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Two isomeric homoleptic Ir(III) complexes with pyridinopyridazine derivative ligands were prepared first. Due to its stronger intramolecular hydrogen bonding and intermolecular interactions, complex IrPPM has a higher decomposition temperature (5% weight loss) of 387°C than IrPPP (354°C). They have similar UV–Vis absorption and photoluminescence spectra in CH2Cl2 solution with photoluminescence peaks around 635–636 nm. However, the emission peak of IrPPM in neat powder obviously red‐shifted to 652 nm, and that of IrPPP blue‐shifted to 626 nm. Simultaneously, complex IrPPM has a lower photoluminescence quantum yield of 0.3 than IrPPP (0.5). Efficient saturated red OLED devices are developed with Commission Internationale de L'Eclairage color coordinates of (0.67, 0.32) and (0.66, 0.32), respectively. The maximum external quantum efficiencies of both devices exceed 11%. These results demonstrate the great potential of pyridinopyridazine derivatives for developing new iridium complexes for OLED applications. [ABSTRACT FROM AUTHOR]

Newborn neurons undergo inside-out migration to their final destinations during neocortical development. Reelin-induced tyrosine phosphorylation of disabled 1 (Dab1) is a critical mechanism controlling cortical neuron migration. However, the roles of Reelin-independent phosphorylation of Dab1 remain unclear. Here, we report that deleted in colorectal carcinoma (DCC) interacts with Dab1 via its P3 domain. Netrin 1, a DCC ligand, induces Dab1 phosphorylation at Y220 and Y232. Interestingly, knockdown of DCC or truncation of its P3 domain dramatically delays neuronal migration and impairs the multipolar-to-bipolar transition of migrating neurons. Notably, the migration delay and morphological transition defects are rescued by the expression of a phospho-mimetic Dab1 or a constitutively active form of Fyn proto-oncogene (Fyn), a member of the Src-family tyrosine kinases that effectively induces Dab1 phosphorylation. Collectively, these findings illustrate a DCC-Dab1 interaction that ensures proper neuronal migration during neocortical development. [ABSTRACT FROM AUTHOR]

Background: Water-forming NADH oxidase can oxidize cytosolic NADH to NAD+, thus relieving cytosolic NADH accumulation in Saccharomyces cerevisiae. Previous studies of the enzyme were conducted under aerobic conditions, as O2 is the recognized electron acceptor of the enzyme. In order to extend its use in industrial production and to study its efect on anaerobes, the efects of overexpression of this oxidase in S. cerevisiae BY4741 and Clostridium aceto- butylicum 428 (Cac-428) under anaerobic conditions were evaluated. Results: Glucose was exhausted in the NADH oxidase-overexpressing S. cerevisiae strain (Sce-NOX) culture after 26 h, while 43.51 ± 2.18 g/L residual glucose was left in the control strain (Sce-CON) culture at this time point. After 30 h of fermentation, the concentration of ethanol produced by Sce-NOX reached 36.28 ± 1.81 g/L, an increase of 56.38 % as compared to Sce-CON (23.20 ± 1.16 g/L), while the byproduct glycerol was remarkably decreased in the culture of Sce-NOX. In the case of the C. acetobutylicum strain (Cac-NOX) overexpressing NADH oxidase, glucose consumption, cell growth rate, and the production of acetone-butanol-ethanol (ABE) all decreased, while the concentrations of acetic acid and butyric acid increased as compared to the control strain (Cac-CON). During fermentation of Cac-CON and Cac-NOX in 100-mL screw-capped bottles, the concentrations of ABE increased with increasing headspace. Additionally, several alternative electron acceptors in C. acetobutylicum fermentation were tested. Nitroblue tetrazo- lium and 2,6-dichloroindophenol were lethiferous to both Cac-CON and Cac-NOX. Methylene blue could relieve the efect caused by the overexpression of the NADH oxidase on the metabolic network of C. acetobutylicum strains, while cytochrome c aggravated the efect. Conclusions: The water-forming NADH oxidase could regulate the metabolism of both the S. cerevisiae and the C. acetobutylicum strains in anaerobic conditions. Thus, the recombinant S. cerevisiae strain might be useful in industrial production. Besides the recognized electron acceptor O2, methylene blue and/or the structural analogs may be the alternative elector acceptor of the NADH oxidase in anaerobic conditions. [ABSTRACT FROM AUTHOR]

Objectives: Paclitaxel (PTX) is frequently used in the clinical treatment of solid tumors. But the PTX-resistance is a great obstacle in cancer treatment. Exploration of the mechanisms of drug resistance suggests that tumor suppressor genes (TSGs) play a key role in the response of chemotherapeutic drugs. TSGs, a set of genes that are often inactivated in cancers, can regulate various biological processes. In this study, an overview of the contribution of TSGs to PTX resistance and their underlying relationship in cancers are reported by using GeneMANIA, a web-based tool for gene/protein function prediction. Methods: Using PubMed online database and Google web site, the terms "paclitaxel resistance" or "taxol resistance" or "drug resistance" or "chemotherapy resistance", and "cancer" or "carcinoma", and "tumor suppressor genes" or "TSGs" or "negative regulated protein" or "antioncogenes" were searched and analyzed. GeneMANIA data base was used to predict gene/protein interactions and functions. Results: We identified 22 TSGs involved in PTX resistance, including BRCA1, TP53, PTEN, APC, CDKN1A, CDKN2A, HIN-1, RASSF1, YAP, ING4, PLK2, FBW7, BLU, LZTS1, REST, FADD, PDCD4, TGFBI, ING1, Bax, PinX1 and hEx. The TSGs were found to have direct and indirect relationships with each other, and thus they could contribute to PTX resistance as a group. The varied expression status and regulation function of the TSGs on cell cycle in different cancers might play an important role in PTX resistance. Conclusion: A further understanding of the roles of tumor suppressor genes in drug resistance is an important step to overcome chemotherapy tolerance. Tumor suppressor gene therapy targets the altered genes and signaling pathways and can be a new strategy to reverse chemotherapy resistance. [ABSTRACT FROM AUTHOR]

The article examines processes for reducing the nitrosamines level in tobacco smoke by microwave irradiation, in relation to efforts to reduce the harm of smoking. The microwave-induced elimination of nitrosamines such as N-nitrosopyrrolidine and N-nitrosodiphenylamine was invesigated and the impact of the presence of water and salt in the medium on the reduction was assessed in detail. The existence of water in the medium was crucial for the microwave-induced reduction of NDPA, because the rapid movement of water molecules under the influence of microwaves strongly affects the adjacent nitrosamines leading to their decomposition.