Nonalcoholic fatty liver disease (NAFLD) is recognized one of the leading metabolic diseases globally, and the younger age population with the disease is rapidly growing, especially in developed countries. Since there has been no approved medicine, losing weight is known to be the only best remedy to control or reverse the disease. Recently, the field of microbiome has attracted much attention to offer more practical choices for patients. Here, we provide experimental evidence that Streptococcus thermophilus LM1012 (LM1012), a safe probiotic strain, is effective for improving NAFLD indexes. In the methionine-choline deficient (MCD) diet induced C57BL/6 mouse model, administration of LM1012 promoted marked reductions of aspartate transaminase (23.8%), total bilirubin (27.8%), hydroxycholesterol (64.2%), triglyceride (29.7%) and IL-1β (68.3%) compared to the MCD diet alone group. Also, the histopathological data imply that LM1012 inhibited fat accumulation and inflammation in the liver, which are the key biomarkers for progression of the disease. Together, these findings suggest that human consumption of LM1012 as a healthy nutritional supplement, may be helpful in reducing the risk of liver damages in NAFLD patients.

Aging is a physiological change that leads to a decline in biological functions from metabolic stress. To investigate the effect of aging on mandibular bone formation, we created SAMP1/Klotho-deficient mice and performed micro-computed tomography (micro-CT) and histology analyses in 4-or 8 week-old SAMP1/kl -/- mice. SAMP1/kl -/- mice exhibited extensive inflammation, tissue calcification, and abnormal mandibular bone development. Using micro-CT analysis, SAMP1/kl -/- mice displayed a loss of incisor roots and irregular dentinal tubule formation, as well as calcification within the pulp root canal. Furthermore, the mandibular ramus showed extensive ground glass appearance in SAMP1/kl -/- mice. In histological analysis, we found calcified skeletal structures and dysplastic bone formation in SAMP1/kl -/- mice. These results provide an understanding of the pathologic alterations of aging-related mandibular bone. SAMP1/kl -/- mice may serve as a novel model for dysosteogenesis in mandibular bone development.

Tissue engineering (TE) has been developed to create functional organs and tissue by combining 3D matrix and cells in vitro. Vascularization and angiogenesis are utmost important for supply of nutrients and oxygen in tissue engineered organs. The present study was performed to isolate and characterize primary endothelial cells (EC) from aorta of alpha 1, 3-enzyme galactosyltransferase knock out (GalT KO) pig, to minimize immune rejection and analyze body immune system for future xenotransplantation studies. Isolation of primary EC from aorta were performed by incubation with dispase for 8-10 min at 37°C. Primary EC were cultured in EC growth medium on different extra cellular matrix (ECM), either collagen or gelation. Primary EC exhibits morphological characteristics and showed positive expressions of EC specific marker proteins i.e. PECAM1, KDR and VWF despite of their ECM surface; however, on collagen based surface they showed increase in mRNA level analyzed by qPCR. Primary EC cultured on collagen were sorted by flow cytometer using KDR marker and cultured as KDR positive cells and KDR negative cells, respectively. KDR positive cells showed dramatically increased in PECAM1 and VWF level as compared to KDR negative cells. Based on the above results, primary EC derived from GalT KO are successfully isolated and survived continuously in culture without becoming overgrown by fibroblast. Therefore, they can be utilize for xeno organ transfer, tissue engineering, and immune rejection study in future.

Reinforced concrete shear walls with deficient reinforcement details are tested under cyclic loading. The deficiency of reinforcement details includes insufficient splice length in U-stirrups at the ends of horizontal reinforcement and boundary column dowel bars found in existing low- to mid-rise Korean buildings designed non-seismically. Three test specimens have rectangular, babel and flanged sections, respectively. Flexure- and shear-controlled models for reinforced concrete shear walls specified in ASCE/SEI 41-13 are compared with the flexural and shear components of force-displacement relation extracted separately from the top displacement of the specimen based on the displacement data measured at diverse locations. Modification of the shear wall models in ASCE/SEI 41-13 is proposed in order to account for the effect of bar slip, cracking loads in flexure and shear. The proposed modification shows better approximation of the test results compared to the original models.

