Experimental Determination of Bubble Size Distributions in Laboratory Scale Sieve Tray with Mesh

Most applications on sieve tray internals were internals additions for increasing bubble area and changing gas liquid contact form to intensify the mass transfer in a tower. An easy improvement to set up a mesh on the sieve tray was proposed in this paper. It was confirmed that foam layer on the sieve tray acts as the main role of mass transfer. The mesh here could turn large bubbles into such small ones that gas would contact with the liquid sufficiently and also could avoid many small bubbles coalescing into large ones. Meanwhile, interfacial area was enlarged greatly, which was of benefit to mass transfer. In addition, the mesh could make small bubbles have a long stay time in trays, an advantage for mass transfer. In this paper, the gas hold-up and tray pressure drop were determined in an air–water system under isothermal conditions. Mean bubble diameter was measured by CCD in a 0.12 m diameter tower, and bubble radial distributions and probability density functions were also determined. The experimental results proved that mesh could obtain more total gas hold-up and reduce the bubble mean diameter greatly but increased the tray pressure drop severely also. The existence of mesh did not change the trend of bubble flow on the tray. The greatest bubbles still concentrated in the center and gradually reduced to the wall along the radial direction; the small bubbles turned into large ones along the height, and the distribution became wider at higher positions

Additional file 1: Figure S1. of MiR-23b controls ALDH1A1 expression in cervical cancer stem cells

MiR-23b is under-expressed in tumorsphere cells derived from Siha and C33A cells. Data is presented as mean ± SEM. *P < 0.05; **P < 0.01. (TIFF 613 kb

Highly Dispersed Mo₂C Nanoparticles Embedded in Ordered Mesoporous Carbon for Efficient Hydrogen Evolution

The development of non-noble metal-based electrocatalysts for the hydrogen evolution reaction (HER) has attracted increasing attention over recent years. As a promising HER catalyst candidate, the preparation of molybdenum carbide requires high temperature for carbothermal reduction, which often causes nanoparticles sintering, leading to low exposed active sites. In this work, highly dispersed β-Mo₂C nanoparticles of approximately 5 nm embedded in ordered mesoporous carbon (Mo₂C@OMC) have been synergistically synthesized. During the synthesis process, the resol precursor for OMC template could serve as carbon source for the formation of Mo₂C and mitigate the sintering of Mo₂C nanoparticles. The resultant well-defined Mo₂C possesses highly exposed active sites of approximately 26.5% and exhibits an excellent performance for the HER in both acidic and alkaline solutions. The synthetic procedure developed in this study may be extended to fabricate other metal carbide@OMC nanocomposites for the HER and other electrocatalytic applications

Morphological Controlled Growth of Nanosized Boehmite with Enhanced Aspect Ratios in an Organic Additive-Free Cationic–Anionic Double Hydrolysis Method

Well-crystallized boehmite nanoparticles showing different sizes and morphologies were fabricated in an organic additive-free cationic–anionic double hydrolysis method using inorganic aluminum chloride salt and sodium aluminate as dual aluminum sources. By adjusting the molar ratios of Al³⁺/AlO₂^– in the synthesis recipe, the boehmite particles’ shapes could be controllably tuned from two-dimensional flakes to one-dimensional (1D) rods, needles, and even fibers with enhanced particles’ aspect ratios. Through X-ray diffraction and high resolution transmission electron microscopy measurements, details of the microstructural features for boehmite particles were gained, and thus the growth habits are discussed, where in strong alkaline synthesis medium with a low Al³⁺/AlO₂^– molar ratio, dispersed nanoflakes grew with (010) and (101) faces as basal and lateral surfaces, while 1D nanoparticles, i.e. nanorods, nanoneedles, and nanofibers preferentially grew along the [100] direction with (100) and (101) faces unexposed when Al³⁺/AlO₂^– molar ratios were gradually raised. Additionally, the impacts of pH values and Cl^– ions in the suspensions to the particles shapes are also discussed. The evolution of boehmite morphologies and the resultant enlargement of aspect ratios led to increased total surface charges (ζ-potential) and higher isoelectric points of boehmite samples which would benefit the stabilization of particles’ suspensions and improvement of surface functionalization abilities

Rcn1 selectively binds to the surface of apoptotic neurons but not healthy neurons.

