• Imaging Science in Dentistry
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• v.30 no.3
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• pp.159-168
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• 2000

Purpose: To elucidate the effects of the irradiation and calcium-deficient diet on expression of interleukin (IL)-1 during tooth formation of rat molar. Materials and Methods: The pregnant three-week-old Spague-Dawley rats were used for the study. The control group was non-irradiation/normal diet group, and the experimental groups were irradiation/normal diet group and irradiation/calcium-deficient diet group. The abdomen of the rats on the 9th day of pregnancy were irradiated with single dose of 350 cGy, The rat pups were sacrificed on the 14th day after delivery and the maxillae tooth germs were taken. The specimen were prepared to make sections for light microscopy, and some of tissue sections were stained immunohistochemically with anti-IL-l antibody. Results: In the irradiation/normal diet group, dental follicle showed fewer blood vessels, mononuclear cells, and fusions of mononuclear cells than in non-irradiation/normal diet group. Alveolar bone showed a few osteoblasts and osteoclasts. Periodontal ligament showed collagen fibers and fibroblasts with irregularity. Weak immunoreactivity for IL-l was shown in dental follicle, alveolar bone, and periodontal ligament. In the irradiation/calcium-deficient diet group, dental follicle showed sparse cellularity. Alveolar bone showed diminished number of osteoblasts. Periodontal ligament showed irregular collagen fibers and atrophy of cementoblasts and fibroblasts. No immunoreactivity for IL-1 was shown in dental follicle, alveolar bone, and periodontal ligament. Conclusion: Irradiation and calcium-deficient diet seems to cause disturbance of the expression of interleukin-l during tooth formation of rat molar.

• IMMUNE NETWORK
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• v.15 no.3
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• pp.125-134
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• 2015

Acute graft-versus-host-disease (GVHD) is characterized by selective damage to the liver, the skin, and the gastrointestinal tract. Following allogeneic hematopoietic stem cell transplantation, donor bone marrow (BM) cells repopulate the immune system of the recipient. We previously demonstrated that the acute intestinal GVHD (iGVHD) mortality rate was higher in MyD88-deficient BM recipients than that in the control BM recipients. In the present study, the role of MyD88 (expressed by donor BM) in the pathophysiology of hepatic GVHD (hGVHD) was examined. Unlike iGVHD, transplantation with MyD88-deficient T-cell depleted (TCD) BM attenuated hGVHD severity and was associated with low infiltration of T cells into the liver of the recipients. Moreover, GVHD hosts, transplanted with MyD88-deficient TCD BM, exhibited markedly reduced expansion of $CD11b^+Gr-1^+$ myeloidderived suppressor cells (MDSC) in the liver. Adoptive injection of the MDSC from wild type mice, but not MyD88-deficient mice, enhanced hepatic T cell infiltration in the MyD88-deficient TCD BM recipients. Pre-treatment of BM donors with LPS increased MDSC levels in the liver of allogeneic wild type BM recipients. In conclusion, hGVHD and iGVHD may occur through various mechanisms based on the presence of MyD88 in the non-T cell compartment of the allograft.

• Journal of Microbiology and Biotechnology
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• v.14 no.2
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• pp.430-434
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• 2004

Three extracellular protease-deficient Bacillus subtilis strains were transformed with the plasmid pCK98 containing the endo-$\beta$-1,4-glucanase (Eng) gene of B. subtilis BSE616. The three transformants, B. subtilis DB104 (pCK98), WB600 (pCK98) and WB700 (pCK98), produced the same high level of enzyme activity and showed similar patterns of cell growth and enzyme production. When B. subtilis DB 104 (pCK98), a two-extracellular protease deficient strain, was cultured for 22 h, almost all the secreted enzyme was found to be in the completely cleaved form by both activity staining and Western blotting studies. B. subtilis WB600 (pCK98), a six-extracellular protease-deficient strain, produced a partially cleaved form in addition to the intact form of the enzyme, although the degree of internal cleavage of the enzyme was greatly reduced. With B. subtilis WB700 (pCK98), a seven-extracellular protease-deficient strain, almost all the enzyme was produced as the intact uncleaved form. This study illustrates that a role of the V pr protease is to degrade foreign proteins produced in B. subtilis and WB700 is a suitable expression system for producing the intact form of the Eng and other foreign proteins that may lose at least part of their efficacy due to internal proteolytic cleavage.

