Defective Tungsten Oxides with Stacking Faults for Proton Exchange Membrane Green-Hydrogen Generation.

Defects can introduce atomic structural modulation and tailor performance of materials. Herein, it demonstrates that semiconductor WO3 with inert electrocatalytic behavior can be activated through defect-induced tensile strains. Structural characterizations reveal that when simply treated in Ar/H2 atmosphere, oxygen vacancies will generate in WO3 and cause defective structures. Stacking faults are found in defects, thus modulating electronic structure and transforming electrocatalytic-inert WO3 into highly active electrocatalysts. Density functional theory (DFT) calculations are performed to calculate *H adsorption energies on various WOx surfaces, revealing the oxygen vacancy composition and strain predicted to optimize the catalytic activity of hydrogen evolution reaction (HER). Such defective tungsten oxides can be integrated into commercial proton exchange membrane (PEM) electrolyser with comparable performance toward Pt-based PEM. This work demonstrates defective metal oxides as promising non-noble metal catalysts for commercial PEM green-hydrogen generation.

Operando Spectroscopy Observation of Mo Clusters-Ti3 C2 TX Catalyst/Support Interface's Dynamic Evolution in Hydrogen Evolution Reaction.

The interaction between catalyst and support plays an important role in electrocatalytic hydrogen evolution (HER), which may explain the improvement in performance by phase transition or structural remodeling. However, the intrinsic behavior of these catalysts (dynamic evolution of the interface under bias, structural/morphological transformation, stability) has not been clearly monitored, while the operando technology does well in capturing the dynamic changes in the reaction process in real time to determine the actual active site. In this paper, nitrogen-doped molybdenum atom-clusters on Ti3 C2 TX (MoACs /N-Ti3 C2 TX ) is used as a model catalyst to reveal the dynamic evolution of MoAcs on Ti3 C2 TX during the HER process. Operando X-ray absorption structure (XAS) theoretical calculation and in situ Raman spectroscopy showed that the Mo cluster structure evolves to a 6-coordinated monatomic Mo structure under working conditions, exposing more active sites and thus improving the catalytic performance. It shows excellent HER performance comparable to that of commercial Pt/C, including an overpotential of 60 mV at 10 mA cm-2 , a small Tafel slope (56 mV dec-1 ), and high activity and durability. This study provides a unique perspective for investigating the evolution of species, interfacial migration mechanisms, and sources of activity-enhancing compounds in the process of electroreduction.

Low-cost synthesis of flowerlike α-Fe2O3 nanostructures for heavy metal ion removal: adsorption property and mechanism.

Flowerlike α-Fe(2)O(3) nanostructures were synthesized via a template-free microwave-assisted solvothermal method. All chemicals used were low-cost compounds and environmentally benign. These flowerlike α-Fe(2)O(3) nanostructures had high surface area and abundant hydroxyl on their surface. When tested as an adsorbent for arsenic and chromium removal, the flowerlike α-Fe(2)O(3) nanostructures showed excellent adsorption properties. The adsorption mechanism for As(V) and Cr(VI) onto flowerlike α-Fe(2)O(3) nanostructures was elucidated by X-ray photoelectron spectroscopy and synchrotron-based X-ray absorption near edge structure analysis. The results suggested that ion exchange between surface hydroxyl groups and As(V) or Cr(VI) species was accounted for by the adsorption. With maximum capacities of 51 and 30 mg g(-1) for As(V) and Cr(VI), respectively, these low-cost flowerlike α-Fe(2)O(3) nanostructures are an attractive adsorbent for the removal of As(V) and Cr(VI) from water.

Synthesis of necklace-like magnetic nanorings.

Necklace-like magnetite and maghemite nanorings, composed of magnetic nanoparticles (NPs) with average size about 40 nm, have been prepared via a solvothermal process in a colloidal solution by a self-assembly process. The composition, phase, and morphology of these nanorings have been characterized by X-ray diffraction, X-ray absorption, and transmission electron microscopy. In this paper, we discuss the influence of reaction conditions on the formation of nanorings structure including the amount of PVP in starting materials, reaction time, and temperature. On the basis of experimental observation, we supposed that magnetite NPs may first assemble into chains by magnetic dipole-dipole interactions. These dipolar chains, which are metastable structures relative to necklace-like nanorings, then produced the rings. So, the stability of chains may determine the yield, size, and morphologies of necklace-like nanorings.

