A synergistic antibacterial platform: combining mechanical and photothermal effects based on Van-MoS2-Au nanocomposites.

Herein, we successfully developed a new multifunctional antibacterial system, which combined mechano-bactericidal (Au-nanostars) and photothermal (MoS2) mechanism. Meanwhile, the targeting molecule of vancomycin was modified on the surface of MoS2-Au nanocomposites (Van-MoS2-Au), that generally yield high efficiency in antibacterial performance due to their effective working radii. Van-MoS2-Au nanocomposites were capable of completely destroying both gram-negative (E. coli) and gram-positive (B. subtilis) bacteria under 808 NIR laser irradiation for 20 min, and nearly no bacterial growth was detected after 12 h incubation. Moreover, these nanocomposites could destruct the refractory biofilm as well, which was a much more difficult medical challenge. The new antibacterial nanomaterials might offer many biomedical applications because of the biocompatibility and strong antibacterial ability.

Surface oxygen vacancy-dependent molecular oxygen activation for propane combustion over α-MnO2.

Oxygen vacancies (OV), as the sites of molecular oxygen adsorption and activation, play an important role in the catalytic combustion process of volatile organic compounds (VOCs). Revealing the relationship between OV concentration and molecular oxygen activation behavior is of significance to construct the efficient catalysts. Herein, α-MnO2 with different OV concentrations was prepared to investigate the molecular oxygen activation for C3H8 combustion. It is disclosed that the enhanced OV concentration in α-MnO2 induced the reconfiguration of surface metal atoms, resulting in the transformation of oxygen activation configuration from end-on mode to side-on mode. Oxygen molecules in side-on mode possessed more localized electron density and weaker coordination bond strength with surrounding Mn atoms, which were more favorable to adsorb C3H8 molecules and activate C-H bond for the improved combustion performance. This work provides a new understanding to reveal that the increased OV concentration contributes to more efficient VOCs combustion.

A DNase-mimetic artificial enzyme for the eradication of drug-resistant bacterial biofilm infections.

The construction of multifunctional nano-enzymes is a feasible strategy for fighting multi-drug resistant (MDR) bacterial biofilm-associated infections. Extracellular DNA (eDNA) is an important functional part of biofilm formation, including the initial adherence of bacteria to subsequent development and eventual maturation. A nano-enzyme platform of graphene oxide-based nitrilotriacetic acid-cerium(IV) composite (GO-NTA-Ce) against bacterial biofilm infection has been developed. When located at the site of bacteria-associated infection, GO-NTA-Ce could inhibit the biofilm formation and effectively disperse the formed biofilm by degrading the eDNA. In addition to Ce-mediated deoxyribonuclease (DNase)-like activity, near-infrared laser irradiation of GO-NTA-Ce could produce local hyperthermia to kill the bacteria that lost the protection by the biofilm matrix. In addition, graphene is also a new green broad-spectrum antimicrobial material that can exert its antimicrobial effects through physical damage and chemical damage. In short, our GO-NTA-Ce nano-enzyme platform is capable of effectively eradicating drug-resistant bacterial biofilm infections through the triple action of DNase-like enzyme properties, photothermal therapy, and graphene-based antimicrobial activity, and the nano-composite has excellent potential for the treatment of MDR bacterial biofilm infections.

Precisely controlled and deeply penetrated micro-nano hybrid multifunctional motors with enhanced antibacterial activity against refractory biofilm infections.

