• The Plant Pathology Journal
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• 제33권6호
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• pp.602-607
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• 2017

Segregation and condensation protein B (ScpB) is essential for replication and segregation in living organisms. Here, we reported the functions of ScpBXv (ScpB-like protein in Xanthomonas campestris pv. vesicatoria) using phenotypic and proteomic analyses. Growth of $Xcv{\Delta}scpBXv$ (ScpBXv knockout mutant) was reduced under both slow and fast growth conditions in rich medium, but comparable to this of the wild-type in plant-mimic conditions. Interestingly, the mutant was significantly less virulent than the wild-type in tomato, indicating that ScpBXv is involved in virulence. To investigate ScpBXv-associated mechanisms, comparative proteomic analyses were carried out and the abundance of 187 proteins was altered. Among them, diverse transcriptional regulators involved in biofilm formation and virulence were abundant in the wild-type. We further showed that biofilm formation of $Xcv{\Delta}scpBXv$ was reduced. This study provides new insights into the functions of ScpBXv in bacterial replication and biofilm formation, which may contribute to the virulence of Xcv.

• 대한약침학회지
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• 제20권3호
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• pp.207-212
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• 2017

Objectives: Study of the mechanisms involved in cancer progression suggests that cyclooxygenase enzymes play an important role in the induction of inflammation, tumor formation, and metastasis of cancer cells. Thus, cyclooxygenase enzymes could be considered for cancer chemotherapy. Among these enzymes, cyclooxygenase 2 (COX-2) is associated with liver carcinogenesis. Various COX-2 inhibitors cause growth inhibition of human hepatocellular carcinoma cells, but many of them act in the COX-2 independent mechanism. Thus, the introduction of selective COX-2 inhibitors is necessary to achieve a clear result. The present study was aimed to determine the growth-inhibitory effects of new analogues of chalcone epoxide as selective COX-2 inhibitors on the human hepatocellular carcinoma (HepG2) cell line. Methods: Estimation of both cell growth and the amount of prostaglandin E2 (PGE2) production were used to study the effect of selective COX-2 inhibitors on the hepatocellular carcinoma cell. Cell growth determination has done by MTT assay in 24 h, 48 h and 72 h, and PGE2 production has estimated by using ELYSA kit in 48 h and 72 h. Results: The results showed growth inhibition of the HepG2 cell line in a concentration and time-dependent manner, as well as a reduction in the formation of PGE2 as a product of COX-2 activity. Among the compounds those analogues with methoxy and hydrogen group showed more inhibitory effect than others. Conclusion: The current in-vitro study indicates that the observed significant growth-inhibitory effect of chalcone-epoxide analogues on the HepG2 cell line may involve COX-dependent mechanisms and the PGE2 pathway parallel to the effect of celecoxib. It can be said that these analogues might be efficient compounds in chemotherapy of COX-2 dependent carcinoma specially preventing and treatment of hepatocellular carcinomas.

• 한국입자에어로졸학회지
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• 제6권1호
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• pp.1-7
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• 2010

Generally, large amounts of DOP(Di-Octyl Phthalate) chemicals are used as plasticizers in PVC compound manufacturing processes. However, it is very important to collect DOP species immediately from a workplace in order to protect worker's heath and recover them. To accomplish these objectives, we need to understand the droplet formation and growth mechanisms of DOP species. In this study, two important parameters such as temperature gradient and residence time were considered to clarify these mechanisms. We found that residence time is very critical to determine the droplet size distribution of DOP, whereas temperature gradient in general operating conditions(less than $-6.8^{\circ}C/cm$) is negligible.

• 한국결정성장학회지
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• 제8권3호
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• pp.454-462
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• 1998

AUC 침전과정중 AUC 입차를 둥글게 제조하는 조건과 기구를 조사하였다. 둥근 AUC 제조는 교반기를 이용한 내부순환 시는 불가능했으나 펌프를 사용한 외부순환 시는 가능했다. 둥근 AUC 제조속도($dn_p$/dt)는 침전조건인 슬러리 밀도($M_t:U/l)$, 슬러리 회전율($T_o$:turn-over ratio), 임펠러 속도(U:Impelle tip velocity)에 비례하여 관계식을 $ dn_p/dt{\propto}M_t{\cdot}T_o{\cdot}U^2$로 표기할 수 있었으며, 이 속도식은 실험결과와 정성적으로 일치하였다. 그리고 두 개의 둥근 AUC 제조 기구가 제시되었는데, 하나는 균일형성기구이고 다른 하나는 etch-pit 형성기구이다. 전자는 AUC 침전과정에서 초기에 발생되고 후자는 침전과정 말기에 발생되는 것으로 확인되었다.

• 한국세라믹학회지
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• 제36권6호
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• pp.655-661
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• 1999

${\beta}$-SiC formation mechanism in Si melt-C-SiC system with varying in size of carbon source was investigated. A continuous reaction sintering process using Si melt infiltration method was adopted to control the reaction sintering time effectively. It was found that ${\beta}$-SiC formation mechanism in Si melt-C-SiC system was directly affected by the size of carbon source. In the Si melt-C-SiC system with large carbon source ${\beta}$-SiC formation mechanism could be divided into two stages depending on the reaction sintering time: in early stage of reaction sintering carbon dissolution in Si melt and precipitation of ${\beta}$-SiC was occurred preferentially and then SIC nucleation and growth was controlled by diffusion of carbon throughy the ${\beta}$-SiC layer formed on graphite particle. Furthmore a dissolution rate of graphite particles in Si melt could be accelerated by the infiltration of Si melt through basal plane of graphite crystalline.

