• Journal of the Korean Institute of Oriental Medical Informatics
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• v.21 no.2
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• pp.11-23
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• 2015

Objectives : Through a comparative study between Sasang constitutional medicine and Syndrome identification and treatment medicine about the theory of diagnosis, the theory of herbal medicine, the theory of prescription, the theory of acupuncture and constitutional medicine to put forward a complementary perfect solution which has good clinical utility. Methods : We compared and sorted out the textbook of Korean Sasang constitutional medicine which named Sasang medicine, and also the textbook of Chinese TCM which was including Basic theory of TCM, Diagnostics of TCM, Science of Chinese materia medica, Pharmacology of traditional Chinese medical formulae, Science of acupuncture and moxibustion, Constitution of TCM, and also related papers. Results : (1) Through a comparative study between Sasang constitutional medicine and Syndrome identification and treatment medicine about diagnosis, herbal medicine, prescription and acupuncture, Sasang constitutional medicine is a medical system which gives priority to balance of organs, when Syndrome identification and treatment medicine is a medical system that gives priority to improve symptom. (2) The prescriptions of Sasang constitutional medicine are used for the treatment of basic pathogenesis in the chronic stage of the disease, which can recover vital qi, when Syndrome identification and treatment medicine are used for the treatment of stage pathogenesis in the acute stage of the disease, which can get rid of pathogenic factors. (3) There are two kind of complementary perfect solution between Sasang constitutional medicine and Syndrome identification and treatment medicine. One perfect complementary medicine is that Sasang constitutional medicine plays a major role when Syndrome identification and treatment medicine plays a supporting role. The other one is that Syndrome identification and treatment medicine plays a major role when Sasang constitutional medicine plays a supporting role. It determined by the usual symptoms and the symptoms now, vital qi and pathogenic factors, symptom and the root cause, acute stage and chronic stage, and the state of pathogenesis. Conclusion : A new perfect complementary medicine can be created which is based on the setting that Sasang constitutional medicine primarily treat the usual symptoms, vital qi, the root cause, chronic stage and basic pathogenesis when Syndrome identification and treatment medicine primarily treat the symptoms now, pathogenic factors, symptom, acute stage and stage pathogenesis.

• Korean Journal of Biological Psychiatry
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• v.9 no.1
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• pp.3-7
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• 2002

Genes involved in the serotonin system are good candidates for the pathogenesis of mood disorder and mood-related disorders, such as eating disorder, obsessive-compulsive disorder, alcoholism, and suicide. Serotonin type 2A(5-HT2A) receptor gene promoter polymorphism(-1438A/G) has been reported. In this article, authors reviewed the literatures regarding association studies between -1438A/G and mood disorder and mood-related disorders. There are controversial results with limited data to date. Further researches on the -1438A/G in psychiatric disorders are required.

• The Plant Pathology Journal
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• v.35 no.3
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• pp.280-286
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• 2019

In this study, PVF11 was selected among 20 candidate pathogenesis-related genes in Burkholderia glumae based on its effect on virulence to rice. PVF11 was found to interact with several plant defense-related WRKY proteins as evidenced through yeast-two hybrid analysis (Y2H). Moreover, PVF11 showed interactions with abiotic and biotic stress response-related rice proteins, as shown by genome-wide Y2H screening employing PVF11 and a cDNA library from B. glumae-infected rice. To confirm the effect of PVF11 on B. glumae virulence, in planta assays were conducted at different stages of rice growth. As a result, a PVF11-defective mutant showed reduced virulence in rice seedlings and stems but not in rice panicles, indicating that PVF11 involvement in B. glumae virulence in rice is stage-dependent.

• The Plant Pathology Journal
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• v.15 no.1
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• pp.8-13
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• 1999

Hypersensitive cell death of plants during incompatible plant-pathogen interactions is one of the efficient defense mechanisms of plants against pathogen infections. For better understanding of the molecular mechanisms involved in the plant hypersensitive response (HR), TMV-induced biotic plant cell death and CuSO4-induced abiotic plant cell death were compared in terms of expression patterns of ten different defense-related genes as molecular markers. The genes include five pathogenesis-related protein genes, two plant secondary metabolite-associated genes, two oxidative stress-related genes and one wound-inducible gene isolated from tobacco. Northern blot analyses revealed that a same set of defense-related genes was induced during both biotic and abiotic cell death but with different time and magnitude. The expression of defense-related genes in tobacco plants was temporarily coincided with the time of cell death. However, when suspension cell cultures was used to monitor the expression of defense-related genes, different patterns of the gene expression were detected. This result implies that three are common and, in addition, also different branches of signaling pathways leading to the induced expression of defense-related genes in tobacco during the pathogen- and heavy metal-induced cell death.

