http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Arash Minai-Tehrani,Young-Chan Park,Soon-Kyung Hwang,Jung-Taek Kwon,장승희,Sung-Jin Park,유경남,김지은,Ji-Young Shin,Ji-Hye Kim,Bitna Kang,Seong-Ho Hong,조명행 대한수의학회 2011 Journal of Veterinary Science Vol.12 No.4
Conventional lung cancer therapies are associated with poor survival rates; therefore, new approaches such as gene therapy are required for treating cancer. Gene therapies for treating lung cancer patients can involve several approaches. Among these, aerosol gene delivery is a potentially more effective approach. In this study, Akt1 kinase-deficient (KD) and wild-type (WT) Akt1 were delivered to the lungs of CMV-LucR-cMyc-IRES-LucF dual reporter mice through a nose only inhalation system using glucosylated polyethylenimine and naphthalene was administrated to the mice via intraperitoneal injection. Aerosol delivery of Akt1 WT and naphthalene treatment increased protein levels of downstream substrates of Akt signaling pathway while aerosol delivery of Akt1 KD did not. Our results showed that naphthalene affected extracellular signal-regulated kinase (ERK) protein levels, ERK-related signaling, and induced Clara cell injury. However, Clara cell injury induced by naphthalene was considerably attenuated in mice exposed to Akt1 KD. Furthermore, a dual luciferase activity assay showed that aerosol delivery of Akt1 WT and naphthalene treatment enhanced cap-dependent protein translation, while reduced cap-dependent protein translation was observed after delivering Akt1 KD. These studies demonstrated that our aerosol delivery is compatible for in vivo gene delivery.
Suppression of A549 lung cancer cell migration by precursor let-7g microRNA.
Park, Sungjin,Minai-Tehrani, Arash,Xu, Cheng-Xiong,Chang, Seung-Hee,Woo, Min-Ah,Noh, Mi-Suk,Lee, Eun-Sun,Lim, Hwang-Tae,An, Gil-Hwan,Lee, Kee-Ho,Sung, Ha-Jung,Beck, George R,Cho, Myung-Haing D. A. Spandidos 2010 MOLECULAR MEDICINE REPORTS Vol.3 No.6
<P>Let-7g miRNAs, short non-coding RNAs approximately 21 nucleotides long, repress protein translation by binding to the 3'UTR of target mRNAs. Aberrant expression of let-7g is associated with the poor prognosis of lung cancer patients. Compared to normal lung cells, let-7g expression is absent in non-small cell lung cancer (NSCLC) cells. Furthermore, K-Ras and HMGA2 are well known as targets of let-7g. In this study, we evaluated the potential role of precursor (pre)-let-7g in lung cancer cell metastasis, focusing on the two targets of let-7g, HMGA2 and K-Ras. We found that pre-let-7g inhibited the migration of A549 lung cancer cells through HMGA2-mediated E2F1 down-regulation. Thus, our results suggest that pre-let-7g could be used as a suitable target for the suppression of lung cancer cell migration.</P>
Acute Pulmonary Toxicity and Body Distribution of Inhaled Metallic Silver Nanoparticles
Kwon, Jung-Taek,Minai-Tehrani, Arash,Hwang, Soon-Kyung,Kim, Ji-Eun,Shin, Ji-Young,Yu, Kyeong-Nam,Chang, Seung-Hee,Kim, Dae-Seong,Kwon, Yong-Taek,Choi, In-Ja,Cheong, Yun-Hee,Kim, Jun-Sung,Cho, Myung-Ha Korean Society of ToxicologyKorea Environmental Mu 2012 Toxicological Research Vol.28 No.1
The purpose of this study was to determine the acute pulmonary toxicity of metallic silver nanoparticles (MSNPs, 20.30 nm in diameter). Acute pulmonary toxicity and body distribution of inhaled MSNPs in mice were evaluated using a nose-only exposure chamber (NOEC) system. Bronchoalveolar lavage (BAL) fluid analysis, Western blotting, histopathological changes, and silver burdens in various organs were determined in mice. Mice were exposed to MSNPs for 6 hrs. The mean concentration, total surface area, volume and mass concentrations in the NOEC were maintained at $1.93{\times}10^7$ particles/$cm^3$, $1.09{\times}10^{10}\;nm^2/cm^3$, $2.72{\times}10^{11}\;nm^3/cm^3$, and 2854.62 ${\mu}g/m^3$, respectively. Inhalation of MSPNs caused mild pulmonary toxicity with distribution of silver in various organs but the silver burdens decreased rapidly at 24-hrs post-exposure in the lung. Furthermore, inhaled MSNPs induced activation of mitogen-activated protein kinase (MAPK) signaling in the lung. In summary, single inhaled MSNPs caused mild pulmonary toxicity, which was associated with activated MAPK signaling. Taken together, our results suggest that the inhalation toxicity of MSNPs should be carefully considered at the molecular level.
