The first GaS nanosheet-based photodetectors are demonstrated on both mechanically rigid and flexible substrates. Highly crystalline, exfoliated GaS nanosheets are promising for optoelectronics due to strong absorption in the UV-visible wavelength region. Photocurrent measurements of GaS nanosheet photodetectors made on SiO2/Si substrates and flexible polyethylene terephthalate (PET) substrates exhibit a photoresponsivity at 254 nm up to 4.2 AW(-1) and 19.2 AW(-1), respectively, which exceeds that of graphene, MoS2, or other 2D material-based devices. Additionally, the linear dynamic range of the devices on SiO2/Si and PET substrates are 97.7 dB and 78.73 dB, respectively. Both surpass that of currently exploited InGaAs photodetectors (66 dB). Theoretical modeling of the electronic structures indicates that the reduction of the effective mass at the valence band maximum (VBM) with decreasing sheet thickness enhances the carrier mobility of the GaS nanosheets, contributing to the high photocurrents. Double-peak VBMs are theoretically predicted for ultrathin GaS nanosheets (thickness less than five monolayers), which is found to promote photon absorption. These theoretical and experimental results show that GaS nanosheets are promising materials for high-performance photodetectors on both conventional silicon and flexible substrates.

Graphical Abstract Highlights d The crystal structure of Mycobacterium smegmatis MmpL3 has been determined d Two Asp-Tyr pairs in the TM region of MmpL3 facilitate proton-translocation d SQ109, an anti-TB drug, binds inside the protontranslocation channel of MmpL3 d Rimonabant, an antagonist for the cannabinoid receptor CB 1 , also inhibits MmpL3

Mononuclear phagocytes are a population of multi-phenotypic cells and have dual roles in brain destruction/reconstruction. The phenotype-specific roles of microglia/macrophages in traumatic brain injury (TBI) are, however, poorly characterized. In the present study, TBI was induced in mice by a controlled cortical impact (CCI) and animals were killed at 1 to 14 days post injury. Real-time polymerase chain reaction (RT-PCR) and immunofluorescence staining for M1 and M2 markers were performed to characterize phenotypic changes of microglia/macrophages in both gray and white matter. We found that the number of M1-like phagocytes increased in cortex, striatum and corpus callosum (CC) during the first week and remained elevated until at least 14 days after TBI. In contrast, M2-like microglia/macrophages peaked at 5 days, but decreased rapidly thereafter. Notably, the severity of white matter injury (WMI), manifested by immunohistochemical staining for neurofilament SMI-32, was strongly correlated with the number of M1-like phagocytes. In vitro experiments using a conditioned medium transfer system confirmed that M1 microglia-conditioned media exacerbated oxygen glucose deprivation-induced oligodendrocyte death. Our results indicate that microglia/macrophages respond dynamically to TBI, experiencing a transient M2 phenotype followed by a shift to the M1 phenotype. The M1 phenotypic shift may propel WMI progression and represents a rational target for TBI treatment.

The worldwide emergence of multidrug-resistant (MDR) and extensively drug-resistant (XDR) tuberculosis threatens to make this disease incurable. Drug resistance mechanisms are only partially understood, and whether the current understanding of the genetic basis of drug resistance in M. tuberculosis is sufficiently comprehensive remains unclear. Here we sequenced and analyzed 161 isolates with a range of drug resistance profiles, discovering 72 new genes, 28 intergenic regions (IGRs), 11 nonsynonymous SNPs and 10 IGR SNPs with strong, consistent associations with drug resistance. On the basis of our examination of the dN/dS ratios of nonsynonymous to synonymous SNPs among the isolates, we suggest that the drug resistance-associated genes identified here likely contain essentially all the nonsynonymous SNPs that have arisen as a result of drug pressure in these isolates and should thus represent a near-complete set of drug resistance-associated genes for these isolates and antibiotics. Our work indicates that the genetic basis of drug resistance is more complex than previously anticipated and provides a strong foundation for elucidating unknown drug resistance mechanisms.