Prostaglandine1 treatment of NZB/NZWF1 hybrid MICE

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

scholarly journals Hybrid Mice Reveal Parent-of-Origin and Cis- and Trans-Regulatory Effects in the Retina

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e109382 ◽  
Author(s):  
Susan Q. Shen ◽  
Ernest Turro ◽  
Joseph C. Corbo
Keyword(s):  
Parent Of Origin ◽  
Regulatory Effects ◽  
Cis And Trans ◽  
Hybrid Mice

Cytoplasmic Genetic Effects and Growth of Hybrid Mice

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

Sex ratio in CBA X C57BL hybrid mice

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

scholarly journals Immunocompetent and Immunodeficient Mouse Models for Enterovirus 71 Pathogenesis and Therapy

Viruses ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 674 ◽  
Author(s):  
Chiaho Shih ◽  
Chun-Che Liao ◽  
Ya-Shu Chang ◽  
Szu-Yao Wu ◽  
Chih-Shin Chang ◽  
...  
Keyword(s):  
Mouse Models ◽  
Viral Entry ◽  
De Novo ◽  
Enterovirus 71 ◽  
Foot And Mouth Disease ◽  
Clinical Isolates ◽  
Transgenic Models ◽  
User Friendly ◽  
Hybrid Mice

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.

The Renal Changes in NZB/B1 and NZB-NZW F1 Hybrid Mice. Light and Electron Microscopic Studies

Nephron ◽  
1967 ◽  
Vol 4 (4) ◽  
pp. 215-230 ◽  
Author(s):  
J.R. Manaligod ◽  
C.L. Pirani ◽  
F. Miyasato ◽  
V.E. Pollak
Keyword(s):  
Electron Microscopic ◽  
Renal Changes ◽  
Microscopic Studies ◽  
Hybrid Mice

Experimental obesity and osteoarthritis

1960 ◽  
Vol 198 (4) ◽  
pp. 765-770 ◽  
Author(s):  
Leon Sokoloff ◽  
Olaf Mickelsen ◽  
Emanuel Silverstein ◽  
George E. Jay ◽  
Richard S. Yamamoto
Keyword(s):  
Weight Gain ◽  
Dietary Restriction ◽  
High Fat Diet ◽  
Deleterious Effect ◽  
Degenerative Joint Disease ◽  
Fat Content ◽  
Joint Disease ◽  
High Fat ◽  
Low Fat ◽  
Hybrid Mice

Experimental obesity was produced in DBA/2JN, STR/N and C57L/HeN mice as well as in Osborne-Mendel rats by several dietary regimens. One of these, containing 60% vegetable fat, increased the amount of degenerative joint disease in the rats and in two strains of mice. No increase of osteoarthritis occurred as a result of a 37.4% fat content in the diet, or from obesity produced by Ingle's diet, which has a relatively low-fat content. The mechanism by which the high-fat diet increased the joint disease is unknown, because neither obesity nor a high-fat diet alone had a deleterious effect on the articulations of the mice. Obese hybrid mice derived from a spontaneously obese and arthritis-prone strain (STR/1N) were resistant to articular degeneration. Dietary restriction of weight gain in the STR/1N mice failed to decrease the osteoarthritis in them.

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