scholarly journals Pure and Hybrid Mice with Finitely Many Woodin Cardinals from Levels of Determinacy Westfälische Wilhelms-Universität Münster, Germany, 2016. Supervised by Ralf-Dieter Schindler

2018 ◽  
Vol 24 (2) ◽  
pp. 198-198
Author(s):  
Sandra Müller
Keyword(s):  
PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e109382 ◽  
Author(s):  
Susan Q. Shen ◽  
Ernest Turro ◽  
Joseph C. Corbo

1989 ◽  
Vol 67 (4) ◽  
pp. 887-894 ◽  
Author(s):  
D. R. Brown ◽  
S. K. DeNise ◽  
R. G. McDaniel
Keyword(s):  

2008 ◽  
Vol 73 (2) ◽  
pp. 369-390 ◽  
Author(s):  
J. R. Steel

In this note we shall proveTheorem 0.1. Letbe a countably ω-iterable-mouse which satisfies AD, and [α, β] a weak gap of. Supposeis captured by mice with iteration strategies in ∣α. Let n be least such that ; then we have that believes that has the Scale Property.This complements the work of [5] on the construction of scales of minimal complexity on sets of reals in K(ℝ). Theorem 0.1 was proved there under the stronger hypothesis that all sets definable over are determined, although without the capturing hypothesis. (See [5, Theorem 4.14].) Unfortunately, this is more determinacy than would be available as an induction hypothesis in a core model induction. The capturing hypothesis, on the other hand, is available in such a situation. Since core model inductions are one of the principal applications of the construction of optimal scales, it is important to prove 0.1 as stated.Our proof will incorporate a number of ideas due to Woodin which figure prominently in the weak gap case of the core model induction. It relies also on the connection between scales and iteration strategies with the Dodd-Jensen property first discovered in [3]. Let be the pointclass at the beginning of the weak gap referred to in 0.1. In section 1, we use Woodin's ideas to construct a Γ-full a mouse having ω Woodin cardinals cofinal in its ordinals, together with an iteration strategy Σ which condenses well in the sense of [4, Def. 1.13]. In section 2, we construct the desired scale from and Σ.


1979 ◽  
Vol 88 (4) ◽  
pp. 1200-1201
Author(s):  
L. D. Udalova
Keyword(s):  

1977 ◽  
Vol 20 (8) ◽  
pp. 1449-1456 ◽  
Author(s):  
Robert B. Zurier ◽  
Ivan Damjanov ◽  
Donna M. Sayadoff ◽  
Naomi F. Rothfield
Keyword(s):  

Viruses ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 674 ◽  
Author(s):  
Chiaho Shih ◽  
Chun-Che Liao ◽  
Ya-Shu Chang ◽  
Szu-Yao Wu ◽  
Chih-Shin Chang ◽  
...  

Enterovirus 71 (EV71) is a global health threat. Children infected with EV71 could develop hand-foot-and-mouth disease (HFMD), encephalitis, paralysis, pulmonary edema, and death. At present, no effective treatment for EV71 is available. We reviewed here various mouse models for EV71 pathogenesis and therapy. Earlier studies relied on the use of mouse-adapted EV71 strains. To avoid artificial mutations arising de novo during the serial passages, recent studies used EV71 clinical isolates without adaptation. Several human receptors for EV71 were shown to facilitate viral entry in cell culture. However, in vivo infection with human SCARB2 receptor transgenic mice appeared to be more limited to certain strains and genotypes of EV71. Efficacy of oral infection in these transgenic models is extremely low. Intriguingly, despite the lack of human receptors, immunodeficient neonatal mouse models can still be infected with EV71 clinical isolates via oral or intraperitoneal routes. Crossbreeding between SCARB2 transgenic and stat1 knockout mice generated a more sensitive and user-friendly hybrid mouse model. Infected hybrid mice developed a higher incidence and earlier onset of CNS disease and death. Different pathogenesis profiles were observed in models deficient in various arms of innate or humoral immunity. These models are being actively used for antiviral research.


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