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Cincinnati, OH, United States

The University of Cincinnati is a comprehensive public research university in Cincinnati, in the U.S. state of Ohio, and a part of the University System of Ohio.Founded in 1819 as Cincinnati College, it is the oldest institution of higher education in Cincinnati and has an annual enrollment of over 40,000 students, making it the second largest university in Ohio and one of the 50 largest universities in the United States. In the 2010 survey by Times Higher Education , the university was ranked in the top 100 universities in North America and as one of the top 200 in the world. Beginning with the 2011 edition of US News and World Report Best Colleges rankings, the University of Cincinnati has been ranked as a Tier One university, ranking as the 129th best overall university and 63rd best public university in the 2015 rankings. This includes being the number 3 ranked university in the nation in the "Up-and-Coming" National Universities section of the 2014 edition. In 2011-2012 academic year the Leiden University ranking put the University of Cincinnati at the 93rd place globally and at the 63rd place in North America by the proportion of top-cited publications. In 2014, US News and World Report ranked UC in the Top-200 of universities worldwide.The university garners nearly $500 million per annum in research funding, ranking 22nd among public universities in the US. Numerous programs across the university are nationally ranked, including: aerospace engineering, anthropology, architecture, classics, composition, conducting, cooperative education, criminal justice, design, environmental science, law, medicine, music, musical theater, neurology, opera, otolaryngology, paleontology, pediatrics, and pharmacy.The school offers over 100 bachelor degrees, over 300 degree granting programs, and over 600 total programs of study, ranging from certificates to doctoral and first professional education. With an economic impact of over $3.5 billion per year, it is the largest single employer in Greater Cincinnati. After extensive renovations through the implementation of the 1989 Master Plan, the university has been recognized by campus planners and architects as one of the most distinguished campus settings in the world. Wikipedia.


Grossman A.W.,University of Cincinnati
Annals of neurology | Year: 2013

We review recent advances in the treatment and prevention of acute ischemic stroke, including the current state of endovascular therapy, in light of 5 randomized controlled trials published this past year. Although no benefit of endovascular therapy over intravenous (IV) recombinant tissue plasminogen activator (rt-PA) has been demonstrated, endovascular therapy is an appropriate treatment for acute ischemic stroke patients within the t-PA window who are ineligible for IV t-PA but have a large vascular occlusion. These trials reveal promises and current limitations of endovascular therapy, and comparison of reperfusion therapies remains an important area of research. One common theme is the strong association between a faster time to reperfusion, improved outcome, and reduced mortality. Primary and secondary stroke prevention trials emphasize the importance of aggressive management of medical risk factors as part of any preventative strategy. New oral anticoagulants, for example, offer cost-effective risk reduction in patients with atrial fibrillation, and may represent an opportunity for those with cryptogenic stroke. We highlight areas of unmet need and promising research in stroke, including the need to deliver proven therapies to more patients, and the need to recruit patients into clinical trials that better define the role of endovascular and other stroke therapies. Finally, improvement in strategies to recover speech, cognition, and motor function has the potential to benefit far more stroke patients than any acute stroke therapy, and represents the greatest opportunity for research in the coming century. Copyright © 2013 American Neurological Association. Source


Ho S.-M.,University of Cincinnati
Journal of Allergy and Clinical Immunology | Year: 2010

Asthma, a chronic inflammatory disorder of the airway, is influenced by interplay between genetic and environmental factors now known to be mediated by epigenetics. Aberrant DNA methylation, altered histone modifications, specific microRNA expression, and other chromatin alterations orchestrate a complex early-life reprogramming of immune T-cell response, dendritic cell function, macrophage activation, and a breach of airway epithelial barrier that dictates asthma risk and severity in later life. Adult-onset asthma is under analogous regulation. The sharp increase in asthma prevalence over the past 2 or 3 decades and the large variations among populations of similar racial/ethnic background but different environmental exposures favors a strong contribution of environmental factors. This review addresses the fundamental question of whether environmental influences on asthma risk, severity, and steroid resistance are partly due to differential epigenetic modulations. Current knowledge on the epigenetic effects of tobacco smoke, microbial allergens, oxidants, airborne particulate matter, diesel exhaust particles, polycyclic aromatic hydrocarbons, dietary methyl donors and other nutritional factors, and dust mites is discussed. Exciting findings have been generated by rapid technological advances and well-designed experimental and population studies. The discovery and validation of epigenetic biomarkers linked to exposure, asthma, or both might lead to better epigenotyping of risk, prognosis, treatment prediction, and development of novel therapies. © 2010 American Academy of Allergy, Asthma & Immunology. Source


