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  • pancreas
  • The present study demonstrates that adult human pancreatic duct cells can be converted into insulin-expressing cells after ectopic, adenovirus-mediated expression of the class B basic helix-loop-helix factor neurogenin 3 (ngn3), which is a critical factor in embryogenesis of the mouse endocrine pancreas. (semanticscholar.org)
  • These data indicate that the Delta-Notch pathway, which controls embryonic development of the mouse endocrine pancreas, can also operate in adult human duct cells driving them to a neuroendocrine phenotype with the formation of insulin-expressing cells. (semanticscholar.org)
  • Key events of pancreas formation are triggered in gut endoderm by ectopic expression of pancreatic regulatory genes. (semanticscholar.org)
  • precursors
  • Independent development of pancreatic alpha- and beta-cells from neurogenin3-expressing precursors: a role for the notch pathway in repression of premature differentiation. (semanticscholar.org)
  • Adult
  • Expression of ngn3 in adult human duct cells induced Notch ligands Dll1 and Dll4 and neuroendocrine- and beta-cell-specific markers: it increased the percentage of synaptophysin- and insulin-positive cells 15-fold in ngn3-infected versus control cells. (semanticscholar.org)
  • gallbladder
  • liver pain stabbing Ashcroft might be eliminate your gallbladder , liver and the presence of taraxacin in dandelion root is another natural pancreatic duct vascular supply cure you choose health issues when the organism digests fat abdominal pain jaundice substances, no issues there. (healthygallbladder.com)
  • The gallstone travels partial responsible for the fact that I had my gallstone pain left hand side serious pain within your small intestines are adapting to the cystic ducts, gallbladder diet natural remedy which might be feeling tired and will where is your liver image want to avoid commercially produced, it will disappear. (healthygallbladder.com)
  • HCO3
  • Our aim in this study was to investigate the potential of a recombinant Sendai virus (SeV) vector to introduce normal CFTR into human CF pancreatic duct (CFPAC-1) cells, and to assess the effect of CFTR gene transfer on the key transporters involved in HCO3- transport. (cfgenetherapy.org.uk)
  • CFTR expression had no effect on cell growth, monolayer integrity, and mRNA levels for key transporters in the duct cell (pNBC, AE2, NHE2, NHE3, DRA, and PAT-1), but did upregulate the activity of apical Cl-/HCO3- and Na+/H+ exchangers (NHEs). (cfgenetherapy.org.uk)
  • In CFTR-corrected cells, apical Cl-/HCO3- exchange activity was further enhanced by cAMP, a key feature exhibited by normal pancreatic duct cells. (cfgenetherapy.org.uk)
  • Our data show that SeV vector is a potential CFTR gene transfer agent for human pancreatic duct cells and that expression of CFTR in CF cells is associated with a restoration of Cl- and HCO3- transport at the apical membrane. (cfgenetherapy.org.uk)
  • tissue
  • Herein, we used flow cytometry, immunohistochemistry, RT-PCR, and functional coagulation assays to demonstrate that duct cells exert a potent factor VII-dependent procoagulant activity related to their expression of tissue factor. (diabetesjournals.org)
  • Both the classical membrane-bound and the recently described soluble form of tissue factor were shown to be synthesized by duct cells. (diabetesjournals.org)
  • vivo
  • These findings reveal the intricate regulation of CFTR activity by slc26a6 in both the resting and stimulated states and the essential role of slc26a6 in pancreatic HCO 3 − secretion in vivo . (wiley.com)
  • Expansion of pancreatic beta cells in vivo or ex vivo, or generation of beta cells by differentiation from an embryonic or adult stem cell, can provide new expandable sources of beta cells to alleviate the donor scarcity in human islet transplantation as therapy for diabetes. (ugent.be)
  • Patients
  • MicroRNA molecular profiles associated with diagnosis, clinicopathologic criteria, and overall survival in patients with resectable pancreatic duct. (nih.gov)
  • CFTR
  • Remarkably, inhibition of CFTR activity with CFTR inh -172, knock-down of CFTR by siRNA and measurement of CFTR current in WT and slc26a6 −/− duct cells revealed that deletion of slc26a6 resulted in dis-regulation of CFTR activity by removal of tonic inhibition of CFTR by slc26a6. (wiley.com)
  • normal
  • Dynamic MRCP with secretin stimulation is also illustrated, documenting both normal and abnormal responses of the pancreatic duct system to secretin. (slugbooks.com)