Acute Pulmonary Toxicity and Body Distribution of Inhaled Metallic Silver Nanoparticles
Jung-Taek Kwon,Arash Minai-Tehrani,Soon-Kyung Hwang,Ji-Eun Kim,Ji-Young Shin,Kyeong-Nam Yu,Seung-Hee Chang,Dae-Seong Kim,Yong-Taek Kwon,In-Ja Choi,Yun-Hee Cheong,Jun Sung Kim,Myung-Haing Cho 한국독성학회 2012 Toxicological Research Vol.28 No.1
The purpose of this study was to determine the acute pulmonary toxicity of metallic silver nanoparticles (MSNPs, 20.30 ㎚ in diameter). Acute pulmonary toxicity and body distribution of inhaled MSNPs in mice were evaluated using a nose-only exposure chamber (NOEC) system. Bronchoalveolar lavage (BAL) fluid analysis, Western blotting, histopathological changes, and silver burdens in various organs were determined in mice. Mice were exposed to MSNPs for 6 hrs. The mean concentration, total surface area, volume and mass concentrations in the NOEC were maintained at 1.93 × 10? particles/㎤, 1.09 × 10<SUP>10</SUP> ㎚²/㎤, 2.72 × 10<SUP>11</SUP> ㎚³/㎤, and 2854.62 ㎍/㎥, respectively. Inhalation of MSPNs caused mild pulmonary toxicity with distribution of silver in various organs but the silver burdens decreased rapidly at 24-hrs post-exposure in the lung. Furthermore, inhaled MSNPs induced activation of mitogen-activated protein kinase (MAPK) signaling in the lung. In summary, single inhaled MSNPs caused mild pulmonary toxicity, which was associated with activated MAPK signaling. Taken together, our results suggest that the inhalation toxicity of MSNPs should be carefully considered at the molecular level.
Kim, You-Kyoung,Minai-Tehrani, Arash,Lee, Jae-Ho,Cho, Chong-Su,Cho, Myung-Haing,Jiang, Hu-Lin Dove Medical Press 2013 International journal of nanomedicine Vol.8 No.-
<P><B>Background</B></P><P>Chitosan and chitosan derivatives have been proposed as alternative and biocompatible cationic polymers for nonviral gene delivery. However, the low transfection efficiency and low specificity of chitosan is an aspect of this approach that must be addressed prior to any clinical application. In the present study, folated poly(ethylene glycol)-chitosan-graft-polyethylenimine (FPCP) was investigated as a potential folate receptor-overexpressed cancer cell targeting gene carrier.</P><P><B>Methods</B></P><P>The FPCP copolymer was synthesized in two steps. In the first step, folate-PEG was synthesized by an amide formation reaction between the activated carboxyl groups of folic acid and the amine groups of bifunctional poly(ethylene glycol) (PEG). In the second step, FPCP was synthesized by an amide formation reaction between the activated carboxyl groups of folate-PEG and amine groups of CHI-g-polyethyleneimine (PEI). The composition of FPCP was characterized by 1H nuclear magnetic resonance.</P><P><B>Results:</B></P><P>FPCP showed low cytotoxicity in various cell lines, and FPCP-DNA complexes showed good cancer cell specificity as well as good transfection efficiency in the presence of serum. Further, FPCP-<I>Pdcd4</I> complexes reduced tumor numbers and progression more effectively than PEI 25 kDa in H-<I>ras</I>12V liver cancer mice after intravenous administration.</P><P><B>Conclusion</B></P><P>Our data suggest that FPCP, which has improved transfection efficiency and cancer cell specificity, may be useful in gene therapy for liver cancer.</P>
