• Journal of the East Asian Society of Dietary Life
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• v.9 no.3
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• pp.302-314
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• 1999

This study was conducted to evaluate nutrient intake, indices of anemia, serum lipids, and their correlations in 40 Korean female college students aged 21 to 25 years. Fasting blood samples were collected in October. 1997 Nutrient intake was investigated by 24-hour recall method for three days. Anthropometric measurements, blood pressure, iron status and serum lipids of the subjects were determined. The mean values for age. height, weight, BMI and blood pressure of the subjects were 22.1 years, 160.6cm, 54.4kg and 109.1/66.9mmHg, respectively. According to the body composition analysis, total body water, % body fat, lean body mass and WHR were 26.7L. 29.5%, 36.5kg and 0.8, respectively. Average daily intake of energy was 1,858.4kcal. Protein, phosphorus, vitamin B$_1$, vitamin B$_2$, niacin and vitamin C intakes were higher than the Korean recommended dietary allowence(RDA), whereas calcium, iron, vitamin A intakes were tower than that. Hemoglobin(Hb), hematocrit(Hct), serum iron(SI) and total iron binding capacity(TIBC) were measured and transferrin saturation (TS%) was calculated from serum. The mean values for Hb, Hct, SI, TIBC and TS were 13.6$\mu\textrm{g}$/㎗, 41.6%,97.8$\mu\textrm{g}$/㎗, 319.6$\mu\textrm{g}$/㎗ and 31.9%, respectively. The Prevalence rates of iron deficiency assessed by Hb and Hct were found to be 10% and 2.5%, respectively. However, when assessed with TIBC, the prevalence rate of iron deficiency was increased to 32.5%. The mean values for serum triglyceride(TG), total cholesterol(TC), HDL-Chol, LDL-Chol concentrations and atherogenic index(AI) were 154.7mg/㎗, 80.0mg/㎗, 47.4mg/㎗, 91.3mg/㎗ and 2.6, respectively. Correlations among indices of anemia. there were positive correlations between Hb and Hct, between SI and TS : negative correlations between TIBC and TS or SI. Correlations among serum lipids, there were positive correlations between TC and TG or LDL-cholesterol. Energy intakes were correlated positively with TIBC(p＜0.05), and vitamin C intakes negatively correlated with Hb(P＜0.05). And vitamin A intakes were negatively correlated with TG(p＜0.01). TC(p＜0.05) and LDL-Chol(p＜0.01). Hb negatively correlated with TG(P＜0.05). Body weights(p＜0.05), lean body mass(p＜0.05) and total body water(p＜0.01) werenegatively correlated with Hb. BMI and WHR correlated with TG and TC(p＜0.01). These results indicated that subjects with higher energy intake and overweight had a tendency to have iron deficiency. Increases in BMI and WHR were related to increases in serum lipids levels and decreases in TIBC. The results also showed that serum lipids were decreased when vitamin A and iron intakes were sufficient.

• BMB Reports
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• v.51 no.7
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• pp.350-355
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• 2018

HnRNPK is a multifunctional protein that participates in chromatin remodeling, transcription, RNA splicing, mRNA stability and translation. Here, we uncovered the function of hnRNPK in regulating the proliferation and differentiation of myoblasts. hnRNPK was mutated in the C2C12 myoblast cell line using the CRISPR/Cas9 system. A decreased proliferation rate was observed in hnRNPK-mutated cells, suggesting an impaired proliferation phenotype. Furthermore, increased G2/M phase, decreased S phase and increased sub-G1 phase cells were detected in the hnRNPK-mutated cell lines. The expression analysis of key cell cycle regulators indicated mRNA of Cyclin A2 was significantly increased in the mutant myoblasts compared to the control cells, while Cyclin B1, Cdc25b and Cdc25c were decreased sharply. In addition to the myoblast proliferation defect, the mutant cells exhibited defect in myotube formation. The myotube formation marker, myosin heavy chain (MHC), was decreased sharply in hnRNPK-mutated cells compared to control myoblasts during differentiation. The deficiency in hnRNPK also resulted in the repression of Myog expression, a key myogenic regulator during differentiation. Together, our data demonstrate that hnRNPK is required for myoblast proliferation and differentiation and may be an essential regulator of myoblast function.

• International Journal of Oral Biology
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• v.45 no.4
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• pp.162-168
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• 2020

Calcium is the most abundant stored mineral in the human body and is especially vital for bone health; thus, calcium deficiency can cause bone-related diseases, such as osteopenia and osteoporosis. However, a high concentration of serum calcium, which is commonly known as hypercalcemia, can also lead to weakened bones and, in severe cases, osteosarcoma. Therefore, it is necessary to maintain the concentration of calcium that is appropriate for bone biology. In the present study, we aimed to elucidate the effects of high concentration of calcium, approximately 2 folds the normal calcium level, on osteoblast differentiation. The CaCl2 treatment showed dose-dependent suppression of the alkaline phosphatase activity and mineralized nodule formation. Calcium showed cytotoxicity at an extremely high concentration, but a moderately high concentration of calcium that results in inhibitory effects to osteoblast differentiation showed no signs of cytotoxicity. We also confirmed that the CaCl2 treatment repressed the mRNA expression and protein abundance of various osteogenic genes and transcriptional factors. Considered together, these results indicate that a high concentration of calcium negatively regulates the osteoblast differentiation of C2C12 cells.

