• Animal Bioscience
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• v.34 no.4
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• pp.575-583
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• 2021

Objective: The aim of the study was to determine the effect of parity and the stage of lactation on the metabolic profile of cows based on the basic chemical milk components and the blood parameters. Methods: The study material consisted of high-yielding Holstein-Friesian cows. In total, 473 cows were examined. According to the parity, cows were divided into four groups: primiparous (P), and multiparous in the second (M2), in the third (M3), and in subsequent lactations (M4). The feeding of cows was based on total mixed ration (TMR) ad libitum. Milk and blood samples were collected individually from each cow three times per standard lactation period. Results: Greater exacerbation of changes in the dynamics of the blood plasma parameters examined was proved for multiparous cows. The highest value of β-hydroxybutyrate acid (0.946 mmol/L) was found for multiparous cows from group M3 at the beginning of lactation. However, it was still in the normal range. The results showed aspartate aminotransferase, and gamma-glutamyl transferase (GGT) activities in dairy cows during lactation had significant variations taking in to account stage of lactation. The highest activity of GGT was found in the group of the oldest cows and measured from 26.36 U/L at the beginning of lactation to 48.75 U/L at the end of the lactation period. Conclusion: The time-related changes in the concentrations of the biochemical parameters described differ markedly among lactating cows, though the housing conditions on the research dairy farm are highly standardised. This indicates that the ability to cope with metabolic stress is mainly affected by the individual predispositions of cows and feed nutrient supply in different stage of lactation. Especially, the feed nutrient supply (in net energy for lactation), which was the best in TMR 1 in comparison TMR 3.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.1
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• pp.69-77
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• 2021

Propofol infusion syndrome characterized by rhabdomyolysis, metabolic acidosis, kidney, and heart failure has been reported in long-term propofol use for sedation. It has been reported that intracellular adenosine triphosphate (ATP) is reduced in rhabdomyolysis. The study aims to investigate the protective effect of ATP against possible skeletal muscle damage of propofol in albino Wistar male rats biochemically and histopathologically. PA-50 (n = 6) and PA-100 (n = 6) groups of animals was injected intraperitoneally to 4 mg/kg ATP. An equal volume (0.5 ml) of distilled water was administered intraperitoneally to the P-50, P-100, and HG groups. One hour after the administration of ATP and distilled water, 50 mg/kg propofol was injected intraperitoneally to the P-50 and PA-50 groups. This procedure was repeated once a day for 30 days. The dose of 100 mg/kg propofol was injected intraperitoneally to the P-100 and PA-100 groups. This procedure was performed three times with an interval of 1 days. Our experimental results showed that propofol increased serum CK, CK-MB, creatinine, BUN, TP I, ALT, AST levels, and muscle tissue MDA levels at 100 mg/kg compared to 50 mg/kg and decreased tGSH levels. At a dose of 100 mg/kg, propofol caused more severe histopathological damage compared to 50 mg/kg. It was found that ATP prevented propofol-induced muscle damage and organ dysfunction at a dose of 50 mg/kg at a higher level compared to 100 mg/kg. ATP may be useful in the treatment of propofol-induced rhabdomyolysis and multiple organ damage.

• Biomolecules & Therapeutics
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• v.31 no.6
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• pp.619-628
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• 2023

In the modern era, chronic kidney failure due to diabetes has spread across the globe. Prunetin (PRU), a component of herbal medicines, has a broad variety of pharmacological activities; these may help to slow the onset of diabetic kidney disease. The anti-nephropathic effects of PRU have not yet been reported. The present study explored the potential nephroprotective actions of PRU in diabetic rats. For 28 days, nephropathic rats were given oral doses of PRU (20, 40, and 80 mg/kg). Body weight, blood urea, creatinine, total protein, lipid profile, liver marker enzymes, carbohydrate metabolic enzymes, C-reactive protein, antioxidants, lipid peroxidative indicators, and the expression of insulin receptor substrate 1 (IRS-1) and glucose transporter 2 (GLUT-2) mRNA genes were all examined. Histological examinations of the kidneys, liver, and pancreas were also performed. The oral treatment of PRU drastically lowered the blood glucose, HbA1c, blood urea, creatinine, serum glutamic-oxaloacetic transaminase, serum glutamic pyruvic transaminase, alkaline phosphatase, lipid profile, and hexokinase. Meanwhile, the levels of fructose 1,6-bisphosphatase, glucose-6-phosphatase, and phosphoenol pyruvate carboxykinase were all elevated, but glucose-6-phosphate dehydrogenase dropped significantly. Inflammatory marker antioxidants and lipid peroxidative markers were also less persistent due to this administration. PRU upregulated the IRS-1 and GLUT-2 gene expression in the nephropathic group. The possible renoprotective properties of PRU were validated by histopathology of the liver, kidney, and pancreatic tissues. It is therefore proposed that PRU (80 mg/kg) has considerable renoprotective benefits in diabetic nephropathy in rats.

