Improving the performance of coupled solid carbon source biofilm carriers through pore-forming methods.

Coupled solid carbon source biofilm carriers (CCBs) was usually utilized to enhance the treatment efficiency of low carbon/nitrogen (C/N) wastewater. However, current CCBs have low carbon release capacity because of its small inner mass transfer coefficient. Therefore, this study innovatively applied pore-forming methods to modify CCBs.

Template-independent genome editing in the Pcdh15 mouse, a model of human DFNB23 nonsyndromic deafness.

Although frameshift mutations lead to 22% of inherited Mendelian disorders in humans, there is no efficient in vivo gene therapy strategy available to date, particularly in nondividing cells. Here, we show that nonhomologous end-joining (NHEJ)-mediated nonrandom editing profiles compensate the frameshift mutation in the Pcdh15 gene and restore the lost mechanotransduction function in postmitotic hair cells of Pcdh15 mice, an animal model of human nonsyndromic deafness DFNB23. Identified by an ex vivo evaluation system in cultured cochlear explants, the selected guide RNA restores reading frame in approximately 50% of indel products and recovers mechanotransduction in more than 70% of targeted hair cells.

Selection and synthesization of multi-carbon source composites to enhance simultaneous nitrification-denitrification in treating low C/N wastewater.

Low carbon/nitrogen ratio (C/N) wastewater is widespread and difficult to treat. To find a resolution to this issue, this study systematically evaluated the constituents of composite solid carbon (i.e.

The potential of electrotrophic denitrification coupled with sulfur recycle in MFC and its responses to COD/SO ratios.

Electrotrophic denitrification is a promising novel nitrogen removal technique. In this study, the performance and the mechanism of electrotrophic denitrification coupled with sulfate-sulfide cycle were investigated under different anodic influent COD/SO ratios. The results showed that electrotrophic denitrification contributed to more than 22% total nitrogen removal in cathode chamber.

PIEZO2 mediates ultrasonic hearing via cochlear outer hair cells in mice.

Ultrasonic hearing and vocalization are the physiological mechanisms controlling echolocation used in hunting and navigation by microbats and bottleneck dolphins and for social communication by mice and rats. The molecular and cellular basis for ultrasonic hearing is as yet unknown. Here, we show that knockout of the mechanosensitive ion channel PIEZO2 in cochlea disrupts ultrasonic- but not low-frequency hearing in mice, as shown by audiometry and acoustically associative freezing behavior.

Mechanisms in cochlear hair cell mechano-electrical transduction for acquisition of sound frequency and intensity.

Sound signals are acquired and digitized in the cochlea by the hair cells that further transmit the coded information to the central auditory pathways. Any defect in hair cell function may induce problems in the auditory system and hearing-based brain function. In the past 2 decades, our understanding of auditory transduction has been substantially deepened because of advances in molecular, structural, and functional studies.

Potential applications of endogenous sulfide for enhanced denitrification of low C/N domestic wastewater in anodic mixotrophic denitrification microbial fuel cell: The mechanism of electrons transfer and microbial community.

Anodic mixotrophic denitrification microbial fuel cell (MFC) was developed for pollutants removal and electricity generation in treatment of low C/N domestic wastewater. The experimental results show that the MFC achieved up to 100% of acetate, 100% of sulfide, and more than 91% of nitrate removal efficiency in all the MFCs. Particularly, thiosulfate was generated as the main intermediate of sulfide oxidation, and the sulfate generation ratio ranged from 66.

Lack of PDZD7 long isoform disrupts ankle-link complex and causes hearing loss in mice.

Usher syndrome (USH) is the most frequent form of combined hereditary deafness-blindness, characterized by hearing loss and retinitis pigmentosa, with or without vestibular dysfunction. PDZD7 is a PDZ domain-containing scaffold protein that was suggested to be a USH modifier and a contributor to digenic USH. In the inner ear hair cells, PDZD7 localizes at the ankle region of the stereocilia and constitutes the so-called ankle-link complex together with three other USH proteins Usherin, WHRN, and ADGRV1.

TMC1 is an essential component of a leak channel that modulates tonotopy and excitability of auditory hair cells in mice.

Hearing sensation relies on the mechano-electrical transducer (MET) channel of cochlear hair cells, in which transmembrane channel-like 1 (TMC1) and transmembrane channel-like 2 (TMC2) have been proposed to be the pore-forming subunits in mammals. TMCs were also found to regulate biological processes other than MET in invertebrates, ranging from sensations to motor function. However, whether TMCs have a non-MET role remains elusive in mammals.

Improved calcium sensor GCaMP-X overcomes the calcium channel perturbations induced by the calmodulin in GCaMP.

GCaMP, one popular type of genetically-encoded Ca indicator, has been associated with various side-effects. Here we unveil the intrinsic problem prevailing over different versions and applications, showing that GCaMP containing CaM (calmodulin) interferes with both gating and signaling of L-type calcium channels (Ca1). GCaMP acts as an impaired apoCaM and Ca/CaM, both critical to Ca1, which disrupts Ca dynamics and gene expression.

Redox regulation of cancer metastasis: molecular signaling and therapeutic opportunities.

Cancer metastasis is the major cause of cancer-related mortality. Accumulated evidence has shown that high-metastasis potential cancer cells have more reactive oxygen species (ROS) accumulation compared with low-metastasis potential cancer cells. ROS can function as second messengers to regulate multiple cancer metastasis-related signaling pathways via reversible oxidative posttranslational modifications of cysteine in key redox-sensitive proteins, which leads to the structural and functional change of these proteins.

Itraconazole suppresses the growth of glioblastoma through induction of autophagy: involvement of abnormal cholesterol trafficking.

Glioblastoma is one of the most aggressive human cancers with poor prognosis, and therefore a critical need exists for novel therapeutic strategies for management of glioblastoma patients. Itraconazole, a traditional antifungal drug, has been identified as a novel potential anticancer agent due to its inhibitory effects on cell proliferation and tumor angiogenesis; however, the molecular mechanisms involved are still unclear. Here, we show that itraconazole inhibits the proliferation of glioblastoma cells both in vitro and in vivo.