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Published in Chad A. Mirkin, Spherical Nucleic Acids, 2020
Aleksandar F. Radovic-Moreno, Natalia Chernyak, Christopher C. Mader, Subbarao Nallagatla, Richard S. Kang, Liangliang Hao, David A. Walker, Tiffany L. Halo, Timothy J. Merkel, Clayton H. Rische, Sagar Anantatmula, Merideth Burkhart, Chad A. Mirkin, Sergei M. Gryaznov
To further elucidate therapeutic potential of IR-SNAs, we sought to determine whether SNA structure exhibited advantages over sequence- and chemistry-matched free unformulated TLR antagonist oligonucleotides in vivo. Nonalcoholic steatohepatitis (NASH) is a fatty liver disease with prevalence as high as 3–5% in the United States. It is characterized by pathologic changes in livers of patients, including steatosis and inflammation, which ultimately progress in a subset of patients to nodular fibrosis, full-blown cirrhosis, and hepatocellular carcinoma (HCC). Currently, there are no FDA-approved treatments for this disease.
Big Data in Medical Image Processing
Published in R. Suganya, S. Rajaram, A. Sheik Abdullah, Big Data in Medical Image Processing, 2018
R. Suganya, S. Rajaram, A. Sheik Abdullah
Accumulation of fat may also be accompanied by a progressive inflammation of the liver (hepatitis), called steatohepatitis. By considering the contribution by alcohol, fatty liver may be termed alcoholic steatosis or non-alcoholic fatty liver disease (NAFLD), and the more severe forms as alcoholic steatohepatitis (part of alcoholic liver disease) and non-alcoholic steatohepatitis (NASH).
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
Another study by Melgert et al. shows kupffer cells targeting of anti-inflammatory drug dexamethasone (Melgert et al., 2001). The researchers realized that kupffer cells are one of the vital players in pathogenesis of inflammatory liver diseases, which if not taken care of may lead to fibrosis. Accordingly, they have coupled mannosylated albumin with dexamethasone and examined its targeting efficiency to kupffer cells in liver employing organ cultures as well as fibrosis induced by bile duct ligation in rats. Their experimental findings suggested that the mannosylated albumin-dexamethasone conjugate could be selectively taken-up by kupffer cells in fibrotic and healthy rats. Significant reduction in intrahepatic ROS in animals and decrease in TNF-alpha production in in-vitro conditions supported better targeting of drug to target cells. So this combination could be treated as a suitable liver macrophage targeting alternative for drug delivery. Apart from inflammatory liver diseases, non-alcoholic fatty liver diseases are also one of the leading causes of death in human beings with chronic liver diseases. This has risen because of bad food habits such as consumption of high caloric carbohydrates which may also lead to non-alcoholic steatohepatitis. Researchers have shown that lipogenetic effects of fructose (high caloric intake) and activation of liver macrophages due to endotoxins are major reasons for development and progression of these liver diseases. In light of these findings, Svendsen et al. investigated kupffer cell targeting by using an anti-CD163-IgG-dexamethasone conjugate (Svendsen et al., 2017). They intended to target the hemoglobin scavenger receptor CD163 in Kupffer cells. A low dose of anti-CD163-IgG-dexamethasone was administered to rats on a high-fructose diet, and within few weeks a significant reduction in hepatocyte ballooning, glycogen deposition, inflammation as well as fibrosis was observed. Dexamethasone alone or dexamethasone conjugated to control-IgG could not produce such therapeutic effect in rats.
Histological and immunohistochemical study of the effect of liraglutide in experimental model of non-alcoholic fatty liver disease
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Mai Salah Nour, Zeinab Abd El-Hay Sakara, Nawal Awad Hasanin, Shereen Mohamed Hamed
The ‘two-hit’ concept is the most widely accepted explanation for how NAFLD develops, despite the fact of its etiology is still unknown. The disruption of fatty acid metabolism, which results in simple steatosis, is the first hit. Steatosis increases the susceptibility of the liver to injury mediated by ‘second hits’, such as inflammatory cytokines/adipokines, mitochondrial dysfunction and oxidative stress, which in turn lead to steatohepatitis and/or fibrosis [8].