• Biomedical Science Letters
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• v.30 no.3
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• pp.101-112
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• 2024

This review provides an overview of carbapenem-resistant Enterobacterales (CRE) studies. CRE, called superbugs, has a high mortality rate and an increased resistance rate in several countries. The bacteria representing CRE are Klebsiella species and Escherichia spp., and they cause urinary tract infections (UTIs) and bloodstream infections (BSIs). CRE acquires resistance due to several mechanisms, typically divided into carbapenemase-producing (CP)-CRE and non-CP-CRE. Furthermore, although there are several antibiotics developed to treat CRE, they have their limitations; thus, antibiotic combination therapies or novel treatments are being developed. Therefore, since research on CRE and the use of appropriate antibiotics is important, some CRE-resistant mechanisms that enhance them are discussed. This review article was written using information obtained from Google Scholar and the National Center for Biotechnology Information website.

• Biomolecules & Therapeutics
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• v.20 no.3
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• pp.256-267
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• 2012

Tamoxifen is a central component of the treatment of estrogen receptor (ER)-positive breast cancer as a partial agonist of ER. It has been clinically used for the last 30 years and is currently available as a chemopreventive agent in women with high risk for breast cancer. The most challenging issue with tamoxifen use is the development of resistance in an initially responsive breast tumor. This review summarizes the roles of ER as the therapeutic target of tamoxifen in cancer treatment, clinical values and issues of tamoxifen use, and molecular mechanisms of tamoxifen resistance. Emerging knowledge on the molecular mechanisms of tamoxifen resistance will provide insight into the design of regimens to overcome tamoxifen resistance and discovery of novel therapeutic agents with a decreased chance of developing resistance as well as establishing more efficient treatment strategies.

• Molecules and Cells
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• v.25 no.1
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• pp.119-123
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• 2008

Pyrimidine antagonists including 5-Fluorouracil (5-FU) have been used in chemotherapy for cancer patients for over 40 years. 5-FU, especially, is a mainstay treatment for colorectal cancer. It is a pro-drug that is converted to the active drug via the nucleic acid biosynthetic pathway. The metabolites of 5-FU inhibit normal RNA and DNA function, and induce apoptosis of cancer cells. One of the major obstacles to successful chemotherapy is the resistance of cancer cells to anti-cancer drugs. Therefore, it is important to elucidate resistance mechanisms to improve the efficacy of chemotherapy. We have used C. elegans as a model system to investigate the mechanism of resistance to 5-FU, which induces germ cell death and inhibits larval development in C. elegans. We screened 5-FU resistant mutants no longer arrested as larvae by 5-FU. We obtained 18 mutants out of 72,000 F1 individuals screened, and mapped them into three complementation groups. We propose that C. elegans could be a useful model system for studying mechanisms of resistance to anti-cancer drugs.

• Integrative Medicine Research
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• v.2 no.4
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• pp.131-138
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• 2013

The skeletal muscle in our body is a major site for bioenergetics and metabolism during exercise. Carbohydrates and fats are the primary nutrients that provide the necessary energy required to maintain cellular activities during exercise. The metabolic responses to exercise in glucose and lipid regulation depend on the intensity and duration of exercise. Because of the increasing prevalence of obesity, recent studies have focused on the cellular and molecular mechanisms of obesity-induced insulin resistance in skeletal muscle. Accumulation of intramyocellular lipid may lead to insulin resistance in skeletal muscle. In addition, lipid intermediates (e.g., fatty acyl-coenzyme A, diacylglycerol, and ceramide) impair insulin signaling in skeletal muscle. Recently, emerging evidence linking obesity-induced insulin resistance to excessive lipid oxidation, mitochondrial overload, and mitochondrial oxidative stress have been provided with mitochondrial function. This review will provide a brief comprehensive summary on exercise and skeletal muscle metabolism, and discuss the potential mechanisms of obesity-induced insulin resistance in skeletal muscle.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.7
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• pp.3191-3194
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• 2014

Adenocarcinoma of lung has high incidence and a poor prognosis, woith chemotherapy as the main therapeutic tool, most commonly with cisplatin. However, chemotherapy resistance develops in the majority of patients during clinic treatment. Mechanisms of resistance are complex and still unclear. Although annexin play important roles in various tumor resistance mechanisms, their actions in cisplatin-resistant lung adenocarcinoma remain unclear. Preliminary studies by our group found that in cisplatin-resistant lung cancer A549 cells and lung adenocarcinoma tissues, both mRNA and protein expression of annexins A1, A2 and A3 is increased. Using a library of annexin A1, A2 and A3 targeting combined molecules already established by ourselves we found that specific targeting decreased cisplatin-resistance. Taken together, the underlined effects of annexins A1, A2 and A3 on drug resistance and suggest molecular mechanisms in cisplatin-resistant A549 cells both in vivo and in vitro. Furthermore, the study points to improved research on occurrence and development of lung adenocarcinoma, with provision of effective targets and programmes for lung adenocarcinoma therapy in the clinic.

