• Journal of Nutrition and Health
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• 제25권6호
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• pp.501-510
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• 1992

식이중에 첨가된 coenzyme ${Q}_{10}이 ADR을 투여한 흰쥐의 심근미세구조 변화에 미치는 영향을 검토하기 위하여 ADR 2수준(1.0 및 2.0mg/kg B.W/week)과 coenzyne ${Q}_{10} 3수준(0, 0.1및 0.5g/kg diet)에 의한 6개의 실험군과 basal diet만을 공급하는 대조군을 설정하여 8주간 실험동물을 사육하였다. 체중증가량은 ADR의 투여수준이 높을수록 유의적으로 감소되었으나 coenzyme ${Q}_{10}급여에 의한 회복효과는 나타나지 않았다. 전자현미경을 통한 관찰결과, ADR투여는 심근세포내 미세구조의 변성을 유도함이 확인 되었고 특히 mitochondria를 비롯한 세포기관의 소실 및 파괴를 관찰할 수 있었으나 coenzyne ${Q}_{10}을 미리 급여한 군에서는 그정도가 완화되었다.

• 한국전기전자재료학회:학술대회논문집
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• 한국전기전자재료학회 2009년도 춘계학술대회 논문집
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• pp.35-36
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• 2009

In this work, we demonstrate 800V 4H-SiC power DMOSFETs with several structural alterations to obtain a low threshold voltage ($V_{TH}$) and a high figure of merit ($V_B^2/R_{SP,ON}$). To optimize the device performance, we consider four design parameters; (a) the doping concentration ($N_{CSL}$) of current spreading layer (CSL) beneath the p-base region, (b) the thickness of p-base ($t_{BASE}$), (c) the doping concentration ($N_J$) and width ($W_J$) of a JFET region, (d) the doping concentration ($N_{EPI}$) and thickness ($t_{EPI}$) of epi-layer. These parameters are optimized using 2D numerical simulation and the 4H-SiC DMOSFET structure results in a threshold voltage ($V_{TH}$) below ~3.8V, and high figure of merit ($V_B^2/R_{SP,ON}$>${\sim}200MW/cm^2$) for a power MOSFET in $V_B$-800V range.

• 한국식품영양과학회지
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• 제18권1호
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• pp.62-70
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• 1989

본 실험은 식이중에 첨가된 coenzyme Q10이 adriamycin (ADR)을 투여한 흰쥐의 심근 미세 구조에 미치는 영향을 규명하기 위하여 실시되었다. 실험군은 모두 ADR 2수준(1.0mg/kg B.W./week, 2.0mg/kg B.W./week)과 coenzyme Q10 3수준(무첨가군, 0.1g / kg diet 및 0.5g / kg diet)에 의한 6개의 실험군과 basal diet만을 공급하는 대조군을 설정하였다. 체중증가량은 ADR의 투여수준이 높을수록 유의적으로 감소되었으며 식이효율에 있어서는 고수준의 ADR 투여시에만 대조군에 비하여 감소되었다. 그러나 coenzyme Q10에 의한 회복효과는 나타나지 않았다. 혈장내 CPK 활성도는 ADR투여로 약간 증가되었으나 유의적인 차이는 없었으며 coenzyme Q10 급여에 대한 영향은 나타나지 않았다. 전자현미경을 통해 심장조직의 형태적변화를 살펴본 결과 ADR투여로 인해 심근세포내 미세구조의 변성을 관찰할 수 있었고 특히 mitochondria 의 변형, myofibil을 비롯한 세포 소기관의 소실 및 파괴로 빈 공간이 형성되어 있었으나 coenzyme Q10 급여군에서는 그 정도가 약화되었다. 고수준의 ADR 투여는 mitochondria 의 volume density와 surface density를 크게 감소시켰지만 고수준의 coenzyme Q10 급여에 의해 이러한 감소가 조절되었다.

• Preventive Nutrition and Food Science
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• 제1권1호
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• pp.134-142
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• 1996

Diabetes carries an increased risk of atherosclerotic disease that is not fully explained by known car-diovascular risk factors. There is accumulating evidence that advanced glycation of structural proteins, and oxidation and glycation of circulating lipoproteins, are implicated in the pathogenesis of diabetic ather-osclerosis. Reactions involving glycation and oxidation of proteins and lipids are believed to contribute to atherogenesis. Glycation, the nonenzymatic binding of glucose to protein molecules, can increase the ather-ogenic potential of certain plasma constituents, including low density lipoptotein(LDL). Glycation of LDL is significant increased in diabetic patients compared with normal subjects, even in the presence of good glycemic control. Metabolic abnormalities associated with glycation of LDL include diminished recognition of LDL by the classic LDL receptor; increased covalent binding of LDL in vessel walls ; enhanced uptake of LDL by the macrophages, thus stimulating foam cell formation ; increased platelet aggregation; formation of LDL-immune complexes ; and generation of oxygen free radicals, resulting on oxidative damage to both the lipid and protein components of LDL and to any nearby macromolecules. Oxidized lipoproteins are characterzied by cytotoxicity, potent stimulation of foam cell formation by macrophages, and procoagulant effects. Combined glycation and oxidation, "glycoxidation" occurs when oxidative reactions affect the initial products of glycation, and results in irreversible structural alterations of proteins. Glycoxidation is of greatest significance in long lived proteins such as collagen. In these proteins, glycoxidation products, believed to be atherogenic, accumulate with advancing age : in diabetes, their rate of accumulate is accelerated. Inhibition of glycation, oxidation and glycoxidation may form the basis of future antiaterogenic strategies in both diabetic and nondiabetic individuals.dividuals.

• Integrative Medicine Research
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• 제3권4호
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• pp.204-210
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• 2014

The aim of this review was to understand the effects of ${\beta}$-adrenergic stimulation on oxidative stress, structural remodeling, and functional alterations in the heart and cerebral artery. Diverse stimuli activate the sympathetic nervous system, leading to increased levels of catecholamines. Long-term overstimulation of the ${\beta}$-adrenergic receptor (${\beta}AR$) in response to catecholamines causes cardiovascular diseases, including cardiac hypertrophy, stroke, coronary artery disease, and heartfailure. Although catecholamines have identical sites of action in the heart and cerebral artery, the structural and functional modifications differentially activate intracellular signaling cascades. ${\beta}AR$-stimulation can increase oxidative stress in the heart and cerebral artery, but has also been shown to induce different cytoskeletal and functional modifications by modulating various components of the ${\beta}AR$ signal transduction pathways. Stimulation of ${\beta}AR$ leads to cardiac dysfunction due to an overload of intracellular $Ca^{2+}$ in cardiomyocytes. However, this stimulation induces vascular dysfunction through disruption of actin cytoskeleton in vascular smooth muscle cells. Many studies have shown that excessive concentrations of catecholamines during stressful conditions can produce coronary spasms or arrhythmias by inducing $Ca^{2+}$-handling abnormalities and impairing energy production in mitochondria, In this article, we highlight the different fates caused by excessive oxidative stress and disruptions in the cytoskeletal proteome network in the heart and the cerebral artery in responsed to prolonged ${\beta}AR$-stimulation.

• Membrane and Water Treatment
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• 제15권2호
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• pp.79-88
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• 2024

Modification of Polyvinylidene fluoride (PVDF) hollow fiber membranes (HFMs) characteristics and performance were investigated via post treatment using different oxidants. sodium hypochlorite (NaOCl), hydrogen peroxide (H₂O₂) and potassium persulfate (KPS). Fourier transform infrared (FTIR) and Proton nuclear magnetic resonance (¹H-NMR) results revealed no structural differences after post treatment. Cross-sectional micrographs show finger-like structures at the outer and inner walls of the HFMs and sponge-like structures in middle, where NaOCl and KPS post treated fibers exhibited a decrease in finger-like structures in addition to aggregates appearing on the surface, consequently leading to an increase in the surface roughness (Ra) from 48 nm to 52.8nm and 56 nm, respectively. Hydrogen peroxide post treatment only was observed to decrease the water contact angle from 98° to 81.4°. It was also observed that the elongation at break and the modulus deceased after NaOCl post treatment from 34.5 to 28.5% and from 19.3 Mpa to 16.6 Mpa, respectively. Moreover, pure water flux after H₂O₂ post treatment increased from 87.8 LMH/bar to 113 LMH/bar at 0.45 bar, while no changes were detected for the methylene blue dye rejection (74%) between raw and hydrogen peroxide post treated fibers at the same pressure. According to the findings hydrogen peroxide post treated PVDF HFMs have the most uniform surfaces, with almost no alterations in structural and mechanical properties or porosities with enhanced hydrophilicity and pure water flux maintaining appropriate rejection. Therefore, it is considered an efficient surface modifying agent for UF/NF membranes or low-pressure separators.

