HOW OUR PAST IS BEING PRESERVED IN DIGITAL STORIES

Tag: 爱上海419IT

first_imgStorytelling has been a human characteristic for thousands of years.We have left our stories wherever we have lived: on mountain sides, on the walls of caves, in the spoken word through myth and song, and synopsised billions of tales through poetry and rhyme. Indeed, everyone has a story to tell…A new, innovative and accessible way of story telling has now emerged in the form of Digital Stories. These anecdotes are short, personal multimedia tales told from the heart which put the narrator at the centre of the process. As such, the audience receive a genuine, unedited, more democratic form of storytelling.In 2013, two groups of service users, the Creative Writing Group from the Rehab Care Resource Centre in Lifford and the Social Group from the Garden Centre in St Conal’s Hospital, Letterkenny, were given the opportunity to create their own digital stories.The project meant the coming together of a number of other agencies, including: the Donegal Education and Training Board, Letterkenny Institute of Technology and the Regional Cultural Centre in Letterkenny. Each agency became an integral part of an overall process which was expertly and sympathetically facilitated by Kevin Mc Monagle.Kevin said: “The digital stories project was transformational for all involved. Creating these autobiographical short narratives allowed us to reflect on the core events in our lives, whilst at the same time providing us with a rare and wonderful view into the real lives of others… For more information on Digital Storytelling, please contact: Mr Seamus Gordon, Social Worker, St Conal’s Hospital Letterkenny – 087 267 1367 HOW OUR PAST IS BEING PRESERVED IN DIGITAL STORIES was last modified: May 29th, 2014 by John2Share this:Click to share on Facebook (Opens in new window)Click to share on Twitter (Opens in new window)Click to share on LinkedIn (Opens in new window)Click to share on Reddit (Opens in new window)Click to share on Pocket (Opens in new window)Click to share on Telegram (Opens in new window)Click to share on WhatsApp (Opens in new window)Click to share on Skype (Opens in new window)Click to print (Opens in new window) Tags:digital storiesdonegaloral history projectlast_img read more


Tag: 爱上海419IT

first_imgLorem ipsum dolor sit amet, consectetur adipisicing elit, sed do eiusmod tempor incididunt ut labore et dolore magna aliqua. Ut enim ad minim veniam, quis nostrud exercitation ullamco laboris nisi ut aliquip ex ea commodo consequat. Duis aute irure dolor in reprehenderit in voluptate velit esse cillum dolore eu fugiat nulla pariatur. Excepteur sint occaecat cupidatat non proident, sunt in culpa qui officia deserunt mollit anim id est laborum.last_img


Tag: 爱上海419IT

first_imgJun 22 2018A surprising form of cell-to-cell communication in glioblastoma promotes global changes in recipient cells, including aggressiveness, motility, and resistance to radiation or chemotherapy.Paradoxically, the sending cells in this signaling are glioblastoma cells that are undergoing programed cell death, or apoptosis, according to research by a team at institutes in the United States, Russia and South Korea.The dying cancer cells send their signals by means of extracellular vesicles induced and released during apoptosis. These vesicles -; small, membrane-bound blobs known as exosomes -; carry components that alter RNA splicing in the recipient glioblastoma cells, and this altered splicing promotes therapy resistance and aggressive migration.This mechanism thus becomes a possible target for new therapies to treat glioblastoma, a primary brain cancer, and the mechanism may apply to other cancer types as well.”Clinically, our data may provide the rationale to the molecular targeting of RNA splicing events or specific splicing factors for novel cancer therapies,” said Ichiro Nakano, M.D., Ph.D., leader of the international study being published in Cancer Cell. “This may lead to decreased acquisition of therapy resistance, as well as reduction in the migration of cancer cells.”Nakano is an academic neurosurgeon at the University of Alabama at Birmingham who conducts both brain tumor translational research and clinical brain tumor surgery. He is professor of neurosurgery in the UAB School of Medicine and a senior scientist for the UAB Comprehensive Cancer Center.Glioblastoma exhibits invasive behavior, abrupt growth and poor patient survival. As the number of the cancer cells rapidly increases, abundant apoptotic tumor cells are intermingled with neighboring proliferating tumor cells. The apoptotic cells can account for up to 70 percent of the tumor cell population.The discovery of this unusual cell-to-cell communication began with a simple experiment -; injecting a combination of lethally irradiated human glioblastoma cells, which makes them apoptotic, and “healthy” glioblastoma cells into a mouse xenograft model. This combination led to much more aggressive tumor growth, as seen in brain scans, compared to “healthy” glioblastoma cells or irradiated glioblastoma cells alone. The combination was also more therapy-resistant.The UAB researchers and colleagues found that, after induction of apoptosis, glioblastoma cells shed significantly higher numbers of exosomes with larger average sizes.Those apoptotic exosomes, when combined with “healthy” glioblastoma cells, significantly increased tumor growth in the xenograft model and cell motility in bench experiments. Also, while the “healthy” glioblastoma cells alone had a clear border between the tumor and adjacent normal tissue in the xenograft, the glioblastoma cells co-injected with apoptotic exosomes invaded into adjacent brain tissue. Exosomes shed by non-apoptotic cells did not have these effects.Related StoriesNew protein target for deadly ovarian cancerResearchers use AI to develop early gastric cancer endoscopic diagnosis systemLiving with advanced breast cancerTo discover the mechanism underlying these changes, the researchers looked at what was inside the apoptotic exosomes. The vesicles were enriched with spliceosomal proteins and several U snRNAs -; parts of the cellular machinery that remove introns from pre-messenger RNA.These are normally confined to the nuclei of cells; but the Nakano team found that, as the glioblastoma cells underwent apoptosis, the spliceosomal proteins were transported out of the nucleus to the cell cytoplasm, where they could be packaged into vesicles for release.Glioblastoma cell subtypes include the proneural subtypes and the mesenchymal subtype. Recent data have shown that, after therapy, glioblastoma cells shift from the less aggressive proneural subtype to the more aggressive and therapy-resistant mesenchymal subtype. The researchers found that apoptotic exosomes induced substantial alternate RNA splicing in recipient cells that resembled the splicing patterns found in the mesenchymal glioblastoma subtype.Part of this was caused by the splicing factor RBM11, which is encapsulated in the vesicles. The researchers found that exogenous RBM11 caused upregulation of endogenous RBM11 in the recipient cells and activated glycolysis. Overexpression of RBM11 increased the migration of glioblastoma cells.They also found that RBM11 altered RNA splicing to produce an isoform of the protein cyclinD1 that promotes DNA repair and an isoform of the protein MDM4 that has significantly higher anti-apoptotic activity. These changes can make the cells more therapy-resistant.Examination of the Cancer Genome Atlas database showed that elevated expression of those two isoforms is associated with poor prognoses for glioblastoma patients.Finally, the Nakano-led team looked at paired glioblastoma specimens of primary and recurrent tumors from matched patients. In most of the 43 pairs of matched samples, the RBM11 protein levels were substantially higher in the recurrent glioblastoma compared to the original, untreated tumors. In two other patient cohorts, they found that the higher RBM11 levels correlated with poor post-surgical survival for glioma patients. Source:http://www.uab.edu/news/research/item/9543-dying-cancer-cells-make-remaining-glioblastoma-cells-more-aggressive-and-therapy-resistantlast_img read more