• 한국응용곤충학회지
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• 제31권3호
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• pp.314-327
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• 1992

Insecticide resistance is a serious is a serious threat to IPM, resulting in various adverse effects not to mention the loss of yield in agriculture. One approach to counter the problem is the disruption of resistance mechanisms. This can be achieved by (1) compounds which show a negative correlation with resistance at the site of action, (2) specific metabolic inhibitors which serve as synergists, or (3) a certain combination of two insecticides producing a joint action. This approach, however, requires certain precautions for the side effects may cause an increase in toxicity to mammals. Owing to the recent advances in theoretical studies on resistance management employing computer simulation and mathematical models, a few principles to reduce the risk of development of resistance have been clarified. They are helpful in designing operational strategies with regard to, for instance, insecticide doses to be applied, mode of application, and choice and nature of the insecticide(s) to be used. For restoration of insecticide susceptibility of a resistant population, reintroduction of susceptible individuals to the resistant population is feasible when certain conditions are met. Natural enemies which developed resistance to insecticides can be an important component of IPM as has been shown in the pest management in apple orchards. After all, the implementation of a successful resistance management program depends upon cooperation between different sigments of the agricutural community. Although resistance is a preadaptive phenomenon, in some cases spontaneous loss of resistance does occur without contamination by susceptible individuals. The instability of resistance in these insects implies the possible existence of a switch machanism controlling the expression of resistance gene(s). Elucidation of such a mechanism may eventually provide us with a new technical approach with which we can combat the problem of insecticide resistance.

• Corrosion Science and Technology
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• 제2권4호
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• pp.202-206
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• 2003

Fusion Bonded Epoxy(FBE) systems have been widely used to protect pipelines for over 30 years. Numerous attempts have so far been made to improve the properties of FBE coatings such as chemical resistance, adhesion, water resistance, cathodic disbondment resistance, impact resistance, and flexibility to protect pipelines at a wet and a high temperature condition. But these attempts have not been successful in reducing some weakness, for instance, in pipeline operating at high temperature due to poor hot water resistance and cathodic protection. The purpose here is to build a basis for getting better corrosion resistance of FBE systems. Cresol-novolac epoxy coating systems were studied compared to bisphenol A type epoxy systems. After the immersion of the film in water at a high temperature for a long period, good adhesion to metal substrate and excellent cathodic disbond resistance were observed in the cresol-novolac epoxy resin systems. It is well known that the adhesion of organic coatings to metal substrate might be decreased due to the disruption of a chemical bond across the film and metal interface induced by water molecules. A high crosslinking density might decrease water permeability and improve cathodic disbonding protection in the coatings. Other factors are studied to understand anti-corrosion mechanism of Cresol-novolac epoxy coatings. In addition, the water absorption rate and the effect of cure temperature on the adhesion and cathodic disbonding resistance ofthe films were studied in different epoxy coatings and the effect of substrate was evaluated. The results of field application are proved that the Cresol-novolac epoxy coating system developed recently is one of the most suitable coatings for protection of pipelines.

• Journal of Microbiology and Biotechnology
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• 제29권3호
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• pp.367-372
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• 2019

Deactivation of aminoglycosides by their modifying enzymes, including a number of aminoglycoside O-phosphotransferases, is the most ubiquitous resistance mechanism in aminoglycoside-resistant pathogens. Nonetheless, in a couple of biosynthetic pathways for gentamicins, fortimicins, and istamycins, phosphorylation of aminoglycosides seems to be a unique and initial step for the creation of a natural defensive structural feature such as a 3',4'-dideoxy scaffold. Our aim was to elucidate the biochemical details on the beginning of these C3',4'-dideoxygenation biosynthetic steps for aminoglycosides. The biosynthesis of istamycins must surely involve these 3',4'-didehydroxylation steps, but much less has been reported in terms of characterization of istamycin biosynthetic genes, especially about the phosphotransferase-encoding gene. In the disruption and complementation experiments pointing to a putative gene, istP, in the genome of wild-type Streptomyces tenjimariensis, the function of the istP gene was proved here to be a phosphotransferase. Next, an in-frame deletion of a known phosphotransferase-encoding gene forP from the genome of wild-type Micromonospora olivasterospora resulted in the appearance of a hitherto unidentified fortimicin shunt product, namely 3-O-methyl-FOR-KK1, whereas complementation of forP restored the natural fortimicin metabolite profiles. The bilateral complementation of an istP gene (or forP) in the ${\Delta}forP$ mutant (or ${\Delta}istP$ mutant strain) successfully restored the biosynthesis of 3',4'-dideoxy fortimicins and istamycins, thus clearly indicating that they are interchangeable launchers of the biosynthesis of 3',4'-dideoxy types of 1,4-diaminocyclitol antibiotics.

