Graphene Oxide Nanoparticle-Loaded Ginsenoside Rg3 Improves Photodynamic Therapy in Inhibiting Malignant Progression and Stemness of Osteosarcoma.

Osteosarcoma serves as a prevalent bone cancer with a high metastasis and common drug resistance, resulting in poor prognosis and high mortality. Photodynamic therapy (PDT) is a patient-specific and non-invasive tumor therapy. Nanoparticles, like graphene oxide have been widely used in drug delivery and PDT. Ginsenoside Rg3 is a principal ginseng component and has presented significant anti-cancer activities. Here, we constructed the nanoparticles using GO linked with photosensitizer (PS) indocyanine green (ICG), folic acid, and polyethylene glycol (PEG), and loaded with Rg3 (PEG-GO-FA/ICG-Rg3). We aimed to explore the effect of PEG-GO-FA/ICG-Rg3 combined with PDT for the treatment of osteosarcoma. Significantly, we found that Rg3 repressed proliferation, invasion, and migration, and enhanced apoptosis and autophagy of osteosarcoma cells, while the PEG-GO-FA/ICG-Rg3 presented a higher activity, in which NIR laser co-treatment could remarkably increase the effect of PEG-GO-FA/ICG-Rg3. Meanwhile, stemness of osteosarcoma cell-derived cancer stem cells was inhibited by Rg3 and PEG-GO-FA/ICG-Rg3, and the combination of PEG-GO-FA/ICG-Rg3 with NIR laser further significantly attenuated this phenotype in the system. Moreover, NIR laser notably improved the inhibitor effect of PEG-GO-FA/ICG-Rg3 on the tumor growth of osteosarcoma cells in vivo. Consequently, we concluded that PEG-GO-FA/ICG-Rg3 improved PDT in inhibiting malignant progression and stemness of osteosarcoma cell. Our finding provides a promising and practical therapeutic strategy for the combined treatment of osteosarcoma.

Self-growth Ni2P nanosheet arrays with cationic vacancy defects as a highly efficient bifunctional electrocatalyst for overall water splitting.

HYPOTHESIS: The transition metal phosphide is one of the promising bifunctional electrocatalysts for overall water splitting. Moreover, the activity of phosphide catalysts can be further enhanced by the cationic vacancy engineering. EXPERIMENTS: The self-growth Ni2P nanosheet arrays with abundant cationic vacancy defects (V-Ni2P/NF) has been synthesized via a facile multi-step reaction process involving hydrothermal, phosphorization and acid-etching of Mn which was doped in Ni2P nanosheets as a sacrificial dopant. Furthermore, the experimental studies and density functional theory (DFT) calculations were carried out to evaluate its electrochemical performance. FINDINGS: The chemical and electrocatalytic property of Ni2P were successfully optimized by cationic vacancy engineering and the obtained V-Ni2P/NF catalyst exhibited superior bifunctional catalytic performance for both hydrogen evolution (HER) and oxygen evolution reaction (OER) compared to pristine Ni2P and Mn-doped Ni2P in alkaline electrolyte. The V-Ni2P/NF can afford the current density of 10 mA cm-2 at a small overpotential of 55 mV for HER and 250 mV for OER. Additionally, the water electrolysis device assembled by the V-Ni2P/NF electrode as both the anode and cathode just requires a small voltage of 1.59 V to achieve 10 mA cm-2 and shows no obvious attenuation for 50 h.

Accelerating effect of bio-reduced graphene oxide on decolorization of Acid Red 18 by Shewanella algae.

In this study, the effects of bio-reduced graphene oxide (BRGO) on the bio-reduction of Acid Red 18 (AR 18) by Shewanella algae were first investigated, and a possible mechanism of BRGO-mediated AR 18 bio-decolorization was proposed. The prepared BRGO was characterized by X-ray photoelectron spectroscopy (XPS), X-ray diffractometer (XRD), infrared spectroscopy (IR), Raman spectra, and transmission electron microscope (TEM), respectively. Moreover, electrochemical experiment demonstrated that BRGO is of good electrical conductivity. AR 18 bio-decolorization could be enhanced in dose-dependent manner of BRGO. The maximum increase in AR 18 removal efficiency was observed at a dose of 0.075 g L(-1) BRGO. Under the same conditions, BRGO could also improve the decolorization rates of Acid Red 88, Acid Red 27, and Acid Red 73. During decolorization, the formation of BRGO and cells composite was observed, which is beneficial for transferring electrons from cells to BRGO. In addition, BRGO could accelerate the bio-decolorization of AR 18 under saline conditions (2-7 %). These findings indicate that BRGO can accelerate the electrons transfer from cells to azo dyes.

Global transcriptome analysis of Escherichia coli exposed to immobilized anthraquinone-2-sulfonate and azo dye under anaerobic conditions.

The immobilization of quinone compounds is regarded as a promising strategy to accelerate anaerobic decolorization of xenobiotic compounds azo dyes in the presence of quinone-reducing microorganisms. However, little is known about the basic response of these microorganisms to immobilized quinones in the presence of azo dyes. In the present study, whole-genome DNA microarrays were used to investigate a quinone-reducing bacterium Escherichia coli K-12 transcription response to immobilized anthraquinone-2-sulfonate (AQSim) reduction and azo dye acid red 18 (AR 18) decolorization. Transcriptome analysis showed that AQSim was more accessible for the cells of E. coli K-12 than AR 18. Despite there being some differences between AQSim and soluble AQS mediated decolorization of AR 18, AQSim reduction and AR 18 decolorization, more similarity could be observed in the four processes. Among over 60 % shared genes, several groups of genes exhibited high expression levels, including those genes encoding terminal reductases, menaquinone biosynthesis, formate dehydrogenases and outer membrane proteins. Especially, nrfABCD, frdBCD and dsmABC encoding terminal reductases were significantly upregulated. Further gene deletion experiments demonstrated that the above three groups of genes were involved in AQSim-mediated AR 18 decolorization. In addition, significant upregulation of stress response genes was observed, which indicated the adaptation of E. coli K-12 to AQSim and AR 18 exposures.

