Zobrazeno 1 - 10
of 19
pro vyhledávání: '"Jessica LaRocca"'
Autor:
Lynea Murphy, Matthew J. LeBaron, Kamin Johnson, Reza J. Rasoulpour, Xiujuan Wang, Jessica LaRocca
Publikováno v:
Frontiers in Toxicology, Vol 3 (2021)
Nitrapyrin, a nitrification inhibitor, produces liver tumors in B6C3F1 mice. In a 2-year oncogenicity study, increased incidence of mice with hepatocellular tumors was observed following exposure to 125 (females only) or 250 mg/kg/day (males and fema
Externí odkaz:
https://doaj.org/article/4739585540144fb7bdb11c9f0f13b2e9
Publikováno v:
PLoS ONE, Vol 6, Iss 9, p e24432 (2011)
Akt1, a serine-threonine protein kinase member of the PKB/Akt gene family, plays critical roles in the regulation of multiple cellular processes, and has previously been implicated in lactation and breast cancer development. In this study, we utilize
Externí odkaz:
https://doaj.org/article/0b50a4382e83421eb3dd7c6bed9cf770
Publikováno v:
Birth defects researchREFERENCES. 114(17)
The dynamics and complexities of in utero fetal development create significant challenges in transitioning from lab animal-centric developmental toxicity testing methods to assessment strategies based on new approach methodologies (NAMs). Nevertheles
Autor:
Jessica R. Weaver, Justin J. Odanga, Kristina K. Wolf, Stephanie Piekos, Mercedes Biven, Mitchell Taub, Jessica LaRocca, Cody Thomas, Alexander Byer-Alcorace, Jingsong Chen, Jung Bok Lee, Edward L. LeCluyse
Publikováno v:
Toxicology in vitro : an international journal published in association with BIBRA. 86
There remains a significant need for a convenient, phenotypically stable long-term culture platform for primary human hepatocytes (PHHs) for use in pharmacological and toxicological applications. Conventional in vitro models are often inconvenient, b
Autor:
Kamin J. Johnson, Eduardo Costa, Valerie Marshall, Shreedharan Sriram, Anand Venkatraman, Kenneth Stebbins, Jessica LaRocca
Publikováno v:
Birth defects research. 114(11)
Traditional developmental toxicity testing practice examines fetal apical endpoints to identify a point of departure (POD) for risk assessment. A potential new testing paradigm involves deriving a POD from a comprehensive analysis of molecular-level
Autor:
B. Bhaskar Gollapudi, David L. Eisenbrandt, Lynea Murphy, Reza J. Rasoulpour, Matthew J. LeBaron, Jessica LaRocca
Publikováno v:
Toxicology Reports
Toxicology Reports, Vol 4, Iss, Pp 586-597 (2017)
Toxicology Reports, Vol 4, Iss, Pp 586-597 (2017)
Graphical abstract
Highlights • Nitrapyrin produces liver tumors in mice via a CAR mode-of-action. • Nitrapyrin does not increase hepatocellular proliferation in CAR knock-out mice. • Nitrapyrin increases cell proliferation in mouse, but n
Highlights • Nitrapyrin produces liver tumors in mice via a CAR mode-of-action. • Nitrapyrin does not increase hepatocellular proliferation in CAR knock-out mice. • Nitrapyrin increases cell proliferation in mouse, but n
Publikováno v:
Current Opinion in Toxicology. 6:87-92
Recent advancements in science and technology have exponentially increased our understanding of epigenetics, and it is important to examine these advancements in the context of potential benefits to safety assessments of chemical products. Product sa
Publikováno v:
Regulatory toxicology and pharmacology : RTP. 113
The derivation of an apical endpoint point of departure (POD) from animal-intensive testing programs has been the traditional cornerstone of human health risk assessment. Replacement of in vivo chronic studies with novel approaches, such as toxicogen
Publikováno v:
Environmental Health Perspectives
Environmental health perspectives, vol 124, iss 3
Environmental health perspectives, vol 124, iss 3
Background There is increasing concern that early-life exposure to endocrine-disrupting chemicals (EDCs) can influence the risk of disease development. Phthalates and phenols are two classes of suspected EDCs that are used in a variety of everyday co
Publikováno v:
Environmental Research. 133:396-406
Genomic imprinting leads to parent-of-origin specific gene expression and is determined by epigenetic modification of genes. The paternally expressed gene insulin-like growth-factor 2 (IGF2) is located about ∼100 kb from the maternally expressed no