Shin, Ji-Young,Lim, Hwang-Tae,Minai-Tehrani, Arash,Noh, Mi-Suk,Kim, Ji-Eun,Kim, Ji-Hye,Jiang, Hu-Lin,Arote, Rohidas,Kim, Doo-Yeol,Chae, Chanhee,Lee, Kee-Ho,Kim, Mi-Sook,Cho, Myung-Haing Oxford University Press 2012 Journal of radiation research Vol.53 No.4
<P>Radiotherapy alone has several limitations for treating lung cancer. Inhalation, a non-invasive approach for direct delivery of therapeutic agents to the lung, may help to enhance the therapeutic efficacy of radiation. Up-regulating beclin1, known as a tumor suppressor gene that plays a major role in autophagy, may sensitize tumors and lead to tumor regression in lungs of K-ras<SUP>LA1</SUP> lung cancer model mice. To minimize the side-effects of radiotherapy, fractionated exposures (five times, 24-h interval) with low dose (2 Gy) of radiation to the restricted area (thorax, 2 cm) were conducted. After sensitizing the lungs with radiation, beclin1, complexed with a nano-sized biodegradable poly(ester amine), was prepared and delivered into the murine lung via aerosol three times/week for four weeks. In a histopathological analysis, animals treated with beclin1 and radiation showed highly significant tumor regression and low progression to adenocarcinoma. An increase in the number of autophagic vacuoles and secondary lysosomes was detected. Dissociation of beclin1-bcl2 stimulated autophagy activation and showed a synergistic anti-tumor effect by inhibiting the Akt-mTOR pathway, cell proliferation and angiogenesis. The combination of radiation with non-invasive aerosol delivery of beclin1 may provide a prospect for developing novel therapy regimens applicable in clinics.</P>
Kim, Ji-Eun,Lim, Hwang-Tae,Minai-Tehrani, Arash,Kwon, Jung-Taek,Shin, Ji-Young,Woo, Chang-Gyu,Choi, Mansoo,Baek, Jongho,Jeong, Dae Hong,Ha, Yoon-Cheol,Chae, Chan-Hee,Song, Kyung-Suk,Ahn, Kang-Ho,Lee, Taylor Francis 2010 Journal of toxicology and environmental health. Pa Vol.73 No.21
<P>Carbon nanotubes (CNT) are known to have widespread industrial applications; however, several reports indicated that these compounds may be associated with adverse effects in humans. In this study, multiwalled carbon nanotubes were administered to murine lungs intratracheally to determine whether acute and chronic pulmonary toxicity occurred. In particular, pristine multiwalled carbon nanotubes (PMWCNT) and acid-treated multiwalled carbon nanotubes (TMWCNT) were used in this study. In broncheoalveolar lavage fluid (BALF) cell analysis, PMWCNT induced more severe acute inflammatory cell recruitment than TMWCNT. Histopathologically, both PMWCNT and TMWCNT induced multifocal inflammatory granulomas in a dose-dependent manner. The observed granulomas were reversible, with TMWCNT-induced granulomas diminishing faster than PMWCNT-induced granulomas. Although the area of granuloma reduced with time, hyperplasia and dysplastic characteristics such as mitotic figures, anisokaryosis, and anisocytosis were still observed. These findings demonstrate that MWCNT induces granulomatous inflammation, and the duration and pattern of inflammation seem to vary depending upon the types of MWCNT to which mice are exposed. Therefore, toxicity studies on various types of CNT are needed as the responsiveness to these compounds differs.</P>