• The Korean Journal of Physiology and Pharmacology
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• 제18권5호
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• pp.411-418
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• 2014

Vascular remodelling is an adaptive mechanism, which counteracts pressure changes in blood circulation. Nicotine content in cigarette increases the risk of hypertension. The exact relationship between nicotine and vascular remodelling still remain unknown. Current study was aimed to determine the effect of clinically relevant dosage of nicotine (equivalent to light smoker) on aortic reactivity, oxidative stress markers and histomorphological changes. Twelve age-matched male Sprague-Dawley rats were randomly divided into two groups, i.e.: normal saline as control or 0.6 mg/kg nicotine for 28 days (i.p., n=6 per group). On day-29, the rats were sacrificed and the thoracic aorta was dissected immediately for further studies. Mean arterial pressure (MAP) and pulse pressure (PP) of nicotine-treated vs. control were significantly increased (p<0.05). Nicotine-treated group showed significant (p<0.05) increase tunica media thickness, and decrease in lumen diameter, suggesting vascular remodelling which lead to prior hypertension state. The phenylephrine (PE)-induced contractile response in nicotine group was significantly higher than control group ($ED_{50}=1.44{\times}10^5M$ vs. $4.9{\times}10^6M$) (p<0.05~0.001). However, nicotine-treated rat showed significantly lower endothelium-dependent relaxation response to acetylcholine (ACh) than in control group ($ED_{50}=6.17{\times}10^7M$ vs. $2.82{\times}10^7M$) (p<0.05), indicating loss of primary vascular function. Malondialdehyde (MDA), a lipid peroxidation marker was significantly higher in nicotine group. Superoxide dismutase (SOD) enzymatic activity and glutathione (GSH) were all reduced in nicotine group (p<0.05) vs. control, suggesting nicotine induces oxidative imbalance. In short, chronic nicotine administration impaired aortic reactivity, probably via redox imbalance and vascular remodelling mechanism.

• 한국콘텐츠학회논문지
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• 제9권4호
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• pp.355-363
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• 2009

비정상적인 미토콘드리아에 의해 산화 스트레스가 증가하면 세포내 신호전달 및 유전자 발현에 손상을 일으켜 인슐린 저항성이나 당뇨병 등의 여러 질환들을 유발한다. 그런데 자식작용은 산화 스트레스로 기능이 저하된 미토콘드리아를 제거하여 인슐린 저항성 등을 억제해준다. 한편 운동도 미토콘드리아 생합성을 강화시켜 조직의 기능저하나 퇴행을 회복시켜준다. 따라서 운동과 자식작용이 서로 연관되어 미토콘드리아 생합성을 유도하는 신호체계로 작용할 가능성이 있고, 이 연구를 통해 운동 혹은 AICAR (aminoimidazole-4-carboxamide-1-${\beta}$-D-ribofuranoside)처치로 활성 화된 AMPK(5'-AMP- activated protein kinase) 신호전달체계가 미토콘드리아 생합성을 증가시키는 경로에 자식작용이 관여하는지의 여부를 확인하고자 하였다. 연구결과에 따르면, 6시간의 급성운동으로 쥐의 골격근에서 PGC-1(peroxisome proliferator-activated receptor gamma coactivator 1)과 mtTFA (mitochondrial transcription factor A)의 mRNA 발현이 유의하게 증가하였다. 하지만 자식작용 표지제인 LC3(microtubule-associated proteinl light chain 3)의 mRNA 발현은 증가경향을 나타냈지만 유의하지 않았다. 한편 C2C12 근세포에서도 AICAR 처치에 의해 PGC-1, mtTFA mRNA 발현이 모두 증가하였지만, 이러한 증가는 LC3 SiRNA에 의해서 억제되지 않는 것으로 나타났다. 이러한 결과들을 통해 자식작용은 AMPK에 의해 조절되는 신호전달 전달체계와는 다른 경로로 미토콘드리아 생합성에 영향을 미칠 것으로 사료된다.

