• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
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• pp.98-98
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• 2003

${\beta}$-(1,3)-D-Glucans have been known to exhibit antitumor and antimicrobial activities. The presence of dectin-1,${\alpha}$, ${\beta}$-glucan receptor of dendritic cell, on macrophage has been controvertial. RT-PCR analysis led to the detection of dectin-1${\alpha}$ and ${\beta}$ in murine macrophage Raw264.7 cell line. Among the various organs of mouse, dectin-1${\alpha}$ and ${\beta}$ were detected in the thymus, lung, spleen, stomach and intestine. To analyze gene expression modulated by ${\beta}$-glucan treated murine Raw264.7 macrophage, total mRNA was applied to cDNA microarray to interrogate the expression of 7,000 known genes. cDNA chip analysis showed that ${\beta}$-glucan of P. osteatus increased gene expressions of immunomodulating genes, membrane antigenic proteins, chemokine ligands, complements, cytokines, various kinases, lectin associated genes and oncogenes in Raw 264.7 cell line. When treated with ${\beta}$-glucan of P. osteatus and LPS, induction of gene expression of TNF-${\alpha}$ and IFN-R1 was confirmed by RT-PCR analysis. Induction of TNF-R type II expression was confirmed by FACS analysis. IL-6 expression was abolished by EDTA in ${\beta}$-glucan and LPS treated Raw264.7 cell line, indicating that ${\beta}$-glucan binds to dectin-l in a Ca$\^$＋＋/ -dependent manner. To increase antitumor efficacy of ${\beta}$-glucan, ginsenoside Rh2 (GRh2) was co-treated with ${\beta}$-glucan in vivo and in vitro tests. IC$\sub$50/ values of GRh2 were 20 and 25 $\mu\textrm{g}$/$m\ell$ in SNU-1 and B16 melanoma F10 cell line, respectively. Co-treatment with ${\beta}$-glucan and GRh2 showed synergistic antitumor activity with cisplatin and mitomycin C both in vitro and in vivo. Single or co-treatment with ${\beta}$-glucan and GRh2 increased tumor bearing mouse life span. Co-treatment with ${\beta}$-glucan and GRh2 showed more increased life span with mitomycin C than that with cisplatin. Antitumor activities were 67% and 72 % by co-injection with ${\beta}$-glucan and GRh2 in the absence or presence of mitomycin C, respectively.

• 마이크로전자및패키징학회지
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• 제19권1호
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• pp.47-53
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• 2012

무연 리플로우 공정 횟수에 따른 organic solderability preservative(OSP) 표면처리 두께변화 및 열화현상을 분석하였다. 무연솔더 접합부의 접합강도에 미치는 OSP 표면처리의 열화특성을 SnPb 표면처리 경우와 비교하여 조사하였다. 또한 리플로우 pass에 따른 무연솔더 접합강도 열화분석을 위해 OSP 및 SnPb 표면처리된 FR-4 재질 PCB를 각각 1-6회 리플로우 처리하였다. 이후 각 리플로우를 거친 PCB 위에 2012 칩 저항기를 실장한 후 접합강도 변화를 측정하였다. 그 결과, 리플로우 공정 중 열 노출에 의해 OSP 코팅두께가 감소되는 것이 관찰되었고, 코팅두께의 변화 및 OSP 코팅 층의 산화를 유발함으로써, 솔더의 젖음성이 감소될 수 있음을 확인할 수 있었다. OSP 열화에 따른 솔더 접합강도는 SnPb 표리처리시 평균 62.2 N 이였으며, OSP의 경우는 약 58.1 N 이였다. 리플로우 공정 노출에 따라 OSP 코팅 층은 열분해 되지만, 솔더 접합부의 접합강도 측면에서는 산업적으로 적용 가능성을 확인할 수 있었다.

• Oncology Letters
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• 제41권6호
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• pp.3464-3474
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• 2019

The EF-hand calcium binding protein tescalcin (TESC) is highly expressed in various human and mouse cancer tissues and is therefore considered a potential oncogene. However, the underlying mechanism that governs TESC expression remains unclear. Emerging evidence suggests that TESC expression is under epigenetic regulation. In the present study, the relationship between the epigenetic modification and gene expression of TESC in gastric cancer was investigated. To evaluate the relationship between the methylation and expression of TESC in gastric cancer, the methylation status of CpG sites in the TESC promoter was analyzed using microarray with the Illumina Human Methylation27 BeadChip (HumanMethylation27_270596_v.1.2), gene profiles from the NCBI Dataset that revealed demethylated status were acquired, and real-time methylation-specific PCR (MSP) in gastric cancer cells was conducted. In the present study, it was demonstrated that the hypermethylation of TESC led to the downregulation of TESC mRNA/protein expression. In addition, 5-aza-2c-deoxycytidine (5'-aza-dC) restored TESC expression in the tested gastric cancer cells except for SNU-620 cells. ChIP assay further revealed that the methylation of the TESC promoter was associated with methyl-CpG binding domain protein (MBD)1, histone deacetylase (HDAC)2, and Oct-1 and that treatment with 5'-aza-dC facilitated the dissociation of MBD1, HDAC2, and Oct-1 from the promoter of TESC. Moreover, silencing of TESC increased MBD1 expression and decreased the H3K4me2/3 level, thereby causing transcriptional repression and suppression of cell survival in NCI-N87 cells; conversely, overexpression of TESC downregulated MBD1 expression and upregulated the H3K4me2 level associated with active transcription in SNU-638 cells. These results indicated that the differential expression of TESC via the modification status of the promoter and histone methylation controled cell survival in gastric cancer cells. Overall, the present study provided a novel therapeutic strategy for gastric cancer.