The use of human cadavers is beneficial in teaching gross human anatomy, training, and development in medicine. Fresh-frozen cadavers initially exhibit natural color, tenderness, and flexibility. They also present innumerable difficulties, including the requirement of freezers for storage and a few weeks’ work time because of fast decay. The risk of infection is also significant. A possible choice for fresh-frozen cadavers is embalmed cadavers. The requested characteristic needed for successful embalming is acceptable long-term structural preservation of organs and tissues with minimal deformity and prevention of outward aspects. Scientists are trying to develop an ideal embalming solution to preserve the human body. Such a solution renders the flexibility of internal organs, preventing dryness, and reducing fungal or bacterial growth. Cadavers should be in a condition comparable to that of an unembalmed cadaver, and the chemicals used in the solution should not be harmful to persons during manipulation. The promising results have been obtained by the use of different embalming techniques by many faculties of medicine as a tool to enhance the teaching of anatomy to students. The use of human cadavers is beneficial in teaching gross human anatomy, training, and development in medicine. Fresh-frozen cadavers initially exhibit natural color, tenderness, and flexibility. They also present innumerable difficulties, including the requirement of freezers for storage and a few weeks’ work time because of fast decay. The risk of infection is also significant. A possible choice for fresh-frozen cadavers is embalmed cadavers. The requested characteristic needed for successful embalming is acceptable long-term structural preservation of organs and tissues with minimal deformity and prevention of outward aspects. Scientists are trying to develop an ideal embalming solution to preserve the human body. Such a solution renders the flexibility of internal organs, preventing dryness, and reducing fungal or bacterial growth. Cadavers should be in a condition comparable to that of an unembalmed cadaver, and the chemicals used in the solution should not be harmful to persons during manipulation. The promising results have been obtained by the use of different embalming techniques by many faculties of medicine as a tool to enhance the teaching of anatomy to students.

The existing in vitro toxicological models lack translational potential, which makes difficult the application of gathered information to clinical usage. To tackle this issue, we built a model with four different types of primary liver cells: hepatic sinusoidal endothelial cells, hepatic stellate cells, Kupffer cells and hepatocytes. We cultured them in different combinations of composition and volumes of cell medium, hepatocyte proportions of total cells and additions of extracellular matrixes. We added rifampicin (RIF), ibuprofen (IBU) and 5-fluorouracil (5-FU) to this model and observed the microanatomy and physiology changes for a week with preclinical and clinical instruments. Among the different model configurations, we selected the feature combination of the in vitro model that had similar biomarker values to those measured in clinical diagnostics. When we exposed the selected model configuration to RIF, IBU and 5-FU, we observed similar glucose, triglyceride and albumin dynamics as in vivo (from clinical data). Therefore, we have built an in vitro liver model that resembles the liver microenvironment, and we have analysed it with clinical instrumentation to facilitate data translation. Furthermore, during these observations, we found that Kupffer and LSEC cells are suitable candidates for the search for clinical diagnostic markers of liver function.

The main focus of in vitro toxicity assessment methods is to assess the viability of the cells, which is usually based on metabolism changes. Yet, when exposed to toxic substances, the cell triggers multiple signals in response. With this in mind, we have developed a promising cell-based toxicity method that observes various cell responses when exposed to toxic substances (either death, division, or remain viable). Based on the collective cell response, we observed and predicted the dynamics of the cell population to determine the toxicity of the toxicant. The method was tested with two different conformations: In the first conformation, we exposed a monoculture model of blood macrophages to UV light, hydrogen peroxide, nutrient deprivation, tetrabromobisphenol A, fatty acids, and 5-fluorouracil. In the second, we exposed a coculture liver model consisting of hepatocytes, hepatic stellate cells, Kupffer cells, and liver sinusoidal endothelial cells to rifampicin, ibuprofen, and 5-fluorouracil. The method showed good accuracy compared to established toxicity assessment methods. In addition, this approach provided more representative information on the toxic effects of the compounds, as it considers the different cellular responses induced by toxic agents.

Analysing the human body by direct observation can lead to misinterpretation of underlying trends, whereas in vitro organ models facilitate their understanding. Likewise, in vitro organ models serve as valuable tools for assessing the toxicity of compounds. However, none of the existing models had the features we considered critical for toxicity assessment, so we developed an in vitro liver model for toxicity assessment. We used four different types of primary liver cells: Hepatic sinusoidal endothelial cells, hepatic stellate cells, Kupffer cells and hepatocytes. We cultured them in different combinations of composition and volume of cell medium, hepatocyte proportion of total cells, and addition of extracellular matrix. We added rifampicin, ibuprofen and 5-fluorouracil to this model and observed the microanatomy and physiology changes for a week with preclinical and clinical instruments. Among the different model configurations, we selected the feature combination of the in vitro model that had similar biomarker values to those measured by the clinical instruments used in clinical diagnostics. When we exposed the selected model configuration to rifampicin, ibuprofen and 5-fluorouracil, the viability of Kupffer cells and liver sinusoidal endothelial cells was significantly lower than in the untreated samples. In contrast, we observed negligible viability of hepatocytes compared to the untreated samples. We have built an in vitro liver model that resembles the liver microenvironment and we have analysed it with clinical instrumentation to facilitate the data translation. In this sense, we have established that Kupffer and LSEC cells are suitable candidates for the search for clinical diagnostic markers of liver function.

The main focus of the in vitro toxicity assessment methods is on the viability of the cells, which is usually based on metabolism changes. Yet, when exposed to toxic substances, the cell triggers multiple signals in response. With this in mind, we have developed a promising cell-based toxicity method that observes various cell responses when exposed to toxic substances (either death, division or remaining viable). Based on the collective cell response, we observed and predicted the dynamics of the cell population to determine the toxicity of the toxicant. The method was tested with two different conformations: In the first conformation, we exposed a monoculture model of blood macrophages to UV light, hydrogen peroxide, nutrient deprivation, tetrabromobisphenol A, fatty acids and 5-fluorouracil. In the second, we exposed a coculture liver model consisting of hepatocytes, hepatic stellate cells, Kupffer cells and liver sinusoidal endothelial cells to rifampicin, ibuprofen and 5-fluorouracil. The method showed good accuracy compared to established toxicity assessment methods. In addition, this approach provided more representative information on the toxic effects of the compounds as it considers the different cellular responses induced by toxic agents.

The negative health effects associated with exposure to heavy metals are of global concern, so their toxic mechanisms and potency should be identified to develop effective prevention. In this sense, we analysed the toxicity of arsenic (+3 and +5 valences) and meHg in intestinal epithelial cells (H4) and blood macrophages (TLT). We performed crystal violet, MTT, proliferation, ROS, H2ax, cell cycle arrest, apoptosis and cell shape assays with different concentrations of these elements to determine the potency and mechanism of their toxicity. The potency of the heavy metals differs in both cell types and among each element. In addition, all the selected heavy metals induced ROS formation and histone exposure, but each element had different pathways associated with their toxicity. For example, each element induced cell cycle arrest in different phases of H4 and TLT cells, and suggest that each element induce different cell death pathways in each cell type. Understanding the mechanisms of toxicity may help to implement effective strategies for the prevention or mitigation of the heavy metal toxicity.