Centrifuge-Free Separation of Solution-Exfoliated 2D Nanosheets via Cross-Flow Filtration.

Solution-processed graphene is a promising material for numerous high-volume applications including structural composites, batteries, sensors, and printed electronics. However, the polydisperse nature of graphene dispersions following liquid-phase exfoliation poses major manufacturing challenges, as incompletely exfoliated graphite flakes must be removed to achieve optimal properties and downstream performance. Incumbent separation schemes rely on centrifugation, which is highly energy-intensive and limits scalable manufacturing. Here, cross-flow filtration (CFF) is introduced as a centrifuge-free processing method that improves the throughput of graphene separation by two orders of magnitude. By tuning membrane pore sizes between microfiltration and ultrafiltration length scales, CFF can also be used for efficient recovery of solvents and stabilizing polymers. In this manner, life cycle assessment and techno-economic analysis reveal that CFF reduces greenhouse gas emissions, fossil energy usage, water consumption, and specific production costs of graphene manufacturing by 57%, 56%, 63%, and 72%, respectively. To confirm that CFF produces electronic-grade graphene, CFF-processed graphene nanosheets are formulated into printable inks, leading to state-of-the-art thin-film conductivities exceeding 104 S m-1 . This CFF methodology can likely be generalized to other van der Waals layered solids, thus enabling sustainable manufacturing of the diverse set of applications currently being pursued for 2D materials.

Neurotrophin-3 signaling maintains maturational homeostasis between neuronal populations in the olfactory epithelium.

Neurons within the olfactory system undergo functional turnover throughout life. This process of cell death and compensatory neurogenesis requires feedback between neuronal populations of different developmental ages. We examined the role of NT-3 in this process. NT-3 was localized within both the olfactory bulb and olfactory epithelium. Mice null for NT-3 showed increased numbers of immature neurons, without change in the number of mature neurons. This was due to compensatory alterations in apoptosis of mature and immature neuronal populations. Using a primary olfactory neuronal culture, NT-3 was found to directly activate the PI3K/Akt pathway and indirectly activate the MAPK and PLC pathways. Activated PI3K/Akt promoted mature neuronal survival and induced the release of secondary factors, which activated the MAPK and PLC pathways to reduce neuronal precursor proliferation and inhibit neuronal maturation. These effects of NT-3 serve to maintain homeostasis between neuronal populations within the olfactory epithelium.

Expression of MeCP2 in olfactory receptor neurons is developmentally regulated and occurs before synaptogenesis.

Rett syndrome, a neurodevelopmental disorder hypothesized to be due to defective neuronal maturation, is a result of mutations in the mecp2 gene encoding the transcriptional repressor methyl-CpG binding protein (MeCP2). We utilized the olfactory system, which displays postnatal neurogenesis, as a model to investigate MeCP2 expression during development and after injury. MeCP2 expression increased postnatally, localizing to mature olfactory receptor neurons (ORNs) and sustentacular supporting cells. The timing of MeCP2 expression was defined by using detergent ablation (to remove the ORNs) and unilateral olfactory bulbectomy (to remove the ORN target), both of which increase neurogenesis. MeCP2 expression in the ORNs reached prelesioning levels as cells matured after ablation, whereas expression was not completely restored after bulbectomy, in which functional synaptogenesis cannot occur. Thus, MeCP2 expression correlates with the maturational state of ORNs, and precedes synaptogenesis. Identifying the time window of MeCP2 expression should help further clarify the biological defects in Rett syndrome.