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Functional and Metabolomic Consequences of KATP Channel Inactivation in Human Islets.
Li C, Ackermann AM, Boodhansingh KE, Bhatti TR, Liu C, Schug J, Doliba N, Han B, Cosgrove KE, Banerjee I, Matschinsky FM, Nissim I, Kaestner KH, Naji A, Adzick NS, Dunne MJ, Stanley CA, De León DD. Li C, et al. Among authors: dunne mj. Diabetes. 2017 Jul;66(7):1901-1913. doi: 10.2337/db17-0029. Epub 2017 Apr 25. Diabetes. 2017. PMID: 28442472 Free PMC article.
Altered Phenotype of β-Cells and Other Pancreatic Cell Lineages in Patients With Diffuse Congenital Hyperinsulinism in Infancy Caused by Mutations in the ATP-Sensitive K-Channel.
Salisbury RJ, Han B, Jennings RE, Berry AA, Stevens A, Mohamed Z, Sugden SA, De Krijger R, Cross SE, Johnson PP, Newbould M, Cosgrove KE, Hanley KP, Banerjee I, Dunne MJ, Hanley NA. Salisbury RJ, et al. Among authors: dunne mj. Diabetes. 2015 Sep;64(9):3182-8. doi: 10.2337/db14-1202. Epub 2015 Apr 30. Diabetes. 2015. PMID: 25931474 Free PMC article.
Increased plasma incretin concentrations identifies a subset of patients with persistent congenital hyperinsulinism without KATP channel gene defects.
Shi Y, Avatapalle HB, Skae MS, Padidela R, Newbould M, Rigby L, Flanagan SE, Ellard S, Rahier J, Clayton PE, Dunne MJ, Banerjee I, Cosgrove KE. Shi Y, et al. Among authors: dunne mj. J Pediatr. 2015 Jan;166(1):191-4. doi: 10.1016/j.jpeds.2014.09.019. Epub 2014 Oct 23. J Pediatr. 2015. PMID: 25444530 Free article.
Atypical Forms of Congenital Hyperinsulinism in Infancy Are Associated With Mosaic Patterns of Immature Islet Cells.
Han B, Mohamed Z, Estebanez MS, Craigie RJ, Newbould M, Cheesman E, Padidela R, Skae M, Johnson M, Flanagan S, Ellard S, Cosgrove KE, Banerjee I, Dunne MJ. Han B, et al. Among authors: dunne mj. J Clin Endocrinol Metab. 2017 Sep 1;102(9):3261-3267. doi: 10.1210/jc.2017-00158. J Clin Endocrinol Metab. 2017. PMID: 28605545 Free PMC article.
159 results