http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Choi, Young Deuk,Ham, Won Sik,Kim, Won Tae,Cho, Kang Su,Lee, Joo Hyoung,Cho, Soung Yong,Seo, Ju Wan,Jin, Ok Hyun Mary Ann Liebert 2009 Journal of endourology Vol.23 No.6
<P>PURPOSE: To evaluate the efficacy and safety of single-session OK-432 sclerotherapy for the treatment of renal cysts. MATERIALS AND METHODS: From October 2005 to November 2006, 48 patients (61 simple renal cysts) were included in the study. Indications were determined as flank discomfort (n = 37) or patient reassurance due to increasing size (n = 11). The simple renal cysts were aspirated under ultrasonography (US), at which point OK-432 was injected into the cyst. Follow-up was performed with US or computed tomography scan every 3 months until 1 year. Complete regression of the renal cyst or more than 70% reduction in size with no symptoms indicated a successful treatment. RESULTS: Among 61 renal cysts of 48 patients, the overall success rate was 98.4%. Complete regression occurred in 46 cysts (75.4%), and more than 90% reduction in size occurred in 6 cysts (9.8%). A size reduction of 80% to 90% and 70% to 80% occurred in five (8.2%) and three cysts (4.9%), respectively. A size reduction less than 70% occurred in only one cyst (1.6%). The success of cyst regression was correlated with cyst volume. Clinical symptoms resolved in 100% of patients with symptomatic cysts, and there was no enlargement of the aspirated cysts at the 1-year follow-up. After the procedure, there were only some minor complications, such as mild fever, flank pain, and leukocytosis, which subsided with the conservative treatment. CONCLUSIONS: Percutaneous OK-432 sclerotherapy is simple, safe, and effective, and it can be an alternative first-line therapy for simple renal cysts.</P>
( Joo Young Lee ),( Hye Suk Han ),( Sung Nam Lim ),( Young Kwang Shim ),( Yong Hyeok Choi ),( Ok Jun Lee ),( Ki Hyeong Lee ),( Seung Taik Kim ) 대한내과학회 2011 대한내과학회 추계학술발표논문집 Vol.2011 No.1
Pneumatosis intestinalis (PI), and portal venous gas (PVG) are relatively rare radiological findings. Although several chemotherapeutic agents and anti-vascular endothelial-growth-factor-agents have been reported to be associated with PI and PVG, no previous report has described an association with anti-epidermal growth factor receptor (EGFR) agents. The present report describes a case of PI and PVG secondary to an EGFR tyrosine kinase inhibitor. A 66-year-old women who had been diagnosed metastatic lung adenocarcinoma presented with nausea, vomiting, and abdominal distension 2 months after commencing gefitinib. A computed tomography scan (CT) of the abdomen revealed PI extending from the ascending colon to the rectum, hepatic PVG, and infarction of the liver. Gefitinib therapy was discontinued immediately and the patient was managed conservatively. A follow-up CT scan 2 weeks later revealed that the PI and hepatic PVG had completely resolved. This is the first report to be issued regarding PI and PVG caused by EGFR tyrosine kinase inhibitor. Although these complications are extremely rare, clinicians should be aware of the risk of PI and PVG in patients undergoing targeted molecular therapy.
Kim, Kyung Eun,Kim, Hwajin,Heo, Rok Won,Shi, Hyun Joo,Yi, Chin-ok,Lee, Dong Hoon,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung,Roh, Gu Seob The Korean Society of Pharmacology 2015 The Korean Journal of Physiology & Pharmacology Vol.19 No.5
Sirtuin 1 (SIRT1) is a mammalian $NAD^+$-dependent protein deacetylase that regulates cellular metabolism and inflammatory response. The organ-specific deletion of SIRT1 induces local inflammation and insulin resistance in dietary and genetic obesity. Macrophage-mediated inflammation contributes to insulin resistance and metabolic syndrome, however, the macrophage-specific SIRT1 function in the context of obesity is largely unknown. C57/BL6 wild type (WT) or myeloid-specific SIRT1 knockout (KO) mice were fed a high-fat diet (HFD) or normal diet (ND) for 12 weeks. Metabolic parameters and markers of hepatic steatosis and inflammation in liver were compared in WT and KO mice. SIRT1 deletion enhanced HFD-induced changes on body and liver weight gain, and increased glucose and insulin resistance. In liver, SIRT1 deletion increased the acetylation, and enhanced HFD-induced nuclear translocation of nuclear factor kappa B (NF-${\kappa}B$), hepatic inflammation and macrophage infiltration. HFD-fed KO mice showed severe hepatic steatosis by activating lipogenic pathway through sterol regulatory element-binding protein 1 (SREBP-1), and hepatic fibrogenesis, as indicated by induction of connective tissue growth factor (CTGF), alpha-smooth muscle actin (${\alpha}$-SMA), and collagen secretion. Myeloid-specific deletion of SIRT1 stimulates obesity-induced inflammation and increases the risk of hepatic fibrosis. Targeted induction of macrophage SIRT1 may be a good therapy for alleviating inflammation-associated metabolic syndrome.
