810 research outputs found
Results of an investigation of plate girders. Proc. Highway Research Board, Vol. 41, 1962, Reprint No. 215 (62-17)
Literature survey on stability of plate girders, Lehigh University, (December 1957); Welded Plate Girders Proposal for a research program, June 20, 1955
VP24-Karyopherin alpha binding affinities differ between Ebolavirus species, nfluencing interferon inhibition and VP24 stability
Zaire ebolavirus (EBOV), Bundibugyo ebolavirus (BDBV), and Reston ebolavirus (RESTV) belong to the same genus but exhibit different virulence properties. VP24 protein, a structural protein present in all family members, blocks interferon (IFN) signaling and likely contributes to virulence. Inhibition of IFN signaling by EBOV VP24 (eVP24) involves its interaction with the NPI-1 subfamily of karyopherin alpha (KPNA) nuclear transporters. Here, we evaluated eVP24, BDBV VP24 (bVP24), and RESTV VP24 (rVP24) interactions with three NPI-1 subfamily KPNAs (KPNA1, KPNA5, and KPNA6). Using purified proteins, we demonstrated that each VP24 binds to each of the three NPI-1 KPNAs. bVP24, however, exhibited approximately 10-fold-lower KPNA binding affinity than either eVP24 or rVP24. Cell-based assays also indicate that bVP24 exhibits decreased KPNA interaction, decreased suppression of IFN induced gene expression, and a decreased half-life in transfected cells compared to eVP24 or rVP24. Amino acid sequence alignments between bVP24 and eVP24 also identified residues within and surrounding the previously defined eVP24-KPNA5 binding interface that decrease eVP24-KPNA affinity or bVP24-KPNA affinity. VP24 mutations that lead to reduced KPNA binding affinity also decrease IFN inhibition and shorten VP24 half-lives. These data identify novel functional differences in VP24-KPNA interaction and reveal a novel impact of the VP24-KPNA interaction on VP24 stability. IMPORTANCE The interaction of Ebola virus (EBOV) VP24 protein with host karyopherin alpha (KPNA) proteins blocks type I interferon (IFN) signaling, which is a central component of the host innate immune response to viral infection. Here, we quantitatively compared the interactions of VP24 proteins from EBOV and two members of the Ebolavirus genus, Bundibugyo virus (BDBV) and Reston virus (RESTV). The data reveal lower binding affinity of the BDBV VP24 (bVP24) for KPNAs and demonstrate that the interaction with KPNA modulates inhibition of IFN signaling and VP24 stability. The effect of KPNA interaction on VP24 stability is a novel functional consequence of this virus-host interaction, and the differences identified between viral species may contribute to differences in pathogenesis
Web buckling tests on welded plate girders, Part 3: Tests on plate girders subjected to shear, WRC Bulletin, 64, (September 1960), Reprint No. 165 (60-5)
Web buckling tests on welded plate girders. Overall introduction and part 1: the test girders.WRC Bulletin, 64, (September 1960), Reprint No. 165 (60-5)
Web buckling tests on welded plate girders. Part 4: tests on plate girders subjected to combined bending and shear. WRC Bulletin, 64, (September 1960), Reprint No. 165 (60-5)
Web buckling tests on welded plate girders, Part 2: Tests on plate girders subjected to bending, WRC Bulletin, 64, (September 1960), Reprint No. 165 (60-5)
Instabilities in Josephson Ladders with Current Induced Magnetic Fields
We report on a theoretical analysis, consisting of both numerical and
analytic work, of the stability of synchronization of a ladder array of
Josephson junctions under the influence of current induced magnetic fields.
Surprisingly, we find that as the ratio of the mutual to self inductance of the
cells of the array is increased a region of unstable behavior occurs followed
by reentrant stable synchronization. Analytic work tells us that in order to
understand fully the cause of the observed instabilities the behavior of the
vertical junctions, sometimes ignored in analytic analyses of ladder arrays,
must be taken into account.Comment: RevTeX, 4 pages, 3 figure
Avalanche of Bifurcations and Hysteresis in a Model of Cellular Differentiation
Cellular differentiation in a developping organism is studied via a discrete
bistable reaction-diffusion model. A system of undifferentiated cells is
allowed to receive an inductive signal emenating from its environment.
Depending on the form of the nonlinear reaction kinetics, this signal can
trigger a series of bifurcations in the system. Differentiation starts at the
surface where the signal is received, and cells change type up to a given
distance, or under other conditions, the differentiation process propagates
through the whole domain. When the signal diminishes hysteresis is observed
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