Search

The Ni–Fe–TiO2 overlayers on mild steel strips were prepared by electrochemical deposition. The layers were characterized morphologically by confocal laser scanning microscopy and scanning electron microscopy (SEM) coupled with energy-dispersive spectroscopy (EDS) analysis. The layers exhibit a quasi-three-dimensional (3D) morphology in which the crystalline, TiO2, is embedded. Electrocatalytic activity of the Ni–Fe–TiO2 layers for the hydrogen evolution reaction (HER) was assessed by using pseudo-steady-state polarization curves and electrochemical impedance spectroscopy (EIS) in alkaline solution. The results were compared with the properties of Ni–Fe electrodes and used for determining the mechanism and kinetics of HER. In comparison with Ni–Fe electrodes, the synthesized Ni–Fe–TiO2 electrodes present higher catalytic activity for HER due to the increase in the real surface area and high intrinsic electrocatalytic activity of titanium dioxide. The present study provides valuable insight for exploring practical applications of Ni-based alloys as hydrogen evolution electrodes. [ABSTRACT FROM AUTHOR]

Introduction Acute respiratory distress syndrome (ARDS), which is the most severe manifestation of acute lung injury, is a clinical syndrome characterized by acute respiratory failure, bilateral pulmonary infiltrates, and edema [...], Acute lung injury is characterized by an increase of inflammatory reaction and severe lung edema. Even if there have been great advances in the identification of genes and signaling pathways involved in acute lung injury, the fundamental mechanisms of initiation and propagation of acute lung injury have not been understood completely. A growing amount of evidence indicates that microRNAs (miRNAs) are involved in various human diseases. However, the expression profile and function of miRNAs in acute lung injury have not been investigated. Here, using real-time polymerase chain reaction analysis, we show that a collection of miRNAs is dynamically regulated in lipopolysaccharide (LPS)-induced mouse acute lung injury. Among them, miR-199a and miR-16 are the most significantly down-regulated miRNAs. To study the role of miR-199a and miR-16 in acute lung injury, an over-expression of miR-199a or miR-16 assay was performed in LPS-treated A549 cells, and then the expression of inflammatory factors was analyzed. Over-expression of miR-199a could not alter the expression level of interleukin (IL)-6 and tumor necrosis factor-alpha (TNFα), while up-regulation of miR-16 could significantly down-regulate IL-6 and TNFα expression level. Using bioinformatic analysis, we show that a 3' untranslational region (UTR) of IL-6 and TNFα contains the binding sites of miR-16. Accordingly, over-expression of miR-16 could significantly suppress the luciferase activity of reporter fusion with the binding sites of TNFα in its 3'UTR region, suggesting that miR-16 played its role in LPS-induced lung inflammation by a direct manner. In this study, we show for the first time that miRNAs are dynamically regulated and play an important function in LPS-induced lung injury. Key words: acute lung injury, microRNA, miR-16, miR-199a, TNFα, inflammation, LPS. La lesion pulmonaire aigue se caracterise par une reaction inflammatoire importante et un oedeme severe du poumon. Malgre des progres considerables dans l'identification des genes et des voies de signalisation impliquees dans la lesion pulmonaire aigue, les mecanismes fondamentaux du declenchement et de la propagation de cette pathologie ne sont pas totalement compris. Un nombre croissant d'etudes indiquent que les microARN (miARN) jouent un role dans diverses maladies touchant les humains. Toutefois, le profil d'expression et la fonction des miARN dans la lesion pulmonaire aigue n'ont pas encore ete examines. Dans la presente etude, utilisant une analyse PCR en temps reel, nous avons montre qu'une collection de miARN a ete dynamiquement regulee dans la lesion pulmonaire aigue induite par les lipopolysaccharides (LPS) chez la souris. Parmi ces miARN, miR-199a et miR-16 ont ete les plus faiblement exprimes. Pour examiner le role de ces deux miARN dans la lesion pulmonaire, nous avons surexprime miR-199a ou miR-16 dans les cellules A549 traitees aux LPS, puis analyse l'expression des facteurs inflammatoires. La surexpression de miR-199a n'a pu modifier le niveau d'expression de l'interleukine (IL)-6 et du facteur de necrose des tumeurs alpha (TNFα), alors que la surexpression de miR-16 a pu diminuer de facon significative les niveaux d'expression de IL-6 et de TNFα. Par une analyse bioinformatique, nous avons montre que la region 3' non traduite (UTR3')de IL-6 et de TNFα contenait les sites de liaison de miR-16. Par consequent, la surexpression de miR-16 a pu supprimer de maniere significative l'activite luciferase de rapporteur fusionnant avec les sites de liaison de TNFα dans sa region UTR3', ce qui donne a penser que miR-16 joue son role de maniere directe dans l'inflammation pulmonaire induite par les LPS. Notre etude est la premiere a montrer que les miARN sont dynamiquement regules et qu'ils ont une fonction importante dans la lesion pulmonaire induite par les LPS. Mots-cles : lesion pulmonaire aigue, microARN, miR-16, miR-199a, TNFα, inflammation, LPS. [Traduit par la Redaction]

