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Fort Lauderdale, FL, United States

Nova Southeastern University, formerly referred to as Nova and now commonly called NSU, is a private, coeducational, nonsectarian, research university located in Broward County, Florida, United States, with its main campus in the town of Fort Lauderdale. The university is the eighth-largest not-for-profit private university in the nation. NSU operates eight Student Educational Centers in Florida, the largest being a 300 acres campus located approximately 24 miles north of Downtown Miami.The university was founded as the Nova University of Advanced Technology on a former Naval Outlying Landing Field built during World War II. The university first offered graduate degrees in the physical and social science. Leo Goodwin, Sr. left a $16 million bequest to the university in 1971 which funded its expansion throughout the 1970s and 1980s. In 1994, the university merged with the Southeastern University of the Health science and assumed its current name.NSU currently consists of 18 colleges and schools offering over 175 programs of study with more than 250 majors. The university offers professional degrees in law, business, osteopathic medicine, allied health, pharmacy, dentistry, optometry, and nursing. Nova Southeastern enrolled 28,457 students in the 2011-2012 academic year and has produced over 145,000 alumni.NSU is classified as a high research and community engaged university by the Carnegie Foundation. The university is accredited by the Southern Association of Colleges and Schools and also has numerous additional specialized accreditations for its colleges and programs.The NSU Sharks compete in the NCAA Division II Sunshine State Conference in seventeen intercollegiate athletic programs. Wikipedia.


Ownby R.L.,Nova Southeastern University
Current Psychiatry Reports | Year: 2010

Cognitive aging describes the changes in mental abilities that occur with increasing age. Although experts disagree on the core underlying processes involved, one factor that links many factors associated with cognitive aging is neuroinflammation. Markers of inflammation are associated directly with deficits in cognitive function and with diseases that are risk factors for cognitive decline. Neuroinflammation is also associated with depression and may account for the complex interaction of depression and cognition in older adults. Interventions that reduce inflammation may improve cognition. Understanding how neuroinflammation affects cognition may provide directions for useful interventions to prevent or treat cognitive decline in older adults. © 2010 Springer Science+Business Media, LLC. Source


Pette G.A.,Nova Southeastern University
The International journal of oral & maxillofacial implants | Year: 2012

Cone beam computed tomography (CBCT) is a three-dimensional radiographic technique used in planning implant therapy to help clinicians determine the volume and dimension of bone available for implant placement, and CBCT images potentially depict coincident findings. Three hundred eighteen patients received CBCT scans prior to receiving implants, which were interpreted by blinded board-certified oral and maxillofacial radiologists. All incidental findings were defined as non-tooth-related pathologies or abnormalities. These findings were categorized and analyzed using descriptive statistics. The patients ranged in age from 16 to 91 years (mean age for men, 64.73 ± 15.05 years; for women, 62.47 ± 15.83 years). Controlling for age, men were 2.13 times more likely to have sinus pathology than women. Patients over age 65 were 5.01 times more likely to demonstrate vascular pathology (eg, carotid artery calcification) than patients ages 41 to 65; the likelihood versus patients ages 16 to 40 was 13.39. Women were 2.63 times more likely to display brain pathology (eg, pineal or pituitary calcifications). Controlling for gender, patients ages 41 to 65 were 3.17 times more likely to exhibit condylar pathology (eg, degenerative changes) than patients ages 16 to 40. Similarly, patients above age 65 were 3.53 times more likely to show condylar pathology than patients ages 16 to 40, and women were 1.61 times more likely to have condylar pathology than men. Versus patients ages 16 to 40, patients ages 41 to 65 were 17.69 times more likely to show signs of vertebral pathology (eg, degenerative disc changes) and patients over age 65 were 28.67 times more likely to display vertebral pathology. CBCT scans frequently reveal non-tooth-related pathologies and/or abnormalities in the head and neck region. Therefore, comprehensive review of the entire CBCT image set is necessary. Source


