In Situ Atomic Force Microscopy (AFM) Study of Oxygen Reduction Reaction on a Gold Electrode Surface in a Dimethyl Sulfoxide (DMSO)-Based Electrolyte Solution

In the present study, the morphological changes on a gold electrode during the oxygen reduction (ORR) and oxygen evolution reaction (OER) processes in a dimethyl sulfoxide (DMSO)-based electrolyte solution were investigated using an electrochemical atomic force microscope (EC-AFM) with the help of vibrational spectroscopy measurements. The growth of the ORR products on the electrode surface, which was mainly assigned to lithium peroxide (Li₂O₂), was directly confirmed by the EC-AFM. It was found that the water concentration in the solution significantly affects the morphology of the ORR products. The growth of anisotropic Li₂O₂ particles on the gold electrode surface has been confirmed to be an electrochemical process. No evidence was found to support the disproportionation growth mechanism. These ORR products were fully decomposed at a potential as high as 4.4 V (vs Li⁺/Li) in the subsequent OER process, more positive than that determined by a surface-enhanced Raman spectroscopy (SERS) measurement. Combined with infrared absorption spectroscopy and SERS measurements, we propose that the oxidation decomposition of the Li₂O₂ deposits first occurs at its interface with the gold electrode surface, while that of the remaining particles takes place at a higher overpotential. On the contrary, the ORR deposits could be fully decomposed at a potential as low as 3.6 V when tetrathiafulvalene (TTF) was included in the solution. We confirmed by EC-AFM that the electrochemically generated TTF⁺ can mediate the decomposition of the Li₂O₂ at a lower potential through a homogeneous oxidation mechanism

Immobilization of Horseradish Peroxidase for Phenol Degradation

The use of enzymes to degrade environmental pollutants has received wide attention as an emerging green approach. Horseradish peroxidase (HRP) can efficiently catalyze the degradation of phenol in the environment; however, free HRP exhibits poor stability and temperature sensitivity and is easily deactivated, which limit its practical applications. In this study, to improve their thermal stability, HRP enzymes were immobilized on mesoporous molecular sieves (Al-MCM-41). Specifically, Al-MCM-41(W) and Al-MCM-41(H) were prepared by modifying the mesoporous molecular sieve Al-MCM-41 with glutaraldehyde and epichlorohydrin, respectively, and used as carriers to immobilize HRP on their surface, by covalent linkage, to form the immobilized enzymes HRP@Al-MCM-41(W) and HRP@Al-MCM-41(H). Notably, the maximum reaction rate of HRP@Al-MCM-41(H) was increased from 2.886 × 105 (free enzyme) to 5.896 × 105 U/min–1, and its half-life at 50 °C was increased from 745.17 to 1968.02 min; the thermal stability of the immobilized enzyme was also significantly improved. In addition, we elucidated the mechanism of phenol degradation by HRP, which provides a basis for the application of this enzyme to phenol degradation

miR-34a inhibits NSCLC tumor growth.

<p>(<b>A</b>) NSCLC cells freshly transfected with miR-34a oligos showed miR-34a levels several orders of magnitude higher than those transfected with miR-NC oligos. The indicated NSCLC cells were transfected with miR-34a or miR-NC oligos, and 48 h later, were harvested and used in tumor experiments (below) whereas a small number of cells were set aside and used in qRT-PCR measurement of miR-34a mRNA levels. Shown are the mean miR-34a levels (in log scale; n = 2) in miR-34a transfected cells relative to those in the miR-NC transfected cells (actual mean values indicated in the bars). (<b>B–D</b>) miR-34a oligo transfection inhibited A549 tumor growth. Indicated are tumor incidence (tumors developed/numbers of injections; %), harvest time (including actual injection and termination dates), mean tumor weight (in grams), and the <i>P</i> values for tumor weights. Gross tumor images are not to the same scale. (<b>E–G</b>) miR-34a oligo transfection inhibited H460 tumor growth. (<b>H–L</b>) miR-34a oligo transfection inhibited H1299 tumor growth.</p

The microRNA miR-34a Inhibits Non-Small Cell Lung Cancer (NSCLC) Growth and the CD44^hi Stem-Like NSCLC Cells

<div><p>Lung cancer is among the most lethal malignancies with a high metastasis and recurrence rate, which is probably due to the existence of lung cancer stem cells (CSCs). CSCs in many tumors including non-small cell lung cancer (NSCLC) have been identified using adhesion molecular CD44, either individually or in combination with other marker(s). MicroRNAs (miRNAs) regulate both normal stem cells and CSCs and dysregulation of miRNAs has been implicated in tumorigenesis. Recently, miR-34a was found to be downregulated in NSCLC cells but the biological functions of miR-34a in regulating NSCLC cell behavior have not been extensively studied. Here we show that transfection of synthetic miR-34a, but not the negative control (NC) miRNA oligonucleotides (oligos) in three NSCLC cell lines, i.e., A549, H460, and H1299, inhibited their holoclone formation, clonogenic expansion, and tumor regeneration in vivo. Furthermore, the lentiviral vector-mediated overexpression of miR-34a in purified CD44^hi H460 cells also inhibited tumor outgrowth. In contrast, expression of miR-34a antagomirs (i.e., antisense oligos) in the CD44^lo H460 cells promoted tumor development. Our study shows that miR-34a is a negative regulator of the tumorigenic properties of NSCLC cells and CD44^hi lung CSCs, and establishes a strong rationale for developing miR-34a as a novel therapeutic agent against NSCLC.</p></div

miR-34a inhibits NSCLC cell clonal and clonogenic properties.

