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Institution

University of Colorado Denver

EducationDenver, Colorado, United States
About: University of Colorado Denver is a education organization based out in Denver, Colorado, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 27444 authors who have published 57213 publications receiving 2539937 citations. The organization is also known as: CU Denver & UCD.


Papers
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Journal ArticleDOI
05 Dec 2007-Allergy
TL;DR: This consensus report recommends strategies that include pharmacological treatment, allergen and trigger avoidance and asthma education that are recommended for clinical practice in Europe as well as in North America.
Abstract: Asthma is the leading chronic disease among children in most industrialized countries. However, the evidence base on specific aspects of pediatric asthma, including therapeutic strategies, is limited and no recent international guidelines have focused exclusively on pediatric asthma. As a result, the European Academy of Allergy and Clinical Immunology and the American Academy of Allergy, Asthma and Immunology nominated expert teams to find a consensus to serve as a guideline for clinical practice in Europe as well as in North America. This consensus report recommends strategies that include pharmacological treatment, allergen and trigger avoidance and asthma education. The report is part of the PRACTALL initiative, which is endorsed by both academies.

560 citations

Journal ArticleDOI
09 Oct 2018-Mbio
TL;DR: The role of complement is tested using a mouse model and it is shown that respiratory disease is significantly reduced in the absence of complement even though viral load is unchanged, suggesting that inhibition of complement signaling might be an effective treatment option following coronavirus infection.
Abstract: Acute respiratory distress syndrome (ARDS) is immune-driven pathologies that are observed in severe cases of severe acute respiratory syndrome coronavirus (SARS-CoV) infection. SARS-CoV emerged in 2002 to 2003 and led to a global outbreak of SARS. As with the outcome of human infection, intranasal infection of C57BL/6J mice with mouse-adapted SARS-CoV results in high-titer virus replication within the lung, induction of inflammatory cytokines and chemokines, and immune cell infiltration within the lung. Using this model, we investigated the role of the complement system during SARS-CoV infection. We observed activation of the complement cascade in the lung as early as day 1 following SARS-CoV infection. To test whether this activation contributed to protective or pathologic outcomes, we utilized mice deficient in C3 (C3–/–), the central component of the complement system. Relative to C57BL/6J control mice, SARS-CoV-infected C3–/– mice exhibited significantly less weight loss and less respiratory dysfunction despite equivalent viral loads in the lung. Significantly fewer neutrophils and inflammatory monocytes were present in the lungs of C3–/– mice than in C56BL/6J controls, and subsequent studies revealed reduced lung pathology and lower cytokine and chemokine levels in both the lungs and the sera of C3–/– mice than in controls. These studies identify the complement system as an important host mediator of SARS-CoV-induced disease and suggest that complement activation regulates a systemic proinflammatory response to SARS-CoV infection. Furthermore, these data suggest that SARS-CoV-mediated disease is largely immune driven and that inhibiting complement signaling after SARS-CoV infection might function as an effective immune therapeutic. IMPORTANCE The complement system is a critical part of host defense to many bacterial, viral, and fungal infections. It works alongside pattern recognition receptors to stimulate host defense systems in advance of activation of the adaptive immune response. In this study, we directly test the role of complement in SARS-CoV pathogenesis using a mouse model and show that respiratory disease is significantly reduced in the absence of complement even though viral load is unchanged. Complement-deficient mice have reduced neutrophilia in their lungs and reduced systemic inflammation, consistent with the observation that SARS-CoV pathogenesis is an immune-driven disease. These data suggest that inhibition of complement signaling might be an effective treatment option following coronavirus infection.

559 citations

Journal ArticleDOI
TL;DR: This guideline is designed to guide screening and clinical care of children with nonalcoholic fatty liver disease and is a management challenge for general pediatric practitioners, subspecialists and for health systems.
Abstract: Nonalcoholic fatty liver disease (NAFLD) is a highly prevalent chronic liver disease that occurs in the setting of insulin resistance and increased adiposity. It has rapidly evolved into the most common liver disease seen in the pediatric population and is a management challenge for general pediatric practitioners, subspecialists, and for health systems. In this guideline, the expert committee on NAFLD reviewed and summarized the available literature, formulating recommendations to guide screening and clinical care of children with NAFLD.

559 citations


Authors

Showing all 27683 results

NameH-indexPapersCitations
Matthew Meyerson194553243726
Charles A. Dinarello1901058139668
Gad Getz189520247560
Gordon B. Mills1871273186451
Jasvinder A. Singh1762382223370
David Haussler172488224960
Donald G. Truhlar1651518157965
Charles M. Perou156573202951
David Cella1561258106402
Bruce D. Walker15577986020
Marco A. Marra153620184684
Thomas E. Starzl150162591704
Marc Humbert1491184100577
Rajesh Kumar1494439140830
Martin J. Blaser147820104104
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20241
202383
2022358
20213,830
20203,913
20193,632