• Korean Journal of Microbiology
• /
• v.50 no.2
• /
• pp.87-94
• /
• 2014

Nitric oxide (NO), which has been recognized as an integral molecule in maintaining homeostasis, plays an important role in host defense against microbes. NO has diverse antimicrobial mechanisms by directly and/or indirectly interacting with microbes. Under the circumstance that there is an urgent need for a new class of antimicrobial agents due to antibiotic resistance, much effort has been made to develop a NO-based antimicrobial agent. In order to make it possible, strategies to store and release NO in a controlled manner are required because NO has a gaseous property and a very short half-life. In this review, we described NO biochemistry and its mechanisms of antimicrobial activity. In additions, we introduced various NO-releasing systems that improve NO's antimicrobial activity.

• CELLMED
• /
• v.4 no.1
• /
• pp.3.1-3.8
• /
• 2014

Spa represents a treatment widely used in many rheumatic diseases (RD). The mechanisms by which immersion in mineral or thermal water ameliorates RD are not fully understood. The net benefit is probably the result of a combination of factors, among which the mechanical, thermal and chemical effects are most prominent. Buoyancy, immersion, resistance and temperature play important roles. According to the gate theory, pain relief may be due to the pressure and temperature of the water on skin; heat may reduce muscle spasm and increase the pain threshold. Mud-bath therapy increases plasma ${\beta}$-endorphin levels and secretion of corticotrophin, cortisol, growth hormone and prolactin. It has recently been demonstrated that thermal mud-bath therapy induces a reduction in circulating levels of prostaglandin E2, leukotriene B4, interleukin-$1{\beta}$ and tumour necrosis factor-${\alpha}$, important mediators of inflammation and pain. Furthermore, balneotherapy has been found to cause an increase in insulin-like growth factor-1, which stimulates cartilage metabolism, and transforming growth factor-${\beta}$. Beneficial anti-inflammatory and anti-degenerative effects of mineral water were confirmed in chondrocytes cultures, too. Various studies in vitro and in humans have highlighted the positive action of mud-packs and thermal baths, especially sulphurous ones, on the oxidant/antioxidant system. Overall, thermal stress has an immunosuppressive effect. Many other non-specific factors may also contribute to the beneficial effects observed after spa therapy in some RD, including effects on cardiovascular risk factors (e.g. adipokines) and changes in the environment, pleasant surroundings and the absence of work duties.

• Preventive Nutrition and Food Science
• /
• v.19 no.4
• /
• pp.247-260
• /
• 2014

The impact of folate on health and disease, particularly pregnancy complications and congenital malformations, has been extensively studied. Mandatory folic acid fortification therefore has been implemented in multiple countries, resulting in a reduction in the occurrence of neural tube defects. However, emerging evidence suggests increased folate intake may also be associated with unexpected adverse effects. This literature review focuses on contemporary issues of concern, and possible underlying mechanisms as well as giving consideration the future direction of mandatory folic acid fortification. Folate fortification has been associated with the presence of unmetabolized folic acid (PteGlu) in blood, masking of vitamin $B_{12}$ deficiency, increased dosage for anti-cancer medication, photo-catalysis of PteGlu leading to potential genotoxicity, and a role in the pathoaetiology of colorectal cancer. Increased folate intake has also been associated with twin birth and insulin resistance in offspring, and altered epigenetic mechanisms of inheritance. Although limited data exists to elucidate potential mechanisms underlying these issues, elevated blood folate level due to the excess use of PteGlu without consideration of an individual's specific phenotypic traits (e.g. genetic background and undiagnosed disease) may be relevant. Additionally, the accumulation of unmetabolized PteGlu may lead to inhibition of dihydrofolate reductase and other enzymes. Concerns notwithstanding, folic acid fortification has achieved enormous advances in public health. It therefore seems prudent to target and carefully monitor high risk groups, and to conduct well focused further research to better understand and to minimize any risk of mandatory folic acid fortification.

• Transactions of the Korean Society of Mechanical Engineers A
• /
• v.37 no.1
• /
• pp.1-8
• /
• 2013

Coolant rubber hoses for automotive radiators can degrade under thermal and mechanical loadings and thus fail owing to the influences of locally formed electricity. In this study, an advanced test method was developed to simulate the failure of a rubber hose. The aging behavior of carbon-black-filled ethylene-propylene diene monomer (EPDM) rubber used as a radiator hose material under a combination of electrochemical stresses and tensile strain was analyzed. The changing behaviors of the current and the resistance as a function of the aging time were analyzed in consideration of the tensile strain, voltage, and aging temperature. Sectioned specimens clarified the failure mechanisms of the aged skin layer under the combined electrochemical stresses.

• Korean Journal of Microbiology
• /
• v.55 no.2
• /
• pp.87-102
• /
• 2019

Most chronic wounds persist in the inflammatory phase during wound healing due to the biofilm. Biofilms are resistant to antibiotics, weakening penetration, resistance to biocides and weakening local immune responses. The biofilm is firmly attached to the surrounding tissues and is very difficult to remove. Therefore, strategies to remove hard biofilms without damaging surrounding tissue are very important. One of possible strategies is dispersal. So many studies have been done to develop new strategies using dispersal mechanisms. In this review paper, especially chemotaxis, phage therapy, polysaccharides, various enzymes (glycosidases, proteases, and deoxyribonucleases), surfactants, dispersion signals, autoinducers, inhibitors were introduced. Combination therapies with other therapies such as antibiotic therapy were also introduced. It is expected that the possibility of treatment of chronic wound infection using the knowledge of the biofilm dispersal mechanisms presented in this paper will be higher.

• Biomolecules & Therapeutics
• /
• v.32 no.5
• /
• pp.577-581
• /
• 2024

Acute myeloid leukemia (AML) is a genetically diverse and challenging malignancy, with mutations in the FLT3 gene being particularly common and deleterious. Gilteritinib, a potent FLT3 inhibitor, has been approved by the U.S. Food and Drug Administration (FDA) for the treatment of relapsed/refractory AML with FLT3 mutations. Although gilteritinib was developed based on its inhibitory activity against FLT3 kinase, it is important to understand the precise mechanisms of its antileukemic activity in managing drug resistance and discovering biomarkers. This study was designed to elucidate the effect of gilteritinib on the FLT3 expression level. The results showed that gilteritinib induced a dose-dependent decrease in both FLT3 phosphorylation and expression. This reduction was particularly pronounced after 48 h of treatment. The decrease in FLT3 expression was found to be independent of changes in FLT3 mRNA transcription, suggesting post-transcriptional regulatory mechanisms. Further studies were performed in various AML cell lines and cells with both FLT3 wild-type and FLT3 mutant exhibited FLT3 reduction by gilteritinib treatment. In addition, other FLT3 inhibitors were evaluated for their ability to reduce FLT3 expression. Other FLT3 inhibitors, midostaurin, crenolanib, and quizartinib, also reduced FLT3 expression, consistent with the effect of gilteritinib. These findings hold great promise for optimizing gilteritinib treatment in AML patients. However, it is important to recognize that further research is warranted to gain a full understanding of these mechanisms and their clinical implications in the context of FLT3 reduction.

• The Plant Pathology Journal
• /
• v.28 no.2
• /
• pp.207-211
• /
• 2012

It has been known that streptomycin resistance in bacteria can occur as a results of chromosomal mutation or through gene acquisition or both. Chromosomal mutations for resistances are point mutations in the rpsL gene, which alter ribosomal protein S12. Acquired resistance has occurred when an $Sm^R$ plasmid carrying transposon Tn5393 with tandem strA-strB gene is transferred by conjugation. A total of 686 isolates of Xanthomonas smithii subsp. citri causal agent of citrus canker disease were collected from 26 citrus orchards in Jeju Island in 2003 and 2004 seasons. Forty-nine of 111 isolates from streptomycin non-sprayed orchards in 2003 season were resistant to streptomycin. Of 107 isolates from orchards sprayed one time with streptomycin, 58 isolates were resistant, and 166 of 221 isolates from orchards sprayed two times with streptomycin were resistant. In 12 orchards sprayed three or more times with streptomycin, 219 of 247 isolates were resistant to streptomycin. Twenty-five isolates of X. smithii subsp. citri were surveyed to identify the mechanisms of streptomycin resistance in this study. Twenty-one of these 25 isolates were resistant to streptomycin, and it was proven by PCR assay that 18 of the 21 streptomycin resistant isolates have the strB gene. In sixteen of the 21 streptomycin resistant isolates, it was occurred a point mutation altered codon lysine (AAG)-41 of rpsL gene to arginine (AGG). The streptomycin-sensitive isolates easily acquired the resistance by mixed culture with resistant isolates. The strB gene was amplified from the isolates that acquired the resistance by mixed culture, and one isolate of them was also point-mutated in codon 41 of rpsL gene to be resistant. In this study, most of the streptomycin-resistant isolates of X. smithii sub sp. citri in Jeju island expressed the resistance by both chromosomal point mutation and gene acquisition, and the resistance was easily acquired through conjugation by culture mixed with streptomycin resistant and sensitive strains.