• Biomolecules & Therapeutics
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• 제31권4호
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• pp.456-465
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• 2023

Cervical tumors represent a prevalent form of cancer affecting women worldwide; current treatment options involve surgery, radiotherapy, and chemotherapy. Angiogenesis, the process of new blood vessel formation, is a crucial factor in cervical tumor growth. The molecular mechanisms underlying the effects of the liver kinase B1 (LKB1/STK11) tumor suppressor protein on tumor angiogenesis have not been elucidated. Therefore, we investigated the role of LKB1 in cervical tumor angiogenesis both in vitro and in vivo in this study. Our results demonstrated that LKB1 inhibited cervical tumor angiogenesis by suppressing the expression of angiogenesis-related factors such as vascular endothelial growth factor (VEGF) and hypoxia inducible factor-1α. LKB1 directly affected both carcinoma and vascular endothelial cells, resulting in a significant reduction in tumor growth and angiogenesis. Furthermore, LKB1 was found to bind to VEGF receptor 2 (VEGFR-2) and target the VEGFR-2-mediated protein kinase B/mechanistic target of rapamycin signaling pathway in endothelial cells, thereby reducing cervical tumor growth and angiogenesis. Our study provides new insights into the molecular mechanisms underlying the anti-tumor and anti-angiogenic effects of LKB1 in cervical cancer. These findings will help develop new therapeutic strategies for cervical cancer.

• 한국어업기술학회:학술대회논문집
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• 한국어업기술학회 2000년도 춘계수산관련학회 공동학술대회발표요지집
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• pp.90-91
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• 2000

The physiological systems that control blood fluidity are both complex and elegant. Blood must remain fluid within the vasculature and yet clot quickly when exposed to nonendothelial surfaces at sites of vascular injury. There are two principle mechanisms to control a delicate balance in higher organisms (Davie & Ratnoff, 1964). Present evidence suggests that the intrinsic pathway play an important role in the growth and maintenance of fibrin formation in the coagulation cascade while a second overlapping mechanism, called the extrinsic pathway, is critical in the initiation of fibrin formation. Coagulation factors is in two mechanisms, and in order to clot blood, they are activated by a cooperation with $Ca^{2+}$, phospholipid and vitamin K etc. For example, the human placental anticoagulant protein (PAP of PAP- I), which is a $Ca^{2+}$ -dependent phospholipid binding protein (Funakoshi et al., 1987) inhibited the activity of factor Xa, so that it prolonged fibrin formation. We wondered whether any other protein was involved in regulation of the coagulant system as an anticoagulant protein from natural organisms. Natural agents would have not harmful side-effects in comparision with chemically synthesized materials such as warfarin, aspirin, phenindione, etc.. But anticoagulant agents from natural, especially marine organisms have hardly been researched except for polysaccharides from marine algae. (omitted)

• Asian Pacific Journal of Cancer Prevention
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• 제14권10호
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• pp.6089-6094
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• 2013

Berberine, a common isoquinoline alkaloid, has been shown to possess anti-cancer activities. However, the underlying molecular mechanisms are still not completely understood. In the current study, we investigated the effects of berberine on cell growth, colony formation, cell cycle distribution, and whether it improved the anticancer efficiency of cisplatin and doxorubicin in human breast cancer estrogen receptor positive (ER+) MCF-7 cells and estrogen receptor negative (ER-) MDA-MB-231 cells. Notably, berberine treatment significantly inhibited cell growth and colony formation in the two cell lines, berberine in combination with cisplatin exerting synergistic growth inhibitory effects. Accompanied by decreased growth, berberine induced G1 phase arrest in MCF-7 but not MDA-MB-231 cells. To provide a more detailed understanding of the mechanisms of action of berberine, we performed genome-wide expression profiling of berberine-treated cells using cDNA microarrays. This revealed that there were 3,397 and 2,706 genes regulated by berberine in MCF-7 and MDA-MB-231 cells, respectively. Fene oncology (GO) analysis identified that many of the target genes were involved in regulation of the cell cycle, cell migration, apoptosis, and drug responses. To confirm the microarray data, qPCR analysis was conducted for 10 selected genes based on previously reported associations with breast cancer and GO analysis. In conclusion, berberine exhibits inhibitory effects on breast cancer cells proliferation, which is likely mediated by alteration of gene expression profiles.

• 한국표면공학회지
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• 제34권5호
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• pp.455-464
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• 2001

Effect of bombardment of the growing film by energetic particles on its properties is know over many years and is widely used for modification of the film properties. Despite of this there are no final answers on such questions as: what is the mechanism of compositional changes that take place for some compound films deposited under the ion bombardment, how the ion bombardment influences the epitaxial growth, what mechanisms govern the growth of the film on its early stages during deposition under the ion bombardment. The role of composition of film-forming species in formation of film structure is barely investigated or even not investigated at all. Experimental evidence and discussion of the influence of ion bombardment and composition of film-forming species on structure and composition of compound films are briefly considered in the review.

• Preventive Nutrition and Food Science
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• 제19권4호
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• pp.299-306
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• 2014

Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of hesperetin are not fully understood. In the present study, we evaluated whether hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs). HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of hesperetin (25, 50, and $100{\mu}M$) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs (P<0.05). Moreover, hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, hesperetin also suppressed microvessel sprouting of mouse aortic rings. Taken together, the findings suggest that hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling.