Mathematical and Pharmacokinetic Approaches for the Design of New 3D Printing Inks Using Ricobendazole

Pharmaceutical Research - 3D printing (3DP) makes it possible to obtain systems that are not achievable with current conventional methods, one of them, sustained release floating systems. Floating...     

Migration of titanium dioxide microparticles and nanoparticles through the body and deposition in the gingiva: an experimental study in rats

The aim of this experimental work was to evaluate deposition of titanium dioxide (TiO₂) microparticles and nanoparticles, which could originate from titanium bioimplants, in the gingiva. Wistar rats were injected intraperitoneally (i.p.) with a suspension of TiO₂ particles of different sizes (150, 10, or 5 nm). The rats were killed 12 months post‐injection, and the buccal and lingual gingivae were resected and evaluated using light and scanning electron microscopy. Energy‐dispersive X‐ray spectroscopy (EDS) was used to confirm the presence of titanium in deposits of microparticles and nanoparticles, and the concentration of titanium in tissues was measured using inductively coupled plasma–mass spectrometry (ICP‐MS). Histological examination showed that all experimental groups exhibited agglomerates, in the gingiva, of titanium particles of micrometer size range, with no associated inflammatory response. Higher concentrations of titanium traces were shown, by ICP‐MS, in both buccal and lingual tissues of all experimental groups compared with their matched controls. Titanium concentrations were significantly higher in the buccal gingiva than in the lingual gingiva, and after injection with 5‐nm particles than with 10‐nm particles in both localizations. Titanium microparticles and nanoparticles deposit in the gingiva, and mostly on the buccal side. Gingival deposition of titanium could be considered a tissue indicator of tribocorrosion processes of titanium bioimplants.     

Sézary Syndrome in a 17‐Year‐Old Boy: Clinicopathologic Features and Genomic Profile

We describe the case of a 17‐year‐old Hispanic boy who had had erythroderma and diffuse lymphadenopathy for approximately 6 months. A diagnosis of Sézary syndrome was made on the basis of the histologic features of the skin; the presence of the same T‐cell clone on the skin, blood, and bone marrow; and the high CD4⁺ lymphocyte count with an aberrant phenotype in peripheral blood; bone marrow involvement was also present. The patient was treated with systemic gemcitabine and achieved partial remission.     

Chronic sleep loss disrupts blood–testis and blood–epididymis barriers,and reduces male fertility

Sleep loss increases blood–brain barrier permeability. As the blood–brain barrier and the blood–tissue barriers in the reproductive tract (blood–testis and blood–epididymis barriers) share common characteristics, we hypothesized that sleep restriction may also modify their barrier function. Previous reports showed that sleep loss decreased sperm viability and progressive fast mobility, which may be a consequence of altered blood–testis and blood–epididymis barrier. Therefore, we quantified changes in blood–testis and blood–epididymis barrier after sleep loss and related them to male fertility. Adult male Wistar rats were sleep restricted using the multiple‐platform technique in a protocol of 20 hr daily sleep deprivation plus 4 hr of sleep recovery in the home‐cage. At the 10th day, barrier permeability assays were performed with Na‐fluorescein, 10 kDa Cascade blue‐dextrans and Evans blue, and the expression of tight junction proteins, actin and androgen receptor was quantified. At the 10th day of sleep restriction and after sleep recovery days 1–7, males were placed with sexually receptive females, sexual behaviour was tested, and the percentage of pregnancies was calculated. Sleep restriction increased the barrier permeability to low‐ and high‐molecular‐weight tracers, and decreased the expression of tight junction proteins, actin and androgen receptor. Concomitantly, sleep restriction reduced the percentage of ejaculating males and the number of pregnancies. Sleep recovery for 2–3 days progressively re‐established fertility, as indicated by a higher percentage of ejaculating males and impregnated females. In conclusion, chronic sleep loss alters fertility concomitantly with the disruption of the blood–tissue barriers at the reproductive tract, the mechanism involves androgen signalling.