Zobrazeno 1 - 10
of 126
pro vyhledávání: '"Pamela A Lucchesi"'
Autor:
Chaitali Misra, Nita Sachan, Caryn Rothrock McNally, Sara N Koenig, Haley A Nichols, Anuradha Guggilam, Pamela A Lucchesi, William T Pu, Deepak Srivastava, Vidu Garg
Publikováno v:
PLoS Genetics, Vol 8, Iss 5, p e1002690 (2012)
Defects of atrial and ventricular septation are the most frequent form of congenital heart disease, accounting for almost 50% of all cases. We previously reported that a heterozygous G296S missense mutation of GATA4 caused atrial and ventricular sept
Externí odkaz:
https://doaj.org/article/8e619ecf80d14f26a44be5766806ce46
Autor:
Flavia M Souza-Smith, Paige S Katz, Aaron J Trask, James A Stewart, Kevin C Lord, Kurt J Varner, Dalton V Vassallo, Pamela A Lucchesi
Publikováno v:
PLoS ONE, Vol 6, Iss 8, p e23337 (2011)
Resistance vessel remodeling is controlled by myriad of hemodynamic and neurohormonal factors. This study characterized structural and molecular remodeling in mesenteric resistance arteries (MRAs) in diabetic (db/db) and control (Db/db) mice.Structur
Externí odkaz:
https://doaj.org/article/327f705fce144702b8555b3c04ed2c40
Autor:
Markus Velten, Kirk R Hutchinson, Matthew W Gorr, Loren E Wold, Pamela A Lucchesi, Lynette K Rogers
Publikováno v:
PLoS ONE, Vol 6, Iss 9, p e24544 (2011)
The impact of the neonatal environment on the development of adult cardiovascular disease is poorly understood. Systemic maternal inflammation is linked to growth retardation, preterm birth, and maturation deficits in the developing fetus. Often pret
Externí odkaz:
https://doaj.org/article/38bcab904fd0471d9cd5402f0e49233b
Publikováno v:
International Journal of Molecular Sciences, Vol 22, Iss 6231, p 6231 (2021)
International Journal of Molecular Sciences
Volume 22
Issue 12
International Journal of Molecular Sciences
Volume 22
Issue 12
A hypofibrotic phenotype has been observed in cardiac fibroblasts (CFs) isolated from a volume overload heart failure model, aortocaval fistula (ACF). This paradoxical phenotype results in decreased ECM synthesis despite increased TGF-β presence. Si
Autor:
Rachel C. Childers, Pamela A. Lucchesi, Ian Sunyecz, Keith J. Gooch, Mary J. Cismowski, T. Aaron West
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 316:H596-H608
Hemodynamic load regulates cardiac remodeling. In contrast to pressure overload (increased afterload), hearts subjected to volume overload (VO; preload) undergo a distinct pattern of eccentric remodeling, chamber dilation, and decreased extracellular
Publikováno v:
Journal of cardiovascular pharmacology. 77(6)
Arachidonic acid-derived lipid mediators play crucial roles in the development and progression of cardiovascular diseases. Eicosanoid metabolites generated by lipoxygenases and cytochrome P450 enzymes produce several classes of molecules, including t
Publikováno v:
Journal of biomechanical engineering. 143(8)
Pressure overload (PO) and volume overload (VO) of the heart result in distinctive changes to geometry, due to compensatory structural remodeling. This remodeling potentially leads to changes in tissue mechanical properties. Understanding such change
Autor:
Bashir M. Rezk, Pamela A. Lucchesi
Publikováno v:
Toxicology and Forensic Medicine – Open Journal. 2:84-87
Autor:
Maarten L. Galantowicz, Pamela A. Lucchesi, Mary J. Cismowski, Aaron J. Trask, Paige S. Katz, Kathryn E. Husarek
Publikováno v:
Vascular Pharmacology. 76:28-36
Cardiovascular complications are a leading cause of morbidity and mortality in type 2 diabetes mellitus (T2DM) and are associated with alterations of blood vessel structure and function. Although endothelial dysfunction and aortic stiffness have been
Autor:
Sakthivel Sadayappan, Kristin Wilson, Anuradha Guggilam, Pamela A. Lucchesi, Xiaojin Zhang, Mary J. Cismowski, Pieter P. de Tombe, Aaron J. Trask, T. Aaron West
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 307:H1605-H1617
Aortocaval fistula (ACF)-induced volume overload (VO) heart failure (HF) results in progressive left ventricular (LV) dysfunction. Hemodynamic load reversal during pre-HF (4 wk post-ACF; REV) results in rapid structural but delayed functional recover