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Chicago Ridge, IL, United States

Loyola University Chicago is a private Jesuit university located in Chicago, Illinois. It was founded by the Roman Catholic Society of Jesus in 1870 under the name of "St. Ignatius College", and has grown to be the largest Jesuit university in the United States with a total enrollment of 15,068 and over 150,000 alumni.Loyola University has six campuses throughout the Chicago metropolitan area, and it also has a permanent overseas campus in Rome, Italy and guest programs in Beijing, China and Ho Chi Minh City, Vietnam. Loyola has twelve undergraduate, graduate, and professional schools offering 71 undergraduate degrees, 85 master's degrees, 31 doctoral degrees, and 26 graduate-level certificate programs.The main campus, the Lake Shore Campus, is located in the Rogers Park and Edgewater neighborhoods of the City of Chicago, located along the shore of Lake Michigan. Loyola University Chicago's intercollegiate sports teams, commonly called the "Loyola Ramblers", compete in National Collegiate Athletic Association Division I and the Missouri Valley Conference. As of 2013, Loyola University is still the only Division I school in the State of Illinois to win a national championship in men's basketball. Wikipedia.


Campbell E.M.,Loyola University Chicago | Hope T.J.,Northwestern University
Nature Reviews Microbiology | Year: 2015

In a mature, infectious HIV-1 virion, the viral genome is housed within a conical capsid core made from the viral capsid (CA) protein. The CA protein and the structure into which it assembles facilitate virtually every step of infection through a series of interactions with multiple host cell factors. This Review describes our understanding of the interactions between the viral capsid core and several cellular factors that enable efficient HIV-1 genome replication, timely core disassembly, nuclear import and the integration of the viral genome into the genome of the target cell. We then discuss how elucidating these interactions can reveal new targets for therapeutic interactions against HIV-1. © 2015 Macmillan Publishers Limited. All rights reserved. Source


Huntsinger J.R.,Loyola University Chicago
Personality and Social Psychology Bulletin | Year: 2014

Four experiments found that positive and negative affect dictated whether primed social categories and trait concepts led to assimilation or contrast. This influence was further found to be flexibly responsive to the momentary activation of a global or local focus. When a global focus was dominant, positive affect resulted in assimilation to primed traits and social categories, and negative affect resulted in contrast. But, when a local focus was dominant, the opposite pattern of assimilation and contrast as a consequence of positive and negative affect was observed. These results are consistent with the more general view that positive and negative affect signal the value of currently accessible response tendencies and are, therefore, flexibly responsive in their influence cognition to changing situations and mental contexts. © 2013 by the Society for Personality and Social Psychology, Inc. Source


Lawson H.A.,University of Washington | Cheverud J.M.,Loyola University Chicago | Wolf J.B.,University of Bath
Nature Reviews Genetics | Year: 2013

Parent-of-origin effects occur when the phenotypic effect of an allele depends on whether it is inherited from the mother or the father. Several phenomena can cause parent-of-origin effects, but the best characterized is parent-of-origin-dependent gene expression associated with genomic imprinting. The development of new mapping approaches applied to the growing abundance of genomic data has demonstrated that imprinted genes can be important contributors to complex trait variation. Therefore, to understand the genetic architecture and evolution of complex traits, including complex diseases and traits of agricultural importance, it is crucial to account for these parent-of-origin effects. Here, we discuss patterns of phenotypic variation associated with imprinting, evidence supporting its role in complex trait variation and approaches for identifying its molecular signatures. © 2013 Macmillan Publishers Limited. All rights reserved. Source


Lukic Z.,Loyola University Chicago
Retrovirology | Year: 2011

The TRIM5 proteins are cellular restriction factors that prevent retroviral infection in a species-specific manner. Multiple experiments indicate that restriction activity requires accessory host factors, including E2-enzymes. To better understand the mechanism of restriction, we conducted yeast-two hybrid screens to identify proteins that bind to two TRIM5 orthologues. The only cDNAs that scored on repeat testing with both TRIM5 orthologues were the proteasome subunit PSMC2 and ubiquitin. Using co-immunoprecipitation assays, we demonstrated an interaction between TRIM5α and PSMC2, as well as numerous other proteasome subunits. Fluorescence microscopy revealed co-localization of proteasomes and TRIM5α cytoplasmic bodies. Forster resonance energy transfer (FRET) analysis indicated that the interaction between TRIM5 and PSMC2 was direct. Previous imaging experiments demonstrated that, when cells are challenged with fluorescently-labeled HIV-1 virions, restrictive TRIM5α orthologues assemble cytoplasmic bodies around incoming virion particles. Following virus challenge, we observed localization of proteasome subunits to rhTRIM5α cytoplasmic bodies that contained fluorescently labeled HIV-1 virions. Taken together, the results presented here suggest that localization of the proteasome to TRIM5α cytoplasmic bodies makes an important contribution to TRIM5α-mediated restriction. Source


Gerding D.N.,Loyola University Chicago
Discovery Medicine | Year: 2013

We are in the midst of a resurgence of Clostridium difficile infection (CDI) in North America and Europe for which morbidity and mortality are higher than ever seen. C. difficile has risen in frequency to become the most common healthcare-associated infection pathogen, exceeding methicillin-resistant Staphylococcus aureus in many hospitals. Protection against CDI is thought to be mediated first by the normal bacterial microbiota, supplemented by an adaptive immune antibody response directed primarily at C. difficile toxins. Treatment of CDI is with antimicrobials that also further disrupt the protective bacterial microbiota leaving the patient susceptible to recurrent CDI. In addition, patients most susceptible to CDI, the advanced elderly, may already have a limited immune response and fail to increase their adaptive immune response with infection. The importance of both of these protective modalities has been demonstrated by 1) the success of fecal microbiota to restore "colonization resistance" for patients with multiple recurrences of CDI, and 2) the marked reduction in CDI recurrences with the use of intravenous monoclonal antibodies directed against toxin A and toxin B as an adjunct to antimicrobial treatment. Anti-toxin vaccines, passive monoclonal anti-toxin antibodies, and non-toxigenic C. difficile (to restore colonization resistance) are already undergoing patient clinical trials. The opportunity to prevent CDI is compelling and future research should focus on understanding the critical elements of the microbiota needed to restore colonization resistance and on development of novel immunologic strategies that include systemic and mucosal vaccines and passive immune modulators. © 2013, Discovery Medicine. Source

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