• Asian-Australasian Journal of Animal Sciences
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• v.4 no.2
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• pp.111-120
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• 1991

A study was conducted to determine the macromineral status of grazing cattle in three climatic regions of the province of South Sulawesi, Indonesia. Soil, forage, blood and rib bone samples were collected within the Western, Central and Eastern regions, respectively, in February-March and August-September of 1987. Calcium and magnesium were not deficient in soil samples. For forages, calcium and phosphorus were deficient for all regions and forage sodium was deficient except for the western region in the dry season. Crude protein was deficient during the dry season. The overall percentage of deficient plasma phosphorus samples was 17 or 23% for the wet and dry seasons, respectively. Based on these analyses, macrominerals most likely deficient in both seasons were phosphorus and calcium in all regions, in addition to sodium in the Central and Eastern regions.

• Biomolecules & Therapeutics
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• v.32 no.4
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• pp.451-459
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• 2024

Apoptosis signal-regulating kinase 1 (ASK1) is an upstream signaling molecule in oxidative stress-induced responses. Because oxidative stress is involved in asthma pathogenesis, ASK1 gene deficiency was investigated in animal models of allergic asthma. However, there is no study to investigate whether ASK1 inhibitors could be applied for asthma to date. Selonsertib, a potent and selective ASK1 inhibitor, was applied to BALB/c mice of an ovalbumin (OVA)-induced allergic asthma model. Selonsertib suppressed antigen-induced degranulation of RBL-2H3 mast cells in a concentration-dependent manner. The administration of selonsertib both before OVA sensitization and OVA challenge significantly reduced airway hyperresponsiveness, and suppressed eosinophil numbers and inflammatory cytokine levels in the bronchoalveolar lavage fluid. Histopathologic examination elucidated less inflammatory responses and reduced mucin-producing cells around the peribronchial regions of the lungs. Selonsertib also suppressed the IgE levels in serum and the protein levels of IL-13 in the bronchoalveolar lavage fluid. These results suggest that selonsertib may ameliorate allergic asthma by suppressing immune responses and be applicable to allergic asthma.

• Molecules and Cells
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• v.43 no.8
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• pp.739-748
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• 2020

Stringent regulation of the chondrocyte cell cycle is required for endochondral bone formation. During the longitudinal growth of long bones, mesenchymal stem cells condense and differentiate into chondrocytes. Epiphyseal chondrocytes sequentially differentiate to form growth-plate cartilage, which is subsequently replaced with bone. Although the importance of nuclear factor 1C (Nfic) in hard tissue formation has been extensively studied, knowledge regarding its biological roles and molecular mechanisms in this process remains insufficient. Herein, we demonstrated that Nfic deficiency affects femoral growth-plate formation. Chondrocyte proliferation was downregulated and the number of apoptotic cell was increased in the growth plates of Nfic^-/- mice. Further, the expression of the cell cycle inhibitor p21 was upregulated in the primary chondrocytes of Nfic^-/- mice, whereas that of cyclin D1 was downregulated. Our findings suggest that Nfic may contribute to postnatal chondrocyte proliferation by inhibiting p21 expression and by increasing the stability of cyclin D1 protein.

• Journal of Nutrition and Health
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• v.42 no.3
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• pp.234-245
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• 2009

Nutritional assessment for the elderly can identify health status and morbidity. However, development of Nutritional Risk Index (NRI) remains limited for elderly because of difficulties in understanding physiological mechanism of elderly. This study was performed to analyze and develop Nutritional Risk Index for Korean elderly Women (Geriatric Nutritional Risk Index, GNRI). Based on literature review, factors for NRI were identified and indices were assessed by a cross-sectional survey. The survey involved Korean elderly women (${\geq}$60, n = 94) in Gwangju area, and sociodemographics, lifestyle characteristics, health conditions, dietary intakes based on 24h- recall, anthropometric measures (wt, ht, BMI, waist, hip, WHR, body protein, body fat, abdominal fat, and triceps skinfold thickness), and clinical biochemistry parameters (systolic blood pressure, diastolic blood pressure, cholesterol, HDL-cholesterol, triglyceride, total protein, albumin, prealbumin, hemoglobin, hematocrit, fasting blood glucose, HbAlc, ferritin, Zn, Ca, Na, K, Vit E, Vit $B_{12}$, folate, C-reactive protein) were examined relation to nutritional risk index. Based on literature review and data analyses, three NRIs were categorized (NRI I, NRI II, NRI III) and used for further analysis. NRI I was related to having metabolic syndrome, NRI II was related to serum albumin and body weight, and NRI III was related to food habit and health concerns. Abdominal fat (%) of elderly was correlated with each NRIs. NRI II was correlated with nutritional deficiency and higher tendency of inflammatory response, and NRI III was correlated with nutritional status which tend to be lower on aging (protein, folate, Vit $B_{12}$). NRI can serve as a useful tools in assessing health risk and nutritional status. Some modification of items in NRI and validity study are need to apply to Korean elderly.

