• The korean journal of orthodontics
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• v.53 no.6
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• pp.345-357
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• 2023

Enamel demineralization represents the most prevalent complication arising from fixed orthodontic treatment. Its main etiology is the development of cariogenic biofilms formed around orthodontic appliances. Ordinarily, oral biofilms exist in a dynamic equilibrium with the host's defense mechanisms. However, the equilibrium can be disrupted by environmental changes, such as the introduction of a fixed orthodontic appliance, resulting in a shift in the biofilm's microbial composition from non-pathogenic to pathogenic. This alteration leads to an increased prevalence of cariogenic bacteria, notably mutans streptococci, within the biofilm. This article examines the relationships between oral biofilms and orthodontic appliances, with a particular focus on strategies for effectively managing oral biofilms to mitigate enamel demineralization around orthodontic appliances.

• IMMUNE NETWORK
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• v.16 no.1
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• pp.1-12
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• 2016

Th2 cell immunity is required for host defense against helminths, but it is detrimental in allergic diseases in humans. Unlike Th1 cell and Th17 cell subsets, the mechanism by which dendritic cells modulate Th2 cell responses has been obscure, in part because of the inability of dendritic cells to provide IL-4, which is indispensable for Th2 cell lineage commitment. In this regard, immune cells other than dendritic cells, such as basophils and innate lymphoid cells, have been suggested as Th2 cell inducers. More recently, multiple independent researchers have shown that specialized subsets of dendritic cells mediate Th2 cell responses. This review will discuss the current understanding related to the regulation of Th2 cell responses by dendritic cells and other immune cells.

• Parasites, Hosts and Diseases
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• v.56 no.2
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• pp.135-145
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• 2018

Due to the critical location and physiological activities of the retinal pigment epithelial (RPE) cell, it is constantly subjected to contact with various infectious agents and inflammatory mediators. However, little is known about the signaling events in RPE involved in Toxoplasma gondii infection and development. The aim of the study is to screen the host mRNA transcriptional change of 3 inflammation-related gene categories, PI3K/Akt pathway regulatory components, blood vessel development factors and ROS regulators, to prove that PI3K/Akt or mTOR signaling pathway play an essential role in regulating the selected inflammation-related genes. The selected genes include PH domain and leucine- rich-repeat protein phosphatases (PHLPP), casein kinase2 (CK2), vascular endothelial growth factor (VEGF), pigment epithelium-derived factor (PEDF), glutamate-cysteine ligase (GCL), glutathione S-transferase (GST), and NAD(P)H: quinone oxidoreductase (NQO1). Using reverse transcription polymerase chain reaction (RT-PCR) and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), we found that T. gondii up-regulates PHLPP2, $CK2{\beta}$, VEGF, GCL, GST and NQO1 gene expression levels, but down-regulates PHLPP1 and PEDF mRNA transcription levels. PI3K inhibition and mTOR inhibition by specific inhibitors showed that most of these host gene expression patterns were due to activation of PI3K/Akt or mTOR pathways with some exceptional cases. Taken together, our results reveal a new molecular mechanism of these gene expression change dependent on PI3K/Akt or mTOR pathways and highlight more systematical insight of how an intracellular T. gondii can manipulate host genes to avoid host defense.

• Korean Journal of Clinical Laboratory Science
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• v.51 no.3
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• pp.323-328
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• 2019

Tuberculosis, a chronic bacterial infection caused by Mycobacterium tuberculosis (MTB), differs in its status latency and activity because of the characteristics of MTB, immune status of the host, and genetic susceptibility. The host defense mechanism against MTB is caused mainly by interactions between macrophages, T cells, and dendritic cells. CD44 is expressed in activated T cells when infected with MTB and regulates lymphocyte migration. In addition, CD44 mediates leukocyte adhesion to the ECM and plays a role in attracting macrophages and $CD4^+$ T cells to the lungs. Therefore, genetic polymorphism of the CD44 gene will inhibit the host cell immune mechanisms against MTB. This study examined whether the genetic polymorphism of the CD44 gene affects the susceptibility of tuberculosis. A total of 237 SNPs corresponding to the CD44 genes were analyzed using the genotype data of 443 tuberculosis cases and 3,228 healthy controls from the Korean Association Resource (KARE). Of these, 17 SNPs showed a significant association with the tuberculosis case. The most significant SNP was rs75137824 (OR=0.231, CI: 1.51~3.56, $P=1.3{\times}10^{-4}$). In addition, rs10488809, one of the 17 significant SNPs, is important for the tuberculosis outbreak can bind to the JUND and FOS transcription factors and can affect CD44 gene expression. This study suggests that polymorphism of the CD44 gene modulates the host susceptibility to tuberculosis in a variety of ways, resulting in differences in the status of tuberculosis.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2022.09a
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• pp.36-36
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• 2022

The molecular understanding of resistance and susceptibility of host plants to scab, a most threatful disease to pome fruit production worldwide, is very limited. Comparing resistant line '93-3-98' to susceptible one 'Sweet Skin' at seven time points of 0, 0.5, 1, 2, 3, 4, 8 days post inoculation, RNA-sequencing data derived from infected and mock-inoculated young leaves were analyzed to evaluate the tolerant response and to mine candidate genes of pear to the scab pathogen Venturia nashicola. Analysis of the mapped reads showed that the infection of V. nashicola led to significant differential expression of 17,827 transcripts with more than 3-fold change in the seven pairs of libraries, of which 9,672 (54%) are up- and 8,155(46%) are down-regulated. These included mainly receptor (NB-ARC domains-containing, CC-NBS-LRR, TIR-NBS-LRR, seven transmembrane MLO family protein) and transcription factor (ethylene responsive element binding, WRKY DNA-binding protein) related gene. An arsenal of defense response of highly resistant pear accessions derived from European pear was probably supposed no sooner had V. nashicola infected its host than host genes related to disease suppression like Polyketide cyclase/dehydrase and lipid transport protein, WRKY family transcription factor, lectin protein kinase, cystein-rich RLK, calcium-dependent phospholipid-binding copine protein were greatly boosted and eradicated cascade reaction induced by pathogen within 24 hours. To identify transcripts specifically expressed in response to V. nashicola, RT-PCRs were conducted and compare to the expression patterns of seven cultivars with a range of highly resistant to highly susceptible symptom. A DEG belonging to the PR protein family genes that were higher expressed in response to V. nashicola suggesting extraordinary role in the resistance response were led to the identification. This study provides the first transcriptional profile by RNA-seq of the host plant during scab disease and insights into the response of tolerant pear plants to V. nashicola.

• Parasites, Hosts and Diseases
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• v.36 no.4
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• pp.261-268
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• 1998

The present study was undertaken to investigate the role of cysteine proteinase of Trichomonas vaginalis in escaping from host defense mechanism. A cysteine proteinase of T. vaginalis was purified by affinity chromatography and gel filtration. Optimum pH for the purified proteinase activity was 6.0. The proteinase was inhibited by cysteine and serine proteinase inhibitors such as E-64, NEM, IAA, leupeptin. TPCK and TLCK, and also by $Hg^{2+}$, but not affected by serine-, metallo-, and aspartic proteinase inhibitors such as PMSF, EDTA and pepstatin A. However, it was activated by the cysteine proteinase activator, DTT. The molecular weight of a purified proteinase was 62 kDa on gel filtration and 60 kDa on SDS-PAGE. Interestingly, the purified proteinase was able to degrade serum IgA, secretory IgA, and serum IgG in time- and dose-dependent manners. In addition, the enzyme also degraded hemoglobin in a dose-dependent manner. These results suggest that the acidic cysteine proteinase of T. vaginalis may play a dual role for parasite survival in conferring escape from host humoral defense by degradation of immunoglobulins, and in supplying nutrients to parasites by degradation of hemoglobin.

