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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].
Introduction to Cancer
Published in Anjana Pandey, Saumya Srivastava, Recent Advances in Cancer Diagnostics and Therapy, 2022
Anjana Pandey, Saumya Srivastava
Another way of sustained angiogenesis is a decreased level of thrombospondin-1 caused by the loss of p53 function, which occurs in most of the human cancerous cells, so it cannot show its inhibitory effect (Sundaram et al., 2011) and angiogenesis in tumor cells sustained.
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.
Polymeric biomaterials for wound healing applications: a comprehensive review
Published in Journal of Biomaterials Science, Polymer Edition, 2022
Ahmed Olanrewaju Ijaola, Damilola O. Akamo, Fouad Damiri, Cletus John Akisin, Emmanuel Anuoluwa Bamidele, Emmanuel Gboyega Ajiboye, Mohammed Berrada, Victor Onyebuchukwu Onyenokwe, Shang-You Yang, Eylem Asmatulu
The cutaneous wound-healing process is a complex biochemical and cellular process. It can be divided into four different overlapping stages: hemostasis, inflammation, proliferation, and remodeling, as illustrated in Figures 1 and 2 [31, 32]. Hemostasis is the first phase of wound healing, that is, the first response to the wound site to stop bleeding and reduce hemorrhage from vascular damage [33]. During hemostasis, the exudates with coagulation factors will congeal at the wound site, which gives mechanical support to the injured tissue [34]. Platelets and inflammatory cells arrive at the wound site by binding to the bare collagen in the extracellular matrix. Subsequently, the secretion of some proteins by platelets takes place to further increase platelet simulation—these proteins include the von Willebrand factor (vWF), fibronectin, thrombospondin, and sphingosine-1-phosphate. Clotting factors are released to stimulate the fibrin matrix deposition in order to form a stable clot, which serves as a provisional matrix for cells moving to the wound bed. Vasoconstriction will be induced due to platelet agglomeration to minimize blood flow to the wound bed [22]. Platelets caught in the clot exude more growth factors, such as interleukin 1 (IL-1), transforming growth factors (TGFs—TGY-α and TGF-), platelet-derived growth factor (PDGF), and insulin growth factor (IGF), to facilitate the next stages of wound healing. Also, TGF- recruits extra cells like macrophages and neutrophils, while PDGF recruits fibroblasts to produce collagen and help with the repair of damaged tissue as well as vascularization [35].