• Journal of Nutrition and Health
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• v.41 no.8
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• pp.691-700
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• 2008

One suggested mechanism underlying copper (Cu) deficiency teratogenicity is a low availability of nitric oxide (NO), signaling molecule which is essential in developmental processes. Increased superoxide anions secondary to decreased activities of Cu-zinc superoxide dismutase (Cu-Zn SOD) in Cu deficiency can interact with NO to form peroxynitrite, which can nitrate proteins at tyrosine residues. In addition, peroxynitrite formation can limit NO bioavailability. We previously reported low NO availability and increased protein nitration in Cu deficient (Cu-) embryos. In the current study, we tested whether Cu deficiency alters downstream signaling of NO by assessing cyclic GMP (cGMP) and phosphorylated vasodilator-stimulating phosphoprotein (VASP) levels, and whether NO supplementation can affect these targets as well as protein nitration. Gestation day 8.5 embryos from Cu adequate (Cu+) or Cu- dams were collected and cultured in either Cu+ or Cu- media for 48 hr. A subset of embryos was cultured in Cu- media supplemented with a NO donor (DETA/NONOate; 20 ${\mu}M$) and/or Cu-Zn SOD. Cu-/Cu- embryos showed a higher incidence of embryonic and yolk sac abnormalities, low NO availability, blunted dose-response in NO concentrations to increasing doses of acetylcholine, low mRNA expression of endothelial nitric oxide synthase (eNOS), increased levels of 3-nitrotyrosine (3-NT) compared to Cu+/Cu+ controls. cGMP concentrations tended to be low in Cu-/Cu- embryos, and they were significantly lower in Cu-/Cu- yolk sacs than in controls. Levels of phosphorylated VASP at serine 239 (P-VASP) were similar in all groups. NO donor supplementation to the Cu- media ameliorated embryonic and yolk sac abnormalities, and resulted in increased levels of cGMP without altering levels of P-VASP and 3-NT. Taken together, these data support the concept that Cu deficiency limits NO availability and alters NO/cGMP-dependent signaling in Cu- embryos and yolk sacs, which contributes to Cu deficiency-induced abnormal development.

• Korean Journal of Animal Reproduction
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• v.10 no.1
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• pp.100-108
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• 1986

Eik-Nes (1966) reported that the mechanism of spermatogenesis is controlled by FSH and LH and maintaned normally in scrotum terperautre which is 3-5$^{\circ}C$ lower than body termperature. But Ojeda and Ramirez (1972) have described that the abdominal testis was shrinked severely and lost its normal function in congenital cryptorchidism or surgically induced cryptorchidism. Ramirez and Sawyer (1974) reported that the compensatory hypertorphy occured in the remaining testis of unilateral castration and the scrotal testis of unilateral cryptorchidism. Cunninham et al. (1978) reported that the serum FSH levle increased after unilateral castration. Frankel and Wright (1982) reported that the serum LH level was unchanged greatly after unilateral castration. Gomes and Jain (1976) reported that the serum testosterone level increased temporarily but not varied after unilateral castration. On the other hand, Kormano et al. (1964) reported that the serum FSH level in unilateral cryptorchidism rat was unchanged in contrast with the control and Risbirdger et al. (1981) reported that the serum LH level was unchanged till 2 weeks after operation and after then increased to 77%. Kim (1984) reported that the serum testosterone level was somewhat lower than that fo control group but there was't significant different. There were many different reports on hormone levels among different investigators when the immarue rats were castrated unilaterally or induced cryptorchidism unilaterally. Liang and Liang (1970) and Cunningham et al. (1978) described that there were no true compenastory hypertrophy in the remaining testis of unilateral castration and scrotal testis of unilateral testis of unilateral cryptorchidism in rat but they grew faster than that of control. Kormano et al.(1964), Damber et al.(1976), Cunningham et al.(1978) and Karpe et al.(1981) reported that the testis weight, germinal epithelia height and seminiferous tubules diameter developed continuously and similarily in the control, the remaining testis of unilateral castration and scrotal testis of unilateral cryptorchidism increased, however, in the abdominal testis of the unilateral cryptorchidism, they were much smaller than those of other groups. In observation of the histological changes in the seminiferous epithelium of control, remaining tesis of unilateral castration and scrotal testis of unilateral cryptorchidism differentiated and developed fully(Cunningham et al., 1978). However, the abdominal testis of unilateral crytorchidism degenerated severely and only the germ cells in early stage and Sertoli cells were found in the seminiferous tubules. (Damber et al., 1976, Gomes and Jain, 1976 and Karpe et al., 1981). By electron microscopic observation, Nagano (1963) and Leason and Leeson (1970) found that the abdominal testis of unilateral cryptorchidism was thicked in boundary tissue, increased lipid droplet in the Sertoli cell, disarranged axial filament complex and increased lipid inclusions in the Sertoli cell.

