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Household and Personal Care Products: Cleaning up and Looking Good
Published in Richard J. Sundberg, The Chemical Century, 2017
The radiation from the sun includes ultraviolet radiation that is classified as UV-B (290–320 nm) and UV-A (340–400 nm). There is also shorter wavelength radiation (<290 nm) called UV-C, but it is absorbed by the ozone layer. Exposure to UV-B radiation leads to demonstrable DNA damage. In most individuals, there is a functioning enzymatic repair mechanism. Individuals with genetic or other impairment of the repair mechanism are very susceptible to skin cancer. As life expectancy has increased so has the incidence of skin cancer. Even young skin suffers damage from exposure to sun. The connecting layer between the epidermis and dermis, known as the basement membrane, seems to be the location of some of the damage. Normally, angiogenesis (formation of blood vessels) is controlled by a protein called thrombospondin-1. In response to wound healing, angiogenesis occurs. Sun exposure also leads to angiogenesis and weakens the epidermis–dermis connection.25 There is a wide variation in individual sensitivity to sunlight, with more highly pigmented skin being both less susceptible to sunburn and less efficient at vitamin D synthesis (see Section 10.1.8). It has been speculated that as humans moved from tropical regions to higher latitudes, vitamin D photosynthesis became more important and resulted in reduced skin pigmentation.
Anti-Cancer and Anti-Angiogenic Properties of Nano-Diamino-Tetrac, A Thyroid Hormone Derivative
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2020
Paul J. Davis, Shaker A. Mousa
A model anti-angiogenesis agent for use in oncology (a) affects multiple blood vessel formation pathways, (b) acts at multiple points in several pathways, e.g., vascular growth factor genes and growth factor receptor function, (c) has some specificity for tumor-related angiogenesis, (d) may stimulate endogenous anti-angiogenesis pathways such as transcription of the thrombospondin-1 (TSP1) gene and (e) has a favorable side effect profile. Tetraiodothyroacetic acid (tetrac) is a novel anti-angiogenic and anti-cancer agent that, formulated covalently via diaminopropane linker to a nanoparticle, e.g., poly (lactic-co-glycolic acid) (PLGA) or to polyethylene glycol (PEG), acts anti-angiogenically at a specific receptor on the extracellular domain of plasma membrane integrin αvβ3. The integrin is overexpressed by dividing endothelial cells and tumor cells. The nanoformulation—Nanotetrac, or nano-diamino-tetrac (NDAT)—disrupts mechanisms of action of vascular growth factors (VEGF, FGF2, PDGF), downregulates expression of the VEGFA gene and the vascular growth factor receptor gene (EGFR) and upregulates anti-angiogenic TSP1. In addition, by multiple downstream mechanisms initiated wholly at tumor cell surface αvβ3, Nanotetrac interrupts cancer cell survival pathways, disrupts the cell cycle, supports apoptosis, and blocks repair of double-strand DNA breaks. The agent also decreases the production of both components of the programmed cell death-1 (PD-l)/PD-ligand 1 (PD-L1) immune checkpoint. Thus, Nanotetrac acts at a single cellular target primarily expressed by cancer cells and attendant blood vessel cells to cause multiple desirable anti-cancer actions. The agent does not affect the reproduction of nonmalignant cells, other than endothelial cells. These anti-angiogenic actions and anti-proliferative effects of Nanotetrac on tumor cells provide support for pharmacological targeting of the thyroid hormone and other small molecule receptor sites on integrin αvβ3 [1].
Anti-Cancer and Anti-Angiogenic Properties of Nano-Diamino-Tetrac, A Thyroid Hormone Derivative
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2019
Paul J. Davis, Shaker A. Mousa
A model anti-angiogenesis agent for use in oncology (a) affects multiple blood vessel formation pathways, (b) acts at multiple points in several pathways, e.g., vascular growth factor genes and growth factor receptor function, (c) has some specificity for tumor-related angiogenesis, (d) may stimulate endogenous anti-angiogenesis pathways such as transcription of the thrombospondin-1 (TSP1) gene and (e) has a favorable side effect profile. Tetraiodothyroacetic acid (tetrac) is a novel anti-angiogenic and anti-cancer agent that, formulated covalently via diaminopropane linker to a nanoparticle, e.g., poly (lactic-co-glycolic acid) (PLGA) or to polyethylene glycol (PEG), acts anti-angiogenically at a specific receptor on the extracellular domain of plasma membrane integrin αvβ3. The integrin is overexpressed by dividing endothelial cells and tumor cells. The nanoformulation—Nanotetrac, or nano-diamino-tetrac (NDAT)—disrupts mechanisms of action of vascular growth factors (VEGF, FGF2, PDGF), downregulates expression of the VEGFA gene and the vascular growth factor receptor gene (EGFR) and upregulates anti-angiogenic TSP1. In addition, by multiple downstream mechanisms initiated wholly at tumor cell surface αvβ3, Nanotetrac interrupts cancer cell survival pathways, disrupts the cell cycle, supports apoptosis, and blocks repair of double-strand DNA breaks. The agent also decreases the production of both components of the programmed cell death-1 (PD-l)/PD-ligand 1 (PD-L1) immune checkpoint. Thus, Nanotetrac acts at a single cellular target primarily expressed by cancer cells and attendant blood vessel cells to cause multiple desirable anti-cancer actions. The agent does not affect the reproduction of nonmalignant cells, other than endothelial cells. These anti-angiogenic actions and anti-proliferative effects of Nanotetrac on tumor cells provide support for pharmacological targeting of the thyroid hormone and other small molecule receptor sites on integrin αvβ3 [1].
