• Journal of Veterinary Clinics
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• v.9 no.1
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• pp.323-332
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• 1992

The present study was carried out to examine the effect of oviduct epithelium and its conditioned medium on e development of early bovine embryos in vitro. Oocytes obtained from ovarian follicles of slaughtered cows were cultured in TCM199 with 10% fetal calf serum for 22-24hrs and then fertillzed in vitro using frozen-thawed semen treated with BO-caffein, BO-BSA(20mM heparin added). Oviduct epithelium was collected in each stage of the estrus cycle and conditioned medium was the medium in which oviduct epithelium in early luteal stage was cultured. In vitro fertilized bovine embryos of 1～2 cell were co-cultured with oviduct epithelium from different estrus cycles, cultured in conditioned medium, and cultured in rabbit oviduct. The cleavage rates of in vitro fertilized early bovine embryos co-cultured with oviduct epithelial cell from early luteal, luteal and follicular phase of estrus cycle(67.2～70.8%) and cultured in conditioned medium(56.7%) were significantly(p<0.05) higher than that of the control(44.2%) The rate of development to morula or blastocyst stage in oviduct epithelial cell co-culture(15.3～32.5%) from three phase of estrus cycles and conditioned medium(14.5%) were significantly(p<0.05) higher than that of the control(5.2%). The oviduct epithelial cell from early luteal phase gave a significantly( p<0.05) higher rate of development to morula or blastocyst stage than both luteal and follicular phase. The results of in vivo culture in rabbit oviduct of early bovine embryos were 52.1% for the cleavage rate and 26.7% for the rate of development to morula or blastocyst stage.

• The Korean Journal of Zoology
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• v.32 no.3
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• pp.290-303
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• 1989

The activities of $\beta$-glucosidase, $\beta$-glucuronidase and N-acetyl-$\beta$-glucosaminidase were measured to investigate the relationships of them to sexual maturity. Peritoneal injections of testosterone and dibutyryl cAMP to rats were carried out. As a result, the activities of $\beta$-glucosidase and N-acetyl-$\beta$-glucosaminidase were significantly decreased from the third day and that of P -glucurondiase on the seventh day in the castrated groups. In addition, ihe activities of these three enzymes were significantly increased in the testosterone treated groups for 7 days. In case of dbcAMP injection, the activities of these three enzymes were similar to those of castrated groups or had a tendency to be decreased. On electron microscopic examination, principal cells, basal cells and narrow cells were observed in all regions of epididymis. Principal cells were general forms of columnar epithelial cells. Narrow cells had a number of small vesicles and light cells showed low electron density in comparison to other epithelial cells in cauda epididymis. Halo cells were migrating leucocytes btween epithelial cells.

• The Korean Journal of Food And Nutrition
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• v.25 no.1
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• pp.64-68
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• 2012

It has been suggested that Helicobacter pylori(H. pylori) infections can promote the development and progression of gastric cancer through the modulation of cell cycle regulators such as $p27^{Kip1}$ and Skp2. $p27^{Kip1}$ is a cyclin-dependent kinase (CDK) inhibitor that blocks the G1/S transition necessary for cell cycle progression. Skp2 is a component of the ubiquitin ligase complex called $SCF^{Skp2}$(SKP1-Cullin-F-box), which specifically binds and promotes the degradation of $p27^{Kip1}$. A low level of $p27^{Kip1}$ and a high level of Skp2 have been reported in many types of cancers, including gastric cancer. In addition, a decrease in $p27^{Kip1}$ has been reported in H. pylori-infected specimens. However, data on Skp2 in H. pylori infections are limited. This study examines the changes in the status of Skp2 in H. pylori-infected gastric epithelial AGS cells. For this, we stimulated AGS cells with H. pylori(NCTC 11637) at the ratio of 300:1(bacterium:cell) for 6 hours. The results of an immunoprecipitation analysis, followed by a western blot, indicate that the interaction between Skp2 and 14-3-3 was elevated 3 hours after the H. pylori treatment. In addition, there was an increase in cytoplasmic Skp2 after 3 hours, whereas there was no change in the nuclear level. Since it has been reported that interaction with 14-3-3 and the subsequent cytoplasmic translocation of Skp2 can increase its protein stability, increases in the interaction with 14-3-3 and the cytoplasmic Skp2 after the H. pylori treatment can increase the level of Skp2 in AGS cells. This phenomenon may explain, at least to some extent, the mechanism underlying the relationship between H. pylori infections and gastric carcinogenesis.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.10
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• pp.5579-5587
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• 2013

