• Journal of Microbiology and Biotechnology
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• v.20 no.3
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• pp.602-608
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• 2010

An atrazine-degrading bacterium, strain KU001, was obtained from a sugarcane field at the Cane and Sugar Research and Development Center at the Kasetsart University, Kamphaeng Saen Campus, Thailand. Strain KU001 had a rod-to-coccus morphological cycle during growth. Biolog carbon source analysis indicated that the isolated bacterium was Arthrobacter histidinolovorans. Sequence analysis of the PCR product indicated that the 16S rRNA gene in strain KU001 was 99% identical to the same region in Arthrobacter sp. The atrazine degradation pathway in strain KU001 consisted of the catabolic genes trzN, atzB, and atzC. Strain KU001 was able to use atrazine as a sole nitrogen source for growth, and surprisingly, atrazine degradation was not inhibited in cells grown on ammonium, nitrate, or urea, as compared with cells cultivated on growth-limiting nitrogen sources. During the atrazine degradation process, the supplementation of nitrate completely inhibited atrazine degradation activity in strain KU001, whereas ammonium and urea had no effect on atrazine degradation activity. The addition of strain KU001 to sterile or nonsterile soils resulted in the disappearance of atrazine at a rate that was 4- to 5-fold more than that achieved by the indigenous microbial community. The addition of citrate to soils resulted in enhanced atrazine degradation, where 80% of atrazine disappeared within one day following nutrient supplementation.

• Solar Energy
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• v.11 no.3
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• pp.53-61
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• 1991

In this research, Octacosane($C_{28}H_{58}$) and Sodium Acetate Trihydrate($CH_3COONa{\cdot}3H_2O$) were selected as latent heat storage materials to store off-peak electricity or waste heat of an industrial plant. Experimental analyses were performed in terms of the variation of phase change temperature and latent heat, phase change stability for the long term utilization. The results were as follows. 1. The phase change temperatures of industrial grade Octacosane and Sodium Acetate Trihydrate were $60.7^{\circ}C$ and $57.4^{\circ}C$, the latent heat were 60.6kcal/kg and 51.1kcal/kg respectively. 2. The latent heat quantity of Octacosane was decreased with the increasing number of phase change cycles. It decreased from 60.6kcal/kg to 47.2kcal/kg upto 200 cycles and then no variation was observed after 200 cycles. 3. To prevent the supercooling of Sodium Acetate Trihydrate, the nucleating agent, Sodium Pyrophosphate Decahydrate of 3 wt% was added, and then the supercooling temperature (Tm-Tsc) was decreased from $25.7^{\circ}C$ to $1^{\circ}C$. The phase separation was disappeared by the addition of CMC-Na of 3 wt% as a thickener. It was found that the optimal quantity of nucleating agent and thickener was 4wt% considering the stability of SAT as a latent heat storage material. 4. The phase change temperature of Sodium Acetate Trihydrate($CH_3COONa{\cdot}3H_2O$) was adjusted from 57.4 to $46.2^{\circ}C$ by the addition of UREA. And then the latent heat quantity was decreased from 51.1 to 38.3kcal/kg. 5. When the heat storage capacities between the sensible and latent heat storage materials were analyzed and compared in heating process from 30 to $90^{\circ}C$, the heat storage capacity of Octacosane was 2.45 times larger than water and 12.5 times than granite at $60.7^{\circ}C$, and the heat storage capacity of Sodium Acetate Trihydrate was 2.53 times larger than water and 12.91 times than granite at $57.4^{\circ}C$.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.29-34
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• 2015

Citrullinemia type1 is an autosomal recessive disorder of the urea cycle characterized by neonatal or late onset of hyperammonemia caused by a deficiency of the enzyme argininosuccinate synthetase (ASS). An ASS1 deficiency demonstrates fatal clinical manifestations that are characterized by the neonatal metabolic coma and early death when untreated. It causes a broad spectrum of effects, ranging from a mild disorder to a severe mental retardation, epilepsy, neurologic deficits. An acute neonatal form is the most common. Infants are normal at birth followed by an acute illness characterized by vomiting, lethargy, seizures and coma. These medical problems are life-threatening in many cases. A later onset form is less frequent and may be milder than the neonatal form. This later-onset form is associated with severe headaches, visual dysfunction, motor dysfunction, and lack of energy. Citrullinemia type1 is caused by mutations in the ASS1 gene located on chromosome 9q34.1 that encodes argininosuccinate synthetase, the third enzyme of the urea cycle catalyzing the formation of argininosuccinic acid from citrulline and aspartic acid. The enzyme is distributed in tissues including liver and fibroblasts. This mutation leads to hyperammonemia, arginine deficiency and elevated citrulline level. In the urea cycle, argininosuccinate synthetase catalyses the conversion of citrulline and aspartate to argininosuccinate.. Here, we describe a female newborn patient with lethargy, rigidity and hyperammonemia who was diagnosed as citrullinemia type1 with a c.[421-2A>G], c.[1128-6_1188dup] mutation.

