Zobrazeno 1 - 10
of 23
pro vyhledávání: '"Alexander Widiapradja"'
Autor:
Alexander Widiapradja, Ainsley O. Kasparian, Samuel L. McCaffrey, Lauren L. Kolb, John D. Imig, Jessica L. Lacey, Giselle C. Melendez, Scott P. Levick
Publikováno v:
Cells, Vol 10, Iss 10, p 2659 (2021)
Reduced levels of the sensory nerve neuropeptide substance P (SP) have been reported in the diabetic rat heart, the consequence being a loss of cardioprotection in response to ischemic post-conditioning. We considered whether this loss of SP also pre
Externí odkaz:
https://doaj.org/article/bd80b6d8c4024f9697b90c293e796785
Autor:
John Thundyil, Silvia Manzanero, Dale Pavlovski, Tanya R Cully, Ker-Zhing Lok, Alexander Widiapradja, Prasad Chunduri, Dong-Gyu Jo, Chie Naruse, Masahide Asano, Bradley S Launikonis, Christopher G Sobey, Mark G Coulthard, Thiruma V Arumugam
Publikováno v:
PLoS ONE, Vol 8, Iss 1, p e53528 (2013)
Ephrin (Eph) signaling within the central nervous system is known to modulate axon guidance, synaptic plasticity, and to promote long-term potentiation. We investigated the potential involvement of EphA2 receptors in ischemic stroke-induced brain inf
Externí odkaz:
https://doaj.org/article/1ea0b0573310427a9bbbd38bfe69e1bc
Autor:
Giselle C. Meléndez, Kylie Kavanagh, Nazli Gharraee, Jessica L. Lacy, Kevin H. Goslen, Masha Block, Jordyn Whitfield, Alexander Widiapradja, Scott P. Levick
Publikováno v:
Biomedicine & Pharmacotherapy. 160:114365
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::5d0f6a0e4e950613ad04381b9886ed53
https://doi.org/10.1016/j.biopha.2023.114365
https://doi.org/10.1016/j.biopha.2023.114365
Autor:
Grace Lim, Alexander Widiapradja, Scott P Levick, Kelly J McKelvey, Xiao-Hui Liao, Samuel Refetoff, Martyn Bullock, Roderick J Clifton-Bligh
Publikováno v:
Endocrinology. 163(12)
Context Foxe1 is a key thyroid developmental transcription factor. Germline deletion results in athyreosis and congenital hypothyroidism. Some data suggest an ongoing role for maintaining thyroid differentiation. Objective We created a mouse model to
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::08dc09ae347f51f5cbd8b08278f3d360
https://pubmed.ncbi.nlm.nih.gov/36156081
https://pubmed.ncbi.nlm.nih.gov/36156081
Autor:
Giselle C Melendez, Kylie Kavanagh, Jessica L Lacy, Masha Block, Nazli Gharraee, Alexander Widiapradja, Scott P Levick
Publikováno v:
Circulation. 144
Introduction: Type 2 diabetes mellitus (T2DM)-associated cardiac fibrosis contributes to heart failure, especially in women. We have data showing that diabetic mice with cardiomyopathy, including cardiac fibrosis, exhibit low levels of the neuropepti
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::be3937078b328bbf154f53b38fe0490c
https://doi.org/10.1161/circ.144.suppl_1.12139
https://doi.org/10.1161/circ.144.suppl_1.12139
Autor:
Heather M. Dehlin, Edward J. Manteufel, Alexander Widiapradja, Bao Lu, Scott P. Levick, Lauren L. Kolb, Joseph S. Janicki, James R. Peña, Paul H. Goldspink, Amit Sharma, John D. Imig
Publikováno v:
Scientific Reports, Vol 9, Iss 1, Pp 1-11 (2019)
Scientific Reports
Scientific Reports
Cardiac fibrosis is an underlying cause of diastolic dysfunction, contributing to heart failure. Substance P (SP) activation of the neurokinin-1 receptor (NK-1R) contributes to cardiac fibrosis in hypertension. However, based on in vitro experiments,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::776edef61f5a8335987be3341c4c3c2e
http://link.springer.com/article/10.1038/s41598-019-47369-0
http://link.springer.com/article/10.1038/s41598-019-47369-0
Autor:
Scott P. Levick, Alexander Widiapradja
Publikováno v:
International Journal of Molecular Sciences
International Journal of Molecular Sciences, Vol 21, Iss 3, p 970 (2020)
International Journal of Molecular Sciences, Vol 21, Iss 3, p 970 (2020)
Diabetic cardiomyopathy involves remodeling of the heart in response to diabetes that includes microvascular damage, cardiomyocyte hypertrophy, and cardiac fibrosis. Cardiac fibrosis is a major contributor to diastolic dysfunction that can ultimately
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9578c331cb5600306f169ba36acbc6f5
https://pubmed.ncbi.nlm.nih.gov/32024054
https://pubmed.ncbi.nlm.nih.gov/32024054
Publikováno v:
European Heart Journal. 40
Introduction Adverse cardiac remodelling is a response of the heart to various stimuli and if left untreated can progress to heart failure. Nr4a1, an orphan nuclear receptor, has been shown to have conflicting contributions to adverse cardiac remodel
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::e894c794e2b4098ef6b92ed420f2d799
https://doi.org/10.1093/eurheartj/ehz745.0869
https://doi.org/10.1093/eurheartj/ehz745.0869
Autor:
Martyn Bullock, Roderick J. Clifton-Bligh, Alexander Widiapradja, William B. Campbell, Samuel L McCaffrey, Scott P. Levick, Ainsley O Kasparian, Grace Lim
Publikováno v:
International Journal of Molecular Sciences, Vol 21, Iss 9757, p 9757 (2020)
International Journal of Molecular Sciences
Volume 21
Issue 24
International Journal of Molecular Sciences
Volume 21
Issue 24
Histamine is a basic amine stored in mast cells, with its release capable of activating one of four histamine receptors. The histamine 3 receptor (H3R) is known to be cardioprotective during acute ischemia by acting to limit norepinephrine release. H
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dd1bdd4debe81f323ec22d71b3477592
https://doi.org/10.3390/ijms21249757
https://doi.org/10.3390/ijms21249757
Publikováno v:
Hypertension. 72
Myocardial remodelling such as fibrosis is a major contributor to heart failure with preserved ejection fraction. We sought to determine the relationship between substance P (SP), a sensory neuropeptide, and this adverse remodelling. Using the angiot
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::69bd267eb9c89e26a5cd5e91770d088a
https://doi.org/10.1161/hyp.72.suppl_1.p321
https://doi.org/10.1161/hyp.72.suppl_1.p321