• Reproductive and Developmental Biology
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• v.36 no.1
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• pp.33-37
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• 2012

Differential capacity of the parthenogenetic embryonic stem cells (PESCs) is still under controversy and the mechanisms of its neural induction are yet poorly understood. Here we demonstrated neural lineage induction of PESCs by addition of insulin-like growth factor-2 (Igf2), which is an important factor for embryo organ development and a paternally expressed imprinting gene. Murine PESCs were aggregated to embryoid bodies (EBs) by suspension culture under the leukemia inhibitory factor-free condition for 4 days. To test the effect of exogenous Igf2, 30 ng/ml of Igf2 was supplemented to EBs induction medium. Then neural induction was carried out with serum-free medium containing insulin, transferrin, selenium, and fibronectin complex (ITSFn) for 12 days. Normal murine embryonic stem cells derived from fertilized embryos (ESCs) were used as the control group. Neural potential of differentiated PESCs and ESCs were analyzed by immunofluorescent labeling and real-time PCR assay (Nestin, neural progenitor marker; Tuj1, neuronal cell marker; GFAP, glial cell marker). The differentiated cells from both ESC and PESC showed heterogeneous population of Nestin, Tuj1, and GFAP positive cells. In terms of the level of gene expression, PESC showed 4 times higher level of GFAP expression than ESCs. After exposure to Igf2, the expression level of GFAP decreased both in derivatives of PESCs and ESCs. Interestingly, the expression level of $Tuj1$ increased only in ESCs, not in PESCs. The results show that IGF2 is a positive effector for suppressing over-expressed glial differentiation during neural induction of PESCs and for promoting neuronal differentiation of ESCs, while exogenous Igf2 could not accelerate the neuronal differentiation of PESCs. Although exogenous Igf2 promotes neuronal differentiation of normal ESCs, expression of endogenous $Igf2$ may be critical for initiating neuronal differentiation of pluripotent stem cells. The findings may contribute to understanding of the relationship between imprinting mechanism and neural differentiation and its application to neural tissue repair in the future.

• Journal of the Korean Society for Aeronautical & Space Sciences
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• v.32 no.7
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• pp.1-12
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• 2004

A flow visualization of the 1st cycle motion of a fling-clapping wing that might be employed by butterflies during flight is performed. In this numerical flow visualization, he time-dependent Navier-Stokes equations are solved for two wing motion types; 'fling followed by clap and pause' and 'clap followed by fling and pause'. The result is observed regarding the main flow features such as the sequential development of the two families of separation vortex pairs and their movement. For the fling followed by clap and pause motion, a strong separation vortex pair of counter-clockwise develops in the opening between the wings in the fling phase and they then move out from the opening in the following clap phase. For the clap followed by fling and pause motion, the separation vortex pair developed in the outside space in the clap phase move into the opening in the following fling phase. The separation vortex pair in the opening developed in the fling phase of the clap followed by fling and pause motion is observed to be stronger than that in the opening developed in the fling phase of the fling followed by clap and pause motion.

• Journal of Food Hygiene and Safety
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• v.22 no.1
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• pp.1-14
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• 2007

