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Institution

Rush University Medical Center

HealthcareChicago, Illinois, United States
About: Rush University Medical Center is a healthcare organization based out in Chicago, Illinois, United States. It is known for research contribution in the topics: Population & Dementia. The organization has 13915 authors who have published 29027 publications receiving 1379216 citations. The organization is also known as: Rush Presbyterian St. Luke's Medical Center.


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Journal ArticleDOI
TL;DR: Current understanding of ICAM‐1 gene regulation is summarized with a particular emphasis on the transcription factors and signal transduction pathways critical for the cell type‐ and stimulus‐specific activation of IC AM‐1 Gene transcription.
Abstract: Intercellular adhesion molecule-1 (ICAM-1, CD54) is an inducible cell adhesion glycoprotein of the immunoglobulin supergene family expressed on the surface of a wide variety of cell types. ICAM-1 interactions with the beta2 integrins CD11a/CD18 (LFA-1) and CD11b/CD18 (MAC-1) on the surface of leukocytes are important for their transendothelial migration to sites of inflammation and their function as costimulatory molecules for T cell activation. ICAM-1 is constitutively expressed on the cell surface and is up-regulated in response to a variety of inflammatory mediators, including proinflammatory cytokines, hormones, cellular stresses, and virus infection. These stimuli increase ICAM-1 expression primarily through activation of ICAM-1 gene transcription. During the past decade much has been learned about the cell type- and stimulus-specific transcription of ICAM-1. The architecture of the ICAM-1 promoter is complex, containing a large number of binding sites for inducible transcription factors, the most important of which is nuclear factor-kappa B (NF-kappaB). NF-kappaB acts in concert with other transcription factors and co-activators via specific protein-protein interactions, which facilitate the assembly of distinct stereospecific transcription complexes on the ICAM-1 promoter. These transcription complexes presumably mediate the induction of ICAM-1 expression in different cell types and in response to different stimuli. In this review, we summarize our current understanding of ICAM-1 gene regulation with a particular emphasis on the transcription factors and signal transduction pathways critical for the cell type- and stimulus-specific activation of ICAM-1 gene transcription.