• BMB Reports
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• v.57 no.6
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• pp.293-298
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• 2024

Microtubule acetylation has been shown to regulate actin filament dynamics by modulating signaling pathways that control actin organization, although the precise mechanisms remain unknown. In this study, we found that the downregulation of microtubule acetylation via the disruption ATAT1 (which encodes α-tubulin N-acetyltransferase 1) inhibited the expression of RhoA, a small GTPase involved in regulating the organization of actin filaments and the formation of stress fibers. Analysis of RHOA promoter and chromatin immunoprecipitation assays revealed that C/EBPβ is a major regulator of RHOA expression. Interestingly, the majority of C/EBPβ in ATAT1 knockout (KO) cells was found in the nucleus as a 27-kDa fragment (referred to as C/EBPβ^p27) lacking the N-terminus of C/EBPβ. Overexpression of a gene encoding a C/EBPβ^p27-mimicking protein via an N-terminal deletion in C/EBPβ led to competitive binding with wild-type C/EBPβ at the C/EBPβ binding site in the RHOA promoter, resulting in a significant decrease of RHOA expression. We also found that cathepsin L (CTSL), which is overexpressed in ATAT1 KO cells, is responsible for C/EBPβ^p27 formation in the nucleus. Treatment with a CTSL inhibitor led to the restoration of RHOA expression by downregulation of C/EBPβ^p27 and the invasive ability of ATAT1 KO MDA-MB-231 breast cancer cells. Collectively, our findings suggest that the downregulation of microtubule acetylation associated with ATAT1 deficiency suppresses RHOA expression by forming C/EBPβ^p27 in the nucleus through CTSL. We propose that CTSL and C/EBPβ^p27 may represent a novel therapeutic target for breast cancer treatment.

• Childhood Kidney Diseases
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• v.25 no.1
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• pp.29-34
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• 2021

C3 glomerulonephritis (C3GN), a rare condition associated with dysregulation of the alternative pathway of the complement system, is histopathologically characterized by isolated or dominant C3 deposition in the renal glomeruli. We report a case of C3GN associated with anti-complement factor H (CFH) autoantibodies and CHF-related protein deficiency in an adolescent male. A 16-year-old adolescent male was admitted to a hospital with a 1-month history of generalized edema prior to presentation. Persistent microscopic hematuria and low serum C3 levels were incidentally detected at 7 and 10 years of age, respectively. Laboratory test results revealed hypoalbuminemia, nephrotic-range proteinuria, microscopic hematuria, and normal serum creatinine levels. The serum C3 and C4 levels were 17 mg/dL (normal 80-150 mg/dL) and 22 mg/mL (17-40 mg/mL), respectively. Renal biopsy showed typical features of C3GN. Further investigations revealed positive results on plasma anti-CFH autoantibody testing and a homozygous deletion of CFHR1 and CFHR3, which encode CFH-related proteins 1 and 3, respectively. Proteinuria persisted despite treatment with intravenous methylprednisolone, mycophenolate mofetil, and angiotensin-receptor blocker; however, his renal function remained stable. In conclusion, anti-CFH autoantibodies serve as important contributors to C3GN. This is the first case report that describes C3GN in an adolescent Korean male with anti-CFH autoantibodies and homozygous CFHR1 and CFHR3 deletion.

• Clinical and Experimental Pediatrics
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• v.48 no.11
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• pp.1252-1255
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• 2005

Abnormalities in the levels of thyroxine-binding globulin (TBG) are not associated with clinical disease and they do not require treatment. Congenital TBG deficiency is inherited in an X-linked manner. To date, some complete and partial TBG variants and one polymorphism have been identified by analysis of the TBG gene. Two male neonates were referred to us because of their low $T_4$ levels that were noted on the neonatal screening test. They showed normal levels of free $T_4$ and TSH. Their serum TBG was not detectable and those values of their parents were within the normal ranges. The genomic DNA was extracted from their white blood cells and the four coding exons of the TBG gene were amplified by using polymerase chain reaction. Sequencing of the four coding regions and all the intron/exon junctions revealed a single nucleotide deletion of the first base of the codon 352 of the mature protein in both of the neonates. This mutation resulted in a frameshift and a premature stop codon (TGA) 374. Their mothers were shown to be heterozygotes. We detected a single nucleotide deletion resulting in a frameshift in two male Korean neonates who had complete TBG deficiency.