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Thus, similar to an "hourglass" model for islet growth (Supplementary Fig. 16), the progeny of the "older" embryonic beta-cells ends up within the posterior half of the islet.
We hypothesized that using the Hnf6 Tg mouse as a model for islet dysmorphogenesis would provide an excellent tool for identifying new genes involved in the cellular processes that establish endocrine pancreatic morphology and architecture.
We present a new model for islet formation that accounts for the morphological transformation from embryonic endocrine cord-like structures into distinct spherical islets of various sizes observed in the adult pancreas.
The results from the quantification of beta-cell proliferation and islet development as well as mathematical analysis on the growth regulation has led us to propose a fission model for islet formation in the developing pancreas.
The current model for islet transplantation has been the Edmonton protocol, which requires at least two donors per transplant.
Two clusters, the euglycemia cluster (P < 0.001) and the hypoglycemia cluster (P = 0.001), were significant factors in the logistic model for islet graft function.
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Mice are widely used as models for islet disease, despite marked differences between rodent and primate islet architecture and innervation [ 31– 31].
Isolated pancreatic islets represent a useful model for studying islet function and hormone secretion.
There are over 600 scientific publications where dogs were the preclinical model for human islet transplantation, and in greater than 250 publications, dogs were recipients.
As described, the model of islet dysmorphogenesis used for these studies was islet-specific Hnf6 transgenic over-expression.
For example, in the rodent model of islet injury induced by the streptozotocin injection, both Schwann cells and pericytes become reactive in response to the islet microstructural and vascular damages (Tang et al., 2013, Teitelman et al., 1998).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com