• Ocean and Polar Research
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• 제26권3호
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• pp.415-423
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• 2004

An experiment was conducted to investigate the differences of total ammonia nitrogen (TAN) excretion rates and feces production rates among the offsprings from cultured Japanese strain (JJ, mean BW; $17.1{\pm}0.1g$), intraspecific hybrid strain between cultured Japanese and selected Korean strain (JK, mean BW: $17.1{\pm}0.1g$) and selected Korean strain(KK, mean BW: $21.5{\pm}0.1g$) of red sea bream in order to compare their dietary protein utilization efficiency. Fish were hand-fed with a commercial diet containing 46.7% crude protein for 2 weeks, three times daily 09:00, 13:00 and 17:00. After daily feeding, the TAN excretion rates reached peaks of 49.03, 58.75 and 36.26mg/kg fish/hr for the JJ, JK and KK strain, respectively, during the daytime. The value of the KK strain was significantly lower than that of the JJ and JX shuin (P<0.05), however daily TAN excretion rates of the JJ, JK and KK strain were not different (P>0.05). When fish were fed at satiation after 4 days of starvation, TAN excretion rates reached the maximum values 4 hours after the feeding fur the KK (31.23 mg/kg fish/hr) and 6 hours after the feeding fur the JJ (44.19 mg/tg fish/hr) and JK strain (41.70 mg/kg fish/hr). After 3 days of starvation, the daily endogenous TAU excretion rates (ETE) for the JJ, JK. and KK strain were 286.91, 215.66 and 179.29mg/kg fish/day, respectively. The value of the KK strain was lower than that of the JJ and JK strain (P<0.05). The total feces production rates of the JJ, JK and KK strain were not significantly different, however the proportions of feces production rates by time for the JJ, JK and KK strain were different (P<0.05). As overall results, efficiency of dietary protein utilization of JJ, JK and KK seems to be different and KK strain could offer a desirable option for aquaculture purpose.

• The Korean Journal of Physiology and Pharmacology
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• 제7권6호
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• pp.333-339
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• 2003

It has been demonstrated that an unidentified cytosolic factor(s) reduces $K_{ACh}$ channel function. Therefore, this study attempted to elucidate the cytosolic factor. Fresh cytosol isolated from normal heart (FC) depressed the $K_{ACh}$ channel activity, but cytosol isolated from the ischemic hearts (IC) did not modulate the channel function. Electrophorectic analysis revealed that a protein of ${\sim}80 kDa was markedly reduced or even lost in IC. By using peptide sequencing analysis and Western blot, this 80 kDa protein was identified as transferrin (receptor-mediated $Fe^{3+}$ transporter, 76 kDa). Direct application of transferrin (100 nM) to the cytoplasmic side of inside-out patches decreased the open probability ($P_o$, 12.7${\pm}6.4%, n=4) without change in mean open time (${\tau}_o$, $98.5{\pm}1.3$%, n=4). However, the equimolar apotransferrin, which is free of $Fe^{3+}$, had no effect on the channel activity (N*$P_o$, $129.1{\pm}13.5$%, n=3). Directly applied $Fe^{3+}$ (100 nM) showed results similar to those of transferrin (N*$P_o$: $21.1{\pm}3.9$%, n=5). However $Fe^{2+}$ failed to reduce the channel function (N*$P_o$, $106.3{\pm}26.8$%, n=5). Interestingly, trivalent cation La3+ inhibited N*$P_o$ of the channel ($6.1{\pm}3.0$%, n=3). Taken together, these results suggest that $Fe^{3+}$ bound to transferrin can modulate the $K_{ACh}$ channel function by its electrical property as a polyvalent cation.

• Journal of Microbiology and Biotechnology
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• 제19권4호
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• pp.416-423
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• 2009

Hepatitis B core antigen(HBcAg) is an important serological marker used in the diagnosis of hepatitis B virus(HBV) infections. In the current study, a fast and efficient preparative purification protocol for truncated HBcAg from Escherichia coli disruptate was developed. The recombinant HBcAg was first captured by anion exchange expanded bed adsorption chromatography integrated with a cell disruption process. This online capture process has shortened the process time and eliminated the "hold-up" period that may be detrimental to the quality of target protein. The eluted product from the expanded bed adsorption chromatography was subsequently purified using size-exclusion chromatography. The results showed that this novel purification protocol achieved a recovery yield of 45.1% with a product purity of 88.2%, which corresponds to a purification factor of 4.5. The recovered HBcAg is still biologically active as shown by ELISA test.

