• International journal of advanced smart convergence
• /
• v.13 no.2
• /
• pp.110-118
• /
• 2024

This study examines factors influencing nonusers' resistance to the adoption of the metaverse, focusing on propagation mechanisms. It elucidates the role of innovation resistance within the metaverse adoption process. We applied the Innovation Resistance Model in the context of the metaverse and considers three major groups of factors influencing resistance to the metaverse: innovation characteristics (perceived usefulness, compatibility, perceived risk, and complexity), consumer characteristics (personal innovativeness), and propagation mechanisms (mass media, online media, and personal communication). An online survey of college students who do not use the metaverse revealed that perceived usefulness, compatibility, personal innovativeness, and online media were negative predictors of resistance to the metaverse. Conversely, perceived risk, mass media, and personal communication were positive predictors of resistance to the metaverse. Furthermore, innovation resistance was found to play a mediating role in the metaverse adoption process. Drawing upon the findings, we suggested marketing strategies to decrease resistance to the metaverse.

• Research in Plant Disease
• /
• v.26 no.1
• /
• pp.1-7
• /
• 2020

The succinate dehydrogenase inhibitor (SDHI) is a class of fungicides, which is widely and rapidly used to manage fungal pathogens in the agriculture field. Currently, fungicide resistance to SDHIs has been developed in many different plant pathogenic fungi, causing diseases on crops, fruits, vegetables, and turf. Understanding the molecular mechanisms of fungicide resistance is important for effective prevention and resistance management strategies. Two different mechanisms have currently been known in SDHI resistance. The SDHI target genes, SdhB, SdhC, and SdhD, mutation(s) confer resistance to SDHIs. In addition, overexpression of ABC transporters is involved in reduced sensitivity to SDHI fungicides. In this review, the current status of SDHI resistance mechanisms in phytopathogenic fungi is discussed.

• Korean Journal of Agricultural Science
• /
• v.44 no.1
• /
• pp.1-15
• /
• 2017

In major field crops, synthetic herbicides have been used to control weeds worldwide. Globally, herbicide resistance in weeds should be minimized because it is a major limiting factor for food security. Cross resistance can occur with herbicides within the same or in different herbicide families and with the same or different sites of action. Multiple resistance refers to evolved mechanisms of resistance to more than one herbicide (e.g., resistance to both ALS-inhibitors and ACCase-inhibitors) and this resistance was brought about by separate selection processes. Target site resistance could occur from changes at the biochemical site of action of one herbicide. Non target site resistance occurs through mechanisms which reduce the number of herbicide molecules that reach the herbicide target site. There are currently 480 unique cases (species ${\times}$ site of action) of herbicide resistance globally in 252 plant species (145 dicots and 105 monocots). To date, resistance in weeds has been reported to 161 different herbicides, involving 23 of the 26 known herbicide sites of action. Finally, it can be concluded that we can protect crops associated to herbicide resistant weeds by applications of biochemical, genetic and crop control strategies.

• Journal of Microbiology and Biotechnology
• /
• v.31 no.1
• /
• pp.1-7
• /
• 2021

Bacterial biofilm is a community of bacteria that are embedded and structured in a self-secreted extracellular matrix. An important clinical-related characteristic of bacterial biofilms is that they are much more resistant to antimicrobial agents than the planktonic cells (up to 1,000 times), which is one of the main causes of antibiotic resistance in clinics. Therefore, infections caused by biofilms are notoriously difficult to eradicate, such as lung infection caused by Pseudomonas aeruginosa in cystic fibrosis patients. Understanding the resistance mechanisms of biofilms will provide direct insights into how we overcome such resistance. In this review, we summarize the characteristics of biofilms and chronic infections associated with bacterial biofilms. We examine the current understanding and research progress on the major mechanisms of antibiotic resistance in biofilms, including quorum sensing. We also discuss the potential strategies that may overcome biofilm-related antibiotic resistance, focusing on targeting biofilm EPSs, blocking quorum sensing signaling, and using recombinant phages.

• Genomics & Informatics
• /
• v.19 no.1
• /
• pp.2.1-2.10
• /
• 2021

BRAF inhibitors (e.g., vemurafenib) are widely used to treat metastatic melanoma with the BRAF V600E mutation. The initial response is often dramatic, but treatment resistance leads to disease progression in the majority of cases. Although secondary mutations in the mitogen-activated protein kinase signaling pathway are known to be responsible for this phenomenon, the molecular mechanisms governing acquired resistance are not known in more than half of patients. Here we report a genome- and transcriptome-wide study investigating the molecular mechanisms of acquired resistance to BRAF inhibitors. A microfluidic chip with a concentration gradient of vemurafenib was utilized to rapidly obtain therapy-resistant clones from two melanoma cell lines with the BRAF V600E mutation (A375 and SK-MEL-28). Exome and transcriptome data were produced from 13 resistant clones and analyzed to identify secondary mutations and gene expression changes. Various mechanisms, including phenotype switching and metabolic reprogramming, have been determined to contribute to resistance development differently for each clone. The roles of microphthalmia-associated transcription factor, the master transcription factor in melanocyte differentiation/dedifferentiation, were highlighted in terms of phenotype switching. Our study provides an omics-based comprehensive overview of the molecular mechanisms governing acquired resistance to BRAF inhibitor therapy.

