Sentence examples for model of accelerated from inspiring English sources

We noted a CMP-mediated potentiation of IHPK1 expression (Table S1: Figure S3) and it has been demonstrated that elevated cortical expression of IHPK1 occurs in an in-bred murine model of accelerated aging (senescence-accelerated mouse/prone 8 (SAMP8: [76]).

SAMP mice such as SAMP1, SAMP2, SAMP3, SAMP6, SAMP7, SAMP8, and SAMP9 are widely used as a murine model of accelerated senescence, and senescence-accelerated mouse-resistant (SAMR) mice such as SAMR1 and SAMR2, that reveal normal aging, are used as a control for SAMP mice [ 36, 37].

Using Sirt3-/ mice as a model of accelerated aging, we investigated the effects of Sirt3 deficiency on NETosis and platelet function, aiming to detect enhancement of thrombosis.

This is the first time that 11β-HSD1 inhavetors have been studied in this broadly-used mouse model of accelerated senescence and late-onset Alzheimer's disease.

In order to allow for a comparative evaluation of the in vivo degeneration of biological and tissue-engineered heart valves and vascular grafts, a small animal model of accelerated cardiovascular calcification is desired.

The aim of this study was to produce a model of accelerated muscle aging by inducing expression of the progerin isoform transcript of the lamin A gene (LMNA) in normal human myoblasts.

Their longevities and aging characteristics have been described, and they have been used for studies on environmental manipulations that increase longevity including caloric restriction and temperature reduction, as well as to generate genetic models of accelerated aging.

Among these are empirical and semi-empirical modeling of accelerated stability studies which can be used to predict product shelf-life (Waterman, Pharm Res 24:780–790, 2007; (Wu et al., AAPS Pharm Sci Tech,16:986–991, 2016); (Lavrich, Rapid Development of Robust Stability Models Using Semi-Empirical Design Space, AAPS Webinar, 2016)).

Human and mouse models of accelerated aging frequently involve heritable defects in genome maintenance mechanisms, implicating spontaneous genotoxic stress as an important causal factor in age-related deterioration and death [2].

Because CCL2 has been implicated in development of atherosclerotic lesions and restenosis, we aimed at testing QC/isoQC-inhibitors in a cuff-model of accelerated atherosclerosis in ApoE3*Leiden mice (Lardenoye et al, 2000).

In support of this, genetic crosses with models of accelerated neuropathology failed to induce somatic instability.