<p>(<b>A–C</b>) Clonal assays. Cells transfected with miR-34a or miR-NC oligos (33 nM) were plated in triplicate at 50 cells/well in 6-well plates. The experiment was terminated at 12 d and wells were Giemsa-stained (A). Shown in B are representative images. Results shown in A and B were representative of two independent experiments. (C) Quantitative presentation of results in A. Bars represent the mean ± S.D. (<b>D–E</b>) Clonogenic assays in MC. A total of 1,000 cells per well were plated for clonogenic assay. Photos were taken on d 15 after plating and shown in D are representative fields. (E) Quantitative presentation of results in D. Bars represent the mean ± S.D.</p

Functional assay (ALDH) and analysis of CD44 and CD133 expression using flow cytometry.

<p>(Top) The Aldefluor assay in 3 NSCLC cells. DEAB-treated samples served as negative controls. ∼1–2% H460 and H1299 cells were Aldefluor-positive whereas >90% of A549 cells were Aldefluor-positive. (Middle) Representative flow cytometry profile of CD44 (FITC) expression in 3 NSCLC cells. Virtually 100% of A549, H460, and H1299 cells were CD44-positive (mean values being 97.2%, 99.3%, and 99.2%, respectively; n = 3). (Bottom) Flow cytometry analysis of CD133 (PE) expression in 3NSCLC cells. There was almost no expression of CD133 in these three NSCLC cell lines.</p

Additional file 1: of The role of increased body mass index in outcomes of sepsis: a systematic review and meta-analysis

The role of increased body mass index in outcomes of sepsis: A systematic review and meta-analysis. (DOCX 385 kb

Effects of miR-34a on the growth of tumors derived from purified CD44^hi or CD44^lo cells.

<p>(<b>A–B</b>) CD44 expression level. (A) Representative diagrams of flow cytometry analysis of CD44 (FITC) expression in H460 cells. (B) CD44 mRNA levels in purified CD44^hi and CD44^lo H460 cells assessed by qRT-PCR. (<b>C, E, F</b>) miR-34a overexpression in purified CD44^hi H460 cells by lentiviral infection inhibited tumor regeneration. (C) Indicated are tumor incidence (tumors developed/numbers of injections; %), harvest time (including actual injection and termination dates), mean tumor weight (in grams, F), and the <i>P</i> values for tumor weights. Gross tumor images are not to the same scale. (E) The tumor growth curve. (<b>D, G–J</b>) Anti-miR-34a promoted tumor growth of purified CD44^lo H460 cells. (D) Indicated are tumor incidence (tumors developed/numbers of injections; %), harvest time (including actual injection and termination dates), mean tumor weight (in grams, G), and the <i>P</i> values for tumor weights. Gross tumor images are not to the same scale. (H–J) The tumor growth curve at three different cell doses.</p

Probing Phonon Dynamics in Individual Single-Walled Carbon Nanotubes

Interactions between elementary excitations, such as carriers, phonons, and plasmons, are critical for understanding the optical and electronic properties of materials. The significance of these interactions is more prominent in low-dimensional materials and can dominate their physical properties due to the enhanced interactions between these excitations. One-dimensional single-walled carbon nanotubes provide an ideal system for studying such interactions due to their perfect physical structures and rich electronic properties. Here we investigated G-mode phonon dynamics in individual suspended chirality-resolved single-walled carbon nanotubes by time-resolved anti-Stokes Raman spectroscopy. The improved technique allowed us to probe the intrinsic phonon information on a single-tube level and exclude the influences of tube–tube and tube–substrate interactions. We found that the G-mode phonon lifetime ranges from 0.75–2.25 ps and critically depends on whether the tube is metallic or semiconducting. In comparison with the phonon lifetimes in graphene and graphite, we revealed structure-dependent carrier–phonon and phonon–phonon interactions in nanotubes. Our results provide new information for optimizing the design of nanotube electronic/optoelectronic devices by better understanding and utilizing their phonon decay channels

Nucleophilic 1,1-Difluoroethylation with Fluorinated Phosphonium Salt

The fluorinated phosphonium salt (Ph₃P⁺CF₂CH₃ BF₄^–) was shown to act as a nucleophilic 1,1-difluoroethylation agent to enable difluoroethylation of aldehydes and imines