Theoretical predictions of the benefits of three-dimensional quantum confinement have provided motivation for the development of quantum-dot lasers. Such lasers, developed in the case of self-assembled quantum dots, have not been successfully demonstrated with quantum-confined colloidal nanocrystals (NCs). Here, using recently developed NC-titania chemistry, we report the successful development of an optically pumped, NC-based distributed feedback laser, in which the narrow gain profiles of these nanoparticles have been matched with the feedback of a second-order distributed feedback laser. This laser, whose output color can be selected by choosing appropriately sized nanocrystals, operates at 80 K and at room temperature.

A central aim of quantum information processing is the efficient entanglement of multiple stationary quantum memories via photons. Among solid-state systems, the nitrogen-vacancy centre in diamond has emerged as an excellent optically addressable memory with second-scale electron spin coherence times. Recently, quantum entanglement and teleportation have been shown between two nitrogen-vacancy memories, but scaling to larger networks requires more efficient spin-photon interfaces such as optical resonators.Here we report such nitrogen-vacancy-nanocavity systems in the strong Purcell regime with optical quality factors approaching 10,000 and electron spin coherence times exceeding 200 ms using a silicon hard-mask fabrication process. This spin-photon interface is integrated with on-chip microwave striplines for coherent spin control, providing an efficient quantum memory for quantum networks.

SummarySarcopenia, the loss of skeletal muscle mass and function during aging, is a major contributor to disability and frailty in the elderly. Previous studies found a protective effect of reduced histone deacetylase activity in models of neurogenic muscle atrophy. Because loss of muscle mass during aging is associated with loss of motor neuron innervation, we investigated the potential for the histone deacetylase (HDAC) inhibitor butyrate to modulate age‐related muscle loss. Consistent with previous studies, we found significant loss of hindlimb muscle mass in 26‐month‐old C57Bl/6 female mice fed a control diet. Butyrate treatment starting at 16 months of age wholly or partially protected against muscle atrophy in hindlimb muscles. Butyrate increased muscle fiber cross‐sectional area and prevented intramuscular fat accumulation in the old mice. In addition to the protective effect on muscle mass, butyrate reduced fat mass and improved glucose metabolism in 26‐month‐old mice as determined by a glucose tolerance test. Furthermore, butyrate increased markers of mitochondrial biogenesis in skeletal muscle and whole‐body oxygen consumption without affecting activity. The increase in mass in butyrate‐treated mice was not due to reduced ubiquitin‐mediated proteasomal degradation. However, butyrate reduced markers of oxidative stress and apoptosis and altered antioxidant enzyme activity. Our data is the first to show a beneficial effect of butyrate on muscle mass during aging and suggests HDACs contribute to age‐related muscle atrophy and may be effective targets for intervention in sarcopenia and age‐related metabolic disease.

Oxidative stress is observed during aging and in numerous age-related diseases. Dietary restriction (DR) is a regimen that protects against disease and extends lifespan in multiple species. However, it is unknown how DR mediates its protective effects. One prominent and consistent effect of DR in a number of systems is the ability to reduce oxidative stress and damage. The purpose of this review is to comprehensively examine the hypothesis that dietary restriction reduces oxidative stress in rodents by decreasing reactive oxygen species (ROS) production and increasing antioxidant enzyme activity, leading to an overall reduction of oxidative damage to macromolecules. The literature reveals that the effects of DR on oxidative stress are complex and likely influenced by a variety of factors, including sex, species, tissue examined, types of ROS and antioxidant enzymes examined, and duration of DR. Here we present a comprehensive review of the existing literature on the effect of DR on mitochondrial ROS generation, antioxidant enzymes and oxidative damage. In a majority of studies, dietary restriction had little effect on mitochondrial ROS production or antioxidant activity. On the other hand, DR decreased oxidative damage in the majority of cases. Although the effects of DR on endogenous antioxidants are mixed, we find that glutathione levels are the most likely antioxidant to be increased by dietary restriction, which supports the emerging redox-stress hypothesis of aging.

SummaryAging is a major worldwide medical challenge. Not surprisingly, identifying drugs and compounds that extend lifespan in model organisms is a growing research area. Here, we present DrugAge (http://genomics.senescence.info/drugs/), a curated database of lifespan‐extending drugs and compounds. At the time of writing, DrugAge contains 1316 entries featuring 418 different compounds from studies across 27 model organisms, including worms, flies, yeast and mice. Data were manually curated from 324 publications. Using drug–gene interaction data, we also performed a functional enrichment analysis of targets of lifespan‐extending drugs. Enriched terms include various functional categories related to glutathione and antioxidant activity, ion transport and metabolic processes. In addition, we found a modest but significant overlap between targets of lifespan‐extending drugs and known aging‐related genes, suggesting that some but not most aging‐related pathways have been targeted pharmacologically in longevity studies. DrugAge is freely available online for the scientific community and will be an important resource for biogerontologists.

Arrays of discrete, lithographically patterned magnetic elements have been proposed as a new generation of ultrahigh density patterned magnetic storage media. Interferometric lithography has been used to make prototype arrays over large areas with periods of 100–200 nm. Arrays of magnetic pillars, pyramids, and dots have been made by electrodeposition, evaporation and liftoff, and etching processes, and the magnetic properties of the particles and their mutual interactions have been measured.

The advancement of quantum optical science and technology with solid-state emitters such as nitrogen-vacancy (NV) centers in diamond critically relies on the coherence of the emitters' optical transitions. A widely employed strategy to create NV centers at precisely controlled locations is nitrogen ion implantation followed by a high-temperature annealing process. We report on experimental data directly correlating the NV center optical coherence to the origin of the nitrogen atom. These studies reveal low-strain, narrow-optical-linewidth (< 500 MHz) NV centers formed from naturally-occurring 14 N atoms. In contrast, NV centers formed from implanted 15 N atoms exhibit significantly broadened optical transitions (> 1 GHz) and higher strain. The data show that the poor optical coherence of the NV centers formed from implanted nitrogen is not due to an intrinsic effect related to the diamond or isotope. These results have immediate implications for the positioning accuracy of current NV center creation protocols and point to the need to further investigate the influence of lattice damage on the coherence of NV centers from implanted ions.

The caseinolytic peptidase P (ClpP) is the endopeptidase component of the mitochondrial matrix ATP-dependent ClpXP protease. ClpP degrades unfolded proteins to maintain mitochondrial protein homeostasis and is involved in the initiation of the mitochondrial unfolded protein response (UPRmt). Outside of an integral role in the UPRmt, the cellular function of ClpP is not well characterized in mammalian cells. To investigate the role of ClpP in mitochondrial function, we generated C2C12 muscle cells that are deficient in ClpP using siRNA or stable knockdown using lentiviral transduction. Reduction of ClpP levels by ~70% in C2C12 muscle cells resulted in a number of mitochondrial alterations including reduced mitochondrial respiration and reduced oxygen consumption rate in response to electron transport chain (ETC) complex I and II substrates. The reduction in ClpP altered mitochondrial morphology, changed the expression level of mitochondrial fission protein Drp1 and blunted UPRmt induction. In addition, ClpP deficient cells showed increased generation of reactive oxygen species (ROS) and decreased membrane potential. At the cellular level, reduction of ClpP impaired myoblast differentiation, cell proliferation and elevated phosphorylation of eukaryotic initiation factor 2 alpha (eIF2α) suggesting an inhibition of translation. Our study is the first to define the effects of ClpP deficiency on mitochondrial function in muscle cells in vitro. In addition, we have uncovered novel effects of ClpP on mitochondrial morphology, cell proliferation and protein translation pathways in muscle cells.