Exact(4)
Several of these intestinal Helicobacter spp. are known to induce colitis in mouse models, yet the mechanisms by which these bacteria induce intestinal inflammation are poorly understood.
This may be caused by higher hydrophobicity since two charges are lost during conversion [ 71]. pE-Aβ has been detected in a variety of AD mouse models, yet the time of first appearance during pathology varies strongly between different mouse models – ranging from 2 months in the APP/PS1KI model [ 72], to 16 months in the Tg2576 model [ 73], to 15 months in the APP23 model [ 20].
Accordingly, the LgDel mouse models yet another clinically significant 22q11DS phenotype: dysphagia – and its impact on growth and health.
There is a long-standing association of gastrin with malignant progression in transgenic mouse models, yet clinical conditions associated with hypergastrinaemia in humans, such as the Zollinger Ellison syndrome, result in the development of hyperplasia of enterochromaffin-like (ECL) cells and carcinoid tumours, not GC, suggesting that the role of gastrin is not critical in gastric carcinogenesis.
Similar(56)
A dose of 2 Gy has been shown to accelerate colon carcinogenesis in susceptible mice models, yet the most sensitive time for radiation exposure differs between studies.
More recently, it has been published that Rett patients presented with a less diverse microbiota than healthy subjects [36], which could affect gastrointestinal function, but this possibility has not been explored in the mouse model yet.
The full potential of such mouse models is yet to be realised and further work is required to derive maximum benefit for cancer patients from these initiatives (Frese and Tuveson, 2007).
However, the precise estimates of over-dispersion are expected to be study-specific; it is plausible they would be smaller in inbred mouse models, smaller yet in cell lines.
Nonetheless, after inclusion of more TP53 mutations, combined with alterations in other oncogenic pathways, careful dissection of the impact of genetic background and extensive use of cancer xenografts, mouse models may yet provide a tremendous contribution to the understanding of the role of p53 in breast cancer.
However, a systematic, large-scale study, elucidating global changes in gene expression during disease progression in the Pkd1 -/- mouse model has yet to be reported.
Although a number of animal models present some of the features similar to those seen in human disease, no mouse model as yet has proven to be a good model in which to study the progression from inflammation to ankylosis in the axial skeleton.
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