<p>(A) Rcn1 is a secreted protein. Rcn1-FLAG with or without the signal peptide was expressed in Neuro-2A cells. Rcn1-FLAG in the conditioned medium of the apoptotic or healthy cells was immunoprecipitated with anti-FLAG mAb and analyzed by Western blot. GFP-FLAG was a non-secretory protein control. (B) Rcn1 selectively binds to apoptotic cells. Rcn1-FLAG was expressed in Neuro-2A cells. Cell surface-bound Rcn1-FLAG was detected for apoptotic and healthy Neuro-2A cells using FITC-labeled anti-FLAG mAb and analyzed by confocal microscopy. FLAG-Tulp1 is a positive control. Apoptotic cells were labeled with propidium iodide. Scale bar = 50 μm. (C) Flow cytometry analysis of Rcn1 binding to apoptotic neurons. Lysates were prepared from cells expressing Rcn1-FLAG, FLAG-Tulp1 (positive control) or GFP-FLAG (negative control), incubated with apoptotic or healthy Neuro-2A cells and analyzed by flow cytometry using FITC anti-FLAG mAb. (D) Rcn1 binds to microglia surface. GST-Rcn1 or GST control was incubated with BV-2 cells and analyzed by flow cytometry using FITC-anti-GST antibody.</p

Rcn1 mediates microglial engulfment via phagocytosis pathway.

<p>Phagocytosis of apoptotic cells by BV-2 microglia was performed as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0126993#pone.0126993.g002" target="_blank">Fig 2A</a>. Phagosome marker Rab7 was detected using anti-Rab7 antibody and FITC-labeled secondary antibody, and analyzed by confocal microscopy. The z-stack images of pHrodo and FITC are co-localized and superimposed with cognate DAPI signals and bright fields. Bar = 10 μm.</p

Rcn1 stimulates microglial phagocytosis.

<p>(A) Expression of Rcn1-FLAG, FLAG-Tulp1 and GFP-FLAG in Neuro-2A cells was verified by Western blot using anti-FLAG mAb. (B) Rcn1 facilitates BV-2 microglial phagocytosis. Rcn1-FLAG, FLAG-Tulp1 (positive control) or GFP-FLAG (negative control) was expressed in Neuro-2A cells. Cells were treated with or without etoposide to induce apoptosis, labeled with pHrodo, incubated with BV-2 microglia for phagocytosis, and analyzed by confocal microscopy. Scale bar = 50 μm. (C) Percentage of BV-2 cells with phagocytosed cargos in (B) were quantified by ImageJ (<u>+</u> s.e.m., *** <i>P</i><0.0001, n = 3, t-test).</p

Rcn1 facilitates macrophage phagocytosis.

<p>(A) Rcn1 stimulates macrophage phagocytosis of apoptotic neurons. Healthy or apoptotic Neuro-2A cells were labeled with pHrodo, incubated with J774 macrophage cells for phagocytosis and analyzed by confocal microscopy as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0126993#pone.0126993.g002" target="_blank">Fig 2A</a>. The z-stack images of pHrodo and DAPI are superimposed with the cognate bright fields to reveal phagocytosed cargos. (B) Percentage of macrophages with phagocytosed cargos in (A) were quantified. Bar = 50 μm (<u>+</u> s.e.m., *** <i>P</i><0.0001, n = 3, t-test).</p

Identification of Rcn1 as a microglial phagocytosis ligand.

<p>(A) Schematics of OPD-NGS. OPD/PFC selection was performed by incubating OPD cDNA library with BV-2 microglial cells at 4°C. After washing, cells were incubated at 37°C for phagocytosis. Surface-bound unphagocytosed phages were removed by stripping with low pH isotonic buffer. Phagocytosed phages were released by cell lysis, amplified and used as input for the next round of selection. After 3 rounds of selection, the cDNA inserts of enriched clones were amplified by PCR and identified by NGS. (B) Verification of Rcn1-Phage phagocytosis by microglia. Clonal Rcn1-Phage, GFP-Phage or Control-Phage was incubated with BV-2 cells at 4°C. After washing, cells were incubated at 37°C to allow bound phages to be phagocytosed. After removal of surface-bound unphagocytosed phage, internalized phages were released by cell lysis and quantified by plaque assay (<u>+</u> s.e.m., *** <i>P</i><0.0001, n = 4, t-test).</p

Reticulocalbin-1 Facilitates Microglial Phagocytosis

<div><p>Phagocytosis is critical to the clearance of apoptotic cells, cellular debris and deleterious metabolic products for tissue homeostasis. Phagocytosis ligands directly recognizing deleterious cargos are the key to defining the functional roles of phagocytes, but are traditionally identified on a case-by-case basis with technical challenges. As a result, extrinsic regulation of phagocytosis is poorly defined. Here we demonstrate that microglial phagocytosis ligands can be systematically identified by a new approach of functional screening. One of the identified ligands is reticulocalbin-1 (Rcn1), which was originally reported as a Ca²⁺-binding protein with a strict expression in the endoplasmic reticulum. Our results showed that Rcn1 can be secreted from healthy cells and that secreted Rcn1 selectively bound to the surface of apoptotic neurons, but not healthy neurons. Independent characterization revealed that Rcn1 stimulated microglial phagocytosis of apoptotic but not healthy neurons. Ingested apoptotic cells were targeted to phagosomes and co-localized with phagosome marker Rab7. These data suggest that Rcn1 is a genuine phagocytosis ligand. The new approach described in this study will enable systematic identification of microglial phagocytosis ligands with broad applicability to many other phagocytes.</p></div