540 citations

Journal ArticleDOI
Francine E. Garrett-Bakelman1, Francine E. Garrett-Bakelman2, Manjula Darshi3, Stefan J. Green4, Ruben C. Gur5, Ling Lin6, Brandon R. Macias, Miles J. McKenna7, Cem Meydan2, Tejaswini Mishra6, Jad Nasrini5, Brian D. Piening8, Brian D. Piening6, Lindsay F. Rizzardi9, Kumar Sharma3, Jamila H. Siamwala10, Jamila H. Siamwala11, Lynn Taylor7, Martha Hotz Vitaterna12, Maryam Afkarian13, Ebrahim Afshinnekoo2, Sara Ahadi6, Aditya Ambati6, Maneesh Arya, Daniela Bezdan2, Colin M. Callahan9, Songjie Chen6, Augustine M.K. Choi2, George E. Chlipala4, Kévin Contrepois6, Marisa Covington, Brian Crucian, Immaculata De Vivo14, David F. Dinges5, Douglas J. Ebert, Jason I. Feinberg9, Jorge Gandara2, Kerry George, John Goutsias9, George Grills2, Alan R. Hargens10, Martina Heer15, Martina Heer16, Ryan P. Hillary6, Andrew N. Hoofnagle17, Vivian Hook10, Garrett Jenkinson9, Garrett Jenkinson18, Peng Jiang12, Ali Keshavarzian19, Steven S. Laurie, Brittany Lee-McMullen6, Sarah B. Lumpkins, Matthew MacKay2, Mark Maienschein-Cline4, Ari Melnick2, Tyler M. Moore5, Kiichi Nakahira2, Hemal H. Patel10, Robert Pietrzyk, Varsha Rao6, Rintaro Saito10, Rintaro Saito20, Denis Salins6, Jan M. Schilling10, Dorothy D. Sears10, Caroline Sheridan2, Michael B. Stenger, Rakel Tryggvadottir9, Alexander E. Urban6, Tomas Vaisar17, Benjamin Van Espen10, Jing Zhang6, Michael G. Ziegler10, Sara R. Zwart21, John B. Charles, Craig E. Kundrot, Graham B. I. Scott22, Susan M. Bailey7, Mathias Basner5, Andrew P. Feinberg9, Stuart M. C. Lee, Christopher E. Mason, Emmanuel Mignot6, Brinda K. Rana10, Scott M. Smith, Michael Snyder6, Fred W. Turek11, Fred W. Turek12 
12 Apr 2019-Science
TL;DR: Given that the majority of the biological and human health variables remained stable, or returned to baseline, after a 340-day space mission, these data suggest that human health can be mostly sustained over this duration of spaceflight.
Abstract: INTRODUCTION To date, 559 humans have been flown into space, but long-duration (>300 days) missions are rare (n = 8 total). Long-duration missions that will take humans to Mars and beyond are planned by public and private entities for the 2020s and 2030s; therefore, comprehensive studies are needed now to assess the impact of long-duration spaceflight on the human body, brain, and overall physiology. The space environment is made harsh and challenging by multiple factors, including confinement, isolation, and exposure to environmental stressors such as microgravity, radiation, and noise. The selection of one of a pair of monozygotic (identical) twin astronauts for NASA’s first 1-year mission enabled us to compare the impact of the spaceflight environment on one twin to the simultaneous impact of the Earth environment on a genetically matched subject. RATIONALE The known impacts of the spaceflight environment on human health and performance, physiology, and cellular and molecular processes are numerous and include bone density loss, effects on cognitive performance, microbial shifts, and alterations in gene regulation. However, previous studies collected very limited data, did not integrate simultaneous effects on multiple systems and data types in the same subject, or were restricted to 6-month missions. Measurement of the same variables in an astronaut on a year-long mission and in his Earth-bound twin indicated the biological measures that might be used to determine the effects of spaceflight. Presented here is an integrated longitudinal, multidimensional description of the effects of a 340-day mission onboard the International Space Station. RESULTS Physiological, telomeric, transcriptomic, epigenetic, proteomic, metabolomic, immune, microbiomic, cardiovascular, vision-related, and cognitive data were collected over 25 months. Some biological functions were not significantly affected by spaceflight, including the immune response (T cell receptor repertoire) to the first test of a vaccination in flight. However, significant changes in multiple data types were observed in association with the spaceflight period; the majority of these eventually returned to a preflight state within the time period of the study. These included changes in telomere length, gene regulation measured in both epigenetic and transcriptional data, gut microbiome composition, body weight, carotid artery dimensions, subfoveal choroidal thickness and peripapillary total retinal thickness, and serum metabolites. In addition, some factors were significantly affected by the stress of returning to Earth, including inflammation cytokines and immune response gene networks, as well as cognitive performance. For a few measures, persistent changes were observed even after 6 months on Earth, including some genes’ expression levels, increased DNA damage from chromosomal inversions, increased numbers of short telomeres, and attenuated cognitive function. CONCLUSION Given that the majority of the biological and human health variables remained stable, or returned to baseline, after a 340-day space mission, these data suggest that human health can be mostly sustained over this duration of spaceflight. The persistence of the molecular changes (e.g., gene expression) and the extrapolation of the identified risk factors for longer missions (>1 year) remain estimates and should be demonstrated with these measures in future astronauts. Finally, changes described in this study highlight pathways and mechanisms that may be vulnerable to spaceflight and may require safeguards for longer space missions; thus, they serve as a guide for targeted countermeasures or monitoring during future missions.