• 한국수정란이식학회지
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• 제31권3호
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• pp.287-291
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• 2016

For evaluating the boar semen quality, sperm motility (MOT) is an important parameter because the movement of spermatozoa indicates active metabolism, membrane integrity and fertilizing capacity. Estrogen receptors 2(ESR2) is involved in estrogen related apoptosis in cell cycle spermatogenesis, but their functions have not been confirmed in pig until now. Therefore, this study was conducted to analyze their association with sperm motility and kinematic characteristics. DNA samples from 105 Duroc pigs with records of semen motility and kinematic characteristics [Total motile spermatozoa (MOT), Curvilinear velocity(VCL), Straight-line velocity(VSL), the ratio between VSL and VCL(LIN), Amplitude of Lateral Head displacement(ALH)] were analyzed. A SNP in coding region of ESR2 g.35547A > G in exon 5 was associated with MOT (p < 0.05) in Duroc population. Therefore, we suggest that the porcine ESR2 gene may be used as a molecular marker for Duroc boar semen quality, although its functional effects were not defined yet. These results might shed new light on the roles of ESR2 in spermatogenesis as candidate gene for boar fertility, but still the lack of association across populations should be considered.

• 한국양식학회지
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• 제15권1호
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• pp.7-13
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• 2002

Since 1993, the White Spot Syndrome Virus (WSSV) disease occurred in China among cultured shrimps resulting in mass mortality. Epizootiological surveys undertaken during the outbreak period of 1993-1994 indicated that all stages of Penaeus chinensis, P. japonicus and P. monodon were infected. Consequent to the transport of contaminated shrimp seedlings and seawater, the disease spread all over the farms of China. The disease was more rapidly transmitted at temperatures above $25^{\circ}C$. Challenge experiments showed the causative agent was highly virulent. White spots appeared on the carapace of both span-taneous and experimentally infected shrimps. Moribund shrimps contained turbid hemolymph, hypertrophied Iymphoid organ and a necrotic mid-gut gland. Electron microscopy showed the presence of viral particles in the gills, stomach, lymphoid organ, and epidermal tissue of the infected shrimp. The visions were slightly ovoid with an envelope and averaged 350 $\times$ 150 nm; nucleocapsids measured 375 $\times$ 157 nm. With discontinuous sucrose gradient of 35, 50 and 60% (w/v), the virus was separated from hemolymph of the infected shrimp. The estimated molecular weight of genomic DNA was 237 Kb with EcoR I, 247 Kb with Hind III and 241kb with Pst I. A total of 9 hybridoma colones secreting monoclonal antibodies (MAbs) were produced from mouse myeloma and spleen cells immunized with WSSV. The immunofluorescence assay of gill tissue showed that the MAbs reacted with diseased but not with healthy shrimp. The MAbs belonged to IgGl, IgG2b subclass and IgM class, all with kappa light Immune-electron-microscopy with colloidal gold marker showed the presence of 5 MAbs epitopes on the envelope and one on the capsid of the virus. Baculoviral mid-gut gland necrosis showed the specificity of the MAbs produced. For diagnosis 5 different methods were selected. Using Kimura primers for PCR, or MAbs for immunoblot, ELISA or FAT method, in situ hybridization was carried out to show the gene. All these methods detected WSSV in the organ samples of the diseased shrimp but not in healthy one.

• BMB Reports
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• 제51권10호
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• pp.508-513
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• 2018

Fibronectin fragments found in the synovial fluid of patients with osteoarthritis (OA) induce the catabolic responses in cartilage. Nuclear high-mobility group protein Box 1 (HMGB1), a damage-associated molecular pattern, is responsible for the regulation of signaling pathways related to cell death and survival in response to various stimuli. In this study, we investigated whether changes induced by 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) in HMGB1 expression influences the pathogenesis of OA via an HMGB1-modulated autophagy signaling pathway. Human articular chondrocytes were enzymatically isolated from articular cartilage. The level of mRNA was measured by quantitative real-time PCR. The expression of proteins was examined by western blot analysis, immnunofluorescence assay, and enzyme-linked immunosorbent assay. Interaction of proteins was evaluated by immunoprecipitation. The HMGB1 level was significantly lower in human OA cartilage than in normal cartilage. Although 29-kDa FN-f significantly reduced the HMGB1 expression at the mRNA and protein levels 6 h after treatment, the cytoplasmic level of HMGB1 was increased in chondrocytes treated with 29-kDa FN-f, which significantly inhibited the interaction of HMGB1 with Beclin-1, increased the interaction of Bcl-2 with Beclin-1, and decreased the levels of Beclin-1 and phosphorylated Bcl-2. In addition, the level of microtubule-associated protein 1 light chain 3-II, an autophagy marker, was down-regulated in chondrocytes treated with 29-kDa FN-f, whereas the effect was antagonized by mTOR knockdown. Furthermore, prolonged treatment with 29-kDa FN-f significantly increased the release of HMGB1 into the culture medium. These results demonstrated that 29-kDa FN-f inhibits chondrocyte autophagy by modulating the HMGB1 signaling pathway.