• Journal of Microbiology
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• 제42권3호
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• pp.228-232
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• 2004

In this paper, we investigated the development of a simplified and rapid primary capture step for the recovery of M13 bacteriophage from particulate-containing feedstock. M13 bacteriophage, carrying an insert, was propagated and subsequently purified by the application of both conventional multiple steps and expanded bed anion exchange chromatography. In the conventional method, precipitation was conducted with PEG/NaCl, and centrifugation was also performed. In the single step expanded bed anion exchange adsorption, UpFront FastLine$\_$TM/20 (20mm i.d.) from UpFront Chromatography was used as the contactor, while 54$m\ell$ (H$\_$o/=15cm) of STREAMLINE DEAE (p=1.2 g/㎤) from Amersham Pharmacia Biotechnology was used as the anion exchanger. The performance of the two methods were evaluated, analysed, and compared. It was demonstrated that the purification of the M13 bacteriophage, using expanded bed anion exchange adsorption, yielded the higher recovery percentage, at 82.86％. The conventional multiple step method yielded the lower recovery percentage, 36.07％. The generic application of this integrated technique has also been assessed.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2007년도 Proceedings of The Convention of The Korean Society of Applied Pharmacology
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• pp.25-44
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• 2007

The glucocorticoid receptor (GR) is an intracellular protein that is widely distributed throughout hippocampal and neocortical brain tissue. Mifepristone (RU486) is a potent GR antagonist that has also been shown to exhibit partial agonist-like effects. The precise location of the GR domain involved in the agonist-like activity of RU486 is unknown. Here, we examine this aspect of GR signaling by comparing human GR (hGR) construct with a Guyanese squirrel monkey GR (gsmGR) construct in which nuclear translocation and transactivation are known to be impaired. Using an objective translocation scoring method, we found that both hGR and gsmGR are translocated by RU486, and that nuclear translocation of hGR is significantly increased compared to gsmGR at 10 nM, 100 nM and 1000 nM RU486 in transiently transfected COS1 cells. While addition of RU486 to the cells transfected with hGR results in a 16-fold dose-dependent increase in transactivation compared to non-treated cells, no significant change in transactivation is observed with gsmGR at doses up to 100 nM RU486. Further experiments using six GR chimeras indicate that replacement of the hGR carboxyl-terminus of tau-1 transactivation domain (C-AF1, amino acids 132-428) with that from gsmGR diminishes hGR transactivation by RU486. These results demonstrate that RU486-induced transactivation of GR is determined in part by amino acids in the C-AF1 domain.

• 대한의생명과학회지
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• 제27권4호
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• pp.208-215
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• 2021

The purpose of this study was to explain the pathology of Alzheimer's disease (AD) and to investigate the correlation between AD and microRNA. AD is the most common type of dementia, accounting for about 80% of all types of dementia, causing dysfunction in various daily activities such as memory loss, cognitive impairment, and behavioral impairment. The typical pathology of AD is explained by the accumulation of beta-amyloid peptide plaques and neurofibrillary tangles containing hyperphosphorylated tau protein. On the other hand, microRNA is small non-coding RNA 22~23 nucleotides in length that binds to the 3' untranslated region of messenger RNA to inhibit gene expression. Many reports explain that microRNAs found in circulating biofluids are abundant in the central nervous system, are involved in the pathogenic mechanism of AD, and act as important factors for early diagnosis and therapeutic agents of AD. Therefore, this paper aims to clarify the correlation between AD and microRNA. In this review, the basic mechanism of miRNAs is described, and the regulation of miRNAs in the pathological processes of AD are highlighted. Furthermore, we suggest that miRNA-based system in development of therapeutic and diagnostic agents of AD can be a promising tool.

• 동의신경정신과학회지
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• 제21권2호
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• pp.171-189
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• 2010

Objectives : This research investigates the effect of the HBSBS on Alzheimer's disease. Specifically, the effects of the HBSBS extract on (1) the behavior (2) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's disease mice induced with $\beta$A were investigated. Methods : The effects of the HBSBS extract suppressed the expression of IL-1$\beta$, IL-6, TNF-$\alpha$ and NOS-II mRNA in BV2 microglial cell line treated with LPS plus $\beta$A were investigated. The effects of the HBSBS extract on the behavior of the memory deficit mice induced by scopolamine were investigated. Results : 1. The HBSBS extract suppressed the expression of IL-1$\beta$, IL-6, TNF-$\alpha$ and NOS-II mRNA in BV2 microglial cell line treated with LPS plus $\beta$A. 2. The HBSBS extract suppressed the expression of $\beta$A protein production in BV2 microglial cell line treated with LPS plus $\beta$A. 3. The HBSBS extract showed significantly inhibitory effect on the scopolamine-induced impairment of memory in the experiment of Morris water maze. 4. The HBSBS group suppressed the over-expression of IL-1$\beta$ protein, TNF-$\alpha$ protein significantly in the mice with Alzheimer's disease induced by $\beta$A. 5. The HBSBS group reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by $\beta$A. 6. The HBSBS group reduced tau protein, and GFAP in the brain tissue of the mice with AD induced by $\beta$A. Conclusions : These results suggest that the HBSBS group may be effective for the treatment of AD. Thus, HBSBS could be considered among the future therapeutic drugs indicated for the treatment of AD.

