R
R.C. Strunk
Researcher at Washington University in St. Louis
Publications - 14
Citations - 1787
R.C. Strunk is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Asthma & Complement factor B. The author has an hindex of 10, co-authored 14 publications receiving 1724 citations. Previous affiliations of R.C. Strunk include Jewish Hospital & Johns Hopkins University.
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Journal ArticleDOI
Long-term effects of budesonide or nedocromil in children with asthma.
Stanley J. Szefler,Scott T. Weiss,James Tonascia,N. Franklin Adkinson,Bruce G. Bender,Reuben M. Cherniack,Michele Donithan,H William Kelly,J. Reisman,Gail G. Shapiro,Alice L. Sternberg,R.C. Strunk,Virginia S. Taggart,Mark L. Van Natta,Robert A. Wise,Margaret Wu,Robert S. Zeiger +16 more
TL;DR: In children with mild-to-moderate asthma, neither budesonide nor nedocromil is better than placebo in terms of lung function, but inhaled budesonides improves airway responsiveness and provides better control of asthma than placebo or nedOCromil.
Iconographies supplémentaires de l'article : Decreased response to inhaled steroids in overweight and obese asthmatic children
TL;DR: Compared with children of normal weight, overweight/obese children in the Childhood Asthma Management Program showed a decreased response to inhaled budesonide on measures of lung function and emergency department visits/hospitalizations for asthma.
Journal ArticleDOI
gamma-Interferon increases expression of class III complement genes C2 and factor B in human monocytes and in murine fibroblasts transfected with human C2 and factor B genes.
TL;DR: Recombinant IFN-gamma increased the synthesis of C2 and factor B in primary cultures of human mononuclear phagocytes and in murine fibroblasts transfected with cosmid DNA bearing the human C2and factor B genes.
Journal ArticleDOI
C1 inhibitor hinge region mutations produce dysfunction by different mechanisms.
A E Davis rd,K. S. Aulak,Richard B. Parad,H P Stecklein,Eric Eldering,C E Hack,J Kramer,R.C. Strunk,John J. Bissler,F S Rosen +9 more
TL;DR: A “hinge” region mutation in C1 inhibitor with a Val to Glu replacement is identified at P14 Val–432, resulting in dysfunction by different mechanisms: in one (P14 Val→Glu), the inhibitor is converted to a substrate, while in the other (P10 Ala→Thr), interaction with target protease is blocked.
Journal ArticleDOI
Dysfunctional C1 inhibitor Ta: deletion of Lys-251 results in acquisition of an N-glycosylation site.
TL;DR: The deletion of nucleotides encoding Lys-251 (AAG) in C1 inhibitor Ta, the dysfunctional C1 inhibitors from a family with type II hereditary angioneurotic edema, is described and it is suggested that this deletion creates a new glycosylation site on SDS/PAGE and very likely interferes with protein function.