The increasing use of nanomaterials has raised concerns about their potential risks to human health. Recent studies have shown that nanoparticles can cross the placenta barrier in pregnant mice and cause neurotoxicity in their offspring, but a more detailed understanding of the effects of nanoparticles on pregnant animals remains elusive. Here, we show that silica and titanium dioxide nanoparticles with diameters of 70 nm and 35 nm, respectively, can cause pregnancy complications when injected intravenously into pregnant mice. The silica and titanium dioxide nanoparticles were found in the placenta, fetal liver and fetal brain. Mice treated with these nanoparticles had smaller uteri and smaller fetuses than untreated controls. Fullerene molecules and larger (300 and 1,000 nm) silica particles did not induce these complications. These detrimental effects are linked to structural and functional abnormalities in the placenta on the maternal side, and are abolished when the surfaces of the silica nanoparticles are modified with carboxyl and amine groups.

Clostridium butyricum MIYAIRI 588 (CBM 588) is a probiotic bacterium that has previously been used to prevent antibiotic-associated diarrhea. However, the underlying mechanism by which CBM 588 protects the gut epithelial barrier remains unclear. Here, we show that CBM 588 increased the abundance of Bifidobacterium, Lactobacillus, and Lactococcus species in the gut microbiome and also enhanced the intestinal barrier function of mice with antibiotic-induced dysbiosis. Additionally, CBM 588 significantly promoted the expansion of IL-17A-producing gdT cells and IL-17A-producing CD4 cells in the colonic lamina propria (cLP), which was closely associated with changes in the intestinal microbial composition. Additionally, CBM 588 plays an important role in controlling antibiotic-induced gut inflammation through upregulation of anti-inflammatory lipid metabolites such as palmitoleic acid, 15d-prostaglandin J 2 , and protectin D 1 . This study reveals a previously unrecognized mechanism of CBM 588 and provides new insights into gut epithelial barrier protection with probiotics under conditions of antibiotic-induced dysbiosis.

This study was conducted to determine whether boys differ from men in their ability to recover from high-intensity exercise. Two groups of volunteers, 8 prepubertal boys (9-12 yr) and 8 young men (19-23 yr), were similar in their peak oxygen uptake (49.6 +/- 6.6 vs. 51.1 +/- 6.6 ml.min-1 x kg-1), adiposity, and activity levels. On three different occasions subjects performed two consecutive 30-s all-out cycling tasks [Wingate anaerobic test (WAnT)], separated by a 1-, 2-, or 10-min recovery interval. In the boys, mean power reached 89.9 +/- 3.6% of the initial value after 1 min of recovery, 96.4 +/- 2.3% after 2 min, and 103.5 +/- 1.3% after 10 min. For the men, the values were 71.2 +/- 2.6, 77.1 +/- 2.4, and 94.0 +/- 1.3%, respectively (boys vs. men, P < 0.0001). Relative to the external work performed during the first WAnT, the boys had a higher net oxygen uptake (exercise--resting) during the test than the men (83.8 +/- 18.4 vs. 57.8 +/- 6.1 ml/kJ). After the WAnT, the net CO2 output and the respiratory exchange ratio were lower in the boys, and they recovered faster. It was concluded that boys recover faster than men from high-intensity short-term exercise. This may reflect a lower reliance on glycolysis during the WAnT in the boys, leading to less acidosis. It is also possible that the boys had a faster postexercise removal of metabolites.

Preeclampsia, a systemic vascular disorder characterized by new-onset hypertension and proteinuria after 20 weeks of gestation, is the leading cause of maternal and perinatal morbidity and mortality. Maternal endothelial dysfunction caused by placental factors has long been accepted with respect to the pathophysiology of preeclampsia. Over the past decade, increased production of placental antiangiogenic factors has been identified as a placental factor leading to maternal endothelial dysfunction and systemic vascular dysfunction. This review summarizes the recent advances in understanding the molecular mechanisms of endothelial dysfunction caused by placental antiangiogenic factors, and the novel clinical strategies based on these discoveries.