• Parasites, Hosts and Diseases
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• v.36 no.2
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• pp.109-120
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• 1998

Mucosal mast cell (MMC) and goblet cell (GC) responses were observed in the small intestine of two strains of mice (BALBfc and C3H) infected with Weodiplostomum seouLehTe, and their roles in the host defense and worm expulsion were studied. From day 3 to 28 post-infection (Pl) with 200 metacercariae, the worm recovery rate from BALB/c mice was consistently and remarkably higher than that from C3H mice. In the duodenum of both strains of mice, the main habitat of the flukes, mastocytosis was pronounced on day 7 Pl but quickly diminished thereafter. Similar kinetics were observed in the jejunum and ileum, although the extent of mastocytosis was lesser in the ileum than other two areas. These MMC kinetics were not different between the ko strains of mice. Moreover, the extent of mastocytosis was stronger in BALB/C mice than in C3H mice. GC hyperplasia was remarkable in the duodenum of BALBlc mice throughout the course of infection except day 14 Pl, whereas it was recognizable only in the jejunum and ileum of C3H mice on day 7 Pl. Mucin activation was evidently demonstrated in both strains of mice throughout the course of infection, but more marked in BALB/c than in C3H mice. The results strongly suggest that mastocytosis and GC hyperplasia are local immune responses against N. seoulense, however, they play a minor role in the host defense and worm expulsion.

• Journal of Life Science
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• v.30 no.4
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• pp.402-409
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• 2020

Nervous necrosis virus (NNV) contains a bi-segmented viral genome, RNA1 (3.4 kb, RdRp), and RNA2 (1.4 kb, capsid protein) in a small particle (25 nm). Despite its extremely compact size, NNV has caused serious damage by infecting approximately 120 fish species worldwide since it was first reported in the late 1980s. In order to minimize the damage caused by NNV infection and develop effective vaccines, it is necessary to understand the intra cellular signaling system according to NNV infection. NNV infection induces cell cycle arrest at the G1 phase via the p53-dependent pathway to use the cellular system for its replication. Otherwise, host cells recognize NNV infection through the RIG-1-like receptor (RLR) signaling pathway to control the virus and infected cells, and then ISGs required for antiviral action are activated via the IFN signaling pathway. Moreover, apoptosis of infected cells is triggered by the unfolded protein response (UPR) through ER stress and mitochondria-mediated cell death. Cell signaling studies on the NNV infection mechanisms are still at an early stage and many pathways have yet to be identified. Understanding the various disease-specific cellular signaling systems associated with NNV infection is essential for rapid and accurate diagnosis and vaccine development.

• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.4
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• pp.365-370
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• 2014

The intrinsic concepts of the three yin and three yang diseases in is unclear yet in spite of considerable controversy. In order to answer these problems, the structures of pathological transmission and anatomical terms used in the text were analyzed first. On these structural bases, the theoretical background and differential therapeutic principles of three yin and three yang disease classification. The organic structures frequently used in the text were heart, stomach, pancreas, blood chamber and urinary bladder, and the important regions in the transmission were chest, flank, epigastrium, abdomen, hypogastrium, groin on the other hand. When a host is invaded by extrinsic pathogen, an affinity is formed between the two based on the similarity of epidermal density condition and nutrient-defense features and existing disorders in the body. And then the symptoms show in 3 stages with 6 patterns in the general infective diseases. The initial stage is the period that the syndrome is limited in the external flesh area, and it mainly corresponds with taiyang bing besides the other exterior patterns of 3 yang and 2 yin bing. The middle stage is to the climax after the end of initial stage and it corresponds with mainly yangming bing including shaoyang and taiyin bing. In the terminal stage, the host gradually falls into exhaustive step or recovery phase, corresponding with shaoyin and jueyin bing. Conclusively, these dual meanings of three yang and yin should be a first guide and principle of treatment against various infective diseases.