• Journal of Korean Academy of Oral and Maxillofacial Radiology
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• v.28 no.1
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• pp.87-109
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• 1998

The present study was designed to elucidate the effects of the Co-60 γ irradiation and/or calcium­deficient diet on the dentin and cementum formation of rat molar. The pregnant three-week old Sprague­Dawley rats were used for the study. The experimental group was divided into two groups, irradiation/normal diet group and irradiation/calcium-deficient diet group. The control group was non­irradiation/normal diet group. The abdomen of the rats at the 19th day of pregnancy were irradiated with single absorbed dose of 350cGy. The rat pups were sacrificed on the 14th day after delivery and the maxillae including molar tooth germ were taken. The specimens including the 1st molar tooth germ were prepared to make tissue sections for light and transmission electron microscopy. Some of tissue sections for light microscopy were stained immunohistochemically with anti-fibronectin antibody. The results were as follows; 1. The Hertwig's epithelial root sheath cells, which are related to the differentiation of the tooth-forming cells, showed irregular cellular arrangement, decrease of intercellular junctional complex, and decreased immunoreactivity to the fibronectin after irradiation. These were more severe in the irradiation/calcium-deficient diet group. 2. The cementoblasts at the cementum-forming area showed chromatin clumpings after irradiation. The immu noreactivity to the fibronectin was weaken after irradiation, especially irradiation/calcium-deficient diet group. 3. The odontoblasts at the dentin-forming area showed increase of lysosomes in the cytoplasm and destruction of intercellular junctional complex. The irradiation/calcium-deficient diet group showed decrease of number and density of the electron dense particles and a large number of vacuoles scattered in the dentin matrix. The immunoreactivity was weaken.

• Molecules and Cells
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• v.43 no.3
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• pp.264-275
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• 2020

Reactive oxygen species (ROS) play a significant role in intracellular signaling and regulation, particularly when they are maintained at physiologic levels. However, excess ROS can cause cell damage and induce cell death. We recently reported that eIF2α phosphorylation protects hepatocytes from oxidative stress and liver fibrosis induced by fructose metabolism. Here, we found that hepatocyte-specific eIF2α phosphorylation-deficient mice have significantly reduced expression of the epidermal growth factor receptor (EGFR) and altered EGFR-mediated signaling pathways. EGFR-mediated signaling pathways are important for cell proliferation, differentiation, and survival in many tissues and cell types. Therefore, we studied whether the reduced amount of EGFR is responsible for the eIF2α phosphorylation-deficient hepatocytes' vulnerability to oxidative stress. ROS such as hydrogen peroxide and superoxides induce both EGFR tyrosine phosphorylation and eIF2α phosphorylation. eIF2α phosphorylation-deficient primary hepatocytes, or EGFR knockdown cells, have decreased ROS scavenging ability compared to normal cells. Therefore, these cells are particularly susceptible to oxidative stress. However, overexpression of EGFR in these eIF2α phosphorylation-deficient primary hepatocytes increased ROS scavenging ability and alleviated ROS-mediated cell death. Therefore, we hypothesize that the reduced EGFR level in eIF2α phosphorylation-deficient hepatocytes is one of critical factors responsible for their susceptibility to oxidative stress.

• Journal of Nutrition and Health
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• v.41 no.4
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• pp.291-298
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• 2008

To study antioxidant role of zinc, the effects of dietary zinc deficiency and vitamin E supplementation on lipid peroxidation were studied. Levels of zinc and vitamin E in blood and liver were also measured. Forty Sprague-Dawley male rats aging 8 weeks old were used as experimental animals. Zinc deficient diet (Zn, 0 ppm), zinc normal diet (Zn,36.5 ppm), and vitamin E supplemented diet (1,000 IU ${\alpha}$-tocopherol/kg of diet) were used as experimental diet. During the first three weeks, rats were divided into zinc normal (ZnN, 8 animals) and zinc deficient (ZnD, 32 animals) group. Eight rats from each group were sacrificed to get blood and liver after 3 weeks of experiment. The remaining 24 zinc deficient rat were then divided into zinc normal (ZnDN), zinc deficient (ZnDD), vitamin E supplemented (ZnDE) diet groups. After another 3 weeks of experiment, all animals were sacrificed as well. Thiobarbituric acid reactive substanc (TBARS) levels in plasma and liver, conjugated diene levels in liver were measured as lipid peroxidation index. There were no significant differences in food intake, body weight gain, and food efficiency ratio among groups. Weights of liver per 100 g body weight were not significantly different. There were no significant differences in Zn levels in serum. Plasma and liver TBARS level, and liver conjugated diene level were significantly lower in ZnDE than in ZnDN or ZnDD, and significantly higher in ZnDD than in ZnDN. Therefore, it seems that lipid peroxidation is accelerated by dietary zinc deficiency and recovered partly by vitamin E supplementation.

