingham in the U.S. state of Alabama. Developed from an academic extension center established in 1936, the institution became an autonomous institution in 1969 and is today one of three institutions in the University of Alabama System. In the fall of 2013, 18,568 students from more than 110 countries were enrolled at UAB pursuing studies in 140 programs of study in 12 academic divisions leading to bachelor's, master's, doctoral, and professional degrees in the social and behavioral science, the liberal arts, business, education, engineering, and health-related fields such as medicine, dentistry, optometry, nursing, and public health.The UAB Health System, one of the largest academic medical centers in the United States, is affiliated with the university. UAB Hospital sponsors residency programs in medical specialties, including internal medicine, neurology, surgery, radiology, and anesthesiology. UAB Hospital is the only ACS verified Level I trauma center in Alabama, as rated by the American College of Surgeons Trauma Program.UAB is the state's largest employer, with more than 18,000 faculty and staff and over 53,000 jobs at the university and in the health system. An estimated 10 percent of the jobs in the Birmingham-Hoover Metropolitan Area and 1 in 33 jobs in the state of Alabama are directly or indirectly related to UAB. The university's overall annual economic impact was estimated to be $4.6 billion in 2010. Wikipedia.
Los Alamos National Security LLC, Beth Israel Deaconess Medical Center, Duke University and University of Alabama at Birmingham | Date: 2017-06-14
The present invention relates, in general, to an immunogenic composition (e.g., a vaccine) and, in particular, to a polyvalent immunogenic composition, such as a polyvalent HIV vaccine, and to methods of using same. The invention further relates to methods that use a genetic algorithm to create sets of polyvalent antigens suitable for use, for example, in vaccination strategies.
Yother J.,University of Alabama at Birmingham
Annual Review of Microbiology | Year: 2011
Capsular polysaccharides and exopolysaccharides play critical roles in bacterial survival strategies, and they can have important medical and industrial applications. An immense variety of sugars and glycosidic linkages leads to an almost unlimited diversity of potential polysaccharide structures. This diversity is reflected in the large number of serologically and chemically distinct polysaccharides that have been identified among both gram-positive and gram-negative bacteria. Despite this diversity, however, the genetic loci and mechanisms responsible for polysaccharide biosynthesis exhibit conserved features and can be classified into a small number of groups. In Streptococcus pneumoniae, capsule synthesis occurs by one of two distinct mechanisms that involve the polymerization of either individual sugars in a processive reaction (synthase dependent) or discrete repeat units in a nonprocessive reaction (Wzy dependent). Characterization of these systems has provided novel insights that are applicable to polymers synthesized by many gram-positive and gram-negative bacteria, as well as eukaryotes. © 2011 by Annual Reviews. All rights reserved.
Sweatt J.,University of Alabama at Birmingham
Neuron | Year: 2013
Over the past 25 years, the broad field of epigenetics and, over the past decade in particular, the emerging field of neuroepigenetics have begun to have tremendous impact in the areas of learned behavior, neurotoxicology, CNS development, cognition, addiction, and psychopathology. However, epigenetics is such a new field that in most of these areas the impact is more in the category of fascinating implications as opposed to established facts. In this brief commentary, I will attempt to address and delineate some of the open questions and areas of opportunity that discoveries in epigenetics are providing to the discipline of neuroscience.
Standaert D.G.,University of Alabama at Birmingham
Neurobiology of Disease | Year: 2011
Dystonia is a clinical syndrome with sustained muscle contraction, twisting, and abnormal postures. A number of different genetic forms have been defined, but most cases are sporadic in nature and of uncertain cause. Relatively few cases of dystonia have been studied pathologically. In primary dystonias, where dystonia is the main symptom, most reports describe little or no detectable neuropathology, although changes in brainstem neurons have been described in some cases. Secondary dystonias are associated with degenerative or destructive diseases of the nervous system; the pathology may be located in the basal ganglia, but in some cases the primary pathological changes are found in the cerebellum or cerebellar outflow pathways, suggesting that both regions may be involved in the pathogenesis of dystonic symptoms. Overall the number of well-documented pathological cases available for study is few, and there is an urgent need for additional postmortem studies. This article is part of a Special Issue entitled "Advances in dystonia". © 2010 Elsevier Inc.
Day J.J.,University of Alabama at Birmingham |
Sweatt J.D.,University of Alabama at Birmingham
Neuron | Year: 2011
Although the critical role for epigenetic mechanisms in development and cell differentiation has long been appreciated, recent evidence reveals that these mechanisms are also employed in postmitotic neurons as a means of consolidating and stabilizing cognitive-behavioral memories. In this review, we discuss evidence for an " epigenetic code" in the central nervous system that mediates synaptic plasticity, learning, and memory. We consider how specific epigenetic changes are regulated and may interact with each other during memory formation and how these changes manifest functionally at the cellular and circuit levels. We also describe a central role for mitogen-activated protein kinases in controlling chromatin signaling in plasticity and memory. Finally, we consider how aberrant epigenetic modifications may lead to cognitive disorders that affect learning and memory, and we review the therapeutic potential of epigenetic treatments for the amelioration of these conditions. © 2011 Elsevier Inc.