Butler D.L.,University of Cincinnati
Nature protocols | Year: 2010

Tendon and ligament injuries are significant contributors to musculoskeletal injuries. Unfortunately, traditional methods of repair are not uniformly successful and can require revision surgery. Our research is focused on identifying appropriate animal injury models and using tissue-engineered constructs (TECs) from bone-marrow-derived mesenchymal stem cells and collagen scaffolds. Critical to this effort has been the development of functional tissue engineering (FTE). We first determine the in vivo mechanical environment acting on the tissue and then precondition the TECs in culture with aspects of these mechanical signals to improve repair outcome significantly. We describe here a detailed protocol for conducting several complete iterations around our FTE 'road map.' The in vitro portion, from bone marrow harvest to TEC collection, takes 54 d. The in vivo portion, from TEC implantation to limb harvest, takes 84 d. One complete loop around the tissue engineering road map, as presented here, takes 138 d to complete. Source


Lam C.K.,University of Cincinnati
Circulation research | Year: 2013

Ischemic heart disease is characterized by contractile dysfunction and increased cardiomyocyte death, induced by necrosis and apoptosis. Increased cell survival after an ischemic insult is critical and depends on several cellular pathways, which have not been fully elucidated. To test the hypothesis that the anti-apoptotic hematopoietic lineage substrate-1-associated protein X-1 (HAX-1), recently identified as regulator of cardiac Ca cycling, also may ameliorate cellular injury with an ischemic insult. We report that cardiac ischemia/reperfusion injury is associated with significant decreases in HAX-1 levels ex vivo and in vivo. Accordingly, overexpression of HAX-1 improved contractile recovery, coupled with reduced infarct size, plasma troponin I level, and apoptosis. The beneficial effects were associated with decreased endoplasmic reticulum (ER) stress response through specific inhibition of the inositol-requiring enzyme (IRE-1) signaling pathway, including its downstream effectors caspase-12 and the transcription factor C/EBP homologous protein. Conversely, HAX-1 heterozygous-deficient hearts exhibited increases in infarct size and IRE-1 activity. The inhibitory effects of HAX-1 were mediated by its binding to the N-terminal fragment of the heat shock protein 90 (Hsp90). Moreover, HAX-1 sequestered Hsp90 from IRE-1 to the phospholamban-sarcoplasmic/endoplasmic reticulum calcium ATPase complex. The HAX-1 regulation was further supported by loss of IRE-1 inhibition in presence of the Hsp90 inhibitor, 17-N-allylamino-17-demethoxygeldanamycin. Cardiac ischemia-reperfusion injury is associated with decreases in HAX-1 levels. Consequently, overexpression of HAX-1 promotes cardiomyocyte survival, mediated by its interaction with Hsp90 and specific inhibition of IRE-1 signaling at the ER/sarcoplasmic reticulum. Source


For over a half century, criminology has been dominated by a paradigm-adolescence-limited criminology (ALC)-that has privileged the use of self-report surveys of adolescents to test sociological theories of criminal behavior and has embraced the view that "nothing works" to control crime. Although ALC has created knowledge, opposed injustice, and advanced scholars' careers, it has outlived its utility. The time has come for criminologists to choose a different future. Thus, a new paradigm is needed that is rooted in life-course criminology, brings criminologists closer to offenders and to the crime event, prioritizes the organization of knowledge, and produces scientific knowledge that is capable of improving offenders' lives and reducing crime. © 2011 American Society of Criminology. Source

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