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Tests on Naturally Voided Body Fluids
Published in Robert B. Northrop, Non-Invasive Instrumentation and Measurement in Medical Diagnosis, 2017
From its origin in the lungs, exhaled breath should ideally contain only water vapor, CO2, O2, N2, and traces of CO, H2, and Ar. Unfortunately, one's breath is not always odorless. Halitosis is a term applied to the general phenomenon of unpleasant, malodorous, or bad breath. The offensive odors can be from several sources and in some cases can be of diagnostic value to a physician or dentist.
Carnosic acid exhibits antiproliferative and proapoptotic effects in tumoral NCI-H460 and nontumoral IMR-90 lung cells
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Amanda Cristina Corveloni, Simone Cristine Semprebon, Adrivanio Baranoski, Bruna Isabela Biazi, Thalita Alves Zanetti, Mário Sérgio Mantovani
Both IMR-90 and NCI-H460 cells demonstrated cell death by apoptosis following exposure to CA. Su et al. (2016) noted that CA inhibited cervical cancer cell growth associated with apoptosis, concomitant with the release of cytochrome c, and upregulation of proapoptotic protein levels, such as Bcl-2, Bax, Bak, Bad, Apaf1, and cleaved caspase-9 and 3. Zhang et al. (2017) found that CA enhanced apoptosis and caspase-3, 8, and 9 activities in HepG2 SMMC-7721 cells. Taj et al. (2012) reported that incubation of human ovarian cancer A2780 cells with rosemary extract (RE) containing CA altered the expression of a number of genes regulating apoptosis. Shi et al. (2017) showed that CA induced apoptosis in HCC827 and H358 lung cancer cells with activation of mitochondrial pathway associated with the rise of cleaved caspase-9 and 3, upregulation of Bax and Bad, and downregulation of Bcl-2 and Bcl-xl. Further, cells also exhibited activation of the extrinsic pathway, with activation of caspase-8 and upregulation of TRAIL, DR4, DR5, and FADD mRNA levels.
Parecoxib exhibits anti-inflammatory and neuroprotective effects in a rat model of transient global cerebral ischemia
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Shaoxing Liu, Yue’e Dai, Chen Zhou, Tao Zhu
Previously He et al. (2019) showed that apoptosis contributes to a significant proportion of neuronal death after cerebral ischemia reperfusion. Similarly, Song et al. (2019) found that apoptosis was involved in cerebral ischemia reperfusion which was accompanied by elevated gene expression of Bax associated with reduction in protein expression of Bcl-2. Shen et al. (2017) reported that the mitochondrial pathway was involved in IL-1β-induced apoptosis of nucleus pulposus cells, as evidenced by elevated expression ratio of Bax/Bcl-2. The Bcl-2 protein family members consist of pro-apoptotic (Bax, Bad) and anti-apoptotic (Bcl-2, Bcl-xl), which are major regulators of the mitochondrial apoptotic pathway after ischemia injury (Cory, Huang, and Adams 2013). It was proposed that Bcl-2/Bax ratio determines whether a cell is protected from, or progresses to, programmed cell death (Guo and Li 2018; Sekerdag, Solaroglu, and Gursoy-Ozdemir 2018). Previously Lipton (1999) showed that necrotic neurons appeared at 6–12 hr and a second peak appeared at 24–72 hr after ischemia reperfusion. In this study, the TUNEL-positive cells, apoptotic rate, and expression of both Bax and Bcl-2 were significantly increased in cortex; however, the ratio of Bcl-2/Bax decreased significantly at 72 hr after tGCI. Our findings demonstrated that parecoxib treatment significantly enhanced Bcl-2 expression accompanied by a fall in Bax expression (i.e., elevated Bcl-2/Bax ratio), attenuating neuronal apoptosis in the prefrontal cortex of tGCI rats.
Ceramide pathway: A novel approach to cancer chemotherapy
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Mahdi Mashhadi Akbar Boojar, Masoud Mashhadi Akbar Boojar, Sepide Golmohammad
In the intrinsic pathway, factors such as environmental stress, heat, hypoxia, lack of growth factors, infections from intracellular masses and caspase-8 which activated in the external pathway of apoptosis results in increased expression of pro-apoptotic proteins of the B-cell lymphoma family such as BAX, BAK, BID, BAD and nitric oxide and attenuation of the anti-apoptosis proteins such as Bcl-2 and Bcl-XL [5,9,12] . The total of these events leads to increased permeability of the mitochondrial membrane and the formation of pores in its surface, resulting in the release of factors such as Cytochrome C and SMAC from mitochondria into the cytoplasm [13]. The release of these agents by generating the apoptosome complex activates Caspase-9, and the activation of Caspase-9 induces caspase 3 which leads to apoptosis [14].