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Discrete Random Variables
Published in William M. Mendenhall, Terry L. Sincich, Statistics for Engineering and the Sciences, 2016
William M. Mendenhall, Terry L. Sincich
Premature aging gene. Ataxia-telangiectasia (A-T) is a neurological disorder that weakens immune systems and causes premature aging. Science News reports that when both members of a couple carry the A-T gene, their children have a 1 in 5 chance of developing the disease. Consider 15 couples in which both members of each couple carry the A-T gene. What is the probability that more than 8 of 15 couples have children that develop the neurological disorder?Consider 10,000 couples in which both members of each couple carry the A-T gene. Is it likely that fewer than 3,000 will have children that develop the disease?
Pinus morrisonicola needles essential oil nanoemulsions as a novel strong antioxidant and anticancer agent
Published in Inorganic and Nano-Metal Chemistry, 2022
Niloufar Khatamian, Mozhgan Soltani, Behnaz Shadan, Ali Neamati, Masoud Homayouni Tabrizi, Bahareh Hormozi
Pinus morrisonicola needles essential oil due to its anticancer phytochemicals such as pinocembrin, chrysin, neophytadiene, and tiliroside has been used successfully in cancer therapy strategies.[10] In this regard, Bing Qiu and et al. revealed more details about Pine oil impacts on HepG2 cancer cell line and demonstrated that the Pinus morrisonicola oil has a significant role in arresting the cells’ cycle in G2/M phase. They approved the role of ATM pathway for G2/M arresting in HepG2 cells by measuring the phosphorylated protein levels of γ-H2A histone family, (p)-ataxia-telangiectasia mutated (ATM), p-p53, p-checkpoint kinase 2, member X, and p-cell division cycle 25 C, which were notably enhanced.[67] Moreover, Peng Ren and et al. indicated the suppressive impacts of Pinus morrisonicola oil on MCF-7 cancer cells. They also showed that it can regulate the MCF-7 cells aggressiveness and apoptosis and even modulate the AMPK/mTOR signaling pathway activity.[68]
Insights into the mechanisms of arsenic-selenium interactions and the associated toxicity in plants, animals, and humans: A critical review
Published in Critical Reviews in Environmental Science and Technology, 2021
Waqar Ali, Hua Zhang, Muhammad Junaid, Kang Mao, Nan Xu, Chuanyu Chang, Atta Rasool, Muhammad Wajahat Aslam, Jamshed Ali, Zhugen Yang
Several researchers have confirmed that AsIII and its metabolites also change the activity of DNA methyltransferase, resulting in the inhibition or stimulation of SAM enzymatic synthesis pathways (Hughes, 2002; Reichard & Puga, 2010; Zhong & Mass, 2001). Interestingly, As induces genotoxicity by affecting the status of protein 53, while similar mechanisms have been reported for cytotoxicity induction (Chowdhury, Chowdhury, Roychoudhury, Mandal, & Chaudhuri, 2009; Shankar & Shanker, 2014). Nevertheless, Se induced genotoxicity by generating ROS and interacting with the thiol group (Letavayova et al., 2006; Ramoutar & Brumaghim, 2007; Valko et al., 2006). Selenium can also induce genotoxicity by inhibiting the cellular DNA repair ability, directly affecting protein 53 and the ataxia-telangiectasia mutation (ATM) (Abul-Hassan, Lehnert, Guant, & Walmsley, 2004; Wei et al., 2001; Zeng & Combs, 2008; Zhou, Xiao, Li, Nur-E-Kamal, & Liu, 2003). Arsenic and Se genotoxicity-induced mechanisms have not yet been clarified; however, most studies have attributed their genotoxicity to their capability to induce oxidative stress (Sun et al., 2014).
Effects of Bisphenol A on Foxl2 gene expression and DNA damage in adult viviparous fish Goodea atripinnis
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Isabel Cervantes-Camacho, Sandra M. Guerrero-Estévez, María Fernanda López, Ernesto Alarcón-Hernández, Eugenia López-López
The typical shape observed in the comets of G. atripinnis analyzed corresponds to a single-strand DNA break, which was reported as the most frequent type of DNA damage (Caldecott 2008; Hulak et al. 2013); therefore, the significant decrease in comet tail length and severity of DNA damage (tail moment) in both sexes of G. atripinnis after 28 days treatment may be related to single strand break DNA repair which is known to reduce DNA migration (Iyama and Wilson 2013; Speit and Hartmann 2005). DNA damage induced by BPA exposure activates DNA-dependent protein kinases, including ATM (ataxia-telangiectasia mutated kinase), which acts upon various phosphorylated substrates such as Chk2 (Xin et al. 2014). The activation of Chk2 stabilizes p53, contributing to DNA binding. Chk2 participates in the arrest of the cell cycle as a repair mechanism and in activation of apoptosis of unrepaired DNA (Xin et al. 2014). Another likely DNA repair mechanism in G. atripinnis may involve ATM/Chk2/p53 signaling pathway once BPA-mediated DNA damage has occurred.