A multistep enzyme catalysis was successfully implemented to produce long-chain α,ω-dicarboxylic and ω-hydroxycarboxylic acids from renewable fatty acids and plant oils. Sebacic acid as well as ω-hydroxynonanoic acid and ω-hydroxytridec-11-enoic acid were produced from oleic and ricinoleic acid.

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Biotransformation of long‐chain fatty acids into medium‐chain α,ω‐dicarboxylic acids or ω‐aminocarboxylic acids could be achieved with biocatalysts. This study presents the production of α,ω‐dicarboxylic acids (e.g., C9, C11, C12, C13) and ω‐aminocarboxylic acids (e.g., C11, C12, C13) directly from fatty acids (e.g., oleic acid, ricinoleic acid, lesquerolic acid) using recombinant Escherichia coli‐based biocatalysts. ω‐Hydroxycarboxylic acids, which were produced from oxidative cleavage of fatty acids via enzymatic reactions involving a fatty acid double bond hydratase, an alcohol dehydrogenase, a Baeyer–Villiger monooxygenase and an esterase, were then oxidized to α,ω‐dicarboxylic acids by alcohol dehydrogenase (ADH, AlkJ) from Pseudomonas putida GPo1 or converted into ω‐aminocarboxylic acids by a serial combination of ADH from P. putida GPo1 and an ω‐transaminase of Silicibacter pomeroyi. The double bonds present in the fatty acids such as ricinoleic acid and lesquerolic acid were reduced by E. coli‐native enzymes during the biotransformations. This study demonstrates that the industrially relevant building blocks (C9 to C13 saturated α,ω‐dicarboxylic acids and ω‐aminocarboxylic acids) can be produced from renewable fatty acids using biocatalysis.magnified image

Zinc‐based metal oxide semiconductors have attracted attention as an alternative to current silicon‐based semiconductors for applications in transparent and flexible electronics. Despite this, metal oxide transistors require significant improvements in performance and electrical reliability before they can be applied widely in optoelectronics. Amorphous indium–zinc–tin oxide (a‐IZTO) has been considered an alternative channel layer to a prototypical indium–gallium–zinc oxide (IGZO) with the aim of achieving a high mobility (>40 cm2 Vs−1) transistors. The effects of the gate bias and light stress on the resulting a‐IZTO field‐effect transistors are examined in detail. Hydrogen impurities in the a‐IZTO semiconductor are found to play a direct role in determining the photo‐bias stability of the resulting transistors. The Al2O3‐inserted IZTO thin‐film transistors (TFTs) are hydrogen‐poor, and consequently show better resistance to the external‐bias‐thermal stress and photo‐bias‐thermal stress than the hydrogen‐rich control IZTO TFTs. First‐principles calculations show that even in the amorphous phase, hydrogen impurities including interstitial H and substitutional H can be bistable centers with an electronic deep‐to‐shallow transition through large lattice relaxation. The negative threshold voltage shift of the a‐IZTO transistors under a negative‐bias‐thermal stress and negative‐bias‐illumination stress condition is attributed to the transition from the acceptor‐like deep interstitial Hi− (or substitutional H‐DX−) to the shallow Hi+ (or HO+) with a high (low) activation energy barrier. Conclusively, the delicate controllability of hydrogen is a key factor to achieve the high performance and stability of the metal oxide transistors.

Hypoxia is a common feature of the tumor microenvironment. Accumulating evidence has demonstrated hypoxia to be an important trigger of tumor cell invasion or metastasizes via hypoxia-signaling cascades, including hypoxia-inducible factors (HIFs). Microfluidic model can be a reliable in vitro tool for systematically interrogating individual factors and their accompanying downstream effects, which may otherwise be difficult to study in complex tumor tissues. Here, we used an in vitro model of microvascular networks in a microfluidic chip to measure the extravasation potential of breast cell lines subjected to different oxygen conditions. Through the use of HIF-1α knock-down cell lines, we also validated the importance of HIF-1α in the transmigration ability of human breast cell lines. Three human breast cell lines derived from human breast tissues (MCF10A, MCF-7 and MDA-MB-231) were used in this study to evaluate the role of hypoxia in promoting metastasis at different stages of cancer progression. Under hypoxic conditions, HIF-1α protein level was increased, and coincided with changes in cell morphology, viability and an elevated metastatic potential. These changes were accompanied by an increase in the rate of extravasation compared to normoxia (21% O2). siRNA knockdown of HIF-1α in hypoxic tumors significantly decreased the extravasation rates of all the cell lines tested and may have an effect on the function of metastatic and apoptotic-related cellular processes.