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Springfield, IL, United States

The University of Illinois at Springfield is a public university in Springfield, Illinois, United States. The university was established in 1969 as Sangamon State University by the Illinois General Assembly and became a part of the University of Illinois system on July 1, 1995. As a public liberal arts college, and the newest campus in the University of Illinois system, UIS is a member of the Council of Public Liberal Arts Colleges. UIS is also part of the American Association of State Colleges and Universities and the American Council on Education. The campus' main repository, Brookens Library, holds a collection of nearly 800,000 books and serials- in addition to accessible resources at the University of Illinois at Chicago and University of Illinois at Urbana-Champaign campuses.The University of Illinois at Springfield serves roughly 5,700 students in 23 undergraduate programs, 20 master's programs, and a doctorate in Public Administration. The university was once one of the two upper-division and graduate universities in Illinois, but now accepts freshmen, transfer and graduate students. Wikipedia.


Elble R.J.,University of Illinois at Springfield
Current Neurology and Neuroscience Reports | Year: 2013

Classic essential tremor is a clinical syndrome of action tremor in the upper limbs (at least 95 % of patients) and less commonly the head, face/jaw, voice, tongue, trunk, and lower limbs, in the absence of other neurologic signs. However, the longstanding notion that essential tremor is a monosymptomatic tremor disorder is being challenged by a growing literature describing associated disturbances of tandem walking, personality, mood, hearing, and cognition. There is also epidemiologic, pathologic, and genetic evidence that essential tremor is pathophysiologically heterogeneous. Misdiagnosis of essential tremor is common because clinicians frequently overlook other neurologic signs and because action tremor in the hands is caused by many conditions, including dystonia, Parkinson disease, and drug-induced tremor. Thus, essential tremor is nothing more than a syndrome of idiopathic tremulousness, and the challenge for researchers and clinicians is to find specific etiologies of this syndrome. © 2013 Springer Science+Business Media New York. Source


Brewer G.J.,University of Illinois at Springfield
Experimental Gerontology | Year: 2010

Harman's free radical theory of aging posits that oxidized macromolecules accumulate with age to decrease function and shorten life-span. However, nutritional and genetic interventions to boost anti-oxidants have generally failed to increase life-span. Furthermore, the free radical theory fails to explain why exercise causes higher levels of oxyradical damage, but generally promotes healthy aging. The separate anti-aging paradigms of genetic or caloric reductions in the insulin signaling pathway is thought to slow the rate of living to reduce metabolism, but recent evidence from Westbrook and Bartke suggests metabolism actually increases in long-lived mice. To unify these disparate theories and data, here, we propose the epigenetic oxidative redox shift (EORS) theory of aging. According to EORS, sedentary behavior associated with age triggers an oxidized redox shift and impaired mitochondrial function. In order to maintain resting energy levels, aerobic glycolysis is upregulated by redox-sensitive transcription factors. As emphasized by DeGrey, the need to supply NAD+ for glucose oxidation and maintain redox balance with impaired mitochondrial NADH oxidoreductase requires the upregulation of other oxidoreductases. In contrast to the 2% inefficiency of mitochondrial reduction of oxygen to the oxyradical, these other oxidoreductases enable glycolytic energy production with a deleterious 100% efficiency in generating oxyradicals. To avoid this catastrophic cycle, lactate dehydrogenase is upregulated at the expense of lactic acid acidosis. This metabolic shift is epigenetically enforced, as is insulin resistance to reduce mitochondrial turnover. The low mitochondrial capacity for efficient production of energy reinforces a downward spiral of more sedentary behavior leading to accelerated aging, increased organ failure with stress, impaired immune and vascular functions and brain aging. Several steps in the pathway are amenable to reversal for exit from the vicious cycle of EORS. Examples from our work in the aging rodent brain as well as other aging models are provided. © 2010 Elsevier Inc. All rights reserved. Source


Bartke A.,University of Illinois at Springfield
Trends in Endocrinology and Metabolism | Year: 2011

Growth hormone (GH) affects somatic growth, sexual maturation, body composition and metabolism, as well as aging and longevity. Mice lacking GH or GH receptor outlive their normal siblings and exhibit symptoms of delayed aging associated with improved insulin signaling and increased stress resistance. Beneficial effects of eliminating the actions of GH are counterintuitive but conform to the concept of antagonistic pleiotropy. Evolutionary selection for traits promoting early-life fitness and reproductive success could account for post-reproductive deficits. Reciprocal relationships between GH signaling and longevity discovered in mutant mice apply also to normal mice, other mammalian species, and perhaps humans. This review summarizes the present understanding of the multifaceted relationship between somatotropic signaling and mammalian aging. © 2011. Source


Bartke A.,University of Illinois at Springfield
Experimental Gerontology | Year: 2011

Longevity of mice can be increased by spontaneous or experimentally induced mutations that interfere with the biosynthesis or actions of growth hormone (GH), insulin-like growth factor 1 (IGF-1), or insulin in the adipose tissue. The effects of GH resistance and deficiency of GH (along with thyrotropin and prolactin) on aging and lifespan are the most pronounced and best established of these mutations. Potential mechanisms linking these endocrine deficits with delayed aging and extended longevity include increased stress resistance, alterations in insulin and mammalian target of rapamycin (mTOR) signaling and metabolic adjustments.Physiological relationships deduced from the extreme phenotypes of long-lived mouse mutants appear to apply broadly, encompassing genetically normal ("wild-type") mice and other mammalian species. The role of GH in the control of human aging continues to be hotly debated, but recent data indicate that reduced somatotropic signaling provides protection from cancer and other age-related diseases and may promote old age survival. © 2010 Elsevier Inc. Source


The reproducibility of pre-clinical research is an important concern that is now being voiced by constituencies that include the National Institutes of Health, the pharmaceutical industry, Congress, the public and the scientific community. An important facet of performing and publishing well-controlled reproducible pre-clinical research is to stabilize and more completely define the environment of the animal subjects. Scientists who use rodents in research generally recognize the importance of maintaining a stable animal environment. However, despite a theoretical and general awareness of these issues, many may lack a true appreciation of how significantly even seemingly minor variations in the environment can affect research outcomes. The purpose of this article is to help investigators gain a more comprehensive and substantiated understanding of the potentially significant impact of even seemingly minor environmental changes on the animals and the data. An important caveat to this article is that the examples presented were selected from a very large literature, admittedly in order to illustrate certain points. The goal of this article is not to provide an overview of the entire literature on how the environment affects rodents but rather to make preclinical scientists more aware of how these factors can potentially influence the experimental data and contribute to poor reproducibility of research. © 2015. Source

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