Genome-wide profiling of mRNA and lncRNA expression in dengue fever and dengue hemorrhagic fever.

Dengue fever (DF) and dengue hemorrhagic fever (DHF) are recurrent diseases that are widespread in the tropics. Here, we identified candidate genes associated with these diseases by performing integrated analyses of DF (GSE51808) and DHF (GSE18090) microarray datasets in the Gene Expression Omnibus (GEO). In all, we identified 7635 differentially expressed genes (DEGs) in DF and 8147 DEGs in DHF as compared to healthy controls (P < 0.05). In addition, we discovered 215 differentially expressed long non-coding RNAs (DElncRNAs) in DF and 225 DElncRNAs in DHF. There were 1256 common DEGs and eight common DElncRNAs in DHF vs DF, DHF vs normal control, and DF vs normal control groups. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that signal transduction (false discovery rate = 8.33E-10), 'toxoplasmosis', and 'protein processing in endoplasmic reticulum' were significantly enriched pathways for common DEGs. We conclude that the MAGED1,STAT1, and IL12A genes may play crucial roles in DF and DHF, and suggest that our findings may facilitate the identification of biomarkers and the development of new drug design strategies for DF and DHF treatment.

[Identification of stage Ib specific related genes in lung squamous cell cancer by oligonucleotide array].

OBJECTIVE: To establish gene expression profile of stage Ib and IIIa primary lung squamous cell cancer (SCC) within whole genome and identify genes specifically expressed in stage Ib of SCC. METHODS: Total RNA was extracted from the normal, stage Ib and IIIa lung SCC tissue. cRNA probes prepared from total RNA were hybridized with pretreatment oligonucleotide chip containing 22215 genes. The resultant data were treated with MSV 5.0 software and looked up on the affymetrix website. RT-PCR examination were used to validated the results from chip analysis. RESULTS: Comparing with the normal lung, difference genes expressed in Ib SCC are totally 1764, among which 571 were upregulated and 1193 were downregulated, and in stage IIIa, they are 554, 128 and 426 genes respectively. Genes specifically expressed in stage Ib were totally 1329, including 482 upregulation genes and 847 downregulation genes, which were classified into different category which included 480 metabolism related genes, 227 signal transduction genes, 136 cell proliferation genes, 136 immune related genes, 94 cell adhere genes, 88 transcription regulation genes, 86 cell cycle genes, 73 cytoskeleton genes, 45 differentiation genes, 42 apoptosis and 31 extracellular matrix genes. RT-PCR examination of FOXM1 and TNXB genes was consistent with the analysis of gene chip. CONCLUSION: Stage Ib and IIIa Gene expression profile of primary SCC within the whole genome were set up and genes specifically expressed in stage Ib of SCC were identified, which lay a foundation for further research on carcinogenesis mechanism and identifying new markers of early diagnosis.

The mechanism of Polydatin in shock treatment.

Polydatin is extracted from a traditional Chinese herbal medicine, Polygonum cuspidatum, and has a special effect in shock treatment. The aim of this study is to explain the cellular and molecular basis of Polydatin in shock treatment. The fluorescent probe techniques, patch clamp method, and cellular flow chamber were used to test intracellular variables of vascular smooth muscle cells (VSMC), myocardial cells (MC), endothelial cells (EC), and white blood cell (WBC). It was shown that Polydatin could inhibit ICAM-1 expression in EC stimulated by lipopolysaccharide (LPS), attenuate WBC-EC adhesion, increase [Ca2+]i in MC with enhancement of MC contraction extent, activate KATP channels of VSMC, and decrease pHi value and [Ca2+]i of VSMC in shock. The study suggests that Polydatin has multiple effects on VSMC, MC, WBC and EC, which are related to the enhancement of heart function and improvement of microcirculatory perfusion in shock.

