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The skin is a tissue constantly exposed to the risk of damage, such as cuts, burns, and genetic disorders. The standard treatment is autograft, but it can cause pain to the patient being extremely complex in patients suffering from burns on large body surfaces. Considering that there is a need to develop technologies for the repair of skin tissue like 3D bioprinting. Skin is a tissue that is approximately 1/16 of the total body weight and has three main layers: epidermis, dermis, and hypodermis. Therefore, there are several studies using cells, biomaterials, and bioprinting for skin regeneration. Here, we provide an overview of the structure and function of the epidermis, dermis, and hypodermis, and showed in the recent research in skin regeneration, the main cells used, biomaterials studied that provide initial support for these cells, allowing the growth and formation of the neotissue and general characteristics, advantages and disadvantages of each methodology and the landmarks in recent research in the 3D skin bioprinting., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

This chapter describes laboratory protocols for TEM and SEM approaches allowing the examination of the dental hard tissues' constituents at the ultrastructural level. TEM has the highest resolution power to examine the cellular and extracellular matrix ultrastructure inside a given sample, detecting the presence, location, and quantification of organelles related to the metabolism of the cell type as well as membrane specializations. SEM allows the observation of the sample surface, for examining dimensional topography and distribution of exposed features.

Background: Although Toxoplasma gondii infection is normally asymptomatic, severe cases of toxoplasmosis may occur in immunosuppressed patients or congenitally infected newborns. When a fetal infection is established, the recommended treatment is a combination of pyrimethamine, sulfadiazine and folinic acid (PSA). The aim of the present study was to evaluate the efficacy of azithromycin to control T. gondii infection in human villous explants., Methods: Cultures of third trimester human villous explants were infected with T. gondii and simultaneously treated with either PSA or azithromycin. Proliferation of T. gondii, as well as production of cytokines and hormones by chorionic villous explants, was analyzed., Results: Treatment with either azithromycin or PSA was able to control T. gondii infection in villous explants. After azithromycin or PSA treatment, TNF-α, IL-17A or TGF-β1 levels secreted by infected villous explants did not present significant differences. However, PSA-treated villous explants had decreased levels of IL-10 and increased IL-12 levels, while treatment with azithromycin increased production of IL-6. Additionally, T. gondii-infected villous explants increased secretion of estradiol, progesterone and HCG+β, while treatments with azithromycin or PSA reduced secretion of these hormones concurrently with decrease of parasite load., Conclusions: In conclusion, these results suggest that azithromycin may be defined as an effective alternative drug to control T. gondii infection at the fetal-maternal interface.

Toxoplasma gondii induces a potent IL-12 response early in infection that results in IFN-γ-dependent control of parasite growth. It was previously shown that T. gondii soluble tachyzoite antigen (STAg) injected 48 hr before intraperitoneal infection reduces lipoxin A4 and 5-lipoxygenase (5-LO)-dependent systemic IL-12 and IFN-γ production as well as hepatic immunopathology. This study investigated the ability of STAg-pretreatment to control the fatal intestinal pathology that develops in C57BL/6 mice orally infected with 100 T. gondii cysts. STAg-pretreatment prolonged the animals' survival by decreasing tissue parasitism and pathology, mainly in the ilea. Protection was associated with decreases in the systemic IFN-γ levels and IFN-γ and TNF message levels in the ilea and with increased TGF-β production in this tissue, but protection was independent of 5-LO and IL-4. STAg-pretreatment decreased CD4(+) T cell, NK cell, CD11b(+) monocyte and CD11b(+)CD11c(+) dendritic cell numbers in the lamina propria and increased CD8(+) T cells in the intestinal epithelial compartment. In parallel, decreases were observed in iNOS and IL-17 expression in this organ. These results demonstrate that pretreatment with STAg can induce the recruitment of protective CD8(+) T cells to the intraepithelial compartment and decrease proinflammatory immune mechanisms that promote intestinal pathology in T. gondii infection.