• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.3
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• pp.214-219
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• 1991

The damaging effect of peroxidized lipid on amino acid was studied in rice bran by determining the free amino acid content in abiological system. The content of free amino acid in the rice bran stored in the controlled atomsphere of $35^{\circ}C$ with relative humidity of 65% for 180 days, increased during the first 60 days of storage, and then decreased as the lipid peroxidation proceeded. The content of free amino acid in the sample exposed to the air of $25-30^{\circ}C$ with relative humidity of 70-90% for 100 days decreased rapidly in the beginning period of the storage. The lipid oxidation developed much faster in the rice bran exposed to the air than in the rice bran stored in the controlled atmosphere. The correlation coefficients between the total content of free amino acid and degree of peroxidation for the samples of both conditions were above -0.8, which is significant(p<0.05). The changes in the concentration of serine, glutamic acid, proline, methionine, lysine, histidine, and arginine were significantly correlated with the degree of lipid oxidation(p<0.05) for the samples stored in the controlled atmosphere and the open air. It was observed that peroxidized lipid has damaging effects on protein in the bilogical system of rice bran.

• Journal of Genetic Medicine
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• v.10 no.2
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• pp.113-116
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• 2013

Alexander disease is a rare degenerative leukodystrophy caused by dominant mutations in glial fibrillary acidic protein (GFAP). The neonatal form of Alexander disease may manifest as frequent and intractable seizures or obstructive hydrocephalus, with rapid progression leading to severe disability or death within two years. We report a case of a 50-day-old male who presented with intractable seizures and obstructive hydrocephalus. His initial magnetic resonance imaging (MRI) suggested a tumor-like lesion in the tectal area causing obstructive hydrocephalus. Despite endoscopic third ventriculostomy and multiple administrations of antiepileptic drugs, the patient experienced intractable seizures with rapid deterioration of his clinical status. After reviewing serial brain MRI scans, Alexander disease was suspected. Subsequently, we confirmed the de novo missense mutation in GFAP (c.1096T>C, Y366H). Although the onset was slightly delayed from the neonatal period (50 days old), we concluded that the overall clinical features were consistent with the neonatal form of Alexander disease. Furthermore, we also suspected that a Y366 residue might be closely linked to the neonatal form of Alexander disease based on a literature review.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.4
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• pp.1539-1544
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• 2014

Purpose: Alpha-fetoprotein (AFP), Lens culinaris agglutinin-reactive fraction of AFP (AFP-L3), and Golgi protein 73 (GP73) levels have been widely used as tumor markers for the diagnosis of hepatocellular carcinoma (HCC). The aim of this study was to investigate whether these tumor markers could be used to monitor short-term treatment response and recurrence of HCC in patients undergoing radiofrequency ablation (RFA). Methods: Between July 2012 and July 2013, 53 consecutive patients with newly diagnosed HCC were prospectively enrolled in this study. Among these, 32 patients underwent RFA, after which they were followed up prospectively at the First Hospital of Jilin University in China. Results: AFP, AFP-L3, and GP-73 values pre-RFA were not associated with tumor size, whereas AFP and GP-73 levels tended to be associated with tumor number, the presence of vascular invasion, deterioration of liver function, advanced-stage disease, and a poor performance status. GP-73 levels were dramatically elevated in the patients with hepatitis C-associated HCC. Neither pre-RFA nor 1-month post-RFA tumor marker values were associated with short-term outcome. The short-term recurrence rate of AFP-positive patients measured 1 month post-RFA was obviously higher than that of AFP-negative patients. Conclusions: AFP and GP-73 values were associated with clinical variables representing tumor growth and invasiveness, and the AFP value measured 1 month post-RFA was a strong predictor of short-term recurrence in patients with HCC.

• Asian-Australasian Journal of Animal Sciences
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• v.29 no.1
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• pp.134-141
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• 2016

To investigate the role of polysaccharide from Acanthopanax senticosus (ASPS) in preventing lipopolysaccharide (LPS)-induced intestinal injury, 18 mice (at 5 wk of age) were assigned to three groups with 6 replicates of one mouse each. Mice were administrated by oral gavage with or without ASPS (300 mg/kg body weight) for 14 days and were injected with saline or LPS at 15 days. Intestinal samples were collected at 4 h post-challenge. The results showed that ASPS ameliorated LPS-induced deterioration of digestive ability of LPS-challenged mice, indicated by an increase in intestinal lactase activity (45%, p<0.05), and the intestinal morphology, as proved by improved villus height (20.84%, p<0.05) and villus height:crypt depth ratio (42%, p<0.05), and lower crypt depth in jejunum (15.55%, p<0.05), as well as enhanced intestinal tight junction proteins expression involving occludin-1 (71.43%, p<0.05). ASPS also prevented intestinal inflammation response, supported by decrease in intestinal inflammatory mediators including tumor necrosis factor ${\alpha}$ (22.28%, p<0.05) and heat shock protein (HSP70) (77.42%, p<0.05). In addition, intestinal mucus layers were also improved by ASPS, as indicated by the increase in number of goblet cells (24.89%, p<0.05) and intestinal trefoil peptide (17.75%, p<0.05). Finally, ASPS facilitated mRNA expression of epidermal growth factor (100%, p<0.05) and its receptor (200%, p<0.05) gene. These results indicate that ASPS can prevent intestinal mucosal barrier injury under inflammatory conditions, which may be associated with up-regulating gene mRNA expression of epidermal growth factor and its receptor.