[Expression of intercellular adhesion molecule-1 in different organs of the mice with endotoxic shock induced by lipopolysaccharide].

To investigate and compare the expression of intercellular adhesion molecule-1 (ICAM-1) in different organs of the mice with endotoxic shock induced by lipopolysaccharide (LPS), protein and mRNA of ICAM-1 were measured by Western blotting and RT-PCR respectively in different organs of BALB/c mice administered intraperitoneally with 5 mg/kg LPS. The results showed that the constitutive expression of ICAM-1 protein and mRNA was the greatest in the lungs, followed by the spleen, kidney and intestine. After LPS stimulation, the upregulation of ICAM-1 was still greatest in the lungs, followed by the liver, spleen, heart, kidney and intestine. Compared with the normal mice, the expression of ICAM-1 protein in endotoxic shocked mice increased by 4.5-fold in the lungs, 3.0-fold in the kidney, 1.5-fold in the spleen; the expression in the liver and heart was negative under normal condition and changed into positive during endotoxic shock; but ICAM-1 expression in the intestine did not change significantly. The expression of ICAM-1 mRNA also increased consistently. These data highlight that LPS can up-regulate ICAM-1 protein and mRNA expression in different tissues of the mice with endotoxic shock. The difference in ICAM-1 expression among the organs may lead to different sensitivity of organ damage in endotoxic shock. This suggests that inhibition of ICAM-1 expression may be a useful principle for prevention and treatment of endotoxic shock.

[Detection of Mycobacterium tuberculosis in lung cancer tissue by indirect in situ nested PCR].

OBJECTIVE: To localize Mycobacterium tuberculosis DNA (TB-DNA) in lung cancer tissue and to investigate the possible relationship of this bacterial infection with the development of lung cancer. METHODS: A sensitive and specific indirect in situ nested PCR (ISNPCR) was used to identify and localize TB-DNA in 15 formalin fixed paraffin-embedded lung cancer tissue specimens, which had been demonstrated to be positive for TB-DNA by conventional PCR. RESULTS: Positive granules of TB-DNA in brown color was found mainly in the cytoplasm of the alveolar epithelial cells, pulmonary macrophages, inflammatory cells and a few tumor cells within lung cancer tissues. CONCLUSION: Mycobacterium tuberculosis infection may play a role in the pathogenesis of lung cancer.

Role of p38 mitogen-activated protein kinase in lipopolysaccharide-induced expression of inducible nitric oxide synthase in human endothelial cells.

OBJECTIVE: To understand the role of p38 mitogen-activated protein kinase (p38MAPK) in the expression of inducible nitric oxide synthase (iNOS) and NO production in human endothelial cells under the stimulation by lipopolysaccharide (LPS). METHODS: NO level in the supernatant of the cell culture media was measured with Griess method, and iNOS protein and mRNA expressions by the cells were detected with immunofluorescence analysis and reverse transcriptase-polymerase chain reaction (RT-PCR) respectively. Immunoprecipitation assay was employed to examine p38 MAPK activity. RESULTS: It was shown that in comparison with the basal level of iNOS expression in cultured endothelial cells line ECV304, iNOS mRNA and protein expressions were significantly increased in the cells after LPS stimulation. In response to LPS treatment, obvious enhancement of p38 MAPK activity in ECV304 took place after the stimulation, with the peak level occurring at 15 min that maintained for approximately 45 min before gradual decline. When treated with SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl) imidazole], a highly specific inhibitor of p38 MAPK, significant inhibition of LPS-induced iNOS protein and mRNA expressions was observed. CONCLUSIONS: p38 MAPK plays an important role in iNOS expression and NO production in ECV304 cells, and, inhibition of the signal transduction pathway may consequently be an effective approach to reduce the production of iNOS and other cytokines for the treatment of septic shock.

[Chromosomal imbalance in primary lung squamous cell carcinoma and their relationship with smoking].