• 한국발생생물학회지:발생과생식
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• 제15권3호
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• pp.265-272
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• 2011

It is well known that adipose tissue or body fat has been proved as a crucial component of brain-peripheral axis which can modulate the activities of reproductive hormonal axis in female mammals including rodents and human. Concerning the male reproduction, however, the role of adipose tissue has not been thoroughly studied. The present study was carried out to elucidate the effect of a high-fat (HF) diet on the reproductive system of postpubertal male rats. The HF diet (45% energy from fat, HF group) was applied to male rats from week 8 after birth for 4 weeks. The blood glucose levels, body and tissue weights were measured. Histological studies were performed to assess the structural alterations in the reproductive tissues. To determine the transcriptional changes of reproductive hormone-related genes in hypothalamus and pituitary, total RNAs were extracted and applied to the semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). Body weights (p<0.01) and blood glucose levels (p<0.01) of HF group were significantly higher than those of control animals. Similarly, the weights of epididymis (p<0.05), prostate (p<0.01), seminal vesicle (p<0.01) in HF group were higher than control levels. The weights of testis were not changed. The weights of kidney (p<0.001) and spleen (p<0.01) were significantly higher than control levels while the adrenal and pancreas weights were not changed. There were only slight alterations in the microstructures of accessory sex organs; the shape of luminal epithelial cells in epididymis from HF group were relatively thicker and bigger than those from control animals. In the semi-quantitative RT-PCR studies, the mRNA levels of hypothalamic GnRH (p<0.05) in HF group were significantly higher than those from the control animals. The mRNA levels of kisspeptin in HF group tend to be higher than control levels, the difference was not significant. Unlike the hypothalamic GnRH expression, the mRNA levels of pituitary $LH{\beta}$ and $FSH{\beta}$ were significantly decreased in HF group (p<0.05). The present study indicated that the 4-weeks feeding HF diet during the postpubertal period can alter the hypothalamus-pituitary (H-P) neuroendocrine reproductive system These results suggest that the increased body fat and the altered leptin input might disturb the H-P reproductive hormonal activities in male rats, and the changed activities seem to be responsible for the changes of tissue weights in accessory sex organs.

• 한국미생물생명공학회:학술대회논문집
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• 한국미생물생명공학회 2002년도 학술발표대회
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• pp.18-25
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• 2002

The pikromycin biosynthetic system in Streptomyces venezuleae is unique for its ability to produce two groups of antibiotics that include the 12-membered ring macrolides methymycin and neomethymycin, and the 14-membered ring macrolides narbomycin and pikromycin. The metabolic pathway also contains two post polyketide-modification enzymes, a glycosyltransferase and P450 hydroxylase that have unusually broad substrate specificities. In order to explore further the substrate flexibility of these enzymes a series of hybrid polyketide synthases were constructed and their metabolic products characterized. The plasmid-based replacement of the multifunctional protein subunits of the pikromycin PKS in S. venezuelae by the corresponding subunits from heterologous modular PKSs resulted in recombinant strains that produce both 12- and 14-membered ring macrolactones with predicted structural alterations. In all cases, novel macrolactones were produced and further modified by the DesVII glycosyltransferase and PikC hydroxylase leading to biologically active macrolide structures. These results demonstrate that hybrid PKSs in S. venezuelae can produce a multiplicity of new macrolactones that are modified further by the highly flexible DesVII glycosyltransferase and PikC hydroxylase tailoring enzymes. This work demonstrates the unique capacity of the S. venezuelae pikromycin pathway to expand the toolbox of combinatorial biosynthesis and to accelerate the creation of novel biologically active natural products. The polyketide backbone of rifamycin B is assembled through successive condensation and ${\beta}$-carbonyl processing of the extender units by the modular rifamycin PKS. The eighth module, in the RifD protein, contains nonfunctional DH domain and functional KR domain, which specify the reduction of the ${\beta}$-carbonyl group resulting in the C-21 bydroxyl of rifamycin B. A four amino acid substitution and one amino acid deletion were introduced in the putative NADPH binding motif in the proposed KR domain encoded by rifD. This strategy of mutation was based on the amino acid sequences of the corresponding motif of the KR domain of module 3 in the RifA protein, which is believed dysfunctional, so as to introduce a minimum alteration and retain the reading frame intact, yet ensure loss of function. The resulting strain produces linear polyketides, from tetraketide to octaketide, which are also produced by a rifD disrupted mutant as a consequence of premature termination of polyketide assembly. Much of the structural diversity within the polyketide superfamily of natural products is due to the ability of PKSs to vary the reduction level of every other alternate carbon atom in the backbone. Thus, the ability to introduce heterologous reductive segments such as ketoreductase (KR), dehydratase (DH), and enoylreductase (ER) into modules that naturally lack these activities would increase the power of the combinatorial biosynthetic toolbox. The dehydratase domain of module 7 of the rifamycin PKS, which is predicted to be nonfunctional in view of the sequence of the apparent active site, was replaced with its functional homolog from module 7 of rapamycin-producing polyketide synthase. The resulting mutant strain behaved like a rifC disrupted mutant, i.e., it accumulated the heptaketide intermediate and its precursors. This result points out a major difficulty we have encountered with all the Amycolatopsis mediterranei strain containing hybrid polyketide synthases: all the engineered strains prepared so far accumulate a plethora of products derived from the polyketide chain assembly intermediates as major products instead of just analogs of rifamycin B or its ansamycin precursors.