The term, "food safety", has traditionally been viewed as a practical science aimed at assuring the prevention acute illnesses caused by biological microorganisms, and only to a minor extent, chronic diseases cause by chronic low level exposures to natural and synthetic chemicals or pollutants. "food safety" meant to prevent microbiological agents/toxins in/on foods, due to contamination any where from "farm to Fork", from causing acute health effects, especially to the young, immune-compromised, genetically-predisposed and elderly. However, today a broader view must also include the fact that diet, perse (nutrients, vitamins/minerals, calories), as well as low level toxins and pollutant or supplemented synthetic chemicals, can alter gene expressions of stem/progenitor/terminally-differentiated cells, leading to chronic inflammation and other mal-functions that could lead to diseases such as cancer, diabetes, atherogenesis and possibly reproductive and neurological disorders. Understanding of the mechanisms by which natural or synthetic chemical toxins/toxicants, in/on food, interact with the pathogenesis of acute and chronic diseases, should lead to a "systems" approach to "food safety". Clearly, the interactions of diet/food with the genetic background, gender, and developmental state of the individual, together with (a) interactions of other endogenous/exogenous chemicals/drugs; (b) the specific biology of the cells being affected; (c) the mechanisms by which the presence or absence of toxins/toxicants and nutrients work to cause toxicities; and (d) how those mechanisms affect the pathogenesis of acute and/or chronic diseases, must be integrated into a "system" approach. Mechanisms of how toxins/toxicants cause cellular toxicities, such as mutagenesis; cytotoxicity and altered gene expression, must take into account (a) irreversible or reversal changes caused by these toxins or toxicants; (b)concepts of thresholds or no-thresholds of action; and (c) concepts of differential effects on stem cells, progenitor cells and terminally differentiated cells in different organs. This brief Commentary tries to illustrate this complex interaction between what is on/in foods with one disease, namely cancer. Since the understanding of cancer, while still incomplete, can shed light on the multiple ways that toxins/toxicants, as well as dietary modulation of nutrients/vitamins/metals/ calories, can either enhance or reduce the risk to cancer. In particular, diets that alter the embryo-fetal micro-environment might dramatically alter disease formation later in life. In effect "food safety" can not be assessed without understanding how food could be 'toxic', or how that mechanism of toxicity interacts with the pathogenesis of any disease.

• Journal of Food Hygiene and Safety
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• v.31 no.4
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• pp.294-298
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• 2016

Natural products are attractive as the source of new drug development. Especially, numerous unknown marine bioresources are an object of attention because the ocean occupies three fourth of the earth. Survival of marine bioresources in extreme environment may induce the production of biological active compounds. As previous study, we examined over 40 specimens of marine sponges collected from Micronesia and screened their anti-proliferative activities in various cancer cell lines. Among them, we investigated Coscinoderma sp.'s activity and mechanism in human colon carcinoma HCT116 and RKO cells. Furthermore, we also used the p53-knockout of HCT116 cells and the p53 loss of RKO cells for elucidating the role of p53. Coscinoderma sp. inhibited cellular viability independently of the p53 status. Therefore, we compared the expression level of cell death-related proteins by Coscinoderma sp. in HCT16 and in HCT116 p53KO cells. Coscinoderma sp. increased p53 level and NOXA levels and induced apoptosis under the condition of p53 existence. On the other hand, Coscinoderma sp. increased p21 and mTOR levels in HCT116 p53KO cells. These results suggest that Coscinoderma sp. induced anti-proliferation effect through different pathway depending on p53 status.

• Proceedings of the Korean Society for Applied Microbiology Conference
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• 2000.04a
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• pp.3-6
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• 2000

Antimicrobial resistance has been a well-recognized problem ever since the introduction of penicillin into clinical use. History of antimicrobial development can be categorized based on the major antibiotics that had been developed against emerging resistant $pathogens^1$. In the first period from 1940 to 1960, penicillin was a dominating antibiotic called as a "magic bullet", although S.aureus armed with penicillinase led antimicrobial era to the second period in 1960s and 1970s. The second stage was characterized by broad-spectrum penicillins and early generation cephalosporins. During this period, nosocomial infections due to gram-negative bacilli became more prevalent, while those caused by S.aureus declined. A variety of new antimicrobial agents with distinct mechanism of action including new generation cephalosporins, monobactams, carbapenems, ${\beta}$-lactamase inhibitors, and quinolones characterized the third period from 1980s to 1990s. However, extensive use of wide variety of antibiotics in the community and hospitals has fueled the crisis in emerging antimicrobial resistance. Newly appeared drug-resistant Streptococcus pneumoniae (DRSP), vancomycin-resistant enterococci (VRE), extended-spectrum ${\beta}$-lactamase-producing Klebsiella, and VRSA have posed a serious threat in many parts of the world. Given the recent epidemiology of antimicrobial resistance and its clinical impact, there is no greater challenge related to emerging infections than the emergence of antibiotic resistance. Problems of antimicrobial resistance can be amplified by the fact that resistant clones or genes can spread within or between the species as well as to geographically distant areas which leads to a global concern$^2$. Antimicrobial resistance is primarily generated and promoted by increased use of antimicrobial agents. Unfortunately, as many as 50 % of prescriptions for antibiotics are reported to be inappropriate$^3$. Injudicious use of antibiotics even for viral upper respiratory infections is a universal phenomenon in every part of the world. The use of large quantities of antibiotics in the animal health industry and farming is another major factor contributing to selection of antibiotic resistance. In addition to these background factors, the tremendous increase in the immunocompromised hosts, popular use of invasive medical interventions, and increase in travel and mixing of human populations are contributing to the resurgence and spread of antimicrobial resistance$^4$. Antimicrobial resistance has critical impact on modem medicine both in clinical and economic aspect. Patients with previously treatable infections may have fatal outcome due to therapeutic failure that is unusual event no more. The potential economic impact of antimicrobial resistance is actually uncountable. With the increase in the problems of resistant organisms in the 21st century, however, additional health care costs for this problem must be enormously increasing.