• The Plant Pathology Journal
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• v.26 no.1
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• pp.8-16
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• 2010

The phytopathogenic fungus Magnaporthe oryzae is a major limiting factor in rice production. To understand the genetic basis of M. oryzae pathogenic development, we previously analyzed a library of T-DNA insertional mutants of M. oryzae, and identified ATMT0879A1 as one of the pathogenicity-defective mutants. Molecular analyses and database searches revealed that a single TDNA insertion in ATMT0879A1 resulted in functional interference with an annotated gene, MGG00056, which encodes a short-chain dehydrogenase/reductase (SDR). The mutant and annotated gene were designated as $MoSDR1^{T-DNA}$ and MoSDR1, respectively. Like other SDR family members, MoSDR1 possesses both a cofactor-binding motif and a catalytic site. The expression pattern of MoSDR1 suggests that the gene is associated with pathogenicity and plays an important role in M. oryzae development. To understand the roles of MoSDR1, the deletion mutant ${\Delta}Mosdr1$ for the gene was obtained via homology-dependent gene replacement. As expected, ${\Delta}Mosdr1$ was nonpathogenic; moreover, the mutant displayed pleiotropic defects in conidiation, conidial germination, appressorium formation, penetration, and growth inside host tissues. These results suggest that MoSDR1 functions as a key metabolic enzyme in the regulation of development and pathogenicity in M. oryzae.

• The Plant Pathology Journal
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• v.25 no.4
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• pp.417-421
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• 2009

The analysis of the full length genome of Korean isolates of Pepper mottle virus (PepMoV) in previous study showed molecular variations and are found to be related to symptom variation and pathogenicity (Kim et al., 2009, Virus Res. 144:83-88). To fully understand the molecular variation of PepMoV in Korea, we further assessed the role of RNA recombination to biological variation and evolution of PepMoV. Full-length genome of a total of 17 Korean-PepMoV and 2 American (CA and FL) isolates were examined for possible detection of genetic recombination using different recombination detections programs and detected 5 and 8 tentative recombination events using RDP3 and Splits Tree4 programs, respectively. Interestingly, tentative recombinants detected such as isolates 57, 134 and 217 were previously identified as severe isolates and 205135 and 205136 as differentiating isolates (Kim et al., 2009, Virus Res. 144:83-88). In addition, recombination was frequently detected in the Vb isolate, the first PepMoV isolate reported in Korea, suggesting significant involvement in the evolution of PepMoV in Korea. These initial results of our recombination analyses among PepMoV isolates in Korea may serve as clues to further investigate the biological variations and evolution of PepMoV brought about by recombination.

• The Plant Pathology Journal
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• v.24 no.2
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• pp.101-111
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• 2008

The fungal genus Alternaria is comprised of many saprophytic and endophytic species, but is most well known as containing many notoriously destructive plant pathogens. There are over 4,000 Alternaria/host associations recorded in the USDA Fungal Host Index ranking the genus 10th among nearly 2,000 fungal genera based on the total number of host records. While few Alternaria species appear to have a sexual stage to their life cycles, the majority lack sexuality altogether. Many pathogenic species of Alternaria are prolific toxin producers, which facilitates their necrotrophic lifestyle. Necrotrophs must kill host cells prior to colonization, and thus these toxins are secreted to facilitate host cell death often by triggering genetically programmed apoptotic pathways or by directly causing cell damage resulting in necrosis. While many species of Alternaria produce toxins with rather broad host ranges, a closely-related group of agronomically important Alternaria species produce selective toxins with a very narrow range often to the cultivar level. Genes that code for and direct the biosynthesis of these host-specific toxins for the Alternaria alternata sensu lato lineages are often contained on small, mostly conditionally dispensable, chromosomes. Besides the role of toxins in Alternaria pathogenesis, relatively few genes and/or gene products have been identified that contribute to or are required for pathogenicity. Recently, the completion of the A. brassicicola genome sequencing project has facilitated the examination of a substantial subset of genes for their role in pathogenicity. In this review, we will highlight the role of toxins in Alternaria pathogenesis and the use of A. brassicicola as a model representative for basic virulence studies for the genus as a whole. The current status of these research efforts will be discussed.

