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Nanotechnology in Molecular Targeting, Drug Delivery, and Immobilization of Enzyme(s)
Published in Vineet Kumar, Praveen Guleria, Nandita Dasgupta, Shivendu Ranjan, Functionalized Nanomaterials I, 2020
Abhishek Sharma, Kishore Kumar, Tanvi Sharma, Shweta Sharma, Shamsher S. Kanwar
NP targeted drug deliver may be potentially used to deliver anti-cancer agents to the tumor site, which provides considerable benefits to cancer patients (Byrne et al., 2008; Sharma et al., 2014). The major advantages of nanomedicine in cancer treatment are that the nanostructures exploit the physiological aspects of tumors and the surrounding tissue inflammation response. Lyp-1 NPs (PEG-PLGA) is a target-specific drug delivery to lymphatic metastasis tumors (Ruoslaht 2017). Silver NPs can act as anti-angiogenic molecules by targeting the activation of the P13K/AKT signaling pathway (Gurunathan et al., 2009). The NP-mediated targeting of phosphatidylinositol-3-kinase signaling inhibits the process of angiogenesis (Harfouche et al., 2009). NPs enable the targeting of the p13K pathway, which resulted in the inhibition of endothelial cell proliferation and tumor angiogenesis (Harfouche et al., 2009). Canine parvo virus (CPV) has a natural affinity for transferrin receptors (TIRs) of canine and human origin, and this property could be harnessed and overexpressed by a variety of human tumor cells (Singh, 2009). Labeling nanocrystals with immune cells acts as a platform technology for nanoimmunotherapy (Conniot et al., 2014). The combination of plasmid DNA encoding a multimeric soluble form of CD40L (Psp-d-CD40L) reduced tumor growth, which could be established through B16F-10 melanoma tumor (Stone et al., 2009). The combination of toll-like receptor (TLR) agonists, C-phosphate-G- (CpG), and poly (I:C) reduces the tumor growth and increases the rate of survival (Kaczanowska et al., 2013). It is also associated with a reduction in intra-tumoral CD11c+ dendritic cells and an influx of CD8 T cells.
Biocompatibility of Powdered Materials: The Influence of Surface Characteristics
Published in Michel Nardin, Eugène Papirer, Powders and Fibers, 2006
Patrick Frayssinet, Patrice Laquerriere
Components of the complement can also bridge the particle to the cells. They can be adsorbed at the material surface due to its chemical properties. Exposure to blood during implantation permits extensive opsonization with the labile fragment C3b and the rapid conversion to its hemolytically inactive, but more stable, form C3bi.3 C3b binds to the monocyte receptor CD35. C3bi is also recognized by CD11b/CD18 and CD11C/CD18, which are receptors found at the surface of macrophages.
The chemistry of chlorogenic acid from green coffee and its role in attenuation of obesity and diabetes
Published in Preparative Biochemistry & Biotechnology, 2020
Vaibhavi Pimpley, Siddhi Patil, Kartikeya Srinivasan, Nivas Desai, Pushpa S. Murthy
Additional information on the same aspect of preventing obesity by supplementing CGA was studied by Yongjie et al.[56] They concentrated not only on obesity, but also on liver steatosis and insulin resistance associated with obesity. Two sets of experiments have been carried out to demonstrate these goals. The first set contained, 6-week old C57BL/6 mice which were fed a regular chow or high-fat diet for fifteen weeks with intra-peritoneal injection of cholorgenic acid (100 mg/kg) or DMSO as a carrier solution, twice per week. 2nd set consisted of obese mice were administered with 100 mg/kg CGA (IP) weekly twice or DMSO for six weeks. The animals were inspected for body weight, body composition and consumption of food. At the end of the study, assessment was also carried out of blood glucose, insulin, lipid levels, accumulation of hepatic lipids and homeostasis of glucose were also assessed. The genes engaged in lipid metabolism and inflammation was also evaluated using PCR in real time. Results manifested that CGA considerably detained the growth of diet induced obesity, but did not influence the obese mice, and also supressed the insulin resistance and heaptic steatosis induced by the high fat diet. Analysis of quantitative PCR showed that CGA suppressed hepatic expression of the Pparπ, Cd36, Fabp4 and Mgat1 genes. The observations also depicted attenuation of liver inflammation and decrease in levels of mRNA of macrophage marker genes in white adipose tissue including F4/80, Cd68, Cd11b, Cd11c, and Tnfα, Mcp-1 and Ccr2 encoding inflammatory proteins.[56]