• Molecules and Cells
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• 제39권5호
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• pp.426-438
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• 2016

Plant disease resistance occurs as a hypersensitive response (HR) at the site of attempted pathogen invasion. This specific event is initiated in response to recognition of pathogen-associated molecular pattern (PAMP) and subsequent PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI). Both PTI and ETI mechanisms are tightly connected with reactive oxygen species (ROS) production and disease resistance that involves distinct biphasic ROS production as one of its pivotal plant immune responses. This unique oxidative burst is strongly dependent on the resistant cultivars because a monophasic ROS burst is a hallmark of the susceptible cultivars. However, the cause of the differential ROS burst remains unknown. In the study here, we revealed the plausible underlying mechanism of the differential ROS burst through functional understanding of the Magnaporthe oryzae (M. oryzae) AVR effector, AVR-Pii. We performed yeast two-hybrid (Y2H) screening using AVR-Pii as bait and isolated rice NADP-malic enzyme2 (Os-NADP-ME2) as the rice target protein. To our surprise, deletion of the rice Os-NADP-ME2 gene in a resistant rice cultivar disrupted innate immunity against the rice blast fungus. Malic enzyme activity and inhibition studies demonstrated that AVR-Pii proteins specifically inhibit in vitro NADP-ME activity. Overall, we demonstrate that rice blast fungus, M. oryzae attenuates the host ROS burst via AVR-Pii-mediated inhibition of Os-NADP-ME2, which is indispensable in ROS metabolism for the innate immunity of rice. This characterization of the regulation of the host oxidative burst will help to elucidate how the products of AVR genes function associated with virulence of the pathogen.

• Biomolecules & Therapeutics
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• 제31권4호
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• pp.446-455
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• 2023

The mechanistic functions of 3-deoxysappanchalcone (3-DSC), a chalcone compound known to have many pharmacological effects on lung cancer, have not yet been elucidated. In this study, we identified the comprehensive anti-cancer mechanism of 3-DSC, which targets EGFR and MET kinase in drug-resistant lung cancer cells. 3-DSC directly targets both EGFR and MET, thereby inhibiting the growth of drug-resistant lung cancer cells. Mechanistically, 3-DSC induced cell cycle arrest by modulating cell cycle regulatory proteins, including cyclin B1, cdc2, and p27. In addition, concomitant EGFR downstream signaling proteins such as MET, AKT, and ERK were affected by 3-DSC and contributed to the inhibition of cancer cell growth. Furthermore, our results show that 3-DSC increased redox homeostasis disruption, ER stress, mitochondrial depolarization, and caspase activation in gefitinib-resistant lung cancer cells, thereby abrogating cancer cell growth. 3-DSC induced apoptotic cell death which is regulated by Mcl-1, Bax, Apaf-1, and PARP in gefitinib-resistant lung cancer cells. 3-DSC also initiated the activation of caspases, and the pan-caspase inhibitor, Z-VAD-FMK, abrogated 3-DSC induced-apoptosis in lung cancer cells. These data imply that 3-DSC mainly increased mitochondria-associated intrinsic apoptosis in lung cancer cells to reduce lung cancer cell growth. Overall, 3-DSC inhibited the growth of drug-resistant lung cancer cells by simultaneously targeting EGFR and MET, which exerted anti-cancer effects through cell cycle arrest, mitochondrial homeostasis collapse, and increased ROS generation, eventually triggering anti-cancer mechanisms. 3-DSC could potentially be used as an effective anti-cancer strategy to overcome EGFR and MET target drug-resistant lung cancer.

• 한국미생물·생명공학회지
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• 제41권1호
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• pp.88-95
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• 2013

Candida 바이오필름은 숙주조직과 의료기기의 표면에 자라는 자가-조직화된 미생물의 군락으로 전통적인 항진균제에 대한 저항성이 높게 나타난다. 황금(Scutellaria baicalensis)의 뿌리는 극동지방에서 의료용 목적으로 널리 사용되어 왔다. 본 연구의 목적은 10 C. albicans 임상 분리균주에 의해 형성된 바이오필름에 대한 황금의 수용성 추출물의 효과를 평가하고, 항바이오필름 활성에 대한 메커니즘을 알아보는 것이다. 바이오필름에 대한 효과는 XTT 환원분석법을 사용하였으며, 조사된 모든 균주에 대한 대사활성은 MIC에서 유의하게 감소($57.7{\pm}17.3$%)하였다. 황금추출물은 (1,3)-${\beta}$-D-글루칸 합성효소의 활성을 저해하였고 C. albicans의 형태에 대한 황금의 효과는 글루칸 합성의 억제로 인한 생장의 변화와 관련이 있었다: 대부분의 세포는 둥글고 팽창되었으며 세포벽이 진하게 염색되거나 파열되었다. 항캔디다 활성은 살진균성이었고, 황금은 C. albicans를 $G_0/G_1$기에 머물게 했다. 데이터는 황금이 목표가 되는 균류에 다중의 치명적인 효과를 내며, (1,3)-${\beta}$-D-글루칸 합성효소의 활성을 저해함을 통해 궁극적으로는 세포벽의 파열과 죽음에 이르게 한다는 것을 나타낸다. 따라서 황금은 바이오필름과 관련된 캔디다의 감염을 치료하고 제거하기 위한 항진균제 개발 후보 물질로서의 가능성을 가진다.