538 citations

Journal ArticleDOI
TL;DR: The objective of this review was to update evidence‐based medicine recommendations for treating motor symptoms of Parkinson's disease with new recommendations for treatment of central nervous system symptoms.
Abstract: Objective The objective of this review was to update evidence-based medicine recommendations for treating motor symptoms of Parkinson's disease (PD). Background The Movement Disorder Society Evidence-Based Medicine Committee recommendations for treatments of PD were first published in 2002 and updated in 2011, and we continued the review to December 31, 2016. Methods Level I studies of interventions for motor symptoms were reviewed. Criteria for inclusion and quality scoring were as previously reported. Five clinical indications were considered, and conclusions regarding the implications for clinical practice are reported. Results A total of 143 new studies qualified. There are no clinically useful interventions to prevent/delay disease progression. For monotherapy of early PD, nonergot dopamine agonists, oral levodopa preparations, selegiline, and rasagiline are clinically useful. For adjunct therapy in early/stable PD, nonergot dopamine agonists, rasagiline, and zonisamide are clinically useful. For adjunct therapy in optimized PD for general or specific motor symptoms including gait, rivastigmine is possibly useful and physiotherapy is clinically useful; exercise-based movement strategy training and formalized patterned exercises are possibly useful. There are no new studies and no changes in the conclusions for the prevention/delay of motor complications. For treating motor fluctuations, most nonergot dopamine agonists, pergolide, levodopa ER, levodopa intestinal infusion, entacapone, opicapone, rasagiline, zonisamide, safinamide, and bilateral STN and GPi DBS are clinically useful. For dyskinesia, amantadine, clozapine, and bilateral STN DBS and GPi DBS are clinically useful. Conclusions The options for treating PD symptoms continues to expand. These recommendations allow the treating physician to determine which intervention to recommend to an individual patient. © 2018 International Parkinson and Movement Disorder Society.

538 citations

Journal ArticleDOI
01 Sep 1984-Sleep
TL;DR: For 24 subjects of this sample, who occupied both major body positions during the evaluation night, the apnea index was found to be twice as high during the time spent sleeping on their backs as it was when they slept in the side position, suggesting sleep position adjustment may be a viable treatment for some nonobese sleep apnea patients.
Abstract: Thirty male patients evaluated sequentially for sleep apnea syndrome by all-night clinical polysomnography were compared for apnea plus hypopnea index (A + HI) during the time in the side versus time in the back sleep posture. For 24 subjects of this sample, who occupied both major body positions during the evaluation night, the apnea index was found to be twice as high during the time spent sleeping on their backs as it was when they slept in the side position. This difference is reliable and inversely related to obesity. Five patients meeting diagnostic criteria for sleep apnea on an all-night basis fell within normal limits while in the side sleep position. This suggests sleep position adjustment may be a viable treatment for some nonobese sleep apnea patients.

538 citations

Journal ArticleDOI
TL;DR: The National Alzheimer's Coordinating Center (NACC) is responsible for developing and maintaining a database of participant information collected from the 29 Alzheimer's Disease Centers (ADCs) by developing data collection forms based on Clinical Task Force definitions, a relational database, and a data submission system accessible by all ADCs.
Abstract: The National Alzheimer's Coordinating Center (NACC) is responsible for developing and maintaining a database of participant information collected from the 29 Alzheimer's Disease Centers (ADCs) funded by the National Institute on Aging (NIA). The NIA appointed the ADC Clinical Task Force to determine and define an expanded, standardized clinical data set, called the Uniform Data Set (UDS). The goal of the UDS is to provide ADC researchers a standard set of assessment procedures, collected longitudinally, to better characterize ADC participants with mild Alzheimer disease and mild cognitive impairment in comparison with nondemented controls. NACC implemented the UDS (September 2005) by developing data collection forms for initial and follow-up visits based on Clinical Task Force definitions, a relational database, and a data submission system accessible by all ADCs. The NIA requires ADCs to submit UDS data to NACC for all their Clinical Core participants. Thus, the NACC web site (https://www.alz.washington.edu) was enhanced to provide efficient and secure access data submission and retrieval systems.

536 citations


Authors

Showing all 14032 results

NameH-indexPapersCitations
John Q. Trojanowski2261467213948
Virginia M.-Y. Lee194993148820
Luigi Ferrucci1931601181199
David A. Bennett1671142109844
Todd R. Golub164422201457
David Cella1561258106402
M.-Marsel Mesulam15055890772
John D. E. Gabrieli14248068254
David J. Kupfer141862102498
Clifford B. Saper13640672203
Pasi A. Jänne13668589488
Nikhil C. Munshi13490667349
Martin B. Keller13154165069
Michael E. Thase13192375995
Steven R. Simon129109080331
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202336
2022166
20212,147
20201,939
20191,708
20181,410