• Biomolecules & Therapeutics
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• 제22권4호
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• pp.275-281
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• 2014

Autophagy is a series of catabolic process mediating the bulk degradation of intracellular proteins and organelles through formation of a double-membrane vesicle, known as an autophagosome, and fusing with lysosome. Autophagy plays an important role of death-survival decisions in neuronal cells, which may influence to several neurodegenerative disorders including Parkinson's disease. Chebulagic acid, the major constituent of Terminalia chebula and Phyllanthus emblica, is a benzopyran tannin compound with various kinds of beneficial effects. This study was performed to investigate the autophagy enhancing effect of chebulagic acid on human neuroblastoma SH-SY5Y cell lines. We determined the effect of chebulagic acid on expression levels of autophagosome marker proteins such as, DOR/TP53INP2, Golgi-associated ATPase Enhancer of 16 kDa (GATE 16) and Light chain 3 II (LC3 II), as well as those of its upstream pathway proteins, AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR) and Beclin-1. All of those proteins were modulated by chebulagic acid treatment in a way of enhancing the autophagy. Additionally in our study, chebulagic acid also showed a protective effect against 1-methyl-4-phenylpyridinium ($MPP^+$) - induced cytotoxicity which mimics the pathological symptom of Parkinson's disease. This effect seems partially mediated by enhanced autophagy which increased the degradation of aggregated or misfolded proteins from cells. This study suggests that chebulagic acid is an attractive candidate as an autophagy-enhancing agent and therefore, it may provide a promising strategy to prevent or cure the diseases caused by accumulation of abnormal proteins including Parkinson's disease.

• Asian Pacific Journal of Cancer Prevention
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• 제16권17호
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• pp.7513-7516
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• 2015

Background: Pyogenic granuloma is a common non-neoplastic connective tissue proliferation. ICAM-1 and VCAM-1 are vascular adhesion molecules and CD34 is a marker for evaluation of angiogenesis. The purpose of this study was to compare the immunohistochemical expression of ICAM-1, VCAM-1 & CD34 in oral pyogenic granuloma and normal gingiva. Materials and Methods: This study was performed on thirty five formalin-fixed, paraffin embedded samples of gingival pyogenic granuloma. Also we used thirty five paraffined blocks of normal gingiva as control group which were taken from crown lengthening surgery. We employed immunohistochemistry staining for our prepared microscopic slides using monoclonal mouse anti-human antibodies against ICAM-1 (CD54), VCAM-1 (CD106) and CD34. Slides were examined under light microscope and then the mean amount of stained vessels also known as microvascular density (MVD) in highly vascularized areas (hot spots) was measured. Paired t-test and repeated measures ANOVA were used to compare the difference between quantitative variables and Chi-square test for qualitative variables in different groups. Pearson correlation coefficient was used to compare relations between quantitative variables. P<0.05 was considered significant. Results: The mean of MVD for ICAM-1, VCAM-1 and CD34 was significantly higher in pyogenic granuloma than normal gingiva (p<0.001 & p<0.001 & p<0.001, respectively). Expression of CD34 in pyogenic granuloma was significantly higher than ICAM-1 and VCAM-1 (P<0.001). Besides, expression of ICAM-1 in normal gingiva, was significantly lower than two other markers (p<0.001). Conclusions: Regarding the results, it seems that ICAM-1, VCAM-1 and CD34 are useful biomarkers in evaluation of vascular and inflammatory lesions such as gingival pyogenic granuloma and the results indicate the role of these biomarkers in pathogenesis of oral pyogenic granuloma.

