Double Bond-Transferring Novel Hydroxylation Reaction Involved in Microbial Metabolism of Plant Essential Oil Eugenol

We isolated a eugenol-degrading bacterium Pseudomonas fluorescens E 118.This strain produced a novel enzyme,eugenol dehydrogenase which catalyzes the formation of coniferyl alcohol from eugenol.The enzyme required an electron acceptor such as phenazione methosulface(PMS).The enzyme was purified 242-fold with a 22.4% overall recovery from the eugenol-induced cells of P.fluorescens E118.The purified enzyme appeared to be homogeneous,judging from the analysis of polyacrylamide gel electrophoresis.The enzyme was a 68.6 kDa protein composed of two different subunits (α　subunit 10.4kDa and βsubunit 58.2kda).The enzyme exhibited a cytochrome c-like absorption.The α subunit containing heme c seemed to play an important role for the dehydrogenation reaction.The enzyme also catalyzes the dehydrogenation of 4-alkylphenol into the corresponding alkyl 1-(4-hydroxyphenyl)-alcohol,and vanillyl alchol into vanillin,respectively.The reaction products were isolated and identified.These reaction seemed to proceed through the same mechanisms.植物精油eugenolは自然界に広く存在し、安価な農業余剰産物である。オイゲノールはPseudomonas属やCorynebacterium属細菌によってFig.1に示したように代謝されることが知られている。この中でオイゲノールからコニフェルアルコールへの変換は二重結合が移動すると同時に酸化されるユニークな反応が予想されるが、この変換に関する酵素化学的知見は全く得られていない。オイゲノール代謝における中間体フェルラ酸は抗酸化剤、医薬品出発原料となり、また、コニフェリルアルコールは高価な香料として知られている。本報ではP.fluorescensE118のオイゲノール代謝について、酵素レベルでの検討を試みた

High-power, continuous-wave, scalable, single-frequency 852nm laser source for 213nm generation

We developed a high-power, continuous-wave (CW), single-frequency 852nm laser source, for the purpose of fourth harmonic generation at 213nm. Our approach is the doubly resonant sum-frequency mixing (DRSFM) with two fiber sources. An in-house single-frequency master oscillator at 1907nm is amplified by an in-house clad-pumped amplifier to 5W, and a commercial single-frequency master oscillator at 1540nm is amplified by a commercial amplifier to 10W. The two beams are combined via a dichroic mirror to a single beam before incident on a dual-wavelength resonator, consisting of one set of dual-wavelength mirrors. The external resonator is locked to the 1907nm laser frequency, and the frequency of the 1540nm is locked to the resonator, realizing double-resonance. With a periodically-poled stoichiometric lithium tantalate in the resonator, the sum-frequency at 852nm is efficiently generated. All 3 waves are in the same polarization (e-ray), allowing the effective use of Brewster-cut device, eliminating reflection loss for all wavelengths without any antireflection coatings. With 4.6W at 1907nm and 7.7W at 1540nm incident onto the resonator, 5.2W at 852nm was generated, representing the efficiency of greater than 40%. The experimental result indicates our current setup will be more efficient with higher input powers at 1907nm. With both fiber sources at 1540nm and 1907nm being scalable in output power, the output at 852nm is also scalable. By the forth harmonic of 852nm, 0.456 W CW 213nm was generated.New Energy and Industrial Technology Development Organization (NEDO) of JapanThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Silenced Expression of NFKBIA in Lung Adenocarcinoma Patients with a Never-smoking History

Nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α (NFKBIA), which is a tumor suppressor gene, was found to be silenced in lung adenocarcinomas. We examined NFKBIA expression, mutations in the EGFR and K-ras genes, and EML4-ALK fusion in 101 resected lung adenocarcinoma samples from never-smokers. NFKBIA expression was evaluated using immunohistochemistry. NFKBIA expression was negative in 16 of the 101 samples (15.8%). EGFR and K-ras mutations and EML4-ALK fusion were detected in 61 (60.5%), 1 (1.0%), and 2 (2.0%) of the 101 samples, respectively, in a completely mutually exclusive manner. Negative NFKBIA expression was observed significantly more frequently among the tumors with none of the three genetic alterations compared to those with such alterations (p＝0.009). In addition, negative NFKBIA expression was significantly more frequent among the EGFR-wild type samples compared to the EGFR-mutant samples (p＝0.013). In conclusion, NFKBIA expression was silenced in adenocarcinomas without EGFR/K-ras mutations or EML4-ALK fusion, suggesting that the silencing of NFKBIA may play an important role in the carcinogenesis of adenocarcinomas independent of EGFR/K-ras mutations or EML4-ALK fusion

Characterization of human UGT2A3 expression using a prepared specific antibody against UGT2A3

UDP-Glucuronosyltransferase (UGT) 2A3 belongs to a UGT superfamily of phase II drug-metabolizing enzymes that catalyzes the glucuronidation of many endobiotics and xenobiotics. Previous studies have demonstrated that UGT2A3 is expressed in the human liver, small intestine, and kidney at the mRNA level; however, its protein expression has not been determined. Evaluation of the protein expression of UGT2A3 would be useful to determine its role at the tissue level. In this study, we prepared a specific antibody against human UGT2A3 and evaluated the relative expression of UGT2A3 in the human liver, small intestine, and kidney. Western blot analysis indicated that this antibody is specific to UGT2A3 because it did not cross-react with other human UGT isoforms or rodent UGTs. UGT2A3 expression in the human small intestine was higher than that in the liver and kidney. Via treatment with endoglycosidase, it was clearly demonstrated that UGT2A3 was N-glycosylated. UGT2A3 protein levels were significantly correlated with UGT2A3 mRNA levels in a panel of 28 human liver samples (r = 0.64, p <0.001). In conclusion, we successfully prepared a specific antibody against UGT2A3. This antibody would be useful to evaluate the physiological, pharmacological, and toxicological roles of UGT2A3 in human tissues. (C) 2019 The Japanese Society for the Study of Xenobiotics. Published by Elsevier Ltd. All rights reserved.Peer reviewe

Scalable Approach for Continuous-Wave Deep-Ultraviolet Laser at 213nm

We present a novel approach for generation at 213nm in continuous-wave, corresponding to the fifth harmonic of common 1064nm laser, in pure continuous-wave mode. The approach is scalable in output power. Starting from two infrared fiber laser sources, we demonstrated 0.456W output at 213nm. (C) 2019 Optical Society of America under the terms of the OSA Open Access Publishing AgreementOpen access journal.This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Preclinical Evaluation of MicroRNA-34b/c Delivery for Malignant Pleural Mesothelioma

The microRNA-34s (miR-34s) have p53 response elements in their 5ʼ-flanking regions and demonstrate tumor-suppressive functions. In malignant pleural mesothelioma (MPM), we previously reported that expression of miR-34b and miR-34c (miR-34b/c) was frequently downregulated by methylation in MPM cell lines and primary tumors. The forced overexpression of miR-34b/c showed significant antitumor effects with the induction of apoptosis in MPM cells. In this study, we examined the in vivo antitumor effects of miR-34b/c using adenovirus vector on MPM. We subcutaneously transplanted NCI-H290, a human MPM cell line, into BALB/C mice and injected adenovirus vector expressing miR-34b/c, luciferase driven by the cytomegalovirus promoter (Ad-miR-34b/c or Ad-Luc), or PBS control into tumors over 5mm in diameter. A statistically significant growth inhibition of the tumor volume was observed in the Ad-miR-34b/c group from day 6 onward compared to the Ad-Luc group. The inhibition rate of Ad-miR-34b/c, compared to the tumor volume treated with Ad-Luc, was 58.6% on day 10 and 54.7% on day13. Our results indicate that adenovirus-mediated miR-34b/c gene therapy could be useful for the clinical treatment of MPM