Air entrapment in coatings by way of a tip-streaming meniscus

Entrapment of small air bubbles is a problem for continuous liquid-film coatings processes. The coating of any surface requires that the surrounding air in contact with it be displaced by an advancing liquid interface. Studies of dynamic wetting suggest that if the interface motion is too rapid, the air is not completely removed and it becomes entrained in the coating material. This process, which can lead to undesirable flaws in the form of bubbles, blemishes or voids, limits the speed at which the substrate can be moved in the production of uniform precision coatings. However, the entrapment process is not understood in detail. Here we report an experimental investigation of air entrapment in high-speed coating operations. Tip streaming--a phenomenon well known in emulsification technology, involving the ejection of a fine filament from the cusped interface between two immiscible fluids--is shown to be the precursor of air entrainment. We demonstrate that tip-streaming air filaments emanating from the contact zone of a dynamic liquid interface give rise to minute (approximately 10 microm) bubbles.     

Alzheimer’s disease: the impact of age-related changes in reproductive hormones

Two classes of ovarian steroids, estrogens and progestins, are potent in protecting neurons against acute toxic events as well as chronic neurodegeneration. Herein we review the evidence for neuroprotection by both classes of steroids, provide plausible mechanisms for these potent neuroprotective activities and indicate the need for further clinical trials of both estrogens and progestins in protection against acute and chronic conditions that cause neuronal death. Estrogens at concentrations ranging from physiological to pharmacological are neuroprotective in a variety of in vitro and in vivo models of cerebral ischemia and brain trauma as well as in reducing key neuropathologies of Alzheimers disease. While the mechanisms of this potent neuroprotection are currently unresolved, a mitochondrial mechanism is involved. Progestins have been recently shown to activate many of the signaling pathways used by estrogens to neuroprotect, and progestins have been shown to protect against neuronal loss in vitro and in vivo in a variety of models of acute insult. Collectively, results of these animal and tissue culture models suggest that the loss of both estrogens and progestins at the menopause makes the brain more vulnerable to acute insults and chronic neurodegenerative diseases. Further clinical assessment of appropriate regimens of estrogens, progestins and their combination are supported by these data.