• Journal of Genetic Medicine
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• v.16 no.2
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• pp.85-89
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• 2019

Hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is a rare autosomal recessive urea cycle disorder. HHH is caused by a deficiency of the mitochondrial ornithine transporter protein, which is encoded by the solute carrier family 25, member 15 (SLC25A15) gene. Recently, government supported Korean newborn screening has been expanded to include a tandem mass spectrometry (MS/MS) measurement of ornithine level. We report a case of a neonate with HHH syndrome showing a normal MS/MS measurement of ornithine level. A female newborn was admitted to neonatal intensive unit due to familial history of HHH syndrome. Her parents were consanguineous Parkistani couple. The subject's older sister was diagnosed with HHH syndrome at age of 30 months based on altered mental status and liver dysfunction. Even though the subject displayed normal ammonia and ornithine levels based on MS/MS analysis, a molecular test confirmed the diagnosis of HHH syndrome. At 1 month of age, amino acid analysis of blood and urine showed high levels of ornithine and homocitrulline. After 11 months of follow up, she showed normal growth and development, whereas affected sister showed progressive cognitive impairment despite no further hyperammonemia after protein restriction and standard therapy. Our report is in agreement with a previous Canadian study, which showed that neonatal samples from HHH syndrome patients demonstrate normal ornithine levels despite having known mutations. Considering the delayed rise of ornithine in affected patients, genetic testing, and repetitive metabolic testing is needed to prevent patient loss in high risk patients.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.18 no.1
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• pp.23-29
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• 2018

Carbamoyl phosphate synthetase 1 deficiency (CPS1D) is a rare autosomal recessive urea cycle disorder characterized by hyperammonemia. CPS1D is caused by mutations in the CPS1 gene on chromosome 2q35. Based on the age of onset, there are two phenotypes: the neonatal type and the delayed-onset type. The severity of clinical manifestation depends on the degree of CPS1 residual enzymatic activity, and can result in hyperammonemia and neurological dysfunction. We report a case of CPS1D in a neonate who developed vomiting, decreased consciousness and hyperammonemia at 25th day after birth. She showed excellent response to treatment including hydration, ammonia-lowering drugs and a low-protein diet without hemodialysis. Her growth, development and neurological outcomes were fair at the last follow-up at 17 months of age.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.18 no.2
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• pp.55-61
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• 2018

Orinithine transcarbamylase (OTC) deficiency is the most common inborn error of the urea cycle with resulting hyperammonemia, which is medical emergency in newborns.We recently had a case of a boy that presented with lethargy, seizure, hyperammonemia and hypocalcemia in neonatal period. He was diagnosed with OTC deficiency by two consequent ways which are initial biochemical phenotype including hyperammonemia and an increased orotic acid in his urine and genetic analysis of the OTC gene. The OTC gene showed a novel hemizygous mutation c.913C>T (p.Pro305Ser). He was treated by low protein intake, sodium benzoate, phenylbutyrate sodium, L-arginine, and continuous renal replacement therapy (CRRT). After discharge, he has a relatively good prognosis without notable developmental delay. For good prognosis, the duration of hyperammonemia should be shorten. And it can be reached by an early diagnosis. For early detection of OTC deficiency, targeted exome sequencing will be a important role as well as biochemical tests.

• Journal of Life Science
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• v.15 no.2 s.69
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• pp.253-260
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• 2005

