Rare earth elements (REE) are widely used in high technologies, medical devices, and military defense systems, and are especially indispensable in emerging clean energy. Along with the growing market of green energy in the next decades, global demand for REE will increase continuously, which will put great pressure on the current REE supply chain. The global REE production is currently mainly concentrated in China and Australia; they respectively contributed 85% and 10% in 2016. However, there are 178 deposits widely distributed in the world, and reported REE resources as of 2017 totaled 478 megaton (Mt) rare earth oxides (REO); 58% of these deposits contained exceed 0.1 Mt REO; 59 deposits have been technically assessed. These resources could sustain the global REE production at the current pace for more than a hundred years. It is noted that REE demand from clean technologies will reach 51.9 thousand metric tons (kt) REO in 2030, Nd and Dy, respectively, comprising 75% and 9%, while these two elements comprise 15% and 0.52% of the global REE resources, respectively. This indicates that Nd and Dy will strongly influence the development of exploring new REE projects and clean technologies in the next decades.

Sevoflurane reduces glycocalyx shedding in the postischemic coronary bed, maintaining the natural cover for endothelial adhesion molecules and, thus, reducing cell adhesion. This may explain beneficial outcomes linked to clinical use of volatile anesthetics after ischemia-reperfusion.

K v 7 channels are enriched at the axonal plasma membrane where their voltage-dependent potassium currents suppress neuronal excitability. Mutations in K v 7.2 and K v 7.3 subunits cause epileptic encephalopathy (EE), yet the underlying pathogenetic mechanism is unclear. Here, we used novel statistical algorithms and structural modeling to identify EE mutation hotspots in key functional domains of K v 7.2 including voltage sensing S4, the pore loop and S6 in the pore domain, and intracellular calmodulin-binding helix B and helix B-C linker. Characterization of selected EE mutations from these hotspots revealed that L203P at S4 induces a large depolarizing shift in voltage dependence of K v 7.2 channels and L268F at the pore decreases their current densities. While L268F severely reduces expression of heteromeric channels in hippocampal neurons without affecting internalization, K552T and R553L mutations at distal helix B decrease calmodulin-binding and axonal enrichment. Importantly, L268F, K552T, and R553L mutations disrupt current potentiation by increasing phosphatidylinositol 4,5-bisphosphate (PIP 2), and our molecular dynamics simulation suggests PIP 2 interaction with these residues. Together, these findings demonstrate that each EE variant causes a unique combination of defects in K v 7 channel function and neuronal expression, and suggest a critical need for both prediction algorithms and experimental interrogations to understand pathophysiology of K v 7-associated EE. Epilepsy is the second most prominent neurological disease (www.epilepsy.com), in which excessive electrical activity within networks of neurons in the brain manifests clinically as recurrent unprovoked seizures 1. Recent discoveries of epilepsy-related genes in multiple laboratories and through large consortia have revealed a diverse array of proteins that may contribute to epileptogenesis 1,2. Among these proteins, neuronal KCNQ/K v 7 potassium (K +) channels have been implicated in epilepsy since mutations in the principle subunits, KCNQ2/K v 7.2 and KCNQ3/K v 7.3, cause Benign Familial Neonatal Epilepsy (BFNE [MIM: 121200]) and Epileptic Encephalopathy (EE [MIM: 613720]) (RIKEE database www.rikee.org). Neuronal K v 7 channels are mainly composed of heterotetramers of K v 7.2 and K v 7.3 3 , which show overlapping distribution in the hippocampus and cortex 4. They generate slowly activating and non-inactivating voltage-dependent K + currents that contribute to resting membrane potential, prevent repetitive and burst firing of action potentials (APs), and modulate AP threshold 3,5-7 .They are enriched at the plasma membrane of axonal initial segments (AIS) and distal axons 8,9 , where APs initiate and propagate 10. Membrane phosphatidylinositol-4,5-bisphosphate (PIP 2) is required for K v 7 channels to open 3 , although its exact binding sites in K v 7.2 and K v 7.3

Organophosphorus pesticides (OPs) can inhibit the activity of acetylcholinesterase (AChE) to induce neurological diseases. It is significant to exploit a rapid and sensitive strategy to monitor OPs. Here, a metal–organic framework (MOF) acted as a carrier to encapsulate AuNCs, which can limit the molecular motion of AuNCs, trigger the aggregation-induced emission (AIE) effect, and exhibit a strong fluorescence with a fluorescence lifetime and quantum yield of 6.83 μs and 4.63%, respectively. Then, the marriage of fluorescence and colorimetric signals was realized on the basis of the dual function of the enzymolysis product from AChE and choline oxidase (CHO) on AuNCs@ZIF-8. First, it can decompose ZIF-8 to weaken the restraint on AuNCs, and thus the fluorescence receded. Second, it can be used as a substrate for the peroxidase mimics of the released AuNCs to oxidize 3,3′,5,5′-tetramethylbenzidine (TMB) and a visible blue appeared. Thus, on the basis of the inhibition of AChE activity by OPs, a fluorescence–colorimetric dual-signal biosensor was established. In addition, colorimetric paper strips were exploited to realize a visual semiquantitative detection, and a smartphone APP was developed to make the visualization results more precise and realize real-time supervision of pesticide contamination.

Lacto-N-neotetraose and its sialyl and fucosyl derivatives including Lewis x (Le(x)) pentasaccharide, sialyl Lewis x (sLe(x)) hexasaccharide and internally sialylated derivatives were enzymatically synthesized from readily available lactoside, commercially available uridine 5'-diphosphate-glucose (UDP-Glc) and the corresponding monosaccharides using a highly efficient sequential one-pot multienzyme (OPME) strategy. The OPME strategy which combines bacterial glycosyltransferases and sugar nucleotide generation enzymes provides easy access to the biologically important complex oligosaccharides at preparative scale. Moreover, the same OPME strategy can be used for the regioselective introduction of sialic acid to the internal galactose unit of LNnT in a designed glycosylation route by simply changing the glycosylation sequence.

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For decades, researchers have endeavored to develop a general automation system to synthesize oligosaccharides comparable to the preparation of oligonucleotides and oligopeptides by commercially available machines. Inspired by the success of automated oligosaccharide synthesis through chemical glycosylation, a fully machine-driven automated system is reported here for oligosaccharides synthesis through enzymatic glycosylation in aqueous solution. The designed full automation system is based on the use of a thermosensitive polymer and a commercially available peptide synthesizer. This study represents a proof-of-concept that the enzymatic synthesis of oligosaccharides can be achieved in an automated manner using a commercially available peptide synthesizer.

Nanosized N-doped graphene oxide (GO) with visible fluorescence in water was prepared by cutting and unzipping of N-doped carbon nanotubes (NCNTs) and used to distinguish between normal and transition metal ions. It is found that the fluorescence is bathochromically shifted as the level of oxidation is increased.