• Microbiology and Biotechnology Letters
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• v.23 no.4
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• pp.384-389
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• 1995

Streptoalloteichus hindustanus ATCC 31219, a nebramycin complex producer, is similar to Streptomyeces tenebrarius in a viewpoint of resistance to a wide range of aminoglycoside antibiotics. S. tenebrarius has resistance mechanisms of 16s rRNA methylation and aminogycoside modification. However, it is not known whether resistance mechanisms of Stall. hindustanus are the same as in S. tenebrarius. Therefore, we have tried to isolate resistance determinants from Stall. hindustanus. Two different types of aminoglycoside resistance determinants were isolated from Stall. hindustanus and expressed in Streptomyces lividans TK24. The apramycin resistance gene (amr) and the tobramycin resistance gene (tmr) isolated from Stall. hindustanus showed broad resistance spectrum against a dozen of aminoglycoside antibiotics. The complete nucleotide sequences of apramycin resistance gene (amr) were determined. The deduced amino acid sequence of the amr gene of Stall hindustanus ATCC 31219 showed extensive sequence homology to the 16s rRNA methylase gene (kamB) of S. tenebrarius.

• Proceedings of the International Microelectronics And Packaging Society Conference
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• 2003.11a
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• pp.195-202
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• 2003

In this study, failure mechanisms of Au stud bumps/ACF flip chip joints were investigated underhigh current stressing condition. For the determination of allowable currents, I-V tests were performed on flip chip joints, and applied currents were measured as high as almost 4.2Amps $(4.42\times10^4\;Amp/cm^2)$. Degradation of flip chip joints was observed by in-situ monitoring of Au stud bumps-Al pads contact resistance. All failures, defined at infinite resistance, occurred at upward electron flow (from PCB pads to chip pads) applied bumps (UEB). However, failure did not occur at downward electron flow applied bumps (DEB). Only several $m\Omega$ contact resistance increased because of Au-Al intermetallic compound (IMC) growth. This polarity effect of Au stud bumps was different from that of solder bumps, and the mechanism was investigated by the calculation of chemical and electrical atomic flux. According to SEM and EDS results, major IMC phase was $Au_5Al_2$, and crack propagated along the interface between Au stud bump and IMC resulting in electrical failures at UEB. Therefore. failure mechanisms at Au stud bump/ACF flip chip Joint undo high current density condition are: 1) crack propagation, accompanied with Au-Al IMC growth. reduces contact area resulting in contact resistance increase; and 2) the polarity effect, depending on the direction of electrons. induces and accelerates the interfacial failure at UEBs.

• Clinical and Experimental Pediatrics
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• v.51 no.10
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• pp.1031-1037
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• 2008

Macrolide antimicrobial agents including erythromycin, roxithromycin, clarithromycin, and azithromycin are commonly used in the treatment of respiratory tract infections in children. Newer macrolides that have structural modifications of older drug erythromycin show improved change in the spectrum of activity, dosing, and administration. However, recent studies reported that increasing use of macrolide antibiotics is the main force driving the development of macrolide resistance in streptococci. In particular, azithromycin use is more likely to select for macrolide resistance with Streptococcus pneumoniae than is clarithromycin use, a possible reflection of its much longer half life. Recently, erythromycin resistance rates of S. pneumoniae and Streptococcus pyogenes are rapidly increasing in Korea. Two main mechanisms of acquired macrolide resistance have been described, altered binding site on the bacterial ribosome encoded by the ermB gene and active macrolide efflux pump encoded by the mef gene. Relationship between the susceptibility of S. pneumoniae and the response to macrolides has been shown in studies of acute otitis media, but less clear in cases of pneumonia. This article reviews the spectrum of activity, pharmacokinetic properties, mechanisms of action and resistance, and clinical implication of resistance on the treatment of respiratory tract infections in children.

• Korean Journal of Microbiology
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• v.26 no.2
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• pp.113-121
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• 1988

Ozone, an atmospheric pollutant, can damage similar UV and X-rays DNA and its components. It is possible then that the KNA damage produced by this gas are similar, to some extent, to those of radiations and that they could be repaired by the same DNA repair mechanisms. It has been observed in Escherichia coli that radiosensitive strains such as lex A, rec A and pol A, all deficient to some extent for DNA repair, are more sensitive to ozone than a wild type strain. We have thendetermined the ozone resistance and host-cell reactivation of ozone-damaged T3 phages for the E. coli double mutants pol A, lex A, uvr B, lex A, uvr A, rec A and rec A lox A. According to the results, the DNA polymerase 1 plays a key role in ozone resistance and Type 11 mechanism and/or shory patch excision repair are the most important for it. The interactions between the different DNA repair mechanisms are secondary. There is a strong correlation between ozone resistance and the capacity to reactivate T3 phages damaged by ozone.

• Journal of IKEEE
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• v.17 no.3
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• pp.229-233
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• 2013

We investigated electrical conduction and resistance switching behavior of the Ag/ZnO/Ti structures for random access memory devices. These films were prepared on glass substrate by dc sputtering technique at room temperature. The resistance switching follows unipolar switching mode with small switching voltages (0.4 V - 0.6 V). Two electrical conduction mechanisms dominating the LRS and HRS are Ohmic and trap-controlled space charge limited current, respectively. These both conductions are consistent with the filamentary model. Based on the filamentary model, the switching mechanism was also interpreted.