The biofilm resistance of microorganisms has severe economic and environmental implications, especially the contamination of facilities associated with human life, including medical implants, air-conditioning systems, water supply systems, and food-processing equipment, resulting in the prevalence of infectious diseases. Once bacteria form biofilms, their antibiotic resistance can increase by 10-1,000-fold, posing a great challenge to the treatment of related diseases. In order to overcome the contamination of bacterial biofilm, destroying the biofilm's matrix so as to solve the penetration depth dilemma of antibacterial agents is the most effective way. Here, a magnetically controlled multifunctional micromotor was developed by using H2O2 as the fuel and MnO2 as the catalyst to treat bacterial biofilm infection. In the presence of H2O2, the as-prepared motors could be self-propelled by the generated oxygen microbubbles. Thereby, the remotely controlled motors could drill into the EPS of biofilm and disrupt them completely with the help of bubbles. Finally, the generated highly toxic •OH could efficiently kill the unprotected bacteria. This strategy combined the mechanical damage, highly toxic •OH, and precise magnetic guidance in one system, which could effectively eliminate biologically infectious fouling in microchannels within 10 min, possessing a wide range of practical application prospects especially in large scale and complex infection sites.

Oxidative damage of copper chloride overload to the cultured rat astrocytes.

Disorders of copper metabolism are associated with neurological dysfunction including Wilson's disease (WD). WD is a autosomal recessive disorder caused by mutations in the ATP7B gene resulting in the inability of the hepatocytes to remove excess copper. Gradual copper accumulation causes damage to liver, brain and other organs manifesting in liver disease, neurological and psychiatric symptoms. Also scond copper-neurometaboic disorder: Menkes disease charaterized with mutated ATP7A gene, is ralated with abnormally neuroal transmission and synaptogenesis. Parkinson's disease and Alzheimer's disease both are refered to some degree of copper/iron metabolism changes. The precise mechanisms by which excess copper causes neurological damage remain to be elucidated. In this study, we aimed to investigate the influence of excessive amounts of Cu(2+) on the oxidative damage response and survival of primary astrocytes from newborn rats. Primary cultured rat astrocytes were divided into three groups: 30 µmol/L CuCl2, 100 µmol/L CuCl2 and control. At 12, 24, 48, 96 and 120 hours of CuCl2 intervention, cell viability, intracellular reduced glutathione level and glutathion reductase activity, and nitric oxide secretion were determined. It was found that 30 µmol/L CuCl2 might stimulate the exaltation and the compensatory proliferation of astrocytes. The survival rate of astrocytes in the 100 µmol/L CuCl2 group was significantly decreased relative to the 30 µmol/L CuCl2 group. At 24 hours of CuCl2 intervention, intracellular reduced glutathione level and glutathion reductase activity were significantly decreased in the 100 µmol/L CuCl2 group compared to the control group. At 120 hours of CuCl2 intervention, nitric oxide secretion in the 100 µmol/L CuCl2 group was significantly greater than in the control group. Under pathological conditions, excessive amounts of Cu(2+) greatly damaged the growth and proliferation of astrocytes, reduced the anti-oxidative capacity of astrocytes by reducing intracellular glutathione level and glutathion reductase activity, worsened oxidative stress, and activated inflammation pathway by increasing nitric oxide secretion. By the way, all these findings might provide potential molecular therapeutic targets for the neurodegenerative diseases related Cu(2+) Metabolic Disorders, e.g., Wilson's disease, Parkinson's disease and Alzheimer's disease.

Downregulation of transketolase activity is related to inhibition of hippocampal progenitor cell proliferation induced by thiamine deficiency.

In animal experiments, hippocampal neurogenesis and the activity of thiamine-dependent transketolase decrease markedly under conditions of thiamine deficiency. To further investigate the effect of thiamine deficiency on the proliferation of hippocampal progenitor cells (HPCs) and the potential mechanisms involved in this effect, we cultured HPCs in vitro in the absence of thiamine and found that proliferation and transketolase activity were both significantly repressed. Furthermore, specific inhibition of transketolase activity by oxythiamine strongly inhibited HPC proliferation in a dose-dependent manner. However, thiamine deficiency itself inhibited the proliferation to a greater degree than did oxythiamine. Taken together, our results suggest that modulation of transketolase activity might be one of the mechanisms by which thiamine regulates the proliferation of hippocampal progenitor cells.