• Clinical and Experimental Pediatrics
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• v.58 no.8
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• pp.283-287
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• 2015

Purpose: We assessed the relationships between iron and vitamin D statuses in breastfed infants and their mothers and evaluated the determinants of iron and vitamin D deficiencies in breastfed infants. Methods: Seventy breastfed infants aged 4-24 months and their mothers participated in this study from February 2012 to May 2013. Complete blood counts, total iron binding capacity, and levels of C-reactive protein, iron, ferritin, calcium, phosphate, alkaline phosphatase, and 25-hydroxyvitamin D (25(OH)D) in infants and their mothers were measured. Results: A history of maternal prepregnancy anemia was associated with lower ferritin and 25(OH)D levels in both infants and their mothers. The 25(OH)D level of infants correlated with maternal 25(OH) D levels. The independent risk factors for iron deficiency in breastfed infants were the duration of breastfeeding (odds ratio [OR], 6.54; 95% confidence interval [CI], 1.09-39.2; P=0.04) and infant body weight (OR, 2.65; 95% CI, 1.07-6.56; P=0.04). The determinants for vitamin D deficiency were the infant's age (OR, 0.15; 95% CI, 0.02-0.97; P=0.046) and maternal 25(OH)D level (OR, 0.74; 95% CI, 0.59-0.92; P=0.01). Conclusion: A maternal history of prepregnancy anemia requiring iron therapy was associated with lower current ferritin and 25(OH)D levels in both infants and their mothers. Therefore, physicians should monitor not only iron but also vitamin D levels in infants who are breastfed by mothers who had prepregnancy anemia.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.6
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• pp.539-547
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• 2019

Anoctamin 5 (ANO5)/TMEM16E belongs to a member of the ANO/TMEM16 family member of anion channels. However, it is a matter of debate whether ANO5 functions as a genuine plasma membrane chloride channel. It has been recognized that mutations in the ANO5 gene cause many skeletal muscle diseases such as limb girdle muscular dystrophy type 2L (LGMD2L) and Miyoshi muscular dystrophy type 3 (MMD3) in human. However, the molecular mechanisms of the skeletal myopathies caused by ANO5 defects are poorly understood. To understand the role of ANO5 in skeletal muscle development and function, we silenced the ANO5 gene in C2C12 myoblasts and evaluated whether it impairs myogenesis and myotube function. ANO5 knockdown (ANO5-KD) by shRNA resulted in clustered or aggregated nuclei at the body of myotubes without affecting differentiation or myotube formation. Nuclear positioning defect of ANO5-KD myotubes was accompanied with reduced expression of Kif5b protein, a kinesin-related motor protein that controls nuclear transport during myogenesis. ANO5-KD impaired depolarization-induced $[Ca2^{+}]_i$ transient and reduced sarcoplasmic reticulum (SR) $Ca^{2+}$ storage. ANO5-KD resulted in reduced protein expression of the dihydropyridine receptor (DHPR) and SR $Ca^{2+}-ATPase$ subtype 1. In addition, ANO5-KD compromised co-localization between DHPR and ryanodine receptor subtype 1. It is concluded that ANO5-KD causes nuclear positioning defect by reduction of Kif5b expression, and compromises $Ca^{2+}$ signaling by downregulating the expression of DHPR and SERCA proteins.

• Journal of Sericultural and Entomological Science
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• v.37 no.2
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• pp.99-108
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• 1995

The experiment was carried out to define the effect of the boron in nutrient solution on the development of mulberry root and cold damage. The length of shoots only attained about 50cm and then stopped in case of boron deficiency, while the mulberry trees developed vigorous and attained over 190cm long under boron supply condition. When boron is deficient, the measles appeared on surface of the stem and the necrosis appeared on the petiole, midribs and veins of leaves. At 70 days after planting, almost all new roots and old roots changed to brown, the lateral roots became necrosis by boron deficiency. After three days of stopping boron supply, many new roots changed to brown and after two days of boron resupply, new roots began to grow out and then new roots normally developed. Content of boron in leaves and barks increased by the increase of boron concentration in nutrient solution and maximum boron content in leaves and barks was obtained with boron-sufficient treatment of 0.5ppm. Treatment of 0.5ppm boron supply indicated that the leaves and barks contained more phospholipid, protein, sugar, RNA and proline than treatment of 0.01ppm boron supply in nutrient solution. The cuttings grown in boron supply nutrition have a sufficient tolerance at -10$^{\circ}C$ and -15$^{\circ}C$ for 24 hours while cuttings grown in boron-deficient nutrition have a weak tolerance at the same condition. As mentioned above, we can conclude that the effect of boron deficiency on root development is much severe and the relationship between the lack of boron and cold damage is very closely related.

