• 한국산학기술학회논문지
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• 제16권3호
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• pp.2165-2171
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• 2015

최근 생활환경의 개선과 의학기술의 발달로 인해 성인병 질환을 앓고 있는 환자의 경우 병원 입원 치료 보다는 통원치료를 통한 주기적인 약물 복용이 증가하고 있다. 이러한 성인병 환자의 경우 주기적인 약물 치료가 유지되기 위해 복약관리에 보다 많은 관심이 요구되고 있다. 본 논문에서는 환자의 주기적이고 안정적인 복약을 위한 NFC 기반의 u-Drug Cap 을 이용한 복약정보 서비스 시스템을 제안하고 개발된 시스템과 테스트 결과를 기술한다. 개발된 시스템은 성인병을 앓고 있는 환자나 고령 환자의 올바른 복약 지도 및 알람을 통해 약품 미복용 및 오복용 방지함으로써 환자의 건강 유지가 가능할 것으로 기대된다.

• 대한의용생체공학회:의공학회지
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• 제33권4호
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• pp.202-206
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• 2012

In this study, we developed transdermal direct drug delivery device using micro-needle painlessly. We has fabricated micro-needle that is 130 ${\mu}m$ thickness and 250 ${\mu}m$length with 10 ${\mu}m$ spiral groove for rolling down drug. Head part of micro-needle device is composed of 20ea micro-needles, an on-off valve and a protective cap. Glass bottle for containing drug is connected to head part of micro-needle device. We examined the puncture characteristic testing using porcine skin and drug delivery testing using porcine, rat skin with Indian Ink.

• Asian Pacific Journal of Cancer Prevention
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• 제15권10호
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• pp.4331-4338
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• 2014

$N^1$-(2, 5-dimethoxyphenyl)-$N^8$-hydroxyoctanediamide (N25) is a novel SAHA cap derivative of HDACi, with a patent (No. CN 103159646). This invention is a hydroxamic acid compound with a structural formula of $RNHCO(CH_2)6CONHOH$ (wherein R=2, 5dimethoxyaniline), a pharmaceutically acceptable salt which is soluble. In the present study, we investigated the effects of N25 with regard to drug distribution and molecular docking, and anti-proliferation, apoptosis, cell cycling, and $LD_{50}$. First, we designed a molecular approach for modeling selected SAHA derivatives based on available structural information regarding human HDAC8 in complex with SAHA (PDB code 1T69). N25 was found to be stabilized by direct interaction with the HDAC8. Anti-proliferative activity was observed in human glioma U251, U87, T98G cells and human lung cancer H460, A549, H1299 cells at moderate concentrations ($0.5-30{\mu}M$). Compared with SAHA, N25 displayed an increased antitumor activity in U251 and H460 cells. We further analyzed cell death mechanisms activated by N25 in U251 and H460 cells. N25 significantly increased acetylation of Histone 3 and inhibited HDAC4. On RT-PCR analysis, N25 increased the mRNA levels of p21, however, decreased the levels of p53. These resulted in promotion of apoptosis, inducing G0/G1 arrest in U251 cells and G2/M arrest in H460 cells in a time-dependent and dose-dependent manner. In addition, N25 was able to distribute to brain tissue through the blood-brain barrier of mice ($LD_{50}$: 240.840mg/kg). In conclusion, our findings demonstrate that N25 will provide an invaluable tool to investigate the molecular mechanism with potential chemotherapeutic value in several malignancies, especially human glioma.