Models of Hepatotoxicity for the Study of Chronic Liver Disease

Chronic liver disease affects globally and has a high morbidity and mortality rate. It is histopathologically characterized by the presence of inflammation, and the progressive destruction and regeneration of the hepatic parenchyma, which can lead to the development of fibrosis, cirrhosis, and hepatocellular carcinoma. Most liver diseases tend to become chronic and can be therefore studied in animal models, as it is possible to quickly develop pathological processes in animals with a high degree of reproducibility and obtain predictive data regarding the different hepatopathies. The development of animal models in the field of hepatology has been geared toward the search for new knowledge meant to favor human well-being and proved useful in translational medicine focused on liver disease. Like any other methodological tool, animal models provide valuable. Obviously, a single model cannot reproduce the complexity and spectrum of all liver diseases, which is why a wide variety are currently employed: they include chemically, immune, diet, surgically, and genetically modified damage in animals and involve biological agents or the use of humanized livers in rodents. This chapter surveys some of the main animal models used in the study of chronic liver disease and the disease characteristics they mimic

Potential Harm of Maltodextrin‐Coated Cadmium Sulfide Quantum Dots in Embryos and Fetuses

Over the past years, there has been significant interest in the study of nanoparticles for clinical applications, particularly quantum dots (QDs). However, previous studies have also shown that QDs can reach the embryo through the placenta, a natural barrier for a large variety of organic substances with diverse molecular structures, and may cause developmental deformities. Due to its essential role in a toxicological profile and its relevance to human safety, knowledge regarding embryotoxicity is of great importance. Previous studies by this research group have shown that CdS‐maltodextrin QDs are biocompatible and nontoxic to cells and animals; however, QDs are able to induce embryotoxic effects. Therefore, as an effort to further address the issue, we studied the effects of CdS‐maltodextrin QDs on embryo and fetus development using an embryotoxicity and teratogenicity assay on chicken embryos. Chicken embryos exposed to CdS‐maltodextrin QDs (0.001, 0.01, 0.1 and 1 µg/kg) in ovo for 72 h showed growth and developmental alterations during the early stage and at the end of their development in a dose‐dependent manner. Decreased development was observed during early stages (Stages 9/10 on the Hamburger‐Hamilton scale) when compared with untreated eggs (Stage 13). Chicken embryos exposed to lower CdS‐maltodextrin QDs doses (0.01, 0.1 and 1 ng/kg) and incubated in ovo for 21 h also showed growth and development alterations during the early stages and at the end of their development in a dose‐dependent manner. However, reduced development was observed at the end of the development period (21 days), and this was associated with death of the chick. Current studies have also shown that CdS‐dextrin induces embryotoxicity and teratogenicity, affecting mainly the CNS, the neural tube and somites in chicken embryos. The nature of the observed abnormalities suggests that these effects could be directly associated with nanoparticle concentrations affecting somitogenesis. Therefore, according to the results, there is a high probability that the prolonged accumulation of QDs in the maternal organism may be potentially harmful on embryo and fetus development. This study is limited to the analysis of embryotoxic and teratogenic effects induced by CdS‐maltodextrin QDs

Delaying surgery for patients with a previous SARS-CoV-2 infection

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