Active interfacial modifier: stabilization mechanism of water in silicone oil emulsions by peptide-silicone hybrid polymers.

We have developed hybrid amphiphilic polymers consisting of a silicone backbone modified with hydrocarbon chains and hydrolyzed silk peptides. These polymers are molecularly soluble neither in water nor in most of organic solvent, but are attractive with these solvents. We assume that this property enables the polymers to form "an independent third phase" between immiscible two liquid phases and stabilize the emulsion system, based on a fundamentally distinguishable mechanism from the approach by conventional surfactants. We have named these amphiphilic polymers "active interfacial modifier (AIM)" and studied physicochemical properties of AIM-stabilized water-in-silicon oil emulsions. The addition of AIM to a mixture of water and decamethylcyclopentasiloxane (D(5)) has achieved preparation of stable W/O emulsions (droplet size = ca. 1 microm) in a wide range of the three components, even under relatively gentle vortex mixing. Interestingly, the prepared W/O emulsions are found to be nearly genuine or quasi Newtonian fluid with low viscosity when water content is in the range from 0 to 36 wt % for the fixed weight ratio of AIM/D(5) = 6/4. This is a good piece of evidence that AIM forms the independent third phase, where the Newtonian shear occurs at the D(5)/AIM interface. The presence of AIM as third phase has also been confirmed by fluorescence probe method with confocal laser scanning microscopy. As such, AIM can activate interfaces by the least amount to cover interfaces as an independent third phase, and hence, this provides a new concept achieving a precise control of interfacial properties.

Dysregulation of the Bmi-1/p16(Ink4a) pathway provokes an aging-associated decline of submandibular gland function.

Bmi-1 prevents stem cell aging, at least partly, by blocking expression of the cyclin-dependent kinase inhibitor p16(Ink4a) . Therefore, dysregulation of the Bmi-1/p16(Ink4a) pathway is considered key to the loss of tissue homeostasis and development of associated degenerative diseases during aging. However, because Bmi-1 knockout (KO) mice die within 20 weeks after birth, it is difficult to determine exactly where and when dysregulation of the Bmi-1/p16(Ink4a) pathway occurs during aging in vivo. Using real-time in vivo imaging of p16(Ink4a) expression in Bmi-1-KO mice, we uncovered a novel function of the Bmi-1/p16(Ink4a) pathway in controlling homeostasis of the submandibular glands (SMGs), which secrete saliva into the oral cavity. This pathway is dysregulated during aging in vivo, leading to induction of p16(Ink4a) expression and subsequent declined SMG function. These findings will advance our understanding of the molecular mechanisms underlying the aging-related decline of SMG function and associated salivary gland hypofunction, which is particularly problematic among the elderly.