Fabrication of Microcapsules for Dye-Doped Polymer-Dispersed Liquid Crystal-Based Smart Windows
Kim, Mingyun,Park, Kyun Joo,Seok, Seunghwan,Ok, Jong Min,Jung, Hee-Tae,Choe, Jaehoon,Kim, Do Hyun American Chemical Society 2015 ACS APPLIED MATERIALS & INTERFACES Vol.7 No.32
<P>A dye-doped polymer-dispersed liquid crystal (PDLC) is an attractive material for application in smart windows. Smart windows using a PDLC can be operated simply and have a high contrast ratio compared to those of other devices that employed photochromic or thermochromic material. However, in conventional dye-doped PDLC methods, dye contamination can cause problems and has a limited degree of commercialization of electric smart windows. Here, we report on an approach to resolve dye-related problems by encapsulating the dye in monodispersed capsules. By encapsulation, a fabricated dye-doped PDLC had a contrast ratio of >120 at 600 nm. This fabrication method of encapsulating the dye in a core–shell structured microcapsule in a dye-doped PDLC device provides a practical platform for dye-doped PDLC-based smart windows.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/aamick/2015/aamick.2015.7.issue-32/acsami.5b04496/production/images/medium/am-2015-044962_0006.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/am5b04496'>ACS Electronic Supporting Info</A></P>
KIM, Wonwoo,SEONG, Jinsil,OH, Hae Jin,KOOM, Woong Sub,CHOI, Kyung-Joo,YUN, Chae-Ok Journal of Radiation Research Editorial Committee 2011 Journal of radiation research Vol.52 No.5
<P>In this study, a novel combination treatment of armed oncolytic adenovirus expressing interleukin 12 (IL-12) and granulocyte-macrophage colony-stimulating factor (GM-CSF) with radiation was investigated for antitumor and antimetastatic effect in a murine hepatic cancer (HCa-I) model. Tumor bearing syngeneic mice were treated with radiation, armed oncolytic virus Ad-ΔE1Bmt7 (dB7) expressing both IL-12 and GM-CSF (armed dB7), or a combination of both. The adenovirus was administered by intratumoral injection 1 × 10<SUP>8</SUP> PFU per tumor in 50 μl of PBS four times every other day. Tumor response to treatment was determined by a tumor growth delay assay. Metastatic potential was evaluated by a lung metastasis model. To understand the underlying mechanism, the level of apoptosis was examined as well as the change in microvessel density and expression of immunological markers: CD4+, CD8+ and Cd11c. The combination of armed dB7 and radiation resulted in significant growth delay of murine hepatic cancer, HCa-1, with an enhancement factor of 4.3. The combination treatment also resulted in significant suppression of lung metastasis. Increase of apoptosis level as well as decrease of microvessel density was shown in the combination treatment, suggesting an underlying mechanism for the enhancement of antitumor effect. Expression of immunological markers: CD4+, CD8+ and Cd11c also increased in the combination treatment. This study showed that a novel combination treatment of radiotherapy with armed oncolytic adenovirus expressing IL-12 and GM-CSF was effective in suppressing primary tumor growth.</P>
Kim, Ok-Hee,Kang, Gun-Hyung,Noh, Hyungjoon,Cha, Ji-Young,Lee, Ho-Jae,Yoon, Jeong-Hwan,Mamura, Mizuko,Nam, Jeong-Seok,Lee, Dae Ho,Kim, Young A.,Park, Young Joo,Kim, Hyeonjin,Oh, Byung-Chul Springer-Verlag 2013 Molecules and cells Vol.36 No.5
<P>Tumor-associated macrophages (TAMs) accumulate in various cancers and promote tumor angiogenesis and metastasis, and thus may be ideal targets for the clinical diagnosis of tumor metastasis with high specificity. However, there are few specific markers to distinguish between TAMs and normal or inflammatory macrophages. Here, we show that TAMs localize in green fluorescent protein-labeled tumors of metastatic lymph nodes (MLNs) from B16F1 melanoma cells but not in necrotic tumor regions, suggesting that TAMs may promote the growth of tumor cells and the progression of tumor metastasis. Furthermore, we isolated pure populations of TAMs from MLNs and characterized their gene expression signatures compared to peritoneal macrophages (PMs), and found that TAMs significantly overexpress immunosuppressive cytokines such as IL-4, IL-10, and TGF-β as well as proangiogenic factors such as VEGF, TIE2, and CD31. Notably, immunological analysis revealed that TIE2(+)/CD31(+) macrophages constitute the predominant population of TAMs that infiltrate MLNs, distinct from tissue or inflammatory macrophages. Importantly, these TIE2(+)/CD31(+) macrophages also heavily infiltrated MLNs from human breast cancer biopsies but not reactive hyperplastic LNs. Thus, TIE2(+)/ CD31(+) macrophages may be a unique histopathological biomarker for detecting metastasis in clinical diagnosis, and a novel and promising target for TAM-specific cancer therapy.</P>