Zobrazeno 1 - 10
of 91
pro vyhledávání: '"Peter J Thompson"'
Autor:
Peter J Thompson, Vered Dulberg, Kyung-Mee Moon, Leonard J Foster, Carol Chen, Mohammad M Karimi, Matthew C Lorincz
Publikováno v:
PLoS Genetics, Vol 12, Iss 10, p e1006390 (2016)
[This corrects the article DOI: 10.1371/journal.pgen.1004933.].
Externí odkaz:
https://doaj.org/article/6beb50761d68402cac2cb07363ed9d53
Autor:
Peter J Thompson, Vered Dulberg, Kyung-Mee Moon, Leonard J Foster, Carol Chen, Mohammad M Karimi, Matthew C Lorincz
Publikováno v:
PLoS Genetics, Vol 11, Iss 1, p e1004933 (2015)
Retrotransposition of endogenous retroviruses (ERVs) poses a substantial threat to genome stability. Transcriptional silencing of a subset of these parasitic elements in early mouse embryonic and germ cell development is dependent upon the lysine met
Externí odkaz:
https://doaj.org/article/6fcd03daa1e3422e917e30e69ef08f57
Publikováno v:
Frontiers in Endocrinology, Vol 15 (2024)
Type 1 Diabetes (T1D) is a chronic metabolic disease resulting from insulin deficiency due to autoimmune loss of pancreatic β cells. In addition to β cell destruction, it is now accepted that β cell stress and dysfunction, such as senescence, play
Externí odkaz:
https://doaj.org/article/b79df56160704070baa4b46aa6ffd100
Publikováno v:
STAR Protocols, Vol 5, Iss 1, Pp 102923- (2024)
Summary: A subpopulation of pancreatic beta cells becomes senescent during type 1 diabetes (T1D) progression, and removal of these populations protects against T1D in mice. Here, we present a protocol to measure senescence in murine pancreatic islet
Externí odkaz:
https://doaj.org/article/bcf47eb9f10e430dafad249751dcd9f7
Publikováno v:
Frontiers in Endocrinology, Vol 14 (2023)
Externí odkaz:
https://doaj.org/article/a0fde109c0534ad1a98ce5307ec69c34
Publikováno v:
Epigenomes, Vol 8, Iss 1, p 10 (2024)
Type 1 diabetes (T1D) is a metabolic disease resulting from progressive autoimmune destruction of insulin-producing pancreatic beta cells. Although the majority of beta cells are lost in T1D, a small subset undergoes senescence, a stress response inv
Externí odkaz:
https://doaj.org/article/54f48bdfe0af447ba7e32edd4b98fd2d
Publikováno v:
Frontiers in Endocrinology, Vol 14 (2023)
Cellular senescence is a response to a wide variety of stressors, including DNA damage, oncogene activation and physiologic aging, and pathologically accelerated senescence contributes to human disease, including diabetes mellitus. Indeed, recent wor
Externí odkaz:
https://doaj.org/article/58636ab6223348a39ce96d539f53c1a2
Publikováno v:
Frontiers in Endocrinology, Vol 13 (2022)
Type 1 Diabetes (T1D) is caused by insulin deficiency, due to progressive autoimmune destruction of pancreatic β cells. Glucagon-secreting α cells become dysfunctional in T1D and contribute to pathophysiology, however, the mechanisms involved are u
Externí odkaz:
https://doaj.org/article/cf42848ddf564ac6977a7bfc049dfb54
Autor:
Hsu Phern Chong, James Hodson, Tara J. Selman, Lucy E. Hudsmith, Peter J. Thompson, Rachel Katherine Morris, Sara Thorne
Publikováno v:
BMC Pregnancy and Childbirth, Vol 19, Iss 1, Pp 1-9 (2019)
Abstract Background Women with cardiac disease are thought to be at increased risk of post-partum haemorrhage. We sought to assess the estimated blood loss (EBL) in our cohort of women with and without cardiac disease (CD) in a quaternary hospital in
Externí odkaz:
https://doaj.org/article/a0f4a0ae98034aa4b653d9c3141c14be
Autor:
Sophie E. Thompson, Chethan Ram Kasargod Prabhakar, Tristan Creasey, Victoria M. Stoll, Leo Gurney, Jennifer Green, Caroline Fox, R. Katie Morris, Peter J. Thompson, Sara A. Thorne, Paul Clift, Lucy E. Hudsmith
Publikováno v:
International Journal of Cardiology. 371:135-139
The Ross procedure, where a pulmonary autograft (neoaorta) replaces the aortic valve, has excellent long-term outcomes in patients with congenital aortic valve disease. However, there are reports of neoaortic dilatation and dissection. An increasing
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4b737f0cf0916f21e17d7d774e31fb25
https://doi.org/10.1016/j.ijcard.2022.09.069
https://doi.org/10.1016/j.ijcard.2022.09.069