• Journal of Life Science
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• v.26 no.1
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• pp.140-145
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• 2016

Genes in multicellular organisms are transcribed in development, differentiation, or tissue-specific manners. The transcription of genes is activated by enhancers, which are transcription regulatory elements located at long distances from the genes. Recent studies have reported that noncoding RNAs are transcribed from active enhancers by RNA polymerase II (RNA Pol II); these are called enhancer RNAs (eRNAs). eRNAs are transcribed bi-directionally from the enhancer core, and are capped on the 5’ end but not spliced or polyadenylated on the 3’ end. The transcription of eRNAs requires the binding of transcription activators on the enhancer and associates positively with the transcription of the target gene. The transcriptional inhibition of eRNAs or the removal of eRNA transcripts results in the transcriptional repression of the coding gene. The transcriptional procedure of eRNAs causes enhancer- specific histone modifications, such as histone H3K4me1/2. eRNA transcripts directly interact with Mediator and Rad21, a cohesin subunit, generating a chromatin loop structure between the enhancer and the promoter of the target gene. The recruitment of RNA Pol II into the promoter and its elongation through the coding region are facilitated by eRNAs. Here, we will review the features of eRNAs, and discuss the mechanism of eRNA transcription and the roles of eRNAs in the transcriptional activation of target genes.

• Korean Journal of Construction Engineering and Management
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• v.16 no.2
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• pp.65-76
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• 2015

The Clean Development Mechanism (CDM) is the multi-lateral 'cap and trade' system endorsed by the Kyoto Protocol. CDM allows developed (Annex I) countries to buy CER credits from New and Renewable (NE) projects of non-Annex countries, to meet their carbon reduction requirements. This in effect subsidizes and promotes NE projects in developing countries, ultimately reducing global greenhouse gases (GHG). To be registered as a CDM project, the project must prove 'additionality,' which depends on numerous factors including the adopted technology, baseline methodology, emission reductions, and the project's internal rate of return. This makes it difficult to determine ex ante a project's acceptance as a CDM approved project, and entails sunk costs and even project cancellation to its project stakeholders. Focusing on hydro power projects and employing UNFCCC public data, this research developed a prediction model using logistic regression and CART to determine the likelihood of approval as a CDM project. The AUC for the logistic regression and CART model was 0.7674 and 0.7231 respectively, which proves the model's prediction accuracy. More importantly, results indicate that the emission reduction amount, MW per hour, investment/Emission as crucial variables, whereas the baseline methodology and technology types were insignificant. This demonstrates that at least for hydro power projects, the specific technology is not as important as the amount of emission reductions and relatively small scale projects and investment to carbon reduction ratios.

• Publications of The Korean Astronomical Society
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• v.24 no.1
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• pp.53-64
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• 2009

MIRIS is the main payload of the STSAT-3 (Science and Technology Satellite 3) and the first infrared space telescope for astronomical observation in Korea. MIRIS space observation camera (SOC) covers the observation wavelength from $0.9{\mu}m$ to $2.0{\mu}m$ with a wide field of view $3.67^{\circ}\times3.67^{\circ}$. The PICNIC HgCdTe detector in a cold box is cooled down below 100K by a micro Stirling cooler of which cooling capacity is 220mW at 77K. MIRIS SOC adopts passive cooling technique to chill the telescope below 200 K by pointing to the deep space (3K). The cooling mechanism employs a radiator, a Winston cone baffle, a thermal shield, MLI (Multi Layer Insulation) of 30 layers, and GFRP (Glass Fiber Reinforced Plastic) pipe support in the system. Optomechanical analysis was made in order to estimate and compensate possible stresses from the thermal contraction of mounting parts at cryogenic temperatures. Finite Element Analysis (FEA) of mechanical structure was also conducted to ensure safety and stability in launching environments and in orbit. MIRIS SOC will mainly perform Galactic plane survey with narrow band filters (Pa $\alpha$ and Pa $\alpha$ continuum) and CIB (Cosmic Infrared Background) observation with wide band filters (I and H) driven by a cryogenic stepping motor.