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Chicago, IL, United States

Rush University Medical Center is a 676-bed academic medical center that includes hospital facilities for adults and children. It also includes the Johnston R. Bowman Health Center . It is affiliated with Rush University. Rush is a not-for-profit health care, education and research enterprise comprising Rush University Medical Center, Rush University, Rush Oak Park Hospital and Rush Health. Rush University is home to one of the first medical colleges in the midwest and includes one of the nation's top-ranked nursing colleges, as well as graduate programs in allied health, health systems management and biomedical research. Rush also offers more than 70 residency and fellowship programs in medical and surgical specialties and subspecialties. Rush is the largest non-governmental employer on Chicago's West Side and is the 20th largest private sector employer in Chicago, with more than 8,000 employees and a payroll of more than $500 million. Wikipedia.

Rasmussen H.,Rush University Medical Center
Journal of the Academy of Nutrition and Dietetics | Year: 2014

It is the position of the Academy of Nutrition and Dietetics (the Academy) that dietary fat for the healthy adult population should provide 20% to 35% of energy, with an increased consumption of n-3 polyunsaturated fatty acids and limited intake of saturated and trans fats. The Academy recommends a food-based approach through a diet that includes regular consumption of fatty fish, nuts and seeds, lean meats and poultry, low-fat dairy products, vegetables, fruits, whole grains, and legumes. These recommendations are made within the context of rapidly evolving science delineating the influence of dietary fat and specific fatty acids on human health. In addition to fat as a valuable and calorically dense macronutrient with a central role in supplying essential nutrition and supporting healthy body weight, evidence on individual fatty acids and fatty acid groups is emerging as a key factor in nutrition and health. Small variations in the structure of fatty acids within broader categories of fatty acids, such as polyunsaturated and saturated, appear to elicit different physiological functions. The Academy recognizes that scientific knowledge about the effects of dietary fats on human health is young and takes a prudent approach in recommending an increase in fatty acids that benefit health and a reduction in fatty acids shown to increase risk of disease. Registered dietitian nutritionists are uniquely positioned to translate fat and fatty acid research into practical and effective dietary recommendations. © 2014 Academy of Nutrition and Dietetics. Source

Kanner A.M.,Rush University Medical Center
Epilepsia | Year: 2011

A bidirectional relation between depressive disorders and epilepsy has been suggested by several population-based studies and is supported by experimental studies. This article reviews the potential pathogenic mechanisms operant in both disorders that may explain such a relation. These mechanisms include a hyperactive hypothalamic-pituitary-adrenal (HPA) axis and its neuroanatomic and neuropathologic complications, as well as disturbances in serotonergic, noradrenergic, γ-aminobutyric acid (GABA)ergic and glutamatergic neurotransmitter systems, all of which may be interrelated. © 2011 International League Against Epilepsy. Source

Gillespie D.,Rush University Medical Center
Nano Letters | Year: 2012

It is proposed that the layering of large ions at the wall/liquid interface of nanofluidic channels can be used to achieve high efficiency (possibly >50%) in the conversion of hydrostatic energy into electrical power. Large ions tend to produce peaks and troughs in their concentration profiles at charged walls, producing high concentrations far from the walls where the ions' pressure-driven velocity is high. This increases the streaming conductance and the energy conversion efficiency. © 2012 American Chemical Society. Source

Boyle P.A.,Rush University Medical Center
Annals of neurology | Year: 2013

The pathologic indices of Alzheimer disease, cerebrovascular disease, and Lewy body disease accumulate in the brains of older persons with and without dementia, but the extent to which they account for late life cognitive decline remains unknown. We tested the hypothesis that these pathologic indices account for the majority of late life cognitive decline. A total of 856 deceased participants from 2 longitudinal clinical-pathologic studies, Rush Memory and Aging Project and Religious Orders Study, completed a mean of 7.5 annual evaluations, including 17 cognitive tests. Neuropathologic examinations provided quantitative measures of global Alzheimer pathology, amyloid load, tangle density, macroscopic infarcts, microinfarcts, and neocortical Lewy bodies. Random coefficient models were used to examine the linear relation of pathologic indices with global cognitive decline. In subsequent analyses, random change point models were used to examine the relation of the pathologic indices with the onset of terminal decline and rates of preterminal and terminal decline (ie, nonlinear decline). Cognition declined a mean of about 0.11 U per year (estimate = -0.109, standard error [SE] = 0.004, p < 0.001), with significant individual differences in rates of decline; the variance estimate for the individual slopes was 0.013 (SE = 0.112, p < 0.001). In separate analyses, global Alzheimer pathology, amyloid, tangles, macroscopic infarcts, and neocortical Lewy bodies were associated with faster rates of decline and explained 22%, 6%, 34%, 2%, and 8% of the variation in decline, respectively. When analyzed simultaneously, the pathologic indices accounted for a total of 41% of the variation in decline, and the majority remained unexplained. Furthermore, in random change point models examining the influence of the pathologic indices on the onset of terminal decline and the preterminal and terminal components of the cognitive trajectory, the common pathologic indices accounted for less than a third of the variation in the onset of terminal decline and rates of preterminal and terminal decline. The pathologic indices of the common causes of dementia are important determinants of cognitive decline in old age and account for a large proportion of the variation in late life cognitive decline. Surprisingly, however, much of the variation in cognitive decline remains unexplained, suggesting that other important determinants of cognitive decline remain to be identified. Identification of the mechanisms that contribute to the large unexplained proportion of cognitive decline is urgently needed to prevent late life cognitive decline. Copyright © 2013 American Neurological Association. Source

Guo T.,Rush University Medical Center
Circulation research | Year: 2012

In cardiac muscle, Ca(2+)-induced Ca(2+) release (CICR) from the sarcoplasmic reticulum (SR) is mediated by ryanodine receptor (RyR) Ca(2+) release channels. The inherent positive feedback of CICR is normally well-controlled. Understanding this control mechanism is a priority because its malfunction has life-threatening consequences. We show that CICR local control is governed by SR Ca(2+) load, largely because load determines the single RyR current amplitude that drives inter-RyR CICR. We differentially manipulated single RyR Ca(2+) flux amplitude and SR Ca(2+) load in permeabilized ventricular myocytes as an endogenous cell biology model of the heart. Large RyR-permeable organic cations were used to interfere with Ca(2+) conductance through the open RyR pore. Single-channel studies show this attenuates current amplitude without altering other aspects of RyR function. In cells, the same experimental maneuver increased resting SR Ca(2+) load. Despite the increased load, Ca(2+) spark (inter-RyR CICR events) frequency decreased and sparks terminated earlier. Spark local control follows single RyR current amplitude, not simply SR Ca(2+) load. Spark frequency increases with load because spontaneous RyR openings at high loads produce larger currents (ie, a larger CICR trigger signal). Sparks terminate when load falls to the point at which single RyR current amplitude is no longer sufficient to sustain inter-RyR CICR. Thus, RyRs that spontaneously close no longer reopen and local Ca(2+) release ends. Source

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