scholarly journals Endochondral Growth Defect and Deployment of Transient Chondrocyte Behaviors Underlie Osteoarthritis Onset in a Natural Murine Model

2016 ◽  
Vol 68 (4) ◽  
pp. 880-891 ◽  
Author(s):  
K. A. Staines ◽  
K. Madi ◽  
S. M. Mirczuk ◽  
S. Parker ◽  
A. Burleigh ◽  
...  
Keyword(s):  
Murine Model ◽  
Growth Defect ◽  
Endochondral Growth

scholarly journals Physiologic Expression of the Candida albicans Pescadillo Homolog Is Required for Virulence in a Murine Model of Hematogenously Disseminated Candidiasis

2012 ◽  
Vol 11 (12) ◽  
pp. 1552-1556 ◽  
Author(s):  
Priya Uppuluri ◽  
Ashok K. Chaturvedi ◽  
Niketa Jani ◽  
Read Pukkila-Worley ◽  
Carlos Monteagudo ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Murine Model ◽  
Critical Role ◽  
Growth Defect ◽  
Mammalian Host ◽  
Developmental Cycle ◽  
Yeast Growth ◽  
Content Type ◽  
Disseminated Candidiasis

ABSTRACT Morphogenetic conversions contribute to the pathogenesis of Candida albicans invasive infections. Many studies to date have convincingly demonstrated a link between filamentation and virulence; however, relatively little is known regarding the role of the filament-to-yeast transition during the pathogenesis of invasive candidiasis. We previously identified the C. albicans pescadillo homolog ( PES1 ) as essential during yeast growth and growth of lateral yeast on hyphae but not during hyphal growth. Furthermore, we demonstrated that PES1 is required for virulence in vivo in a Galleria mellonella larva model of candidiasis. Here, we have used a regulatable tetO-PES1 / pes1 strain to assess the contribution of C. albicans PES1 to pathogenesis in the commonly used and clinically relevant murine model of hematogenously disseminated candidiasis. Our results indicate that a physiologically controlled level of PES1 expression is required for full virulence in this animal model, with virulence defects observed both when PES1 is overexpressed and and when it is depleted. The pathogenetic defect of cells depleted of PES1 is not due to a general growth defect, as demonstrated by the fact that PES1 -depleted cells still kill Caenorhabditis elegans as efficiently as the wild type due to hyphal outgrowth through worm tissues. Our results suggest a critical role of lateral yeast growth in the ability of C. albicans to normally proliferate within tissues, as well as a pivotal role for Pes1 in the normal developmental cycle of C. albicans within the mammalian host during infection.

scholarly journals STR/ORT mice exhibit an inherent endochondral growth defect and redeploy transient chondrocyte behaviours prior to osteoarthritis onset

2014 ◽  
Vol 22 ◽  
pp. S357
Author(s):  
K.A. Staines ◽  
S. Parker ◽  
B. Poulet ◽  
S. Mirczuk ◽  
R.C. Fowkes ◽  
...  
Keyword(s):  
Growth Defect ◽  
Endochondral Growth

Anti-OX40ligand treatment as a novel therapeutic strategy in a murine model of colitis

2001 ◽  
Vol 120 (5) ◽  
pp. A685-A685
Author(s):  
B SINGH ◽  
V MALMSTROM ◽  
F POWRIE
Keyword(s):  
Murine Model ◽  
Therapeutic Strategy ◽  
Novel Therapeutic

404: Immune Mediated Survival Advantage and Primary Tumor Control of Cryoablation Compared to Nephrectomy in a Murine Model of Advanced Renal Cancer

2006 ◽  
Vol 175 (4S) ◽  
pp. 132-132 ◽  
Author(s):  
Sean P. Hedican ◽  
Eric R. Wilkinson ◽  
Thomas F. Warner ◽  
Fred T. Lee ◽  
Stephen Y. Nakada
Keyword(s):  
Renal Cancer ◽  
Murine Model ◽  
Primary Tumor ◽  
Survival Advantage ◽  
Tumor Control ◽  
Advanced Renal Cancer ◽  
Immune Mediated
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