Research indicates that a small population of cancer cells is highly tumorigenic, endowed with the capacity for self-renewal, and has the ability to differentiate into cells that constitute the bulk of tumors. These cells are considered the "drivers" of the tumorigenic process in some tumor types, and have been named cancer stem cells (CSC). Epithelial-mesenchymal transition (EMT) appears to be involved in the process leading to the acquisition of stemness by epithelial tumor cells. Through this process, cells acquire an invasive phenotype that may contribute to tumor recurrence and metastasis. CSC have been identified in human head and neck squamous cell carcinomas (HNSCC) using markers such as CD133 and CD44 expression, and aldehyde dehydrogenase (ALDH) activity. Head and neck cancer stem cells reside primarily in perivascular niches in the invasive fronts where endothelial-cell initiated events contribute to their survival and function. Clinically, CSC enrichment has been shown to be enhanced in recurrent disease, treatment failure and metastasis. CSC represent a novel target of study given their slow growth and innate mechanisms conferring treatment resistance. Further understanding of their unique phenotype may reveal potential molecular targets to improve therapeutic and survival outcomes in patients with HNSCC. Here, we discuss the state-of-the-knowledge on the pathobiology of cancer stem cells, with a focus on the impact of these cells on head and neck tumor progression, metastasis and recurrence due to treatment failure.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.3
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• pp.781-784
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• 2012

The aim of this study was to evaluate the effect of the adenovirus-mediated double suicide gene (CD/TK) for selective killing of gastric cancer cells. Gastric cancer cells SCG7901 and normal gastric epithelial cell lines were infected by adenoviruses Ad-survivin/GFP and Ad-survivin/CD/TK. GFP expression and CD-TK were detected by fluorescence microscopy and reverse transcriptase polymerase chain reaction (RT-PCR), respectively. After treatment of the infected cells with the pro-drugs ganciclovir (GCV) and/or 5-FC, the cell growth status was evaluated by methyl thiazolyl tetrazolium assay. Cell cycle changes were detected using flow cytometry. In nude mice bearing human gastric cancer, the recombinant adenovirus vector was injected directly into the tumor followed by an intraperitoneal injection of GCV and/or 5-FC. The subsequent tumor growth was then observed. The GFP gene driven by survivin could be expressed within the gastric cancer line SCG7901, but not in normal gastric epithelial cells. RT-PCR demonstrated the presence of the CD/TK gene product in the infected SCG7901 cells, but not in the infected normal gastric epithelial cells. The infected gastric cancer SCG7901, but not the gastric cells, was highly sensitive to the pro-drugs. The CD/TK fusion gene system showed significantly greater efficiency than either of the single suicide genes in killing the target cells (P<0.01). Treatment of the infected cells with the pro-drugs resulted in increased cell percentage in G0-Gl phase and decreased percentage in S phase. In nude mice bearing SCG7901 cells, treatment with the double suicide gene system significantly inhibited tumor growth, showing much stronger effects than either of the single suicide genes (P<0.01). The adenovirus-mediated CD/TK double suicide gene driven by survivin promoter combined with GCV an 5-FC treatment could be an effective therapy against experimental gastric cancer with much greater efficacy than the single suicide gene CD/TK combined with GCV or 5-FC.

