The development of chemically recyclable polymers offers a solution to the end-of-use issue of polymeric materials and provides a closed-loop approach toward a circular materials economy. However, polymers that can be easily and selectively depolymerized back to monomers typically require low-temperature polymerization methods and also lack physical properties and mechanical strengths required for practical uses. We introduce a polymer system based on γ-butyrolactone (GBL) with a trans-ring fusion at the α and β positions. Such trans-ring fusion renders the commonly considered as nonpolymerizable GBL ring readily polymerizable at room temperature under solvent-free conditions to yield a high-molecular weight polymer. The polymer has enhanced thermostability and can be repeatedly and quantitatively recycled back to its monomer by thermolysis or chemolysis. Mixing of the two enantiomers of the polymer generates a highly crystalline supramolecular stereocomplex.

Many efforts are recently devoted on improving thermoelectric SnTe as an environment-friendly alternative to conventional PbTe and successful approaches include valence band convergence, nanostructuring, and substantial/interstitial defects. Among these strategies, alloying SnTe with MnTe enables the most effective reduction in the valence band offset (between L and Σ) for a convergence due to its high solubility of ≈15%, yet there is no indication that the solubility of MnTe is high enough for fully optimizing the valence band structure and thus for maximizing the electronic performance. Here, a strategy is shown to increase the MnTe solubility up to ≈25% by alloying with 5% GeTe, which successfully locates the composition (20% MnTe) to optimize the valence band structure by converging a more degenerated Λ (as compared with band L) and Σ valence bands. Through a further alloying with Cu 2 Te, the resultant Cu-interstitial defects enable a sufficient reduction in lattice thermal conductivity to its amorphous limit (0.4 W m −1 K −1 ). These electronic and thermal effects successfully realize a record-high thermoelectric figure of merit, zT of 1.8, strongly competing with that of PbTe. This work demonstrates the validity of band manipulation and interstitial defects for realizing extraordinary thermoelectric performance in SnTe.

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GeTe alloys have recently attracted wide attention as efficient thermoelectrics. In this work, a single-leg thermoelectric device with a conversion efficiency as high as 14% under a temperature gradient of 440 K was fabricated on the basis of GeTe-Cu2Te-PbSe alloys, which show a peak thermoelectric figure of merit (zT) > 2.5 and an average zT of 1.8 within working temperatures. The high performance of the material is electronically attributed to the carrier concentration optimization and thermally due to the strengthened phonon scattering, the effects of which all originate from the defects in the alloys. A design of Ag/SnTe/GeTe contact successfully enables both a prevention of chemical diffusion and an interfacial contact resistivity of 8 microhm·cm2 for the realization of highly efficient devices with a good service stability/durability. Not only the material’s high performance but also the device’s high efficiency demonstrated the extraordinariness of GeTe alloys for efficient thermoelectric waste-heat recovery.

The membrane-anchored ubiquitin ligase gp78 promotes degradation of misfolded endoplasmic reticulum (ER) proteins and sterol-regulated degradation of HMG-CoA reductase. It was known previously that Ufd1 plays a critical role in ER-associated degradation (ERAD) together with Npl4 and VCP. The VCP-Ufd1-Npl4 complex recognizes polyubiquitin chains and transfers the ubiquitinated proteins to the proteasome. Here we show that Ufd1 directly interacts with gp78 and functions as a cofactor. Ufd1 enhances the E3 activity of gp78, accelerates the ubiquitination and degradation of reductase, and eventually promotes receptor-mediated uptake of low-density lipoprotein. Furthermore, we demonstrate that the monoubiquitin-binding site in Ufd1 is required for the enhancement of gp78 activity and that the polyubiquitin-binding site in Ufd1 is critical for a postubiquitination step in ERAD. In summary, our study identifies Ufd1 as a cofactor of gp78, reveals an unappreciated function of Ufd1 in the ubiquitination reaction during ERAD, and illustrates that Ufd1 plays a critical role in cholesterol metabolism.

We propose an experimental scheme to implement a strong photon blockade with a single quantum dot coupled to a nanocavity. The photon blockade effect can be tremendously enhanced by driving the cavity and the quantum dot simultaneously with two classical laser fields. This enhancement of photon blockade is ascribed to the quantum interference effect to avoid two-photon excitation of the cavity field. Comparing with Jaynes-Cummings model, the second-order correlation function at zero time delay g(2)(0) in our scheme can be reduced by two orders of magnitude and the system sustains a large intracavity photon number. A red (blue) cavity-light detuning asymmetry for photon quantum statistics with bunching or antibunching characteristics is also observed. The photon blockade effect has a controllable flexibility by tuning the relative phase between the two pumping laser fields and the Rabi coupling strength between the quantum dot and the pumping field. Moreover, the photon blockade scheme based on quantum interference mechanism does not require a strong coupling strength between the cavity and the quantum dot, even with the pure dephasing of the system. This simple proposal provides an effective way for potential applications in solid state quantum computation and quantum information processing.

Much effort has recently been directed at advancing thermoelectric SnTe as an alternative to PbTe. Effective methods include energy band convergence, nanostructures, and substitutional and interstitial defects. Among these strategies, it is shown that CdTe alloying effectively reduces the energy offset between valence bands for an enhanced thermoelectric figure of merit, zT. However, its solubility of only ∼6% might limit this effect on a full zT optimization in SnTe−CdTe alloys. Here, we show an effective approach for increasing CdTe solubility up to ∼20%, with the help of the existence of 5% GeTe. This leads the valence bands to be further converged for improving electronic performance. In addition, Cu 2 Te alloying is used to create interstitial defects for reducing the lattice thermal conductivity. Eventually, the increase of CdTe solubility and the creation of Cu interstitials enable a significantly enhanced zT, indicating the importance of solubility manipulation for engineering the band structure in thermoelectric SnTe alloys.

Fragile X syndrome, the most common form of inherited mental retardation, is caused by the absence of the fragile X mental retardation protein FMRP. The RNA-binding FMRP represses translation of the microtubule (MT)-associated protein 1B (MAP1B) during synaptogenesis in the brain of the neonatal mouse. However, the effect of FMRP on MTs remains unclear. Mounting evidence shows that the structure and the function of FMRP are well conserved across species from Drosophila to human. From a genetic screen, we identified spastin as a dominant suppressor of rough eye caused by dfmr1 over-expression. spastin encodes an MT-severing protein, and its mutations cause neurodegenerative hereditary spastic paraplegia. Epistatic and biochemical analyses revealed that dfmr1 acts upstream of or in parallel with spastin in multiple processes, including synapse development, locomotive behaviour and MT network formation. Immunostaining showed that both loss- and gain-of-function mutations of dfmr1 result in an apparently altered MT network. Western analysis revealed that the levels of α-tubulin and acetylated MTs remained normal in dfmr1 mutants, but increased significantly when dfmr1 was over-expressed. To examine the consequence of the aberrant MTs in dfmr1 mutants, we analysed the MT-dependent mitochondrial transport and found that the number of mitochondria and the flux of mitochondrial transport are negatively regulated by dfmr1. These results demonstrate that dFMRP plays a crucial role in controlling MT formation and mitochondrial transport. Thus, defective MTs and abnormal mitochondrial transport might account for, at least partially, the pathogenesis of fragile X mental retardation.