• KIPS Transactions on Software and Data Engineering
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• v.3 no.10
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• pp.421-428
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• 2014

Like Alzheimer's disease, Parkinson's Disease(PD) is one of the most common neurodegenerative brain disorders. PD results from the deterioration of dopaminergic neurons in the brain region called the substantia nigra. Currently there is no cure for PD, but diagnosing in its early stage is important to provide treatments for relieving the symptoms and maintaining quality of life. Unlike many diagnosis methods of PD which use a single biomarker, we developed a diagnosis method that uses both biochemical biomarkers and imaging biomarkers. Our method uses ${\alpha}$-synuclein protein levels in the cerebrospinal fluid and diffusion tensor images(DTI). It achieved an accuracy over 91.3% in the 10-fold cross validation, and the best accuracy of 72% in an independent testing, which suggests a possibility for early detection of PD. We also analyzed the characteristics of the brain fiber pathways of Parkinson's disease patients and normal elderly people.

• Ocean Science Journal
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• v.42 no.2
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• pp.129-134
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• 2007

Increasing industrial development in the Masan Bay area of Korea over the past decades increased the risk for the survival of marine organisms in the bay area by the deterioration of the water quality. Since living organisms have the ability to adapt contamination-associated stimuli by the alteration of gene expression, changes in proteins can be used as an important criterion for assessing the levels of environmental conditions. In this study, therefore, alterations of the expression of proteins in the muscle of Limanda yokohamae from Dukdong and Dotsum in the bay area were surveyed and characterized as compared with Haegumgang, which served as a control site. The results demonstrated that the twenty spots detected from Dukdong and Dotsum were similar to each other. Fifteen proteins were found to be predicted or undefined proteins, while five proteins were identified as heavy polypeptide 11 of myosin, apolipoprotein A-I, fibroblast growth factor 17b precursor, G protein-coupled receptor kinase 1 b and bonnie and clyde. These data suggest that local fish in the bay area have dysfunction in muscle physiology including contraction, lipid metabolism, proliferation and differentiation and nervous system.

• Childhood Kidney Diseases
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• v.22 no.2
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• pp.52-57
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• 2018

Purpose: Rhabdomyolysis is a metabolic disorder in which the content of damaged muscle cells is released into plasma. Its manifestations include asymptomatic, myalgia, gross hematuria, and complications of acute kidney injury. Because of limited data on rhabdomyolysis in children, we performed this study to determine clinical characteristics of rhabdomyolysis in children. Methods: We retrospectively reviewed the records of patients with rhabdomyolysis who were treated at the Pusan National University Children's hospital from January 2011 to July 2016. The diagnostic criteria were serum myoglobin level of ${\geq}80ng/mL$, exclusive of acute myocardial injury, cardiac arrest, and brain damage. Results: Forty-five patients were enrolled; mean age, $116{\pm}68$ months. Of these, 35 were boys and 10 were girls. Twenty-six patients experienced myalgia and 12 patients showed gross hematuria. Among these, seven patients initially had both myalgia and gross hematuria. The most common causes of rhabdomyolysis were infection, physical exertion, prolonged seizures, metabolic abnormalities, and drug addiction. Acute kidney injury (AKI) was the most common complication, followed by disseminated intravascular coagulation. Thirty-seven patients improved with sufficient fluid supply but two patients underwent hemodialysis due to deterioration of kidney function. Gross hematuria, positive occult blood test, and positive urine protein were more common in patients with AKI than in those without AKI. Conclusions: In children, infection was the most common cause of rhabdomyolysis. Most patients recovered by sufficient fluid therapy. However, in severe cases, especially in patients with underlying kidney disease, hemodialysis may be necessary in the present study.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.11 no.1
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• pp.88-98
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• 2011