• Journal of Plant Biotechnology
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• v.36 no.4
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• pp.397-402
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• 2009

Ornithinine carbamoyltransferase (OTC) is an enzyme that catalyzes the key step in arginine biosynthesis in bacteria and plants. OTC is also involved in the urea cycle and deficiency of the enzyme in human leads to disease. The argF gene encoding OTC has been reported in many bacteria and few plants. Here we report the characterization of a gene encoding OTC from rice (OsOTC). Analysis of a cDNA sequence from rice revealed that the full-length open reading frame of OsOTC consisted of 367 amino acids, corresponding to a protein of approximately 39.7 kDa. The predicted amino acid sequence of OsOTC harbor distinct five OTC signature sites and is highly homologous to that of enzymes of plants, animals and many bacterial OTCs. Expression of OsOTC in argF mutants of Escherichia coli showed that the gene was able to functionally complement to the mutant. These results suggest that the OsOTC encode a protein for ornithine carbamoyltransferase in rice.

• BMB Reports
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• v.57 no.7
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• pp.330-335
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• 2024

Arginine methylation, which is catalyzed by protein arginine methyltransferases (Prmts), is known to play a key role in various biological processes. However, the function of Prmts in osteogenic differentiation of mesenchymal stem cells (MSCs) has not been clearly understood. In the current study, we attempted to elucidate a positive role of Prmt7 in osteogenic differentiation. Prmt7-depleted C3H/10T1/2 cells or bone marrow mesenchymal stem cells (BMSCs) showed the attenuated expression of osteogenic specific genes and Alizarin red staining compared to the wild-type cells. Furthermore, we found that Prmt7 deficiency reduced the activation of bone morphogenetic protein (BMP) signaling cascade, which is essential for the regulation of cell fate commitment and osteogenesis. Taken together, our data indicate that Prmt7 plays important regulatory roles in osteogenic differentiation.

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.57-57
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• 2003

In growing number of diseases it has been shown that aggregation of specific proteins has an important role in pathogenesis of the disorder. This has been demonstrated in structural details with the liver cirrhosis of ${\alpha}$$_1$-antitrypsin deficiency, and it is now believed that similar protein aggregation underlies many neurodegenerative disorders such as autosomal dominant Parkinson disease, prion diseases, Alzheimer disease, and Huntington disease. ${\alpha}$$_1$-Antieypsin, a member of serine pretense inhibitor (serpin) family, functions as an inhibitor of neutrophil elastase.

• Biomedical Science Letters
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• v.10 no.4
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• pp.375-383
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• 2004

It has been reported that osteoporosis induced by the deficiency of estrogens in menopause is associated with the unbalance of Ca/sup 2+/ and Pi levels. Proximal tubule is very important organ to regualte Ca/sup 2+/ and Pi level in the body. However, the effect of estrogens on Ca/sup 2+/ and Pi regulation was not elucidated. Thus, we examined the effect of 17-β estradiol (E₂) on Ca/sup 2+/ and Pi uptake in the primary cultured rabbit renal proxiaml tubule cells. In the present study, E₂(> 10/sup -9/M) decreases Ca/sup 2+/uptake and stimulates Pi uptake over 3 days. E₂-induced decrease of Ca/sup 2+/ uptake and stimulation of Pi uptake were blocked by actinomycin D (a gene transcription inhibitor), cycloheximide (a protein synthesis inhibitor). tamoxifen, and progesterone (estrogen receptor antagonists). E₂-induced decrease of Ca/sup 2+/ uptake and stimulation of Pi uptake were blocked by SQ22536 (an adenylate cyclase inhibitor), Rp-cAMP (a cAMP antagonist), and PKI (a protein kinase A inhibitor). Indeed, E₂ increased cAMP formation. In addition, E₂-induced decrease of Ca/sup 2+/ uptake and stimulation of Pi uptake were blocked by staurosporine, H-7, and bisindolylmaleimide I (protein kinase C inhibitors) and E₂ translocated PKC from cytoslic fraction to membrane fraction. In conclusion, E₂ decreased Ca/sup 2+/ uptake and stimulated Pi uptake via cAMP and PKC pathway in the PTCs.

