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MOF-based Electrochemical Sensors for Protein Detection
Published in Ram K. Gupta, Tahir Rasheed, Tuan Anh Nguyen, Muhammad Bilal, Metal-Organic Frameworks-Based Hybrid Materials for Environmental Sensing and Monitoring, 2022
Yang Liu, Juanhua Zhou, Shiyu Zhang, Hongye Wang
Cardiovascular diseases are common diseases that seriously threaten human health and rank first among various causes of death. C-reactive protein (CRP) can be an indicator of cardiovascular diseases in clinical diagnosis. Wang et al. synthesized size/morphology adjustable NH2-Ni-MOFs as electrocatalysts and realized highly sensitive detection of CRP based on an aptamer binding induced DNA walker–antibody sandwich assay [64]. Furthermore, an innovative label-free CRP immunosensor was constructed on biocompatible ZnO/MPC composite which was prepared by pyrolysis of a mixed ligand MOF [65]. This kind of novel carbon material possessed charming electrochemical properties and could be a potential carrier of load identification units. Moreover, galectin-3 (Gal-3) was associated with heart failure closely. There was a sandwich-type electrochemical immunosensor for detecting Gal-3 based on N-doped graphene nanoribbon immobilized Fe-based-Metal-organic frameworks deposited with Au nanoparticles (N-GNRs-Fe-MOFs@Au NPs) [66].
Macrophage Targeting: A Promising Strategy for Delivery of Chemotherapeutics in Leishmaniasis and Other Visceral Diseases
Published in Sarwar Beg, Mahfoozur Rahman, Md. Abul Barkat, Farhan J. Ahmad, Nanomedicine for the Treatment of Disease, 2019
Jaya Gopal Meher, Pankaj K. Singh, Yuvraj Singh, Mohini Chaurasia, Anita Singh, Manish K. Chourasia
Macrophages involved in fibrotic disease including liver fibrosis are well known to overexpress Galectin–3 protein (gal–3 receptors) which has the ability to bind terminal galactose residues in glycoproteins. However, it is also reported that expression of gal–3 receptors is very low in normal liver. Taking this fact into consideration Traber and team hypothesized that targeting the gal–3 receptors in liver macrophages would be a suitable strategy in delivery drug to liver macrophages (Traber and Zomer, 2013). In continuation to their hypothesis, researchers employed GM-CT–01 and GR-MD–02 as inhibitors for treatment of fibrosis in murine model. As per their findings, these inhibitors could efficiently target liver macrophages and reduce gal–3 activated macrophage-related complications as well as hepatocyte ballooning, collagen deposition, inflammatory infiltration at intra-portal and intra-lobular level and fat accumulation. In various physiological conditions, activation of macrophages leads to release of pro-inflammatory cytokines like TNF which can aggravate progression of liver diseases. Under such conditions, anti-TNF antibody (e.g., infliximab) is given, but it suffers from lack of specificity and in many cases can immunocompromise the treated patient causing development of bacterial infections. So a target-specific strategy is needed, and delivery of siRNA against TNF has been found to be the best option. He et al. have developed mannose-modified trimethyl chitosan-cysteine (MTC) conjugate nanoparticles (He et al., 2013). They have employed TNF-α siRNA for gene silencing of TNF, and the nanoformulations were developed by ionic gelation technique. This unique delivery system was equipped with trimethyl, thiol, and mannose groups along with a chitosan backbone, which were altogether programmed in such a way that they could be activated at different time as well as environmental conditions ensuring the protection of TNF-α siRNA and delivery at target site. The researchers found that that the delivery system could efficiently deliver TNF-α siRNA to liver macrophages via a clathrin-independent endocytosis. Similar effects were also observed after oral administration in mice as they were protected against acute hepatic injury caused by inflammation-induced liver damage.
Potential adverse cardiac remodelling in highly trained athletes: still unknown clinical significance
Published in European Journal of Sport Science, 2018
Luigi Gabrielli, Marta Sitges, Mario Chiong, Jorge Jalil, María Ocaranza, Silvana Llevaneras, Sebastian Herrera, Rodrigo Fernandez, Rodrigo Saavedra, Fernando Yañez, Luis Vergara, Alexis Diaz, Sergio Lavandero, Pablo Castro
The repetitive cycle of oxidative stress increase and heart muscle mechanical deformation during extreme exercise (Krip, Gledhill, Jamnik, & Warburton, 1997) might induce cardiomyocyte cell membrane damage that correlates with an elevation of multiple cardiac injury biomarkers such as myoglobin, cardiac troponin-I, creatine kinase MB and B-type natriuretic peptide (Fortescue et al., 2007). These biomarkers could stimulate immune cells recruitment – including lymphocytes, macrophages and mast cells – toward the damage area (Scherr et al., 2011). Then, immune cells would secrete pro-inflammatory cytokines, such as interleukin-6, which work as extracellular signals to induce fibroblast to myofibroblast differentiation with the subsequent secretion of procollagen (Benito et al., 2011). This phenomenon could be responsible for fibrosis deposited in patches in the myocardium and larges arteries (Figure 1(D)) (La Gerche et al., 2012). In fact, in rat models, prolonged strenuous exercise increased expression of transforming growth factor β-1 (TGF β-1) – the main mediator of fibroblast activation and cardiac fibrosis – in the right and left atria and right ventricle resulting in increased cardiac stiffness (Benito et al., 2011). Interestingly, this mechanism could be correlated with the elevation of galectin-3 plasma level and cardiac fibrosis in human (Hattasch et al., 2014).