Lesch-Nyhan syndrome is a X-linked recessive disorder caused by a deficiency of the enzyme hypoxanthine-guanidine phosphoribosyltransferase (HPRT), enzyme to recycle purines. Case history: born induced vaginal delivery at 40 weeks complicated by premature membrane ruputure, body weight 2.820 gm. He showed failure to thrive showing severe protein aversion like milk products and pink daper. Developmental delay revealing rolling over at 10.5 month, followed by regression. Seizure at 2 months, His poor oral feeding was lifelong problem. Weak crying, spastic, choreoathetoid movement. Self mutilating behavior noted and diagnosed at age 3 years. No family history of consanguinity and neurological disorders. Method: Laboratory test, physical exam, imaging study and molecular. Clinical follow up Treat ment with allopurinol. Result: uric acid 10.5 mg/dL (N 3.5-7.9), APRT 151.1uM/ min/ml pro(25.7-101), HPRT 7.6 (N 233.5-701) and c.151C>T hemizygote (p,Arg51X). Abdominal sonogram showed staghorn calculi in both kidneys, brain MRI brain atrophy. Clinical follow up showed, seizure at 2 mo, developmental delay (head control and, rolling over at at 11mo, pointing body part at 2 yr 7 mo, eye hand coordination at 2 y 11mo,creeping at 3 y 7 mo, speaking words at 6 y 6 mo ),and developmental regression at 3 yr of age. Sleeping problem including insomnia and severe constipation. Self mutilating behavior (lip bite) started at 2.5 yr, neurologic sx including intermittent upward gaze accompanied by swallowing difficulty at 3 y 7 mo grand mal seizure at 4.5 yr and spastic extremity and trunchal hypotonia and choleoathetoid movement and ataxia at 6.5 yr. Scoliosis with severe spasticity at 9 yr 9 mo. Acute life threatening episode with irregular breathing at 9 yr and 9 mo, Emaciation and nephrolithiasis and recurrent pneumonia. Died suddenly at 10 yr 3 mo. Conclusion: life long feeding problem, chronic gut motility dysfunction, sleeping difficulty and progressing neurologic deterioration and nephrolithiasis despite normal serum uric acid maintence by allopurinol treatment.

• Environmental Analysis Health and Toxicology
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• v.18 no.3
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• pp.209-217
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• 2003

To investigate the effects of low dosed microcystin -LR (MCLR) on the initial stage of subacute hepatotoxicity in vivo, male Sprague-Dawley rats after weanling were divided in four groups. The orally treated group (OG) was administered orally by 1 $\mu\textrm{g}$/kg B.W. at an interval of three days. The free group (FG) has taken the drinking water including 1 $\mu\textrm{g}$/L freely and the control group (CC) was only treated with 0.9％ saline solution All groups were treated for a period of 3 weeks. There was a significant correlation in body growth rate between OG and FC and especially, a deterioration of the growth of spleen was observed in the FG after 5 days. The protein levels were also decreased in OG and FG after 9 days. Level of total fat was increased to the 9th day but again decreased up to the initial level. High hemolysis of the isolated erythrocytes occurred only in OG. Activities of ${\gamma}$-G7 of 0G and FG were higher twice-fold than CG, but the values of OG were already higher at the first treatment day. No significant change in aspartate aminotransferase (AST) activity was shown in all groups, but the activity of alanine aminotransferase (ALT) was slightly increased at the beginning state. There were much similarities in the results of OG and FG. except the growth inhibition of spleen in FG. It may be concluded that long -term effects of the low doses of mycrocystins in animals including human being can lead to serious health problems, especially to liver and spleen.

• Journal of Ginseng Research
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• v.42 no.4
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• pp.540-548
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• 2018

Background: Acute hepatic failure is a life-threatening critical condition associated with rapid deterioration of liver function and liver transplantation. Several studies have shown that Panax ginseng Mayer has antidiabetic and hepatoprotective effects. However, the hepatoprotective effect of ginseng berry is still unveiled. In this study, we evaluated the hepatoprotective effects of ultrasonication-processed ginseng berry extract (UGBE) on acute hepatic failure model in rats. Methods: Ginseng berry extract (GBE) was ultrasonically processed. The GBE, silymarin, and UGBE were orally administered to male Sprague-Dawley rats for 4 wk. Twenty-four h after the last administration, rats were challenged with D-galactosamine (D-GalN)/lipopolysaccharide (LPS). Results: After ultrasonication, the component ratio of ginsenosides Rg2, Rg3, Rh1, Rh4, Rk1, Rk3, and F4 in GBE had been elevated. Administration of UGBE significantly increased the survival rate of D-GalN/LPS-challenged rats. Pretreatment with UGBE significantly decreased serum alanine aminotransferase, aspartate aminotransferase, and total bilirubin levels in D-GalN/LPS-challenged rats in a dose-dependent manner. The levels of enzymatic markers for oxidative stress (superoxide dismutase, glutathione peroxidase, catalase, and glutathione) were increased by UGBE treatment in a dose-dependent manner. Tumor necrosis factor alphalevel, inducible nitric oxide synthase activities, and nitric oxide productions were reduced by UGBE treatment. In addition, hemeoxygenase-1 levels in liver were also significantly increased in the UGBE-treated group. The protein expression of toll-like receptor 4 was decreased by UGBE administration. Hematoxylin and eosin staining results also supported the results of this study showing normal appearance of liver histopathology in the UGBE-treated group. Conclusion: UGBE showed a great hepatoprotective effect on D-GalN/LPS-challenged rats via the toll-like receptor 4 signaling pathway.