• KOREAN JOURNAL OF CROP SCIENCE
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• v.25 no.2
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• pp.6-14
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• 1980

One of the physiological disease, sudden wiliting of Yushin variety suggested that low sunlight, excessive nitrogen application, and highly reduced soil condions either singly or combined, might be possible causes of the disorder. Some visual symptom of sudden wilting are discoloration of leaves, development of nodal roots above the soil surface, total root rot, and lodging. Those observations led to the hypothesis that suffocation of root tissues was a direct cause of the wilting. The oxygen transport characteristics of Yushin, IR262 and Tongil were examined by two methods. First, Soil-cultured plants of the three varieties were subjected to paraffin treatment to decrease the oxygen supply from the air to root tissues through the soil-water system, liquid paraffin was applied to the water surface in the pots at panicle formation stage. In this experiment, sudden wilting was observed of Yushin and IR262 at about a week after the treatment, but Tongil remained green and healthy. Wilting-resistant variety Tongil had higher oxygen release, whereas the susceptible Yushin and IR262 had lower oxygen release. Second, the number and size of the air spaces in each internode were investigated in the 5th internode from the top, all three varieties have a similar number of air spaces, although the air spaces of Thongil were larger. In the 4th internode, Tongil had plenty air spaces, Yushin and one of the Yushin's parents IR262 had scanty or none. The observations indicated that the ability of Yushin and IR262 for oxygen transport is very limited compared with that of Tongil. The limited oxygen supply due to poor development of air space in internode of rice plants may cause suffocation of root tissues, weaken metabolic activity of the tissues, and induce root rot, subsequently inducing sudden wilting and lodging under unfavorable weather, soil and cultural conditions.

• Journal of Genetic Medicine
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• v.4 no.1
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• pp.72-79
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• 2007

Purpose : Glycogen storage disease type III (GSD-III) is a rare autosomal recessive disorder of glycogen metabolism. The affected enzyme, amylo-1,6-glucosidase, 4-alpha-glucanotransferase (AGL, glycogen debranching enzyme), is responsible for the debranching of the glycogen molecule during catabolism. The disease shows clinical and biochemical heterogeneity, reflecting genotype-phenotype heterogeneity among different patients. In this study, we aim at analyzing mutations of the AGL gene in three unrelated Korean GSD-III patients, and characterizing their clinical and laboratory findings. Methods : We characterized the clinical features of three unrelated Korean GSD-III patients by biochemical, histological and imaging studies. The 35 exons and part of exon-intron boundaries of AGL were analyzed by direct sequencing using genomic DNA extracted from the peripheral leukocytes of patients. Results : Diverse clinical features were observed in these patients including hepatomegaly (all patients), seizures (patient 2), grow th failure (patients 1 and 2), hyperlipidemia (patients 1 and 3), raised transaminase and creatine kinase concentrations (all patients), and mild cardiomyopathy (patient 2). Liver transplantation w as performed in patient 2 due to progressive hepatic fibrosis. A dministration of uncooked corn starch maintained normoglycemia and improved biochemical and growth profiles. DNA sequence analysis revealed mutations in 5 out of 6 alleles. Patient 1 was a compound heterozygote of c.1282 G>A (p.R428K) and c.1306delA (p.S603PfsX6), patient 2 had c.1510_1511insT (p.Y 504L fsX 10), and patient 3 had c.3416 T >C (p.L 1139P) and c.1735+1 G>T (p.Y 538_R578delfsX 4) mutations. A part from the p.R428K mutation, the 4 other substitutions identified w ere nov el. Conclusion : GSD-III patients display variable phenotypic characteristics resembling those of GSD-Ia. Molecular defects in the AGL gene of Korean GSD-III patients are genetically heterogeneous.

• Food Engineering Progress
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• v.21 no.4
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• pp.318-325
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• 2017

Alcoholic steatosis is a fundamental metabolic disorder and may precede the onset of more severe forms of alcoholic liver disease. In this study, we isolated enzymatichydrolysate from Semisulcospira libertine by alcalase hydrolysis and investigated the protective effect of Semisulcospira libertine hydrolysate on liver injury induced by alcohol in the mouse model of chronic and binge ethanol feeding (NIAAA). In an in vitro study, the hydrolysate protects HepG2 cells from ethanol toxicity. Liver damage was assessed by histopathological examination, as well as by quantitating activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). After the administration of S. libertina hydrolysate, fat accumulation and infiltration of inflammatory cells in liver tissues were significantly decreased in the NIAAA mouse model. The elevated levels of serum AST, ALT, and ALP activities, along with the lipid contents of a damaged liver, were recovered in experimental mice administrated with S. libertina hydrolysate, suggesting its role in blood enzyme activation and lipid content restoration within damaged liver tissues. Moreover, treatment with S. libertine hydrolysate reduced the expression rate of cyclooxygenase (COX-2), interleukin $(IL)-1{\beta}$, and IL-6, which accelerate inflammation and induces tissue damage. All data showed that S. libertine hydrolysate has a preventive role against alcohol-induced liver damages by improving the activities of blood enzymes and modulating the expression of inflammation factor, suggesting S. libertine hydrolysate could be a commercially potential material for the restoration of hepatotoxicity.