Copper is an essential micronutrient whose deficiency is often seen to occur in humans. Although many biomedical studies have focused on the use of nanoparticles, the nutritional effects of nano-sized copper oxide particles are not well known. This aim of this study was to investigate the nutritional bioavailability of nano- and micro-sized copper oxide (CuO) particles in copper-deficient (CuD) mice. Copper deficiency was induced in mice by feeding a CuD diet (0.93 mg Cu/kg diet) for 7 weeks. After the induction of copper deficiency, nano- or micro-sized copper oxide particles were administered orally at two different doses (0.8 and 4.0 mg CuO/kg body weight) to mice in the following groups: (1) normal control (NC), (2) CuD, (3) low dose micro-sized CuO, (4) high dose micro-sized CuO, (5) low dose nano-sized CuO, and (6) high dose nano-sized CuO. The hepatic copper concentration in the CuD group was significantly lower than that in the NC group. Compared to the NC group, the CuD group exhibited lower serum ceruloplasmin (CP) activity and CP level. The copper/zinc-superoxide dismutase activity in the CuD group was significantly lower than that in the NC group. Treatment with nano- or micro-sized copper oxide particles for 2 weeks restored the hepatic copper levels and serum CP activities to values similar to those observed in the NC group. The CP levels and copper/zinc-superoxide dismutase activities in all the copper oxide treatment groups also recovered to normal values after 3 weeks of copper oxide treatment. These results show that oral administration of either nano- or micro-sized copper oxide particles for 2–3 weeks restored the normal condition in previously CuD mice.

We investigated the change of growth characters by over-expressing OsPT6 (OsPT6-OX) under phosphorus (Pi) deficient condition in rice. In analyzing the change of growth rate according to Pitreatment for two weeks, shoot growth rate of OsPT6-OX was increased in Pi deficient condition than in Pi sufficient condition. Therefore, the chlorophyll content of leaf in OsPT6-OXs did not increase even decreased in the youngest leaf. However growth rate of wild type plant in Pi deficient condition showed significant reduction with increment of chlorophyll content. In analyzing agronomic characters, the tiller number of OsPT6-OX less decreased than those of wild type plant in Pi deficient condition. Panicle number and ripening rate of wild type plant were changed according to Pi treatment. However those of OsPT6-OX did not change in such conditions. Resulting of changes in agronomic characters, yield of wild type plant decreased about 10 % in Pi deficient condition. That of OsPT6-OX did not show significant difference in Pi deficient condition. The results obtained this study demonstrated that over-expression of OsPT6 could increase phosphorus deficient stress resistance in rice.

The objective of this study was to identify the nutritional risk factors by blood analysis, in 1,083 preschool children of age 3 to 6 years. The frequency of anemic children was 7.3% with Hb<11.1 g/dL, 29.9% with ferritin<20 ng/mL, and 16.7% with transferrin Fe saturation(%)<15%. The prevalence of anemia in these children were 12.8% for those with MCV<79 fL, and it was 71% for those with TIBC>400 μg/dL. Serum ferritin concentration was 20 ng/mL in the normal children. Thirty two percent of the children had anemia with Hb<12 g/dL, which is below the normal range of Hb. Exactly 15.4% of the children had serum Fe concentration of 60 μg/dL. The transferrin Fe saturation of the children (16.3%) was >15%. The serum ferritin concentration showed low correlations with Hb, Fe, transferrin Fe saturation, and MCV. The transferrin Fe saturation, higher Hb concentration, MCV, and Hct values were increased significantly. Consequently, iron-deficiency anaemia was thus defined as having Hb concentration <12 g/dL accompanied by ferritin concentration <20 ng/mL or Hct <33%.

