Ó Sheán Clárach Mac Domhnaill go dtí Nioclás Tóibín: traidisiún na hamhránaíochta ins na Déise

Féachann an tráchtas seo le solas a chaitheamh ar an amhránaíocht mar a chleachtaítí agus mar a chleactaítear fós i gcontae Phort Láirge í. Ardaítear ann ceisteanna a bhaineann le seachadadh agus le sealbhú na n-amhrán I measc an phobail i gceantar na nDéise sa tréimhse c.1750-1960, ó aimsir Sheáin Chláraigh go dtí an ré sin ina raibh Nioclás Tóibín, ‘rí-amhránaí Éireann’, ar bhuaic a réime. Cuirtear spéis anseo i bhfás agus i dteacht chun cinn an Rómánsachais agus (a leathchúpla) an náisiúnachais ar Mhór-roinn na hEorpa in earr an 18ú haois agus amach san 19ú haois; ar thionchar na ngluaiseachtaí sin i bhfad ó bhaile ar Éirinn i gcoitinne san aimsir úd; orthu sin a raibh díolamaí amhrán á gcur in eagar acu in Éirinn san 19ú agus amach san 20ú haois; agus, ar deireadh, ar an stór amhrán mar atá le clos inniu I measc na ndaoine i nGaeltacht na Déise.

Study of insulin-like growth factor signaling in mitochondrial function

Insulin-like Growth Factor-1 (IGF-1) signalling promotes cell growth and is associated with cancer progression, including metastasis, epithelial-mesenchymal transition (EMT), and resistance to therapy. Mitochondria play an essential role in cancer cell metabolism and accumulating evidence demonstrates that dysfunctional mitochondria associated with release of mitochondrial reactive oxygen species (ROS) can influence cancer cell phenotype and invasive potential. We previously isolated a mitochondrial UTP carrier (PNC1/SLC25A33) whose expression is regulated by IGF-1, and which is essential for mitochondrial maintenance. PNC1 suppression in cancer cells results in mitochondrial dysfunction and acquisition of a profound ROS-dependent invasive (EMT) phenotype. Moreover, over-expression of PNC1 in cancer cells that exhibit an EMT phenotype is sufficient to suppress mitochondrial ROS production and reverse the invasive phenotype. This led us to investigate the IGF-1-mitochondrial signalling axis in cancer cells. We found that IGF-1 signalling supports increased mitochondrial mass and Oxphos potential through a PI3K dependant pathway. Acute inhibition of IGF-1R activity with a tyrosine kinase inhibitor results in dysfunctional mitochondria and cell death. We also observed an adaptive response to IGF-1R inhibition upon prolonged exposure to the kinase inhibitor, where increased expression of the EGF receptor can compensate for loss of mitochondrial mass through activation of PI3K/mTOR signalling. However, these cells exhibit impaired mitochondrial biogenesis and mitophagy. We conclude that the IGF-1 is required for mitochondrial maintenance and biogenesis in cancer cells, and that pharmacological inhibition of this pathway may induce mitochondrial dysfunction and may render the cells more sensitive to glycolysis-targeted drugs.