Lymperopoulos A.,Nova Southeastern University | Rengo G.,University of Naples Federico II | Koch W.J.,Temple University
Circulation Research | Year: 2013

Heart failure (HF), the leading cause of death in the western world, develops when a cardiac injury or insult impairs the ability of the heart to pump blood and maintain tissue perfusion. It is characterized by a complex interplay of several neurohormonal mechanisms that become activated in the syndrome to try and sustain cardiac output in the face of decompensating function. Perhaps the most prominent among these neurohormonal mechanisms is the adrenergic (or sympathetic) nervous system (ANS), whose activity and outflow are enormously elevated in HF. Acutely, and if the heart works properly, this activation of the ANS will promptly restore cardiac function. However, if the cardiac insult persists over time, chances are the ANS will not be able to maintain cardiac function, the heart will progress into a state of chronic decompensated HF, and the hyperactive ANS will continue to push the heart to work at a level much higher than the cardiac muscle can handle. From that point on, ANS hyperactivity becomes a major problem in HF, conferring significant toxicity to the failing heart and markedly increasing its morbidity and mortality. The present review discusses the role of the ANS in cardiac physiology and in HF pathophysiology, the mechanisms of regulation of ANS activity and how they go awry in chronic HF, methods of measuring ANS activity in HF, the molecular alterations in heart physiology that occur in HF, along with their pharmacological and therapeutic implications, and, finally, drugs and other therapeutic modalities used in HF treatment that target or affect the ANS and its effects on the failing heart. © 2013 American Heart Association, Inc. Source


Giese M.J.,4148 NW 19th Terrace | Speth R.C.,Nova Southeastern University
Pharmacology and Therapeutics | Year: 2014

The renin-angiotensin system (RAS) is most well-known for its role in regulation and dysregulation of blood pressure as well as fluid and electrolyte homeostasis. Due to its ability to cause cardiovascular disease, the RAS is the target of a multitude of drugs that antagonize its pathophysiological effects. While the "classical" RAS is a systemic hormonal system, there is an increasing awareness of the existence and functional significance of local RASs in a number of organs, e.g., liver, kidney, heart, lungs, reproductive organs, adipose tissue and adrenal. The eye is one of these organs where a compelling body of evidence has demonstrated the presence of a local RAS. Individual components of the RAS have been shown to be present in many structures of the eye and their potential functional significance in ocular disease states is described. Because the eye is one of the most important and complex organs in the body, this review also discusses the implications of dysregulation of the systemic RAS on the pathogenesis of ocular diseases and how pharmacological manipulation of the RAS might lead to novel or adjunctive therapies for ocular disease states. © 2013 Elsevier Inc. All rights reserved. Source


Lymperopoulos A.,Nova Southeastern University
Frontiers in Physiology | Year: 2013

Heart failure (HF), the leading cause of death in the western world, ensues in response to cardiac injury or insult and represents the inability of the heart to adequately pump blood and maintain tissue perfusion. It is characterized by complex interactions of several neurohormonal mechanisms that get activated in the syndrome in order to try and sustain cardiac output in the face of decompensating function. The most prominent among these neurohormonal mechanisms is the adrenergic (or sympathetic) nervous system (ANS), whose activity and outflow are greatly elevated in HF. Acutely, provided that the heart still works properly, this activation of the ANS will promptly restore cardiac function according to the fundamental Frank-Starling law of cardiac function. However, if the cardiac insult persists over time, this law no longer applies and ANS will not be able to sustain cardiac function. This is called decompensated HF, and the hyperactive ANS will continue to "push" the heart to work at a level much higher than the cardiac muscle can handle. From that point on, ANS hyperactivity becomes a major problem in HF, conferring significant toxicity to the failing heart and markedly increasing its morbidity and mortality. The present review discusses the role of the ANS in cardiac physiology and in HF pathophysiology, the mechanisms of regulation of ANS activity and how they go awry in chronic HF, and, finally, the molecular alterations in heart physiology that occur in HF along with their pharmacological and therapeutic implications for the failing heart. © 2013 Lymperopoulos. Source

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