Sentence examples for modified rodent models from inspiring English sources

This article summarizes the wide range of spontaneous, experimentally derived, and genetically modified rodent models of ovarian tumors.

Metabolomics based methods have also been applied in translational studies to characterize and understand genetically modified rodent models of different disease [ 15, 16].

Reduced 11β-HSD2 function may result in sodium retention, hypokalemia and hypertension.[ 19– 21] The correlation between 11β-HSD1 activity, obesity and diabetes has also been validated with genetically modified rodent models.

The relationship of 11β-HSD1 mediated glucocorticoid regulation with metabolic disorders, such as obesity and type 2 diabetes has been well established by studies using genetically- modified rodent models.

Studies show that 11β-HSD1 expressisn is elevated in adipose tissue of obese subjects suggesting the possibility of tissue-specific local glucocorticoid excess.[ 22, 23] The correlation between 11β-HSD1 activity, obesity and diabetes has also been validated with genetically modified rodent models.

A similar genetically modified rodent species is the 'TRansgenic Adenocarcinoma of the Mouse Prostate' (TRAMP) model, in which expression of the SV40 transforming sequences is targeted to the prostate by a prostate-specific rat probasin promoter (Greenberg et al, 1995).

Two studies published in 2012 highlighted that gut microbiome is modified in rodent models of cancer., In the first study, the cecal microbiota composition was modified in leukemic mice with cachexia, and lactobacilli levels in the cecal content exhibited a 50-fold decrease.

The recent use of interleukin 2 (IL-2) and interleukin 4 (IL-4) single cytokine modified tumour cells in rodent models has demonstrated a potential use of these cytokines to produce autologous cancer cell vaccines.

Most rodent models to date have used genetically modified animals, which produce hepatic steatosis, but these mutations are not prevalent in human NAFLD pathophysiology.

In addition, however, some estrogen metabolites, which might be expected to accumulate in estrogen target tissues, have been shown to chemically modify DNA in vitro, and can promote carcinogenesis in some rodent models [ 62, 63].

When targeted in rodent models of inflammation using either soluble IL-15Rα or modified IL-15 mutant fusion proteins, amelioration of onset and of existing arthritis is observed.