• Journal of Microbiology and Biotechnology
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• v.27 no.1
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• pp.161-170
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• 2017

Meningitis caused by Streptococcus suis serotype 2 (S. suis 2) is a great threat to the pig industry and human health. Virulence factors associated with the pathogenesis of meningitis have yet to be clearly defined, even though many potential S. suis 2 virulence factors have been identified. This greatly hinders the progress of S. suis 2 meningitis pathogenesis research. In this study, a co-culture blood-brain barrier (BBB) model was established using primary porcine brain microvascular endothelial cells and astrocytes, and the whole genome library of S. suis 2 was constructed using phage display technology. Finally, a total of 14 potential virulence factors contributing to S. suis 2 adherence to and invasion of the BBB were selected by analyzing the interactions between the phage library and the co-culture model. Twelve of these factors have not been previously reported in meningitis-related research. The data provide valuable insight into the pathogenesis of S. suis 2 meningitis and potential targets for the development of drug therapies.

• Molecules and Cells
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• v.28 no.2
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• pp.105-109
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• 2009

We reported previously that overexpression of a salicylic acid (SA) methyltransferase1 gene from rice (OsBSMT1) or a SA glucosyltransferase1 gene from Arabidopsis thaliana (AtSAGT1) leads to increased susceptibility to Pseudomonas syringae due to reduced SA levels. To further examine their roles in the defense responses, we assayed the transcript levels of AtBSMT1 or AtSAGT1 in plants with altered levels of SA and/or other defense components. These data showed that AtSAGT1 expression is regulated partially by SA, or nonexpressor of pathogenesis related protein1, whereas AtBSMT1 expression was induced in SA-deficient mutant plants. In addition, we produced the transgenic Arabidopsis plants with RNAi-mediated inhibition of AtSAGT1 and isolated a null mutant of AtBSMT1, and then analyzed their phenotypes. A T-DNA insertion mutation in the AtBSMT1 resulted in reduced methyl salicylate (MeSA) levels upon P. syringae infection. However, accumulation of SA and glucosyl SA was similar in both the atbsmt1 and wild-type plants, indicating the presence of another SA methyltransferase or an alternative pathway for MeSA production. The AtSAGT1-RNAi line exhibited no altered phenotypes upon pathogen infection, compared to wild-type plants, suggesting that (an)other SA glucosyltransferase(s) in Arabidopsis plants may be important for the pathogenesis of P. syringae.

• Biomolecules & Therapeutics
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• v.28 no.1
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• pp.98-103
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• 2020

Marfan syndrome (MFS), a connective tissue disorder caused by mutations in the fibrillin-1 (Fbn1) gene, has vascular manifestations including aortic aneurysm, dissection, and rupture. Its vascular pathogenesis is assumed to be attributed to increased transforming growth factor β (TGFβ) signaling and blockade of excessive TGFβ signaling has been thought to prevent dissection and aneurysm formation. Here, we investigated whether galunisertib, a potent small-molecule inhibitor of TGFβ receptor I (TβRI), attenuates aneurysmal disease in a murine model of MFS (Fbn1^C1039G/+) and compared the impact of galuninsertib on the MFS-related vascular pathogenesis with that of losartan, a prophylactic agent routinely used for patients with MFS. Fbn1^C1039G/+ mice were administered galunisertib or losartan for 8 weeks, and their ascending aortas were assessed for histopathological changes and phosphorylation of Smad2 and extracellular signal-regulated kinase 1/2 (Erk1/2). Mice treated with galunisertib or losartan barely exhibited phosphorylated Smad2, suggesting that both drugs effectively blocked overactivated canonical TGFβ signaling in Fbn1^C1039G/+ mice. However, galunisertib treatment did not attenuate disrupted medial wall architecture and only partially decreased Erk1/2 phosphorylation, whereas losartan significantly inhibited MFS-associated aortopathy and markedly decreased Erk1/2 phosphorylation in Fbn1^C1039G/+ mice. These data unexpectedly revealed that galunisertib, a TβRI inhibitor, showed no benefits in aneurysmal disease in MFS mice although it completely blocked Smad2 phosphorylation. The significant losartan-induced inhibition of both aortic vascular pathogenesis and Smad2 phosphorylation implied that canonical TGFβ signaling might not prominently drive aneurysmal diseases in MFS mice.