• Preventive Nutrition and Food Science
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• 제19권3호
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• pp.145-155
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• 2014

Vascular dementia is characterized by white matter lesions involving the demyelination and activation of astrocytes and microglia. In a previous study, we showed that the supernatant of a laboratory-scale, hot water extract of ground whole wheat (TALE) attenuated white matter injury and astrocytic activation in a rat model of bilateral common carotid artery occlusion (BCCAO). In the present study, we made several modifications to the hot water extraction process to remove starch and enable large-scale production. We used wheat bran (WB), which contains less starch, instead of ground whole wheat. In addition, we removed starch granules with a decanter before hot water extraction. The final product, wheat bran extract (WBE), contained 2.42% arabinose, a surrogate marker of arabinoxylan, which is an active constituent of WBE. Supplementation of the rat model of BCCAO with WBE (400 mg/kg/day) for 33 days attenuated white matter injury, which was assessed by Luxol Fast Blue staining, in the corpus callosum (cc) and optic tract (opt) regions. Attenuation of white matter injury in the opt region was accompanied by improvement of the pupillary light reflex. Immunochemical staining revealed that supplementation with WBE reduced astrocytic activation in the cc and opt regions and reduced microglial activation in the opt region. These findings indicate that supplementation with WBE is effective at attenuating white matter injury accompanied by the inhibition of astrocytic and microglial activation. Therefore, extracts from WB, a cheap by-product of wheat milling, can be developed as a nutraceutical to prevent vascular dementia, a disease for which there is no approved pharmaceutical treatment.

• Journal of Crop Science and Biotechnology
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• 제10권3호
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• pp.193-200
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• 2007

Mungbean plants generally have a relatively close canopy, thus a large amount of self-shading can reduce yield due to poor light penetration. Modification of leaflet type can affect leaf canopy and could alter seed yield. Two multiple leaflet mutants were obtained from gamma-ray irradiation and used to study the mode of inheritance related to leaflet types and to evaluate their agronomic features. The cross between large-heptafoliate leaflet with small-pentafoliate leaflet mutants produce all $F_1$ plants with normal trifoliate leaflets. The $F_2$ plants segregated in leaflet size and leaflet number into a 9:3:3:1 ratio of large-trifoliate: large-heptafoliate: small-pentafoliate: small-heptafoliate plants, suggesting that independent loci control leaflet size and leaflet number. Regarding leaflet number, the $F_2$ population can be classified into normal-trifoliate, small-pentafoliate, large-heptafoliate, and small-heptafoliate at the dihybrid ratio of 9:3:3:1. The gene symbols $N_1,n_1$ and $N_2,n_2$ are proposed to represent leaflet number. Since no plant was found with large-pentafoliate leaflets, we hypothesize that the $N_2$ allele expresses pleiotropic effect on both leaflet number and leaflet size. Another possibility is that an additional locus with S and s alleles controls leaflet size and S is tightly linked with $N_2$. The effect of multifoliate leaflet on yield and yield components was evaluated in four mungbean families each with four leaflet isolines under three environments. Averaging across the families and environments, the normal-trifoliate and large-heptafoliate lines gave higher yield than small pentafoliate and heptafoliate ones. These two large leaflet lines also had higher leaf area per plant than the other multifoliate lines. Therefore, the mungbean lines with a greater leaf area, which were likely to intercept more sunlight, gave greater yield. Three AFLP markers that were found to be linked to number of leaflets per leaf, corresponded to the N1 allele of the smallpentafoliate parent.

• Nuclear Engineering and Technology
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• 제4권4호
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• pp.331-339
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• 1972

트리티움 표지 형광도료의 원료인 고 비방사능의 트리티움 표지 폴리스타이렌을 얻기 위하여 테슬라 방전법, 윌즈바크 노출법, 감마선 조사법, 자외선 조사법 등 여러 방법들을 비교 검토하였다. 테슬라 방전 또는 자외선 조사법으로 얻은 polystyrene-T(G)의 비방사능은 1-l.2mCi/mg로써 다른 방법에 의한 생성물의 값보다 높았다. Polystyrene-T(G)와 ZnS:Cu 형광체를 무게비로 1:4가 되게 혼합하면 광도가 가장 컸다. 30mg의 형광도료 혼합물을 1ml의 바인다(시판 니스 1g을 100m1의 벤젠에 녹인 것)를 써서 바르는 경우 최대 장도는 약 20$\mu$L이었으며 갱내 표지판이나 암실내 광원으로 유효하게 사용될 수 있음을 확인하였다.