Peroxiredoxin Ⅱ (Prdx Ⅱ; a typical 2-Cys Prdx) has been originally isolated from erythrocytes, and its structure and peroxidase activity have been adequately studied. Prdx Ⅱ has been reported to protect a wide range of cellular environments as antioxidant enzyme, and its dysfunctions may be implicated in a variety of disease states associated with oxidative stress, including cancer and aging-associated pathologies. But, the precise mechanism is still obscure in various aspects of aging containing ovarian aging. Identification and relative quantification of the increased proteins affected by Prdx Ⅱ deficiency may help identify novel signaling mechanisms that are important for oxidative stress-related diseases. To identify the increased proteins in Prdx Ⅱ—/— mice, we performed RBC comparative proteome analysis in membrane fraction and cytosolic fractions by nano-UPLC-MSE shotgun proteomics. We found the increased 86 proteins in membrane (32 proteins) and cytosolic (54 proteins) fractions, and analyzed comparative expression pattern in healthy RBCs of Prdx Ⅱ+/+ mice, healthy RBCs of Prdx Ⅱ—/— mice, and abnormal RBCs of Prdx Ⅱ—/— mice. These proteins belonged to cellular functions related with RBC lifespan maintain, such as cellular morphology and assembly, cell-cell interaction, metabolism, and stress-induced signaling. Moreover, protein networks among the increased proteins were analyzed to associate with various diseases. Taken together, RBC proteome may provide clues to understand the clue about redox-imbalanced diseases.

Red blood cells (RBCs) have been studied as models for infectious diseases, various symptoms of anemia, hemolysis, and erythrocyte aging. Although do not directly affect RBCs, other diseases may cause RBC physiological alterations that could be advanced for diagnostic aim or to convince better understanding of a certain pathological pattern. In this study, comparative RBC proteomics between healthy and abnormal conditions involve to promote aging related‐biomarker discovery. Peroxiredoxin II (Prdx II; a typical 2‐Cys Prdx) has been originally isolated from erythrocytes, and its structure and peroxidase activity have been adequately studied. Mice absent to Prdx II proteins had heinz bodies in their peripheral blood, and morphologically aged cells were detected in the dense RBC fractions, which contained markedly higher levels of reactive oxygen species (ROS). In addition, a labeling experiment with the thiol‐modifying reagent biotinylated iodoacetamide (BIAM) in Prdx II‒/‒ mice revealed that a variety of RBC proteins were highly oxidized. To identify oxidation‐sensitive proteins in Prdx II‒/‒ mice, we performed RBC comparative proteome analysis by nano‐UPLC‐MSE shotgun proteomics with relative protein quantitative analysis. We found oxidation‐sensitive 18 membrane and 41 cytosol proteins from 32 and 85 peptides containing cysteine oxidation, and analyzed comparative expression pattern in healthy RBCs of Prdx II+/+ mice (W1), healthy RBCs of Prdx II‒/‒ mice (K1), and abnormal RBCs of Prdx II‒/‒ mice (K2). These proteins belonged to cellular functions related with RBC lifespan maintain, such as cytoskeleton, stress‐induced proteins, amino acid/nucleic acid metabolic enzymes, signal transduction, and molecular transporters. Furthermore, protein networks among identified oxidation sensitive proteins were analyzed to associate with aging consequence. Consequently, we expected that RBC proteome may provide clues to understand redox‐imbalanced diseases.

