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Studies in animal models that spontaneously exhibit features of the human syndrome contribute to the identification of causative genes for components of the cardio-metabolic syndrome.
The colon mucus in animal models that spontaneously develop colitis and in patients with active UC allows bacteria to penetrate and reach the epithelium.
Penetration of the mucus layer was observed in animal models that spontaneously developed colitis, as well as in patients with active UC where bacteria were observed to reach the intestinal epithelium.
The use of genetically modified animal models that spontaneously develop gliomas, therefore, seems a powerful approach [ 5, 59] and quite recently the generation of a mouse GBM model in a region- and cell type-specific manner using intracerebral lentiviral transduction was reported [ 92].
We comment here on the peptide P140 able to delay the development of lupus in mouse models that spontaneously develop the disease and that has been evaluated in multicenter double-blind phase IIb clinical trials including lupus patients.
These include mouse models that spontaneously develop mammary tumors, carcinogen-treated mouse models, xenograft models, transgenic mice and gene knockout mice that develop mammary tumors.
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In addition, an animal model that spontaneously develops FSGS is discussed.
Hence, the present study was designed to evaluate the effects of TRC150094 in an animal model that spontaneously displays a phenotype akin to patients with the aforementioned cluster of nontraditional CV risk factors.
In the present study, we have employed obese ZSF1 rats, an animal model that spontaneously develops obesity and dysglycemia as well as an associated clinically relevant constellation of comorbidities.
Thus, for the first time in an animal model that spontaneously establishes LTBI similar to that in human, we show that once bacillary growth is controlled, the sustained upregulation of genes associated with activation of T cells and associated networks is dispensable to maintain latency in the host.
Major insights into the molecular mechanisms of inflammatory arthritis recently emerged from the study of murine models of RA-like disease using genetically deficient or transgenic mice or a combined murine model (K/BxAg7) that spontaneously develops both RA-like disease and atherosclerosis [ 33].
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