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Three weeks following treatment, mice treated with DC/sIL-4 had sparsely infiltrated islets, with a majority of islets demonstrating no mononuclear cell infiltration or peri-insulitis (Figure 3A & B).

Intriguingly, Pax8 immunostaining also persisted in the majority of islets cells of neonatal animals (Fig.  2A; h).

As indicated in Fig. 2a, b, the majority of islets in animals treated with B 9-23/IFA were minimally inflamed or had mild peri-insulitis.

Importantly, pancreatic islets following 14 days of c-Myc reactivation showed no signs of tumour regression but rather progression of islet tumourigenesis, with the vast majority of islets showing more pronounced invasion (adenocarcinoma).

Finally, we assessed islet viability after electroporation by ethidium bromide incorporation, and found that although electroporation caused a modest increase in the number of non-viable islets, the majority of islets 75-800%) remained impermeable, indicating good viability.

Similar(55)

Although cSN50 treatment eliminated the majority of islet-reactive lymphocytes and facilitated reduction of insulitis, these islet-reactive and invading immune cells did not completely vanish following intense 1- or 4- day delivery of cSN50 peptide via ip injection or osmotic pump, respectively.

As in the angiography literature, the majority of islet cell tumours are hypervascular and will be best seen after intravenous injection of contrast medium.

The study of human islets is hindered by obstacles including difficulty of maintaining islet cells in vitro but within their native complex tissue environment, the intact islet, and difficulty modulating gene expression in a majority of islet cells without significantly damaging islet viability, function and architecture.

Overall, sustained graft survival is achieved in the majority of islet transplant recipients, with >70% of them retaining C-peptide levels, normalized A1C, nearly-absent severe hypoglycemia, and significantly reduced insulin requirements (∼50% from pretransplant dose) at 5 years under the Edmonton Protocol (1, 5).

A majority of the islets from the diabetic mice showed a slightly elevated basal pHi and/or poor recovery from acid/base load.

We conclude that during post-embryonic growth, a majority of the islet's anterior beta-cell mass is produced by the differentiation of post-embryonic progenitors.

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