• The Korean Journal of Physiology and Pharmacology
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• 제5권4호
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• pp.333-342
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• 2001

Adriamycin is a commonly used chemotherapeutic agent for cancer, including acute leukemia, lymphoma, and a number of solid human tumors. However, recent studies have recognized severe cardiotoxicity after an acute dose, which are likely the result of generation of free radicals and lipid peroxidation. Therefore, the clinical uses of adriamycin have been limited. Melatonin, the pineal gland hormone known for its ability to modulate circardian rhythm, has recently been studied in its several functions, including cancer growth inhibition, stimulating the immune system, and acting as an antioxidant and radical scavenging effects. In the present study, we evaluated the effect of melatonin administration on adriamycin-induced cardiotoxicity in rat. Heart slices were prepared using a Stadie-Riggs microtome for the measurement of malondialdehyde (MDA) content used as an index of lipid peroxidation and lactate dehydrogenase (LDH) release as an indicator of lethal cell injury. Serious adriamycin-induced lethality was observed in rat by a single intraperitoneal injection in a dose-dependent manner. A single injection of adriamycin (25 mg/kg, i.p.) induced a lethality rate of 86%, with melatonin (10 mg/kg s.c. for 6 days) treatment reducing the adriamycin-induced lethality rate to 20%. The severe body weight loss caused by adriamycin was also significantly attenuated by melatonin treatment. Treatment of melatonin marked reduced adriamycin-induced the levels of MDA formation and LDH release. A cell damage indicated by the loss of myofibrils, swelling of the mitochondria as well as cytoplasmic vacuolization was seen in adriamycin-treated group. Melatonin attenuated the adriamycin-induced structural alterations. These data provide evidence that melatonin prevents adriamycin-induced cardiotoxicity and might serve as a combination with adriamycin to limit free radical-mediated cardiotoxicity.

• 대한치과보철학회지
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• 제14권1호
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• pp.41-46
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• 1976

The purpose of the current study was to investigate histologic changes in the alveolar bone of the lower molar region subsequent to the loss of their opposite molars, and to characterize chemical alterations by utilization of histochemical procedures. Twenty five rats(Sprague Dawley), approximately 150-200gm body weight, were used in this experiment. In the treated animals, upper molars were removed. The animals were decapitated by groups at the following intervals after teeth removals: 10th, 20th, 50th, 70th and 100th day. The normal, untreated rats were used as controls. The molar region of lower jaw, including the intact alvelar bone and teeth was dissected and specimens were decalcified in 3% formic acid. After the tissues were fully decalcified, the specimens were embedded in celloidin and sectioned in mesiodistal plane. These sections were stained in the following staining methods. Mallory azan stain and hematoxylin-eosin stain were utilized for structural evaluation. Polysaccharides were demonstrated by means of the PAS reaction. Acidmucopolysaccharides were studied by means of the colloidal iron stain. Alloxan-Schiff reaction was used for protein. The results were as follows: 1) In the control animals, bone resorption was noted in the distal alveolar bone proper and bone apposition was shown in the mesial alveolar bone proper. But in the treated animals, bone apposition was observed on the mesial and distal walls of the alveolus and osteoclastic activity was not noted in any walls. 2) Bone apposition was most prominent from the 10th to 20th day after treatment. 3) Appositional growth of cementum along the surface of root was prominent from the 50th to 70th day after treatment. 4) In the area where osteoblastic activity was apparent, osteoblasts were stained strongly in the PAS and alloxan-Schiff reaction. A plastic resorption line showed strong alloxan-Schiff reaction. 5) In the colloidal iron stain, the alveolar wall adjacent to the cementum apposition area was stained more strongly than the other areas.