Highly Porous Carbon Materials Filled with Nickel Hydroxide Nanoparticles; Synthesis, Study, Application in Electrochemistry

Nickel hydroxide was deposited on the surface of the porous carbon to obtain a cathode material for  supercapacitors. This work is the first part of the study of Ni(OH)2/С composite, which considers the conditions of its synthesis using two types of porous carbon matrices with a highly developed specific surface area (1000–3000 m2/g) and two types of precursors (NiCl2*6H2O and Ni(N3)2). The morphology of the systems, in particular the shape and size characteristics of the hydroxide filler particles, was examined using the scanning electron microscopy, X-ray diffraction, and nitrogen adsorption-desorption at 77 K. The measurements of capacity of the Ni(OH)2/С-electrodes were made in 6 M KOH using an asymmetric two-electrode cell (a porous carbon material with known electrode characteristics was employed as the counter electrode). The capacity was shown to decrease by 22–56% with increasing the scanning rate from 10 to 80 mV/s. A maximum capacity of the composite was obtained at a scanning rate of 10 mV/s was 346 F/g

Benzothiazinones kill Mycobacterium tuberculosis by blocking arabinan synthesis

New drugs are required to counter the tuberculosis (TB) pandemic. Here, we describe the synthesis and characterization of 1,3-benzothiazin-4-ones (BTZs), a new class of antimycobacterial agents that kill Mycobacterium tuberculosis in vitro, ex vivo, and in mouse models of TB. Using genetics and biochemistry, we identified the enzyme decaprenylphosphoryl-beta-d-ribose 2'-epimerase as a major BTZ target. Inhibition of this enzymatic activity abolishes the formation of decaprenylphosphoryl arabinose, a key precursor that is required for the synthesis of the cell-wall arabinans, thus provoking cell lysis and bacterial death. The most advanced compound, BTZ043, is a candidate for inclusion in combination therapies for both drug-sensitive and extensively drug-resistant TB

Depletion of Dendritic Cells Enhances Innate Anti-Bacterial Host Defense through Modulation of Phagocyte Homeostasis

Dendritic cells (DCs) as professional antigen-presenting cells play an important role in the initiation and modulation of the adaptive immune response. However, their role in the innate immune response against bacterial infections is not completely defined. Here we have analyzed the role of DCs and their impact on the innate anti-bacterial host defense in an experimental infection model of Yersinia enterocolitica (Ye). We used CD11c-diphtheria toxin (DT) mice to deplete DCs prior to severe infection with Ye. DC depletion significantly increased animal survival after Ye infection. The bacterial load in the spleen of DC-depleted mice was significantly lower than that of control mice throughout the infection. DC depletion was accompanied by an increase in the serum levels of CXCL1, G-CSF, IL-1α, and CCL2 and an increase in the numbers of splenic phagocytes. Functionally, splenocytes from DC-depleted mice exhibited an increased bacterial killing capacity compared to splenocytes from control mice. Cellular studies further showed that this was due to an increased production of reactive oxygen species (ROS) by neutrophils. Adoptive transfer of neutrophils from DC-depleted mice into control mice prior to Ye infection reduced the bacterial load to the level of Ye-infected DC-depleted mice, suggesting that the increased number of phagocytes with additional ROS production account for the decreased bacterial load. Furthermore, after incubation with serum from DC-depleted mice splenocytes from control mice increased their bacterial killing capacity, most likely due to enhanced ROS production by neutrophils, indicating that serum factors from DC-depleted mice account for this effect. In summary, we could show that DC depletion triggers phagocyte accumulation in the spleen and enhances their anti-bacterial killing capacity upon bacterial infection

Regulatory (pan-)genome of an obligate intracellular pathogen in the PVC superphylum.

Like other obligate intracellular bacteria, the Chlamydiae feature a compact regulatory genome that remains uncharted owing to poor genetic tractability. Exploiting the reduced number of transcription factors (TFs) encoded in the chlamydial (pan-)genome as a model for TF control supporting the intracellular lifestyle, we determined the conserved landscape of TF specificities by ChIP-Seq (chromatin immunoprecipitation-sequencing) in the chlamydial pathogen Waddlia chondrophila. Among 10 conserved TFs, Euo emerged as a master TF targeting >100 promoters through conserved residues in a DNA excisionase-like winged helix-turn-helix-like (wHTH) fold. Minimal target (Euo) boxes were found in conserved developmentally-regulated genes governing vertical genome transmission (cytokinesis and DNA replication) and genome plasticity (transposases). Our ChIP-Seq analysis with intracellular bacteria not only reveals that global TF regulation is maintained in the reduced regulatory genomes of Chlamydiae, but also predicts that master TFs interpret genomic information in the obligate intracellular α-proteobacteria, including the rickettsiae, from which modern day mitochondria evolved

Effect of ionizing radiation on the protein-synthesizing system of brain neurons of ground squirrels in different functional states

Using fluorescence and electron microscopy, it is shown that the physiological state of ground squirrels exposed to ionizing radiation at different stages of the torpor-awakeness (hypothermia-normothermia) cycle is the main factor responsible for changes in the protein-synthesizing system of neurons in the hippocampus (fields CA1 and CA3) and the sensomotor cortex. The neurons of animals irradiated in the state of awakeness are less radioresistant and recover more slowly than neurons of animals irradiated in torpor, with the difference being more distinct in neurons of the CA1 field. The effect of irradiation is weak in animals entering torpor and reaches a peak in awakening animals. It is proposed that the inhibition of protein synthesis in the latter case takes place at the elongation stage, with heavy polysomes formed in the cytoplasm of neurons