• Molecules and Cells
• /
• v.47 no.3
• /
• pp.100007.1-100007.11
• /
• 2024

Recent evidence establishes a pivotal role for obesity-induced inflammation in precipitating insulin resistance and type-2 diabetes. Central to this process is the proinflammatory M1 adipose-tissue macrophages (ATMs) in epididymal white adipose tissue (eWAT). Notably, natural killer (NK) cells are a crucial regulator of ATMs since their cytokines induce ATM recruitment and M1 polarization. The importance of NK cells is shown by the strong increase in NK-cell numbers in eWAT, and by studies showing that removing and expanding NK cells respectively improve and worsen obesity-induced insulin resistance. It has been suggested that NK cells are activated by unknown ligands on obesity-stressed adipocytes that bind to NKp46 (encoded by Ncr1), which is an activating NK-cell receptor. This was supported by a study showing that NKp46-knockout mice have improved obesity-induced inflammation/insulin resistance. We therefore planned to use the NKp46-knockout mice to further elucidate the molecular mechanism by which NKp46 mediates eWAT NK-cell activation in obesity. We confirmed that obesity increased eWAT NKp46⁺ NK-cell numbers and NKp46 expression in wild-type mice and that NKp46-knockout ablated these responses. Unexpectedly, however, NKp46-knockout mice demonstrated insulin resistance similar to wild-type mice, as shown by fasting blood glucose/insulin levels and glucose/insulin tolerance tests. Obesityinduced increases in eWAT ATM numbers and proinflammatory gene expression were also similar. Thus, contrary to previously published results, NKp46 does not regulate obesity-induced insulin resistance. It is therefore unclear whether NKp46 participates in the development of obesity-induced inflammation and insulin resistance. This should be considered when elucidating the obesity-mediated molecular mechanisms that activate NK cells.

• Journal of Animal Science and Technology
• /
• v.66 no.4
• /
• pp.663-681
• /
• 2024

Co-infection with porcine reproductive and respiratory syndrome virus (PRRSV) and Haemophilus parasuis (HPS) has severely restricted the healthy development of pig breeding. Exploring disease resistance of non-coding RNAs in pigs co-infected with PRRSV and HPS is therefore critical to complement and elucidate the molecular mechanisms of disease resistance in Kele piglets and to innovate the use of local pig germplasm resources in China. RNA-seq of lungs from Kele piglets with single-infection of PRRSV or HPS and co-infection of both pathogens was performed. Two hundred and twenty-five differentially expressed long non-coding RNAs (DElncRNAs) and 30 DEmicroRNAs (DEmiRNAs) were identified and characterized in the PRRSV and HPS co-infection (PRRSV-HPS) group. Compared with the single-infection groups, 146 unique DElncRNAs, 17 unique DEmiRNAs, and 206 target differentially expressed genes (DEGs) were identified in the PRRSV-HPS group. The expression patterns of 20 DEmiRNAs and DElncRNAs confirmed by real-time quantitative polymerase chain reaction (RT-qPCR) were consistent with those determined by high-throughput sequencing. In the PRRSV-HPS group, the target DEGs were enriched in eight immune Gene Ontology terms relating to two unique DEmiRNAs and 16 DElncRNAs, and the unique target DEGs participated the host immune response to pathogens infection by affecting 15 immune-related Kyoto Encyclopedia of Genes and Genomes enrichment pathways. Notably, competitive endogenous RNA (ceRNA) networks of different groups were constructed, and the ssc-miR-671-5p miRNA was validated as a potential regulatory factor to regulate DTX4 and AEBP1 genes to achieve innate antiviral effects and inhibit pulmonary fibrosis by dual-luciferase reporter assays. These results provided insight into further study on the molecular mechanisms of resistance to PRRSV and HPS co-infection in Kele piglets.

• Journal of Industrial Technology
• /
• v.21 no.B
• /
• pp.331-339
• /
• 2001

Zero to tension fatigue tests and strain controlled fatigue tests were carried out to find how initial strain induced martensite, ${\alpha}^{\prime}$ affects low and high cycle fatigue behavior and fatigue crack growth mechanisms. Microscopic study and phase analysis were carried out with TEM, SEM, EDAX, Optical Microscope, Ferriscope, and X-ray diffractometry. The amount of Initial ${\alpha}^{\prime}$ was controlled from 0% to 33% by controlling the temperatures for cold working and heat treatment. Lower contents of initial ${\alpha}^{\prime}$ showed higher fatigue resistance in low cycle fatigue but lower fatigue resistance in high cycle fatigue because it is ascribed to the more transformation of ${\alpha}^{\prime}$ martensite during low cycle fatigue and higher ductility. In high cycle fatigue, fatigue life is attributed to the strength and phase transformation of austenite into ${\alpha}^{\prime}$ during fatigue was negligible. ${\gamma}$ boundary, ${\gamma}/twin$ boundary, and ${\gamma}/{\alpha}^{\prime}$ boundary were found to be the preferred site of fatigue crack initiation.