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Sustainable Green Polymeric Nanoconstructs for Active and Passive Cancer Therapeutics
Published in Vladimir Torchilin, Handbook of Materials for Nanomedicine, 2020
Ankit Rochani, Sreejith Raveendran, D. Sakthi Kumar
In the previous subsections, we have seen various biomaterials like proteins and polysaccharides that self-assemble to form NPs for the delivery of drugs and metal ions like iron and gold NPs for getting synergistic modes of cancer therapy. Ferritin is a natural example of symmetrically assembled carrier protein. It is a universally expressed protein and naturally works as a storage of iron in prokaryotes and eukaryotes. Ferritin is around 450 kDa protein that consists of 24 protein subunits that form a nanocage-like structure (as shown in Fig. 7.2b). The nanocage is typically around 8 and 12 nm in size for internal and external diameter, respectively. Ferritin naturally helps in maintaining the balance of free and bound form of iron atoms in plasma. Usually, ferritin can carry around 2–4000 Fe atoms/protein cage. Eventually, the ferritin proteins get damaged and it exposes Fe atoms to cytoplasmic reducing agents, initiates redox reaction and produces hemosiderin (also known as insoluble cellular iron) [183, 184]. Pharmacokinetics and dynamics of iron-complexed ferritin NPs is a naturally driven phenomenon. Hence, it becomes obvious to explore this system as a natural nanodrug delivery system for therapeutic benefits.
Effects of continuous and pulsatile flows generated by ventricular assist devices on renal function and pathology
Published in Expert Review of Medical Devices, 2018
Takuma Miyamoto, Jamshid H. Karimov, Kiyotaka Fukamachi
ARF may occur during severe episodes of hemoglobinuria. Persistent severe hemoglobinuria is also associated with substantial proximal tubule hemosiderin deposition. In a typical course of CF LVAD support, severe hemoglobinuria did not occur unless there were complications leading to hemolysis, such as device thrombosis. However, some amount of hemolysis occurs during CF LVAD support due to extraphysiologic shear stress. Rother et al. [50] proposed the existence of hemolysis-associated smooth muscle dystonia, vasculopathy, and endothelial dysfunction. Nitric oxide reacts with hemoglobin in an extremely fast and irreversible reaction that produces an inactive oxidation product nitrate (NO3) and methemoglobin. The authors propose that the release of hemoglobin during intravascular hemolysis results in excessive consumption of nitric oxide, subsequent reduction in guanylate cyclase activity, smooth muscle contraction, vasoconstriction, and platelet activation/aggregation. John et al. [51] investigated changes in the endothelial system in CF LVAD recipients. They found no significant differences in the number of circulating endothelial cells in either CF LVAD recipients or control patients (patients who underwent non-LVAD cardiac surgery) compared with those in the normal range. However, markers of endothelial activation (including vascular cell adhesion molecule-1, intercellular adhesion molecule, E-selectin, and tissue factor) were all significantly higher at baseline in CF LVAD recipients. All these markers further peaked on POD 7 and remained significantly elevated until POD 180. Nascimbene et al. [52] focused on microparticles. A persistent and systemic generation of microparticles can lead to a sustained pro-inflammatory and pro-coagulant state and can cause activation of the endothelium, which responds to microparticle-bound tissue factor. Phosphatidylserine plus microparticle levels were higher in patients at baseline than in healthy controls. After CF LVAD implantation, phosphatidylserine plus microparticle levels were high in patients at post-surgery baseline, at discharge after implantation, and at 3 months. Ahmad et al. [53] examined long-term changes in commonly measured laboratory parameters in 37 consecutive patients, aged 18 years and older, who required MCS with a CF LVAD. Median concentrations of neutrophil gelatinase-associated lipocalin – a diagnostic biomarker of early AKI, also considered a risk marker of atherosclerosis [54] – did not change significantly, despite concomitant decreases in Cre after CF LVAD support.