BACKGROUND & OBJECTIVE: Chromosomal imbalance plays an important role in tumorigenesis of lung cancer, and may be influenced by different carcinogens. This study was to examine chromosomal imbalance in primary lung squamous cell carcinoma (LSCC), and their association with smoking. METHODS: Chromosomal gains and losses in 39 specimens of LSCC were identified by comparative genomic hybridization (CGH), the association between chromosomal imbalances in LSCC and smoking was analyzed. RESULTS: The most frequent chromosomal gains of LSCC were detected on chromosomal arms 3q (74.4%, 29/39), 5p (66.7%, 26/39), 1q (43.6%, 17/39), 8q (41.0%, 16/39), 12p (42.6%, 18/39), 2p (38.5%, 15/39), and 18p (33.3%, 13/39), with minimal amplified regions (MAR) at 3q26.2-29 (74.4%, 29/39), 5p14.3-15.3 (66.7%, 26/39), 1q41-44(41.0%, 16/39), 8q23 (41.0%, 16/39), 12p13 (41.0%, 16/39), and 18p11.2 (33.3%, 13/39)u high-copy-number amplification at chromosomal arms 3q, and 5p were found in 15 (38.5%), and 6 (15.4%) patients. Chromosomal losses mainly involved chromosomal arms 3p (56.4%, 22/39), 5q (53.8%, 21/39), 13q (51.3%, 20/39), 8p (46.1%, 18/39), 4p (43.6%, 17/39), 4q (43.6%, 17/39), 1p (41.0%, 16/39), 2q (38.5%, 15/39), 9q (35.9%, 14/39), 13p (35.9%, 14/39), 16p (35.9%, 14/39) ,6p (33.3%, 13/39), and 6q (30.7%, 12/39), with minimal deleted regions (MDR) at 3p14.2-21.2 (51.3%, 20/39), 5q15-22 (51.3%, 20/39), 13q14.2-21.2 (48.7%, 19/39), 8p21.1-22 (43.6%, 17/39), 2q32 (35.9%, 14/39), and 16p12-13.1 (33.3%, 13/39). Amplification rates of chromosomal arms 3q, and 8q in smoking LSCC patients were significantly higher than those in non-smoking LSCC patients (P=0.002,P=0.031). While high incidences of gains at chromosomal arms 5p and 12p, and of losses at chromosomal arms 3p, 4q, and 5q were the common feature of chromosomal changes of smoking and non-smoking LSCC patients. CONCLUSION: 3q, 5p, 1q, 8q, 12p, 2p, 18p gains and 3p, 5q, 13q, 8p, 4p, 4q, 1p, 2q, 9q, 13p,16p, 6p, 6q loses might be involved in tumorigenesis and/or progression of LSCC, smoking-induced lung cancer may be associated with 3q, 8q gains.

Recurrent chromosomal imbalances in nonsmall cell lung carcinoma: the association between 1q amplification and tumor recurrence.

BACKGROUND: Lung carcinoma is a leading cause of cancer deaths worldwide. To better understand this disease, the authors studied genetic alterations in nonsmall cell lung carcinoma (NSCLC) and the association between genetic changes and clinical features. METHODS: Genetic alterations in 30 patients with adenocarcinoma (AC) and 39 patients with squamous cell carcinoma (SCC) were analyzed by comparative genomic hybridization. The genetic changes in patients with AC and SCC were compared and the associations of these changes with clinical features were studied. RESULTS: A gain of 3q with a minimal amplified region at 3q25.3-qter was significantly higher in patients with SCC compared with patients with AC (72% vs. 27%; P < 0.001). A gain of 20q and loss of chromosome 9 were detected more frequently in patients with AC compared with patients with SCC (P < 0.05). Gains of 5p and 20q and loss of 5q were significantly correlated with an advanced stage of NSCLC (P < 0.05). Amplification of 1q was significantly associated with NSCLC recurrence (P = 0.04). CONCLUSIONS: The results of the current study suggested that different chromosomal aberrations may contribute to the types and pathologic stages of NSCLC.