Endothelial cells are a vital constituent of most mammalian organs and are required to maintain the integrity of these tissues. These cells also play a major role in angiogenesis, inflammatory reactions, and in the regulation of thrombosis. Angiogenesis facilitates pulp formation and produces the vessels which are essential for the maintenance of tooth homeostasis. These vessels can also be used in bone and tissue regeneration, and in surgical procedures to place implants or to remove cancerous tissue. Furthermore, endothelial cell regeneration is the most critical component of the tooth generation process. The aim of the present study was to stimulate endothelial regeneration at a site of acute cyclophosphamide (CP)-induced endothelial injury by treatment with human umbilical cord-derived endothelial/mesenchymal stem cells (hEPCs). We randomly assigned 16 to 20-week-old female NOD/SCID mice into three separate groups, a hEPC (1 × 105 cells) transplanted, 300mg/kg CP treated and saline (control) group. The mice were sacrificed on days 5 and 10 and blood was collected via the abdominal aorta for analysis. The alanine transaminase (ALT), aspartate aminotransferase (AST), serum alkaline phosphatase (s-ALP), and albumin (ALB) levels were then evaluated. Tissue sections from the livers and kidneys were stained with hematoxylin and eosin (HE) for microscopic analysis and were subjected to immunohistochemistry to evaluate any changes in the endothelial layer. CP treatment caused a weight reduction after one day. The kidney/body weight ratio increased in the hEPC treated animals compared with the CP only group at 10 days. Moreover, hEPC treatment resulted in reduced s-ALP, AST, ALT levels compared with the CP only group at 10 days. The CP only animals further showed endothelial injuries at five days which were recovered by hEPC treatment at 10 days. The number of CD31-positive cells was increased by hEPC treatment at both 5 and 10 days. In conclusion, the CP-induced disruption of endothelial cells is recovered by hEPC treatment, indicating that hEPC transplantation has potential benefits in the treatment of endothelial damage.

Selenium (Se) obtained from dietary sources is an essential micronutrient for normal body function and it functions as an essential constituent of selenoproteins. We investigated the influence of Se on the formation of colonic aberrant crpyt foci (ACF) and tumor formation induced by azoxymethane (AOM) and dextran sodium sulfate (DSS) in male ICR mice. Five-week old ICR mice were acclimated for one week and fed on the low iron diet (LFe, 4.5 ppm) and different Se diet [Lse (0.02 ppm), Normal Se (0.1 ppm), HSe (0.5 ppm)] for 12 weeks. Animals received intraperitoneal injections of AOM (10㎎/㎏ B.W. in saline weekly for 3 weeks), followed by 2% DSS (molecular weight 36,000～50,000) in the drinking water for a week. There were five experimental groups, including a normal control group, AOM/DSS, LFe+AOM/DSS, LFe+AOM/DSS+LSe, LFe+AOM/DSS+HSe. After sacrifice of animals, the total numbers of AC and ACF were measured in the colonic mucosa. The number of mice bearing tumors was expressed as tumor incidence rate. The iron and selenium liver concentration was measured using ICP-AES. Glutathione peroxidase (GPx) activity was determined using a GPx assay kit in the liver and colon. TUNEL and proliferating cell nuclear antigen (PCNA) staining were performed to examine the cell apoptosis and cell proliferation. In addition, immunohistochemistry of β-catenin was also performed on the mucous membrane tissue of colon. In AOM/DSS-induced colon carcinogenesis animal model, LFe diet decreased the number of 2.95±2.5 ACF/cm2 to 1.85±1.1 ACF/cm2 but it increased the total number of 5.06±4.2 AC/cm2 to 6.19±4.8 AC/cm2 compared with normal iron diet. In the iron-deficient mice, selenium did not affect the either the number of ACF or AC. The tumor incidence rate was higher in LFe diet groups than in normal iron diet group and high selenium diet weakly reduced the tumor incidence. Low selenium diet decreased the activity of GPx in the liver and colon. Apoptotic positive cells were decreased in the low selenium diet group. In addition, on the β-catenin staining, positive cells were increased in the low selenium diet group while they were decreased in the high selenium diet group. These findings indicate that the dietary levels of selenium was not highly enough to exhibit a significant protection against colon carcinogenesis in the iron-deficient mice. However, our results also indicate that dietary selenium might exert a protecting effect against colon cancer by increasing GPx activity and apoptosis and by inhibiting cell proliferation and β-catenin over-expression.