Mitotic centromere-associated kinesin (MCAK), which is a member of the Kin I (internal motor domain) subfamily of kinesin-related proteins, is known to play a role in mitotic segregation of chromosome during M phase of the cell cycle. In the present study, we have produced a rat polyclonal antibody using human MCAK (HsMCAK) expressed in E. coli as the antigen. The antibody specifically recognized the HsMCAK protein (81 kDa), and could detect its nuclear localization in human Jurkat T cells and 293T cells by Western blot analysis. The specific stage of the cell cycle was obtained through blocking by either hydroxyl urea or nocodazole and subsequent releasing from each blocking for 2, 4, and 7 h. While the protein level of HsMCAK reached a maximum level in the S phase with slight decline in the $G_{2}-M$ phase, the electrophoretic mobility shift from $p81^{MCAK}\;to\;p84^{MCAK}$ began to be induced in the late S phase and reached a maximum level in the $G_{2}/M $ phase, and then it disappeared as the cells enter into the $G_{1}$ phase. Immunocytochemical analysis revealed that HsMCAK protein localized to centrosome and nucleus at the interphase, whereas it appeared to localize to the spindle pole, centromere of the condensed mitotic DNA, spindle fiber, or midbody, depending on the specific stage of the M phase. These results demonstrate that a rat polyclonal antibody raised against recombinant HsMCAK expressed in E. coli specifically detects human MCAK, and indicate that the electrophoretic mobility shift from $p81^{MCAK}\;to\;p84^{MCAK}$, which may be associated with its differential intracellular localization during the cell cycle, fluctuates with a maximum level of the shift at the $G_{2}-M$ phase.

• Journal of Animal Reproduction and Biotechnology
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• v.36 no.4
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• pp.230-238
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• 2021

This study attempted to determine the characteristic features of postpartum dairy cows during their return to estrus. Moreover, it investigated the effects of abnormal ovarian cycles (AOC) on subsequent reproductive performance and the relationship between normal ovarian cycles (NOC) and the blood urea nitrogen (BUN) level postpartum. Incidentally, 56.3% of the Holstein cows and 66.7% of the Jersey cows had NOC, whereas the 43.7% and 33.3% of the Holstein and Jersey, respectively, had AOC. Within 100 days of calving, the cows with AOC had significantly lower rates of artificial insemination (AI) submission as well as pregnancy and a significantly longer interval to first AI, as compared to that in the cows with NOC. Additionally, the cows with NOC had a significantly higher first AI conception rate than that in the cows with AOC. In this study, of the 32 Holstein cows, 8 resumed their ovarian cycle within 20 days of calving, 10 resumed the cycle with 21-40 days of calving, 8 within 41-60 days of calving, while the remaining 6 did not resume their ovarian cycles until 60 days postpartum. Furthermore, the likelihood ratios of incidence of NOC are 0.93, 1.94, and 0.38, respectively, in the groups with BUN levels < 15, 15-19.9, and ≥ 20 mg/dl. In conclusion, AOC postpartum adversely affects reproductive performance such as AI submission rate, pregnancy rate, interval to first AI and first AI conception rate; moreover, an increase or decrease in the BUN levels beyond 15-19.9 mg/dL leads to the AOC postpartum.

• The Journal of Pediatrics of Korean Medicine
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• v.30 no.1
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• pp.1-8
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• 2016

Objectives The purpose of this study is to report the case of nocturnal enuresis in two children treated by using hypothesis that awareness during sleep may improves symptoms. Methods Enuresis children usually are not even aware of nocturnal urea due to excessive sleep. During the sleep cycle, enuresis children do not tend to have sleep-wake transition period compared to normal children. Ephedrine, the main ingredient of Ephedra sinica (麻黃), has a wakening effect. Two pediatric patients, who were suffering from nocturnal enuresis, were administered by Tosatang-gamibang (菟絲湯加味方) added Ephedra sinica (麻黃) or Boatang-gamibang (補兒湯加味方) added Ephedra sinica (麻黃) while correcting unhealthy voiding habit. Results As a result of the treatment, two pediatric patients were recovered without relapse. Conclusions In this report, we have proven that Tosatang-gamibang (菟絲湯加味方) added Ephedra sinica (麻黃) or Boatang-gamibang (補兒湯加味方) added Ephedra sinica (麻黃) and correcting voiding habit can considerably be effective in recovering nocturnal enuresis.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.16 no.3
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• pp.123-134
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• 2016

Mitochondrial disease is a group of disorders caused by dysfunctional mitochondria, the organelles that generate energy for the cell. Diagnosis of mitochondrial disease is difficult, subtle, and has many problems. It is more likely to miss the diagnosis of mitochondrial disease, especially in borderline cases where the symptoms of the disease are not severe. In this regard, urine organic acid analysis is noninvasive and can increase the sensitivity and specificity through repeated load test with few changes according to the specimen. And, It is considered to be suitable as a screening test for mitochondrial diseases because it has a great advantage of distinguishing from organic aciduria, urea cycle disorder and fatty acid oxidation disorder which may have similar symptoms. The purpose of this study was to investigate the clinical features and age distribution of mitochondrial diseases diagnosed by organic acid analysis and to establish the policy of diagnosis and treatment based on this study.