• Molecules and Cells
• /
• v.42 no.3
• /
• pp.237-244
• /
• 2019

Understanding the mechanisms of cancer drug resistance is a critical challenge in cancer therapy. For many cancer drugs, various resistance mechanisms have been identified such as target alteration, alternative signaling pathways, epithelial-mesenchymal transition, and epigenetic modulation. Resistance may arise via multiple mechanisms even for a single drug, making it necessary to investigate multiple independent models for comprehensive understanding and therapeutic application. In particular, we hypothesize that different resistance processes result in distinct gene expression changes. Here, we present a web-based database, CDRgator (Cancer Drug Resistance navigator) for comparative analysis of gene expression signatures of cancer drug resistance. Resistance signatures were extracted from two different types of datasets. First, resistance signatures were extracted from transcriptomic profiles of cancer cells or patient samples and their resistance-induced counterparts for >30 cancer drugs. Second, drug resistance group signatures were also extracted from two large-scale drug sensitivity datasets representing ~1,000 cancer cell lines. All the datasets are available for download, and are conveniently accessible based on drug class and cancer type, along with analytic features such as clustering analysis, multidimensional scaling, and pathway analysis. CDRgator allows meta-analysis of independent resistance models for more comprehensive understanding of drug-resistance mechanisms that is difficult to accomplish with individual datasets alone (database URL: http://cdrgator.ewha.ac.kr).

• Tuberculosis and Respiratory Diseases
• /
• v.79 no.4
• /
• pp.248-256
• /
• 2016

Somatic mutations that lead to hyperactivation of epidermal growth factor receptor (EGFR) signaling are detected in approximately 50% of lung adenocarcinoma in people from the Far East population and tyrosine kinase inhibitors are now the standard first line treatment for advanced disease. They have led to a doubling of progression-free survival and an increase in overall survival by more than 2 years. However, emergence of resistant clones has become the primary cause for treatment failure, and has created a new challenge in the daily management of patients with EGFR mutations. Identification of mechanisms leading to inhibitor resistance has led to new therapeutic modalities, some of which have now been adapted for patients with unsuccessful tyrosine kinase inhibitor treatment. In this review, we describe mechanisms of tyrosine kinase inhibitor resistance and the available strategies to overcoming resistance.

• Tuberculosis and Respiratory Diseases
• /
• v.75 no.5
• /
• pp.188-198
• /
• 2013

Over the past decade, several kinase inhibitors have been approved based on their clinical benefit in cancer patients. Unfortunately, in many cases, patients develop resistance to these agents via secondary mutations and alternative mechanisms. To date, several major mechanisms of acquired resistance, such as secondary mutation of the epidermal growth factor receptor (EGFR) gene, amplification of the MET gene and overexpression of hepatocyte growth factor, have been reported. This review describes the recent findings on the mechanisms of primary and acquired resistance to EGFR tyrosine kinase inhibitors and acquired resistance to anaplastic lymphoma kinase inhibitors, primarily focusing on non-small cell lung carcinoma.

• Molecular & Cellular Toxicology
• /
• v.3 no.1
• /
• pp.11-18
• /
• 2007

Mechanisms of insecticide resistance found in insects may include three general categories. Modified behavioral mechanisms can let the insects avoid the exposure to toxic compounds. The second category is physiological mechanisms such as altered penetration, rapid excretion, lower rate transportation, or increased storage of insecticides by insects. The third category relies on biochemical mechanisms including the insensitivity of target sites to insecticides and enhanced detoxification rate by several detoxifying mechanisms. Insecticides metabolism usually results in the formation of more water-soluble and therefore more readily eliminated, and generally less toxic products to the host insects rather than the parent compounds. The representative detoxifying enzymes are general esterases and monooxygenases that catalyze the toxic compounds to be more water-soluble forms and then secondary metabolism is followed by conjugation reactions including those catalyzed by glutathione S-transferases (GSTs). However, a change in the resistant species is not easily determined and the levels of mRNAs do not necessarily predict the levels of the corresponding proteins in a cell. As genomics understands the expression of most of the genes in an organism after being stressed by toxic compounds, proteomics can determine the global protein changes in a cell. In this present review, it is suggested that the environmental proteomic application may be a good approach to understand the biochemical mechanisms of insecticide resistance in insects and to predict metabolomic changes leading to physiological changes of the resistant species.

• Mycobiology
• /
• v.29 no.1
• /
• pp.19-26
• /
• 2001

Defense mechanisms against anthracnose disease caused by Colletotrichum orbiculare on the leaf surface of cucumber plants after pre-treatment with plant growth promoting rhizobacteria(PGPR), amino salicylic acid(ASA) or C. orbiculare were compared using a fluorescence microscope. Induced systemic resistance was mediated by the pre-inoculation in the root system with PGPR strain Bacillus amylolquefaciens EXTN-1 that showed direct antifungal activity to C. gloeosporioides and C. orbiculare. Also, systemic acquired resistance was triggered by the pre-treatments on the bottom leaves with amino salicylic acid or conidial suspension of C. orbiculare. The protection values on the leaves expressing SAR were higher compared to those expressing ISR. After pre-inoculation with PGPR strains no change of the plants was found in phenotype, while necrosis or hypersensitive reaction(HR) was observed on the leaves of plants pre-treated with ASA or the pathogen. After challenge inoculation, inhibition of fungal growth was observed on the leaves expressing both ISR and SAR. HR was frequently observed at the penetration sites of both resistance-expressing leaves. Appressorium formation was dramatically reduced on the leaves of plants pre-treated with ASA, whereas EXTN-1 did not suppress the appressorium formation. ASA also more strongly inhibited the conidial germination than EXTN-1. Conversely, EXTN-1 significantly increased the frequency of callose formation at the penetration sites, but ASA did not. The defense mechanisms induced by C. orbiculare were similar to those by ASA. Based on these results it is suggested that resistance mechanisms on the leaf surface was different between on the cucumber leaves expressing ISR and SAR, resulting in the different protection values.