Assessment of a PCL-3D Printing-Dental Pulp Stem Cells Triplet for Bone Engineering: An In Vitro Study.

The search of suitable combinations of stem cells, biomaterials and scaffolds manufacturing methods have become a major focus of research for bone engineering. The aim of this study was to test the potential of dental pulp stem cells to attach, proliferate, mineralize and differentiate on 3D printed polycaprolactone (PCL) scaffolds. A 100% pure Mw: 84,500 ± 1000 PCL was selected. 5 × 10 × 5 mm3 parallelepiped scaffolds were designed as a wood-pilled structure composed of 20 layers of 250 µm in height, in a non-alternate order ([0,0,0,90,90,90°]). 3D printing was made at 170 °C. Swine dental pulp stem cells (DPSCs) were extracted from lower lateral incisors of swine and cultivated until the cells reached 80% confluence. The third passage was used for seeding on the scaffolds. Phenotype of cells was determined by flow Cytometry. Live and dead, Alamar blue™, von Kossa and alizarin red staining assays were performed. Scaffolds with 290 + 30 µm strand diameter, 938 ± 80 µm pores in the axial direction and 689 ± 13 µm pores in the lateral direction were manufactured. Together, cell viability tests, von Kossa and Alizarin red staining indicate the ability of the printed scaffolds to support DPSCs attachment, proliferation and enable differentiation followed by mineralization. The selected material-processing technique-cell line (PCL-3D printing-DPSCs) triplet can be though to be used for further modelling and preclinical experiments in bone engineering studies.

Distribution and expression of GnRH 1, kiss receptor 2, and estradiol α and ß receptors in the anterior brain of females of Chirostoma humboldtianum.

Reproduction in vertebrates is a complex process regulated by many hormones, and by paracrine factors and their receptors. This study aimed to examine the expression of pjGonadotropin-releasing hormone (GnRH 1), the kisspeptin receptor 2 (kissr2), and estradiol receptors α and ß (ER α and ER ß) during different stages of the sexual cycle and their distribution within the anterior brain of females of Chirostoma humboldtianum. Among these molecules, the kissr2 showed the maximal variation in expression, while GnRH 1 showed minimal variation of expression, and ERß and ERα had intermediate variation of expression. The distribution of these molecules in the anterior brain was consistent with their levels of expression; kissr2 was widely distributed throughout the telencephalon and diencephalon, while ER and GnRH 1 showed more restricted distributions. No coexpression of kissr2 and ER in GnRH 1ergic neurons, suggesting that regulation of this GnRH variant is indirectly mediated by kisspeptin and estradiol.

Food-grade titanium dioxide (E171) induces anxiety, adenomas in colon and goblet cells hyperplasia in a regular diet model and microvesicular steatosis in a high fat diet model.

Food-grade titanium dioxide (E171) is a white additive widely used in solid and liquid food products. There is still debate about E171 toxic effects after oral consumption since this additive is deposited in colon, liver, spleen, testis and brain. The consumption of E171 commonly occurs with Western diets that are characterized by a high fat content. Thus, E171 could worsen adverse effects associated with a high fat diet (HFD) such as anxiety, colon diseases and testicular damage. We aimed to evaluate the effects of E171 on anxiety-like behavior, colon, liver and testis and to analyze if the administration of a HFD could exacerbate adverse effects. E171 was administered at ~5 mg/kgbw by drinking water for 16 weeks and mice were fed with a Regular Diet or a HFD. E171 promoted anxiety, induced adenomas in colon, goblet cells hypertrophy and hyperplasia and mucins overexpression, but had no toxic effects on testicular tissue or spermatozoa in regular diet fed-mice. Additionally, E171 promoted microvesicular steatosis in liver in HFD fed-mice and the only HFD administration decreased the spermatozoa concentration and motility. In conclusion, E171 administration increases the number of adenomas in colon, induces hypertrophy and hyperplasia in goblet cells and microvesicular steatosis.