• Parasites, Hosts and Diseases
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• v.61 no.1
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• pp.2-14
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• 2023

Trichomonas vaginalis is a flagellated protozoan that causes trichomoniasis, a common nonviral sexually transmitted infection. T. vaginalis infection is asymptomatic in most infected men but can lead to chronic infection. The inflammatory response to chronic T. vaginalis infection may contribute to prostatic diseases, such as prostatitis and benign prostatic hyperplasia (BPH); however, studies on the relationship between T. vaginalis infection and prostate diseases are scarce. In this review, we discuss evidence from our studies on the involvement of T. vaginalis in the pathogenesis of prostate diseases, such as prostatitis and BPH. Studies of prostatitis have demonstrated that the attachment of T. vaginalis trophozoite to prostate epithelial cells (PECs) induces inflammatory cytokine production and inflammatory cell migration, leading to prostatitis. T. vaginalis also causes pathological changes, such as inflammatory cell infiltration, acinar changes, interstitial fibrosis, and mast cell infiltration, in prostate tissues of infected rats. Thus, T. vaginalis is considered an infectious agent that triggers prostatitis. Meanwhile, studies of prostatic hyperplasia revealed that mast cells activated by T. vaginalis-infected prostate cells secreted inflammatory mediators, such as β-hexosaminidase and tryptase, which promoted proliferation of prostate stromal cell (PSC). Moreover, interleukin-6 produced by proliferating PSCs induced the multiplication of BPH-1 epithelial cells as a result of stromal-epithelial interaction, suggesting that the proliferation of T. vaginalis-infected prostate cells can be induced through crosstalk with mast cells. These collective findings suggest that T. vaginalis contributes to the progression of prostatitis and prostatic hyperplasia by creating an inflammatory microenvironment involving PECs and PSCs.

• Journal of fish pathology
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• v.36 no.2
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• pp.415-422
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• 2023

In veterinary medicine for mammals, studies are being conducted to confirm the effects of antioxidants using pathological toxicity model studies, and are also used to confirm the effect of mitigating liver or kidney toxicity of specific substances. It was considered necessary to study such a toxicity model for domestic farmed fish, so thioacetamide (TAA), a toxic substance that causes tissue damage by mitochondrial dysfunction, was injected into rainbow trout (Oncorhynchus mykiss), a major farmed freshwater fish species in Korea. The experiment was conducted with 40 rainbow trout (Oncorhynchus mykiss) weighting 53 ± 0.6 g divided into two groups. Thioacetamide(TAA) 300mg/kg of body weight was intraperitoneally injected into rainbow trout and samples were taken 1, 3, 5, 7 days after peritoneal injection. As a result, in serum biochemical analysis, AST levels related to liver function decreased 3 and 5 days after intraperitoneal injection and increased after 7 days, and ALT levels also increased after 7 days. In addition, creatinine related to renal malfunction increased 3 and 5 days after TAA injection. In histopathological analysis, pericholangitis and local lymphocyte infiltration were observed in the liver from 1 day after intraperitoneal injection of TAA, and hepatic parenchymal cell necrosis was also observed from 3 days after intraperitoneal injection. Hyaline droplet in renal tubular epithelial cell was observed from 1 day after TAA injection, and acute tubular damage such as tubular epithelial cell necrosis appeared from 3 days after TAA injection. Accordingly, it is thought that it will be able to contribute to studies that require a toxicity model.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.142-142
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• 2002

Many studies have identified the phosphatidylinositol 3-kinase (PI3K) as a key regulator for various cellular functions including cell survival, growth and motility. We have previously shown that H-ras, but not N-ras, induces invasiveness and motility in human breast epithelial cells (MCF10A), while both H-ras and N-ras induce transformed phenotype.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.141-141
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• 2003

Ras expression has been suggested as a marker for tumor aggressiveness of breast cancer, including the degrees of invasion and tumor recurrence. We previously showed that p38 MAPK is a key signaling molecule differentially regulated by H-ras and N-ras, leading to H-ras-specific cell invasive and migrative phenotypes in human breast epithelial cells (Cancer Res.: 63, 5454-5461, 2003).(omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.153.2-154
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• 2003

Extracts of Artemisia asiatica Nakai (Asteraceae) possess anti-inflammatory and anti-oxidative activities. Eupatilin (5,7-dihydroxy-3,4,6-tri-methoxy-flavone), one of the pharmacologically active ingredients derived from Artemisia asiatica, was shown to induce apoptosis in human promyelocytic leukemia (HL-60) cells (H.-J. Seo and Y.-J. Surh, Mutat. Res., 496, 191-198, 2001). In the present study, we examined the cytostatic effects of eupatilin in H-ras-transformed human breast epithelial (MCF10A-ras) cells. (omitted)