Dwivedi Y.,University of Alabama at Birmingham
Progress in Neuro-Psychopharmacology and Biological Psychiatry | Year: 2016
As a class of noncoding RNAs, microRNAs (miRNAs) regulate gene expression by inhibiting translation of messenger RNAs. These miRNAs have been shown to play a critical role in higher brain functioning and actively participate in synaptic plasticity. Pre-clinical evidence demonstrates that expression of miRNAs is differentially altered during stress. On the other hand, depressed individuals show marked changes in miRNA expression in brain. MiRNAs are also target of antidepressants and electroconvulsive therapy. Moreover, these miRNAs are present in circulating blood and can be easily detected. Profiling of miRNAs in blood plasma/serum provides evidence that determination of miRNAs in blood can be used as possible diagnostic and therapeutic tool. In this review article, these aspects are critically reviewed and the role of miRNAs in possible etiopathogenesis and therapeutic implications in the context of major depressive disorder is discussed. © 2015 Elsevier Inc.
Watkins S.,University of Alabama at Birmingham
Trends in neurosciences | Year: 2012
Gliomas are terrifying primary brain tumors for which patient outlook remains bleak. Recent research provides novel insights into the unique biology of gliomas. For example, these tumors exhibit an unexpected pluripotency that enables them to grow their own vasculature. They have an unusual ability to navigate tortuous extracellular pathways as they invade, and they use neurotransmitters to inflict damage and create room for growth. Here, we review studies that illustrate the importance of considering interactions of gliomas with their native brain environment. Such studies suggest that gliomas constitute a neurodegenerative disease caused by the malignant growth of brain support cells. The chosen examples illustrate how targeted research into the biology of gliomas is yielding new and much needed therapeutic approaches to this challenging nervous system disease. Copyright © 2012 Elsevier Ltd. All rights reserved.
Zhou D.,University of Alabama at Birmingham
Nature genetics | Year: 2010
We show that knockdown of KLF1 in human and mouse adult erythroid progenitors markedly reduces BCL11A levels and increases human gamma-globin/beta-globin expression ratios. These results suggest that KLF1 controls globin gene switching by directly activating beta-globin and indirectly repressing gamma-globin gene expression. Controlled knockdown of KLF1 in adult erythroid progenitors may provide a method to activate fetal hemoglobin expression in individuals with beta-thalassemia or sickle cell disease.
Tolwani A.,University of Alabama at Birmingham
New England Journal of Medicine | Year: 2012
Acute limb ischemia due to a perioperative type B (distal) thoracic aortic dissection develops in a 90-kg, 20-year-old man with Marfan's syndrome who is admitted to the hospital for elective aortic-valve replacement. On postoperative day 1, he undergoes endovascular repair of the thoracic aorta. On postoperative day 4, his urine output decreases to 420 ml over a 24-hour period. He requires mechanical ventilation with a fraction of inspired oxygen (FIO2) of 0.70; his mean arterial pressure is 74 mm Hg with vasopressor support. He has had a positive fluid balance of 9.8 liters since admission. The serum creatinine level has increased from a baseline of 0.6 mg per deciliter (53.0 μmol per liter) to 4.4 mg per deciliter (389.0 μmol per liter). The bicarbonate level is 19 mmol per liter despite bicarbonate infusion, and the potassium level is 6.1 mmol per liter. The creatine kinase level has increased to 129,040 U per liter. An intensive care specialist evaluates the patient and recommends initiation of continuous renal-replacement therapy. Copyright © 2012 Massachusetts Medical Society.
Calhoun D.A.,University of Alabama at Birmingham
Annual Review of Medicine | Year: 2013
Resistant hypertension affects an estimated 10-15 million American adults and is increasing in prevalence. The etiology of resistant hypertension is almost always multifactorial, including obesity, older age, high dietary salt, chronic kidney disease, and aldosterone excess. Classical primary aldosteronism and lesser degrees of aldosterone excess, possibly originating from visceral adipocytes, contribute broadly to antihypertensive treatment resistance. Treatment of resistant hypertension is predicated on appropriate lifestyle changes and use of effective combinations of antihypertensive agents from different classes. Blockade of aldosterone with spironolactone has been shown to be particularly effective for treatment of resistant hypertension. The antihypertensive benefit of spironolactone is not limited to patients with demonstrable hyperaldosteronism but instead can be effective in resistant hypertensive patients regardless of aldosterone levels. Chlorthalidone is a potent, long-acting thiazide-like diuretic and should be used preferentially to treat resistant hypertension as it is superior to normally used doses of hydrochlorothiazide. Copyright © 2013 by Annual Reviews.