The dynamics of isolated air bubbles crossing the horizontal interface separating two Newtonian immiscible liquids initially at rest are studied both experimentally and computationally. High-speed video imaging is used to obtain a detailed evolution of the various interfaces involved in the system. The size of the bubbles and the viscosity contrast between the two liquids are varied by more than one and four orders of magnitude, respectively, making it possible to obtain bubble shapes ranging from spherical to toroidal. A variety of flow regimes is observed, including that of small bubbles remaining trapped at the fluid-fluid interface in a film-drainage configuration. In most cases, the bubble succeeds in crossing the interface without being stopped near its undisturbed position and, during a certain period of time, tows a significant column of lower fluid which sometimes exhibits a complex dynamics as it lengthens in the upper fluid. Direct numerical simulations of several selected experimental situations are performed with a code employing a volume-of-fluid type formulation of the incompressible Navier-Stokes equations. Comparisons between experimental and numerical results confirm the reliability of the computational approach in most situations but also points out the need for improvements to capture some subtle but important physical processes, most notably those related to film drainage. Influence of the physical parameters highlighted by experiments and computations, especially that of the density and viscosity contrasts between the two fluids and of the various interfacial tensions, is discussed and analysed in the light of simple models and available theories.

The placenta exchanges nutrients between the mother and the fetus and requires a constant abundant energy supply. Adiponectin (a cytokine produced primarily by adipose tissue) controls glucose and lipid homeostasis. It is well-known that maternal serum adiponectin levels are inversely related to birth weight, suggesting that adiponectin has a negative effect on fetal growth. This effect appears to be related to the control of nutrient transporters in human placenta. However, the underlying molecular mechanisms have not yet been characterized. In the present work, we studied adiponectin's direct effect on human primary cytotrophoblasts from first-trimester placenta. Our result showed that in placental cells, adiponectin 1) inhibits the expression of the major glucose transporters (GLUT1 and GLUT12) and sodium-coupled neutral amino acid transporters (SNAT1, SNAT2, and SNAT4), 2) enhances total ATP production but decreases lactate production, 3) inhibits mitochondrial biogenesis and function, and 4) stimulates cell death by enhancing the expression of the pro-apoptotic B-cell lymphoma-2 (BCL-2)-associated X protein (BAX) and tumor protein P53 (TP53) gene expression and inducing the caspase activity. Small-interfering RNA mediating the down-regulation of adiponectin receptors (ADIPOR1 and ADIPOR2) was used to demonstrate that adiponectin effects on placental nutrient transport and apoptosis seemed to be essentially mediated by these specific receptors. Taken as a whole, these results strongly suggest that adiponectin regulates human placental function by limiting nutrient transporter expression and inducing apoptosis. These findings may help us to better understand adiponectin's role in placental pathologies such as intrauterine growth restriction, which is characterized by fetal weight loss and drastic apoptosis of placental cells.

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Infertility now affects one in seven couples, and the prevalence of this condition continues to increase. Ovulatory defects and unknown causes account for more than half of the cases of infertility. It has been postulated that a significant proportion of these cases are directly or indirectly related to obesity, since the presence of excess adipose tissue has a variety of effects on reproductive function. Here, we review on the effects of the two major adipokines (leptin and adiponectin) on fertility, with a focus on the first steps in embryo implantation and the key components of fetal-maternal interface (the placenta and the endometrium). These adipokines are reportedly involved in the regulation of cell proliferation and differentiation, and as such affect local angiogenesis, immune tolerance and inflammatory processes in placental and endometrial tissues. In placental cells, leptin and adiponectin also modulate trophoblast invasiveness and the nutrient supply. These observations strongly suggest by interfering with the placenta and endometrium, adipokines can create a favorable environment for embryo implantation and have a key role in fetal-maternal metabolism, fetal-maternal communication, and gestation. Given that reproductive functions are tightly coupled to the energy balance, metabolic abnormalities may lead to the development of complications of pregnancy and changes in fetal growth. In this context, we suggest that the leptin/adiponectin ratio may be a clinically valuable marker for detecting a number of pathologies in pregnancy.