Benzo[a]pyrene osteotoxicity and the regulatory roles of genetic and epigenetic factors: A review
Published in Critical Reviews in Environmental Science and Technology, 2022
Jiezhang Mo, Doris Wai-Ting Au, Jiahua Guo, Christoph Winkler, Richard Yuen-Chong Kong, Frauke Seemann
MiR-let-7e promotes the fusion of OCP by targeting thrombospondin-1 (THBS1) or integrin alpha 4 (ITGA4) (de la Rica et al., 2015). Additionally, the upregulation of DC-STAMP is supported by the downregulation of miR-7b. Moreover, miR-26a targets connective tissue growth factor (CTGF), which promotes OC maturation by upregulating the expression of DC-STAMP (Dou et al., 2014). Additionally, MiR-29 inhibits OC maturation by targeting C-FOS and MMP2 (Rossi et al., 2013), while MiR-31 inhibits actin ring formation and bone resorption in MOCs by targeting Ras homolog family member A (RHOA) (Mizoguchi et al., 2013). MiR-20a targets autophagy-related 16-like 1 (ATG16L1) and inhibits the packaging and secretion of proteases at the ruffled border (Sun et al., 2015), while miR-365 and miR-186 negatively regulate the expression of MMP9 and CTSK, respectively (Li et al., 2015; Ma et al., 2018). MiR-21 promotes OC survival and inhibits OC apoptosis by targeting the cell-surface death-receptor FAS ligand (FASLG) (Sugatani & Hruska, 2013) or the programmed cell death 4 (PDCD4) mRNA (Sugatani et al., 2011). It should also be noted that the biogenesis, maturation, and function of miRNAs are also subjected to epigenetic regulation (Hassan et al., 2015).
Indoor air pollution aggravates asthma in Chinese children and induces the changes in serum level of miR-155
Published in International Journal of Environmental Health Research, 2019
Qingbin Liu, Wei Wang, Wei Jing
MicroRNA, small non-coding RNA of 18–25 nucleotides, can affect gene expression (Cai et al. 2018) and has been used as biomarkers in human diseases. miR-98 reduces the levels of thrombospondin 1 (THBS1), which plays an important role in regulating cellular immunity activity in allergic asthma (Chen et al. 2017). miR-19b can reduce the levels of oxidative stress by reducing thymic stromal lymphopoietin in an animal asthma model (Ye et al. 2017). MiR-155, one of the most studied miRNAs, has been found to be associated with complex cellular activities. Allergy is often caused by hyperactive CD4+ Th2 cells, and miR-155 has a T cell-intrinsic role in cellular immunity. MiR-155 is a potential therapy target to reduce Th2-modulated inflammatory activities (Okoye et al. 2014) and plays an important role in asthma progression (Zhou et al. 2016). Detecting microRNA will be a simple non-invasive way for the diagnosis of pediatric asthma. We seek to explore the relationship between the changes of serum miR-155 and air pollution-induced asthma.
Cylindrospermopsin toxicity in mice following a 90-d oral exposure
Published in Journal of Toxicology and Environmental Health, Part A, 2018
N. Chernoff, D.J. Hill, I. Chorus, D.L. Diggs, H. Huang, D. King, J.R. Lang, T.-T. Le, J.E. Schmid, G.S. Travlos, E.M. Whitley, R.E. Wilson, C.R. Wood
Changes in hepatic gene expression were determined for a series of genes known to be affected following i.p. administration of CYN (Chernoff et al. 2010; personal communication). Gene expression data and general functions of genes are summarized in Table 6. There was a significant upregulation of the pro-apoptotic Bcl-2-associated X gene (Bax) at all doses in females and at 150 and 300 µg/kg doses in males which was a dose-related effect in both genders. The fatty acid-binding protein 4 (Fabp4) gene involved with fatty acid uptake and metabolism was significantly downregulated at all dose levels with the exception of high-dose males. Nuclear protein-1, a gene associated with pancreatic disease, exhibited significant upregulation in the female 300 µg/kg group. Ribosomal protein L6 (Rpl6), which is associated with liver regeneration, was significantly upregulated at all dose levels in both genders in a dose-related manner. Both c-Jun that protects against apoptosis and Trp53 that initiates apoptosis were not markedly affected in a consistent pattern. The expression of genes known to be involved in the production of key proteins in the coagulations system was determined. Protein C (Proc) which functions as an anticoagulant by suppressing coagulation factors Va and VIIIa was significantly downregulated in both males and females. Kalikrein (Klkb1) which functions as an activator of plasminogen resulting in the production of plasmin and the dissolution of clots was significantly downregulated at all dose levels in a dose-related manner. Thrombospondin-1 (Thbs-1) and thrombopoietin (Thpo) are genes that regulate platelet formation, aggregation, and clot strengthening, and neither of the genes exhibited biologically consistent altered expressions.