The effect of an intestinal microflora consisting of selected microbial species on myoelectric activity of small intestine was studied using germ-free rat models, with recording before and after specific intestinal colonization, in the unanesthetized state. Intestinal transit, neuropeptides in blood (RIA), and neuromessengers in the intestinal wall were determined. Clostridium tabificum vp 04 promoted regular spike burst activity, shown by a reduction of the migrating myoelectric complex (MMC) period from 30.5 +/- 3.9 min in the germ-free state to 21.2 +/- 0.14 min (P < 0.01). Lactobacillus acidophilus A10 and Bifidobacterium bifidum B11 reduced the MMC period from 27.9 +/- 4.5 to 21.5 +/- 2.1 min (P < 0.02) and accelerated small intestinal transit (P < 0.05). Micrococcus luteus showed an inhibitory effect, with an MMC period of 35.9 +/- 9.3 min compared with 27.7 +/- 6.3 min in germ-free rats (P < 0.01). Inhibition was indicated also for Escherichia coli X7 gnotobiotic rats. No consistent changes in slow wave frequency were observed. The concentration of neuropeptide Y in blood decreased after introduction of conventional intestinal microflora, suggesting reduced inhibitory control. Intestinal bacteria promote or suppress the initiation and aboral migration of the MMC depending on the species involved. Bacteria with primitive fermenting metabolism (anaerobes) emerge as important promoters of regular spike burst activity in small intestine.

Graphical Abstract Highlights d UHRF1 maintains cancer-specific DNA methylation through its chromatin reader domains d PHD and SRA domain mutants phenocopy UHRF1 depletion to reverse DNA hypermethylation d Disrupting PHD or SRA domain functions impairs key oncogenic properties of CRC cells d The maintenance function of overexpressed UHRF1 in CRC has prognostic significance SUMMARY UHRF1 facilitates the establishment and maintenance of DNA methylation patterns in mammalian cells. The establishment domains are defined, including E3 ligase function, but the maintenance domains are poorly characterized. Here, we demonstrate that UHRF1 histone-and hemimethylated DNA binding functions, but not E3 ligase activity, maintain cancer-specific DNA methylation in human colorectal cancer (CRC) cells. Disrupting either chromatin reader activity reverses DNA hypermethylation, reactivates epigenetically silenced tumor suppressor genes (TSGs), and reduces CRC oncogenic properties. Moreover, an inverse correlation between high UHRF1 and low TSG expression tracks with CRC progression and reduced patient survival. Defining critical UHRF1 domain functions and its relationship with CRC prognosis suggests directions for, and value of, targeting this protein to develop therapeutic DNA demethylating agents.

Thermal evaporation and characterization of superstrate CdS/Sb2Se3 solar cells Appl. Phys. Lett. 104, 173904 (2014); 10.1063/1.4874878 Photoelectric performance of TiO 2 nanotube array photoelectrodes cosensitized with CdS/CdSe quantum dots Appl. Phys. Lett. 96, 153104 (2010); 10.1063/1.3386525 Effect of internal surface area on the performance of Zn O ∕ In 2 S 3 ∕ Cu SCN solar cells with extremely thin absorber Appl. Phys. Lett. 92, 153107 (2008);

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Sb2Se3 has attracted great research interest very recently as a promising absorber material for thin film photovoltaics due to its suitable bandgap, high absorption coefficient, and non‐toxic, low cost, and earth abundant nature. In this work, a significant efficiency improvement to 4.8% of superstrate cadmium sulfide (CdS)/Sb2Se3 solar cells is obtained by the controlled addition of oxygen during thermal evaporation of Sb2Se3 films. Systematic materials and device physics characterization reveal that oxygen addition during Sb2Se3 film evaporation significantly improves the CdS/Sb2Se3 heterojunction quality through effective passivation of interfacial defect states, resulting in a substantial enhancement in device circuit voltage and short circuit current density. The 4.8% device is the highest efficiency thus far reported for Sb2Se3 thin film solar cells. Copyright © 2015 John Wiley & Sons, Ltd.

Solid–solid reactions are very effective for solving the main challenges of lithium–sulfur (Li–S) batteries, such as the shuttle effect of polysulfides and the high dependence of electrolyte consumption. However, the low sulfur content and sluggish redox kinetics of such cathodes dramatically limit the practical energy density of Li–S batteries. Here a rationally designed hierarchical cathode to simultaneously solve above‐mentioned challenges is reported. With nanoscale sulfur as the core, selenium‐doped sulfurized polyacrylonitrile (PAN/S7Se) as the shell and micron‐scale secondary particle morphology, the proposed cathode realizes excellent solid–solid reaction kinetics in a commercial carbonate electrolyte under high active species loading and a relatively low electrolyte/sulfur ratio. Such an approach provides a promising solution toward practical lithium sulfur batteries.

Tumor cell-derived microparticles (T-MP) contain tumor antigen profiles as well as innate signals, endowing them with vaccine potential; however, the precise mechanism by which DCs present T-MP antigens to T cells remains unclear. Here, we show that T-MPs activate a lysosomal pathway that is required for DCs presenting tumor antigens of T-MPs. DCs endocytose T-MPs to lysosomes, where T-MPs increase lysosomal pH from 5.0 to a peak of 8.5 via NOX2-catalyzed reactive oxygen species (ROS) production. This increased pH, coupled with T-MP-driven lysosomal centripetal migration, promotes the formation of MHC class I-tumor antigen peptide complexes. Concurrently, endocytosis of T-MPs results in the upregulation of CD80 and CD86. T-MP-increased ROS activate lysosomal Ca channel Mcoln2, leading to Ca release. Released Ca activates transcription factor EB (TFEB), a lysosomal master regulator that directly binds to CD80 and CD86 promoters, promoting gene expression. These findings elucidate a pathway through which DCs efficiently present tumor antigen from T-MPs to CD8 T cells, potentiating T-MPs as a novel tumor cell-free vaccine with clinical applications. .

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