[Decolorization of azo dyes using quinone reductase and quinoid compounds].

Using quinoid redox mediator and bacterial cellular quinone reductase, we investigated the decolorization ability of gene-engineered strain Escherichia coli YB and the effects of methylhydroquinone (MHQ) pretreatement on decolorization performance of E. coli JM109 and anaerobic sludge. The results indicate that lawsone is an effective accelerator for azo dye decolorization by E. coli YB overexpressing cellular quinone reductase AZR. In the presence of 0.2 mmol x L(-1) lawsone, 75% Amaranth (1 mmol x L(-1)) can be decolorized in 2 h. E. coli YB can also decolorize high concentration of azo dye in the presence of lawsone. Around 50% Amaranth (5 mmol x L(-1)) is decolorized in 8 h. Compared to lawsone, menadione is a less effective mediator. E. coli YB takes 12 h to reach 70% decolorization in the presence of 2.5 mmol x L(-1) menadione. Repeated decolorization studies showed that E. coli YB had stable decolorizing ability in the presence of lawsone. Four rounds of repeated decolorization can be completed in 12 h. Lawsone can also accelerate the decolorization of azo dyes with complex structures such as Acid Scarlet GR and Reactive Brilliant Red K-2BP. With the optimal LQ concentrations, 70% Acid Scarlet GR and Reactive Brilliant Red K-2BP are decolorized in 9 h and 30 h,respectively. Decolorization performances of E. coli JM109 and anaerobic sludge pretreated with MHQ are improved. After MHQ pretreatment,in the presence of lawsone, 80% Amaranth (1 mmol x L(-1)) can be decolorized in 5 h by E. coli JM109, while more than 75% Amaranth can be removed in 11 h by sludge.

Ab initio/DFT and AIM studies on dual hydrogen-bonded complexes of 2-hydroxypyridine/2-pyridone tautomerism.

The second-order Møller-Plesset (MP2) and density functional theory (DFT) calculations have been carried out to investigate the structures and stabilities of hydrogen (H-) bonded 2-hydroxypyridine (2HP)/2-pyridone (2PY) dimeric forms as well as 2HP-2PY complexes. The results on single-point counterpoise (CP) correction of these complexes were compared against CP-optimized correction. The nature of the intermolecular contacts in the sense of normal H-bond or blue-shifting H-bond was determined on the basis of harmonic vibrational, atom-in-molecule (AIM), and natural bond orbital (NBO) analysis. A blue-shifting C-H...N H-bond was found and NBO analysis revealed a slight decrease in the population of the contacting sigmaC-H* antibonding orbital as the primary reason of the C-H contraction. Good correlations have been established between the interaction energies and the H-bond distances versus other characteristic H-bond parameters.

Bis[bis(methoxycarbimido)amine-kappa2N,N']bis(perchlorato-kappaO)copper(II) bis[bis(methoxycarbimido)amine-kappa2N,N']bis(methanol-kappaO)copper(II) bis(perchlorate) methanol disolvate.

The title compound, [Cu(ClO4)2(C4H9N3O2)2][Cu(C4H9N3O2)2(CH4O)2](ClO4)2.2CH3OH, comprises two independent Cu(II) species lying on different inversion sites. In the Cu complexes, a distorted octahedral geometry arises (from basic square-planar N4 coordination) from the weak coordination of two perchlorate ions (as Cu-O) in one species and two methanol molecules in the other (also as Cu-O). Interactions between the O atoms of the perchlorate anions or methanol groups and the imide or amine NH groups afford an extensive intermolecular hydrogen-bonding network.

Lgf-YL-9 induces apoptosis in human epidermoid carcinoma KB cells and multidrug resistant KBv200 cells via reactive oxygen species-independent mitochondrial pathway.

Pyrazolon derivatives were reported to have cytotoxicity to some tumour cells. In the present study, we investigated the effect of Lgf-YL-9 on cytotoxicity and cell apoptosis in human epidermoid carcinoma drug-sensitive parental KB cells and multidrug resistant (MDR) KBv200 cells. Lgf-YL-9 exhibited potent cytotoxicity not only to KB cells but also to KBv200 cells, and the IC(50) were 3.81 and 3.45 microg/mL in KB cells and KBv200 cells, respectively. Importantly, Lgf-YL-9 effectively inhibited tumour growth of KB cell xenografts in nude mice. Lgf-YL-9-induced cell apoptosis was confirmed by chromatin condensation, DNA fragmentation, Annexin-V and propidium iodide (PI) double-staining assay and poly(ADP-ribose) polymerase (PARP) cleavage. Furthermore, Lgf-YL-9-mediated apoptosis in KB cells and KBv200 cells was accompanied by the loss of mitochondrial membrane potential (DeltaPsi(m)), the release of cytochrome c, and the activation of caspases-3, -7, and -9, but not by intercalating to DNA. Although Lgf-YL-9-induced apoptosis was associated with the decrease of DeltaPsi(m), reactive oxygen species (ROS) reduction was interestingly observed in both cell lines. The data suggest that Lgf-YL-9 has similar cytotoxicity to drug-sensitive parental KB cells and MDR KBv200 cells. Lgf-YL-9-induced apoptosis is involved in a new ROS-independent mitochondrial dysfunction pathway, but not in intercalating to DNA.