• Laboraroty Animal Research
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• v.34 no.4
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• pp.295-301
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• 2018

Nucleotide-binding domain 1 (Nod1) is a cytosolic receptor that is responsible for the recognition of a bacterial peptidoglycan motif containing meso-diaminophimelic acid. In this study, we sought to identify the role of Nod1 in host defense in vivo against pulmonary infection by multidrug resistant Acinetobacter baumannii. Wildtype (WT) and Nod1-deficient mice were intranasally infected with $3{\times}10^7CFU$ of A. baumannii and sacrificed at 1 and 3 days post-infection (dpi). Bacterial CFUs, cytokines production, histopathology, and mouse ${\beta}$-defensins (mBD) in the lungs of infected mice were evaluated. The production of cytokines in response to A. baumannii was also measured in WT and Nod1-deficient macrophages. The bacterial clearance in the lungs was not affected by Nod1 deficiency. Levels of IL-6, $TNF-{\alpha}$, and $IL-1{\beta}$ in the lung homogenates were comparable at days 1 and 3 between WT and Nod1-deficient mice, except the $TNF-{\alpha}$ level at day 3, which was higher in Nod1-deficient mice. There was no significant difference in lung pathology and expression of mBDs (mBD1, 2, 3, and 4) between WT and Nod1-deficient mice infected with A. baumannii. The production of IL-6, $TNF-{\alpha}$, and NO by macrophages in response to A. baumannii was also comparable in WT and Nod1-deficient mice. Our results indicated that Nod1 does not play an important role in host immune responses against A. baumannii infection.

• Communications of the Korean Mathematical Society
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• v.30 no.2
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• pp.93-101
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• 2015

In this paper, we study the uniqueness of entire functions concerning differential polynomials and deficient value. The results extend and improve Theorem 2 in Yi [13].

• Proceedings of the Korean Ceranic Society Conference
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• 2003.10a
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• pp.174.1-174
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• 2003

• Journal of the Korean Applied Science and Technology
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• v.3 no.2
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• pp.49-64
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• 1986

This experiment is carried out to study effect of choline-deficient diet on serum and liver lipid contents of male rats. The experimental animals use 36 male Sprague-Dawley rats weighing about $100{\pm}3g$. They are classified into 7 groups and fed to experimental diets which are composed of 0.8% choline-supplement of deficient diets in addition to 14% corn oil, 14% corn margarine and 14% lipids mixed with 4% corn oil and 10% corn margarine, respectively. After feeding for 4 weeks, I measure lipid concentration of serum and liver, and the result are as follows. 1. The choline-deficient diet group decreases slightly the rates of weight gain and feed efficiency as compared with those of the choline-supplement diet group, but increases liver weight. 2. The choline-dificient diet group decreases the serum concentrations of total cholesterol (TC), free cholesterol, HDL-choelsterol, VLDL, LDL-cholesterol and phospholipid (PL), but increases the contents of triglyceride and the ratios of cholesterol/HDL-cholesterol and triglyceride/PL, and indicates no remarkable-difference in the ratio of TC/PL. 3. As compared with the choline-supplement diet group, the choline-deficient diet group contains the higher liver contents of total lipids, free cholesterol and triglyceride, and gives little difference in the liver contents of total cholesterol and phospholipid(PL), and presents the higher ratios of VLDL, LDL-cholesterol/HDL-cholesterol and TG/PL in the liver.4. In the choline-deficient diet group, the coutents of serum and liver lipid is not influenced by the kind of dietary fat. On the other hand, the choline-supplemented diet group indicates a significantly lower content of phospholipid in the corn margarine-added diet group than in the corn oil-added diet group. As aforementioned results, I think that the choline-deficient diet induces fatty liver in male rats without relation to kind of fatty acid, and cholines-upplement diet with saturated fatty acid makes the more decrease of liver phospholipid than that with polyunsaturated fatty acid.