• 한국식품영양과학회지
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• 제45권4호
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• pp.542-550
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• 2016

굴 가수분해물의 이취 제거를 위한 가수분해 및 발효의 최적 조건과 이의 항산화 효과를 검토하였다. 이취 제거를 위한 굴 가수분해물의 최적 추출 조건은 Neutrase를 이용하여 E/S 3.3%, $50^{\circ}C$, 8.3시간이었으며, 발효 공정은 $24^{\circ}C$에서 glucose 0.5%와 Saccharomyces cerevisiae를 5% 접종하였다. 굴 가수분해 발효물의 구성 아미노산은 25.7%에 해당하였으며, Glu, Asp, Lys, Leu, Arg, Gly 및 Ala이 전체의 61.2%를 차지하였다. 유리 아미노산 조성의 경우 Leu, Ala, Phe, Val 및 Tau의 순으로 높게 나타났다. 또한 무기질 함량은 Na, P, K, Zn, Fe이 높게 나타났으며, 정상 간세포주인 Chang cell에 대한 독성은 나타나지 않았다. 이상의 결과로 미루어 S. cerevisiae에 의해 수산물의 이미취를 masking 할 수 있으나, 기능성 원료로 사용하기 위해 최종 제품의 카드뮴 함량을 저감시킬 대책이 필요하다.

• Journal of Microbiology and Biotechnology
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• 제32권9호
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• pp.1154-1167
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• 2022

In this study, we investigated the anti-amnesic effect of Korean red pine (Pinus densiflora) bark extract (KRPBE) against amyloid beta_1-42 (Aβ_1-42)-induced neurotoxicity. We found that treatment with KRPBE improved the behavioral function in Aβ-induced mice, and also boosted the antioxidant system in mice by decreasing malondialdehyde (MDA) content, increasing superoxide dismutase (SOD) activities, and reducing glutathione (GSH) levels. In addition, KRPBE improved the cholinergic system by suppressing reduced acetylcholine (ACh) content while also activating acetylcholinesterase (AChE), regulating the expression of choline acetyltransferase (ChAT), postsynaptic density protein-95 (PSD-95), and synaptophysin. KRPBE also showed an ameliorating effect on cerebral mitochondrial deficit by regulating reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and ATP levels. Moreover, KRPBE modulated the expression levels of neurotoxicity indicators Aβ and phosphorylated tau (p-tau) and inflammatory cytokines TNF-α, p-IκB-α, and IL-1β. Furthermore, we found that KRPBE improved the expression levels of neuronal apoptosis-related markers BAX and BCl-2 and increased the expression levels of BDNF and p-CREB. Therefore, this study suggests that KRPBE treatment has an anti-amnestic effect by modulating cholinergic system dysfunction and neuroinflammation in Aβ_1-42-induced cognitive impairment in mice.

• 동의신경정신과학회지
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• 제24권3호
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• pp.309-320
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• 2013

Objectives : There is a possibility LRE as remedy in Alzheimer disease (AD), but it's nerve protection effect and mechanism have to be elucidate. In this research, we applied LRE on $A{\beta}_{25-35}$ pre-treated SH-SY5Y cells, to find out the nerve protection effect and mechanism in AD cell model. Methods : We tried to confirm that effect by experimenting with 20, 50, and $100{\mu}g/ml$ concentration of LRE as a medicine. Next experiment, we assessed damage effect which induced $A{\beta}_{25-35}$, known to cause AD, on SH-SY5Y cell. In addition, cellular viability test is executed under $H_2O_2$ treatment condition in a SH-SY5Y cell. Results : 1. In $A{\beta}_{25-35}$ treated SH-SY5Y cell, LRE exhibited an anti-phosphorylation effect about tau protein, JNK, and IKB. 2. LRE prevent nerve cell apoptosis, which indued $A{\beta}_{25-35}$ and oxidative stress, modify JNK engaged synaptic structure and $NF{\kappa}B$ induced p75-neurotrophin receptor polymorphism. Conclusions : We found that LRE prevented oxidative stress-induced cellular destruction, for example, increased SOD activity of $A{\beta}_{25-35}$ treated SH-SY5Y cell and reduced toxicity of oxygen free radical. Consequently, the ingredients of LRE have a role as a catalyzer for $A{\beta}_{25-35}$ clearance and as scavenger for active oxygen free radical.