Epithelial-mesenchymal transition (EMT) is an essential step for cancer metastasis. MicroRNAs (miRNAs) are small non-coding RNAs that regulate target-mRNAs post-transcriptionally. The expression and function of miRNAs in EMT of HT-29 colonic cells remain elusive. This study looks at expression of miRNAs in EMT and explores the effects of miRNAs on EMT in HT-29 cell line. HT-29 was treated with TGF β to establish an EMT model, in which a collection of miRNAs was dynamically regulated by real-time PCR (qPCR) analysis. Among them, miR-21 and miR-27 were significantly upregulated, while miR-22, miR-26, miR-30, miR-181, miR-200b, miR-200c and miR-214 were markedly downregulated. MiRNA-inhibitors were used to knockdown miRNAs in HT-29 and EMT markers were determined by qPCR to monitor the effects of miRNAs on EMT process. Results showed that miR-22 could not alter the expression of EMT markers, while knockdown of miR-200b could significantly increase that of epithelial markers, N-cadherin, Vimentin, α-Sma and Twist1 and decrease that of mesenchymal marker, E-cadherin. Bioinformatic analysis and Western blot showed that ZEB1 was directly suppressed by miR-200b. In conclusion, miRNAs are dynamically regulated in TGF β-induced EMT of HT-29 and miR-200b was essential for EMT by suppressing the expression of ZEB1 in HT-29. [ABSTRACT FROM AUTHOR]

This report presents the extracorporeal membrane oxygenation (ECMO)-assisted surgical as a treatment of benign double tracheoesophageal fistula. The patient was a 43-year-old woman who presented the airway obstruction for 3 weeks after the esophagus metal stent implantation for the tracheoesophageal fistula 1 year ago. The airway obstruction was due to the expansion and piercing of the metal stent through the upper part of the esophagus into the tracheal cavity. In view of the failure of endotracheal intubation, we finally used ECMO-assisted surgery to remove the stent. And at the same time, cervical esophagostomy externa, exclusion of the thoracic tracheoesophageal fistulas and gastrostomy were performed.

The asymmetric unit of the title compound, (C(13)H(11)Cl(2)N(2))(2)[Ni(C(4)N(2)S(2))(2)], contains one-half of a centrosymmetric [Ni(mnt)(2)] anion (where mnt is maleonitrile-dithiol-ate or 1,2-dicyano-1,2-ethyl-enedithiol-ate) and an (E)-1-(3,4-dichloro-benzyl-ideneamino)-4-methyl-pyridinium cation. In the anion, the coordination around the Ni atom is a distorted square. In the cation, the aromatic rings are oriented at a dihedral angle of 7.81 (3)°. In the crystal structure, inter-molecular C-H⋯N hydrogen bonds link the cations and anions. π-π Contacts between the nickel dithiol-ene and pyridine rings and between the benzene and pyridine rings, [centroid-centroid distances = 3.682 (3) and 3.643 (3) Å, respectively] may further stabilize the structure.

The asymmetric unit of the title compound, (C(6)H(9)N(2))(2)[Ni(C(4)N(2)S(2))(2)], contains one half of an [Ni(mnt)(2)](2-) anion (mnt is maleonitrile-dithiol-ate or 1,2-dicyano-ethene-1,2-dithiol-ate) and one 1-amino-4-methyl-pyridinium cation. The Ni(II) atom is located on an inversion centre. In the crystal structure, inter-molecular N-H⋯N hydrogen bonds link the mol-ecules.