• The Korean Journal of Medicine
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• v.99 no.1
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• pp.50-56
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• 2024

Nocardiosis is uncommon. Immunocompromising conditions predispose individuals to pulmonary and disseminated nocardiosis of the brain, skin, and subcutaneous tissues. The most common pathogens are Nocardia cyriacigeorgica, Nocardia nova, and Nocardia farcinica. The speciation of Nocardia to determine antimicrobial susceptibility is difficult using traditional biochemical methods. Here, we report the case of a 73-year-old man with chronic obstructive lung disease who developed a rapidly progressing intramuscular abscess around the left hip and thigh. Within 3 days, the lesions progressed to an epidural abscess at the L4 to S1 level. Although he was treated with broad-spectrum antibiotics and extensive incision and drainage, he died of rapidly progressive respiratory failure. Nocardia abscessus (N. abscessus) was identified in pus samples using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). This case shows that the diagnosis of an intramuscular abscess caused by N. abscessus is challenging and that using MALDI-TOF MS may facilitate the diagnosis and ensure appropriate treatment.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.60 no.5
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• pp.540-547
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• 2006

Background : Vital stability and right side heart failure are major prognostic factors of acute pulmonary thromboembolism. While it is important to recognize right side heart failure, it is often difficult in real practice. Recently, several studies have described early diagnostic tools for detecting right side heart failure including echocardiography and biochemical markers. This study, we evaluated the prognostic role of the B-type natriuretic peptide (BNP) in an acute pulmonary thromboembolism. Methods : Thirty-four patients with a diagnosis of acute pulmonary thromboembolism were enrolled in the study. The BNP levels were measured and echocardiography was performed at the Emergency Department. Data on the prognostic factors including ventilatory support, vital stability, pulmonary artery pressure, degree of tricuspid valve regurgitation, complications and death was collected from the patients' medical records. The patients with an acute pulmonary thromboembolism were divided into two groups based on the vital stability and the BNP level and the cutoff values and prognostic factors of the two groups were compared. Results : The predictors of the vital stability that influence the prognosis of patients with acute pulmonary thromboembolism were the BNP level, ventilatory support and death. The plasma BNP levels showed a strong correlation with the vital stability, ventilatory support, thrombolytic therapy and death. When the BNP cutoff level was set to 377.5 pg/dl in a ROC curve, the sensitivity and the specificity for differentiating between the groups with stable or unstable vital signs was 100% and 90%, respectively. Conclusion : This study indicates that a measurement of the plasma BNP levels may be a useful prognostic marker in patients with an acute pulmonary thrombo-embolism.

• Tuberculosis and Respiratory Diseases
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• v.41 no.4
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• pp.405-412
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• 1994

Background: In Korea, the prevalence of tuberculosis and hepatitis is high, and combined therapy with rifampicin and pyrazinamide is used in tuberculosis, so drug induced hepatitis is not only problem of tuberculosis therapy but also cause of treatment failure. However most of recent reports on drug induced hepatitis during antituberculosis medication have dealt with its pathogenesis and have stressed the biochemical, and histopathological aspects of the disorder, whereas this study was designed primarily to provide information on the clinical features. Method: The subjects of study were 1414 patients treated with antituberculosis drugs on the department of chest medicine at National Medical Center during the 5-year 6-month period from January 1, 1988, to June 30, 1993. Retrospective analysis of clinical features for the 29 patients who developed drug induced hepatitis was done. Results: 1) The incidence of antituberculosis drug induced hepatitis was 2.1%. 2) Male to fema1e ratio of antituberculosis drug induced hepatitis was 2:1, but case rates among males and females were not significantly different. 3) Rates of drug induced hepatitis according to age distribution shows the most common incidence between 35 to 49 year old age group, but rates among groups of age were not significant1y different. 4) Drug induced hepatitis was most common in the case of moderate advanced pulmonary tuberculosis(rate is 2.78%), but rates among types of tuberculosis were not significant1y different. 5) 18 cases(62%) of antituberculosis drug induced hepatitis patients had no signs or symptoms. In remaining cases, they were nausea, vomiting, jaundice, hepatomegaly, icteric sclera, right upper quadrant tenderness in order. 6) 22 cases(76%) of antituberculosis drug induced hepatitis cases had occured within the first month. 7) The duration of abnormal liver function was $28{\pm}5$(Mean${\pm}$SD), ranged from 5 days to 180 days. 8) One case of antituberculosis drug induced hepatitis died. 9) The levels of abnormal GOT ranged from 64 to 1055U/L and GPT from 68 to 931U/L. Conclusion: There are no dicided predisposing factors of antituberculosis drug induced hepatitis, so it should be done biochemical monitoring as well as close monitoring for overt signs or symptoms of hepatitis to avoid the development of irreversible hepatic reaction, especially at the treatment of the first month.