• Journal of Nutrition and Health
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• v.18 no.1
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• pp.5-13
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• 1985

The purpose of this study was to provide the proper nutritional management, and help to improve the health of girl students in a rural area. The nutritional survey, and blood sampling was conducted for five days, from April 26 to 30, 1983. The subjects of this survey were 110 students of girl's high school in Cheongyang area. The results were summerized as follows; 1) The daily food intake was 842.3g and that of animal foods was 34.4g. The average intake of calorie, protein, Ca, Fe, thiamin, riboflavin and niacin except Vit. A and Vit. C was below the RDA. Total calorie intake was l,802kcal. The ratio of carbohydrate, protein and fat was 81:11:8. 2) The extent of malnutrition was explained in terms of the amount of calorie, protein, Ca, Fe, and Vit. C. The predicted percentage of deficiency was 47.3% in calorie, 46.4% in protein, 61.8% in Ca, 48.2% in Fe, and 15.5% in Vit C of total subjects. 3) The mean values of Hgb, Hct and MCHC were 13.15g/dl, 39.57% and 33.2%, thus, the anemic prevalences were 10.9%, 2% and 78.2% respectively. The mean values of SI.TIBCand TS were $109.86{\mu}g$/61, $317.11{\mu}g/dl$ and 34.59%. 4) The correlation between the economic levels and nutrients intake was significant. Correlation between weight and nutrients intake was also significant but nutrients intake was not significantly correlated to blood contents.

• Journal of Life Science
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• v.19 no.2
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• pp.284-288
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• 2009

The innate immune system is important for the first line of host defence against infectious agents, which have penetrated the mechanical barriers. Mannose-binding lectin (MBL or mannan-binding protein, MBP) is a serum protein that is synthesized in the liver as a part of the acute phase response. MBL binds to carbohydrate structures presented by a wide range of pathogenic bacteria, viruses, fungi, and parasites. MBL is synthesized as a monomer that has a carboxy-terminal carbohydrate recognition domain, a neck region and a collagen region. Low MBL level was reported to be the most frequent immuno-deficiency syndrome. Although extensive studies have yielded detailed information on the structure of MBL, functions of the MBL complex are not fully understood yet. We, here, present cloning process of MBL cDNA from the rat liver and production of truncated recombinant MBL protein using a bacterial expression system in order to produce anti-MBL polyclonal antibody. Anti-MBL polyclonal antibody was raised in a New Zealand rabbit and its affinity was tested against recombinant protein using western blot technique. MBL cDNA, recombinant protein and anti-MBL antibody could be used as great arsenals to dissect cellular biochemistry of MBL.

• Clinical and Experimental Pediatrics
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• v.52 no.6
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• pp.721-724
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• 2009

Meningococcal infections can be associated with abnormalities of the complement system, which contains 5 terminal complement proteins. Furthermore, deficiencies in 1 of these 5, complement component 7 (C7), leads to the loss of complement lytic function, and affected patients show increased susceptibility to recurrent meningococcal meningitis and systemic Neisseria gonorrhoeae infection. In September 2003, an 11-year-old female patient presented at our outpatient department with high fever, lower leg pain, headache, and petechiaes. She rapidly progressed to coma but later achieved full recovery due to prompt treatment. Her final diagnosis was meningococcal sepsis and arthritis. Her elder brother also had a similar bacterial meningoencephalitis history, which encouraged us to perform analyses for complement component and gene mutations. Resultantly, both the brother and sister were found to have the same mutation in the C7 gene. Subsequently, vaccinations of the meningococcal vaccine meningococcal vaccine ($Menomune^{(R)}$) were administered. However, in September 2006, the brother expired due to acute micrococcus meningoencephalitis. At present, the 16-year-old female patient is healthy. Here, we report a Korean family with a hereditary C7 deficiency with susceptibility to meningococcal infections due to C7 gene mutation.