FT Report: Derry City 2 St Pats 2 Pinterest The Taoiseach has come under pressure from members of his own party to move the country to Level 2 Covid-19 restrictions for Christmas.Yesterday, Micheal Martin said the aim was Level 3 from the 1st of December to allow businesses to re-open.However, at a meeting of the Fianna Fail parliamentary party last night, there was a ‘general consensus’ to go further and allow domestic travel and more visitors to homes.The National Public Health Emergency Team meet later to discuss the current progress with Level 5.Professor of Public Health at the University of Bristol, Gabriel Scally, says it’s important not to get ahead of ourselves when reopening next month: Derry draw with Pats: Higgins & Thomson Reaction Google+ WhatsApp Facebook Important message for people attending LUH’s INR clinic Previous articleStill no decision on extending restrictions in NorthNext articleCouncil to look at traffic issues at Mountain Top News Highland DL Debate – 24/05/21 Taoiseach under pressure to move country to Level 2 for Christmas Twitter By News Highland – November 12, 2020 Facebook Google+ Pinterest News, Sport and Obituaries on Monday May 24th WhatsApp AudioHomepage BannerNews Twitter Harps come back to win in Waterford RELATED ARTICLESMORE FROM AUTHOR
Editing genes at the source Related Harvard scientists receive grant funding through NIH program Breakthrough research shows that stem cell genes can be edited in living systems Harvard University stem-cell researchers led by Amy Wagers, the Forst Family Professor of Stem Cell and Regenerative Biology, are embarking on a major study of Duchenne muscular dystrophy (DMD). Supported by research funding from Sarepta Therapeutics, under a multiyear collaboration agreement coordinated by Harvard’s Office of Technology Development (OTD), the project aims to use in vivo genome editing in mouse models of DMD to fully and precisely restore the function of a protein crucial for proper muscular growth and development. Approaches validated by this work may point the way to an eventual therapeutic strategy to reverse DMD in humansDuchenne muscular dystrophy is a genetic disease caused by the lack of a protein called dystrophin that normally helps support the structural integrity of muscle fibers, including those in the heart. Without dystrophin, cells are weaker and degenerate more quickly. Over time, affected individuals — boys, typically, as DMD is a recessive X-linked disorder — lose their capacity to move independently.“It’s really a devastating disease; it robs young boys of their capacity to be young boys,” said Wagers, who is co-chair of the Department of Stem Cell & Regenerative Biology and an executive committee member of Harvard Stem Cell Institute. “Though it is early days, I’m hopeful that through this work we may identify and validate new avenues for therapy to completely rescue the proper expression and function of the dystrophin protein and regenerate healthy muscle tissue.”Researchers worldwide have pursued a variety of promising approaches — such as cell and gene therapies, small-molecule therapies, and others — to lessen or prevent the disease and improve patients’ quality of life. “[Duchenne muscular dystrophy] is really a devastating disease; it robs young boys of their capacity to be young boys.” — Amy Wagers The strategy pursued by the Wagers Lab at Harvard aims to fully correct the genetic template for dystrophin at its source, in the DNA of stem cells (satellite cells) that create and regenerate muscle cells. Combining cutting-edge CRISPR/Cas9 genome-editing technologies with a deep knowledge of stem-cell science and regenerative biology, this approach if successful might offer a permanent restoration of muscle function.“In skeletal muscle, muscle fibers are terminally post-mitotic, meaning they cannot divide and they cannot reproduce themselves,” Wagers explains. “If you lose muscle fibers, the only way to produce new muscle is from stem cells, specifically the satellite cells. The satellite cells are self-renewing, self-repairing, and ready to spring into action to create new muscle fibers. So we expect that a satellite cell with the corrected DMD gene would quite quickly and continuously propagate the edited gene throughout the muscle tissue.”At present, research conducted in mice has shown promising results. In June, the Wagers Lab published the results of editing stem cells in vivo, demonstrating that stem-cell genes can be edited in living systems, not only in a dish. In that work, Wagers and her team delivered genome-editing molecules to the cells using adeno-associated viruses (AAVs). Her lab has also successfully used gene editing in heart, muscle, and satellite cells to partially restore the function of the DMD gene that encodes dystrophin, by chopping out faulty sequences of code that are disrupting the proper reading frame.The new stem-cell approach pursued in collaboration with Sarepta would build on these achievements and use more precise genome-editing approaches, in animal models of DMD, to entirely replace genetic mutations in the DMD gene with correctly encoded sequences. The project will also explore alternate delivery methods and strategies to mitigate immune effects of in vivo genome editing.“This ambitious project will benefit greatly from the resources and insights of a company with deep clinical experience in the development of therapeutics for muscular dystrophy,” said Vivian Berlin, managing director of strategic partnerships at Harvard OTD. “Preclinical discoveries by Harvard researchers may open entirely new possibilities for lifesaving treatments in the long run, offering much-needed hope to patients and families in the future. We’re grateful to be able to sustain the important momentum already established in Professor Wagers’ lab, through this collaboration.”“As we work to bring forward new treatments for patients with DMD, Sarepta is excited to support Professor Wagers and her lab to accelerate the development of a gene-editing approach, which has shown significant potential in early studies,” said Louise Rodino-Klapac, Sarepta’s senior vice president of gene therapy. “This multiyear collaboration is part of Sarepta’s broader commitment to pursuing all therapeutic modalities and advancing our scientific understanding of gene editing in order to maximize the potential of this approach to help patients.”Under the terms of the agreement between Harvard and Sarepta, the company will have the exclusive option to license any arising intellectual property for the purpose of developing products to prevent and treat human disease. As with any research agreement facilitated by OTD, the right of academic and other not-for-profit researchers to use the technology in further scholarly work is preserved. Seven recognized for high-risk, high-reward research
Before Wieskamp’s game-winner, Geo Baker made a 3 with 3.2 seconds remaining to give the Scarlet Knights (12-13, 5-10) a one-point lead.MORE: Don’t sleep on P.J. Washington in All-America raceIowa is one of the better teams in the Big Ten and isn’t on the NCAA Tournament bubble at the moment, but a close loss at Rutgers would have been tough. Wieskamp helped the Hawkeyes escape that fate. Give the backboard assist on this one.Iowa wins on the INSANE banked game winner! pic.twitter.com/G2RLltRXT9— Sporting News (@sportingnews) February 17, 2019The Hawkeyes have now won consecutive games on buzzer-beaters. Jordan Bohannon sank one Sunday to stun Northwestern. For the second game in a row, No. 21 Iowa snatched victory from the jaws of defeat.Joe Wieskamp’s prayer corner 3 off a deflected pass somehow went into the basket, giving the Hawkeyes (20-5, 9-5 Big Ten) a 71-69 victory over Rutgers on Saturday.