• Molecules and Cells
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• v.37 no.7
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• pp.547-553
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• 2014

Glioblastoma multiforme (GBM) is one of the most common brain malignancies and has a very poor prognosis. Recent evidence suggests that the presence of cancer stem cells (CSC) in GBM and the rare CSC subpopulation that is resistant to chemotherapy may be responsible for the treatment failure and unfavorable prognosis of GBM. A garlic-derived compound, Z-ajoene, has shown a range of biological activities, including anti-proliferative effects on several cancers. Here, we demonstrated for the first time that Z-ajoene specifically inhibits the growth of the GBM CSC population. CSC sphere-forming inhibition was achieved at a concentration that did not exhibit a cytotoxic effect in regular cell culture conditions. The specificity of this inhibitory effect on the CSC population was confirmed by detecting CSC cell surface marker CD133 expression and biochemical marker ALDH activity. In addition, stem cell-related mRNA profiling and real-time PCR revealed the differential expression of CSC-specific genes, including Notch, Wnt, and Hedgehog, upon treatment with Z-ajoene. A proteomic approach, i.e., reverse-phase protein array (RPPA) and Western blot analysis, showed decreased SMAD4, p-AKT, 14.3.3 and FOXO3A expression. The protein interaction map (http://string-db.org/) of the identified molecules suggested that the AKT, ERK/p38 and $TGF{\beta}$ signaling pathways are key mediators of Z-ajoene's action, which affects the transcriptional network that includes FOXO3A. These biological and bioinformatic analyses collectively demonstrate that Z-ajoene is a potential candidate for the treatment of GBM by specifically targeting GBM CSCs. We also show how this systemic approach strengthens the identification of new therapeutic agents that target CSCs.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.6 no.1
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• pp.15-23
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• 2006

Purpose: Glycogen storage disease type III (GSD-III), is a rare autosomal recessive disorder of glycogen metabolism. The affected enzyme is amylo-1,6-glucosidase, 4-alpha-glucanotransferase (AGL, glycogen debranching enzyme), which is responsible for the debranching of the glycogen molecule during catabolism. The disease has been demonstrated to show clinical and biochemical heterogeneity, reflecting the genotype-phenotype heterogeneity among different patients. In this study, we analyzed mutations of the AGL gene in three unrelated Korean GSD-III patients and discussed their clinical and laboratory implications. Methods: We studied three GSD-III patients and the clinical features were characterized. Sequence analysis of 35exons and part exon-intron boundaries of the AGLgene in patients were carried out by direct DNA sequencing method using genomic DNA isolated from patients' peripheral leukocytes. Results: The clinical features included hepatomegaly (in all patients), seizures (in patient 2), growth failure (in patients 1), hyperlipidemia (in patients 1 and 3), raised transaminases and creatinine kinase concentrations (in all patients) and mild EKG abnormalities (in patients 2). Liver transplantation was performed in patient 2due to progressive hepatic fibrosis. Administration of raw-corn-starch could maintain normoglycemia and improve the condition. 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 with c.1510_1511insT (p.Y504LfsX10), and patient 3 with c.3416 T>C (p.L1139P) and c.l735+1 G>T (Y538_R578delfsX4) mutations. Except R428K mutation, 4 other mutations identified in3 patients were novel. Conclusion: GSD-III patients have variable phenotypic characteristics resembling GSD-Ia. The molecular defects in the AGL gene of Korean GSD-III patients were genetically heterogeneous.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.26 no.1
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• pp.5-17
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• 2000

To evaluate the possible therapeutic effects of growth hormone and vitamin C on multiorgan failure, a rat model was developed for LPS-induced sepsis. Using this model, the effects of growth hormone and vitamin C on tissue damages, catalase and i-NOS activities, and MDA levels were examined in the lung and liver. The level of TNF- in plasm was also examined. Male, Sprague-Dawley rats were injected with LPS intraperitoneally then divided into 3 groups : positive controls injected with LPS only, the ones injected with growth hormone or vitamin C immediately after the LPS injections. The lung and the liver were then isolated, blood samples were collected at 24 or 48 hours after the LPS injection, then examined for histopathological and biochemical changes. The results obtained were as follows. 1. LPS induced sinusoid vasodilation and mild destruction of lobular structure in the liver. In the lung, alveolar structure appeared to be thickened and interstitial edema was observed. The levels of MDA in the liver and the lung was increased by LPS, while the activity of catalase was decreased. The activity of i-NOS of those tissues was also increased, which was more pronounced at 24 hr. The level of TNF- in plasm was increased by LPS 2. In the lung, vitamin C suppressed lymphocyte and neutrophil infiltration, alveolar wall thickening and interstitial edema. In the liver, vitamin C protected against the destruction of the lobular structure. The activity of catalase reduced by LPS was reversed partly by vitamin C. The activity of i-NOS enhanced by LPS was also reversed by vitamin C. The level of TNF- in plasm reduced in some animals by vitamin C, which however was not significant statistically(p<0.05). 3. Growth hormone showed similar protective effects against inflammation and damages in the liver and lung tissues. Growth hormone reversed partly the LPS effects on the level of MDA, the activity of catalase and i-NOS induction in the liver and the lung. Growth hormone reduced plasma level of TNF-${\alpha}$ substantially, which contrasted from vitamin C. Besides this, overall protective effects of growth hormone against LPS-induced experimental sepsis were similar to those of vitamin C. From this results, the mechanism of growth hormone on suppression of LPS-induced tissue damage might be associated with production of antioxidative enzyme and suppression of plasma TNF- level.