Phenyl 2‐pyridyl ketoxime induces cellular senescence‐like alterations via nitric oxide production in human diploid fibroblasts

Yang, Kyeong Eun,Jang, Hyun&#x2010,Jin,Hwang, In&#x2010,Hu,Chung, Young&#x2010,Ho,Choi, Jong&#x2010,Soon,Lee, Tae&#x2010,Hoon,Chung, Yun&#x2010,Jo,Lee, Min&#x2010,Seung,Lee, Mi Young,Yeo, Eui&#x2010,J BLACKWELL PUBLISHING 2016 AGING CELL Vol.15 No.2

<P><B>Summary</B></P><P>Phenyl‐2‐pyridyl ketoxime (PPKO) was found to be one of the small molecules enriched in the extracellular matrix of near‐senescent human diploid fibroblasts (HDFs). Treatment of young HDFs with PPKO reduced the viability of young HDFs in a dose‐ and time‐dependent manner and resulted in senescence‐associated β‐galactosidase (SA‐β‐gal) staining and G2/M cell cycle arrest. In addition, the levels of some senescence‐associated proteins, such as phosphorylated ERK1/2, caveolin‐1, p53, p16<SUP>ink4a</SUP>, and p21<SUP>waf1</SUP>, were elevated in PPKO‐treated cells. To monitor the effect of PPKO on cell stress responses, reactive oxygen species (ROS) production was examined by flow cytometry. After PPKO treatment, ROS levels transiently increased at 30 min but then returned to baseline at 60 min. The levels of some antioxidant enzymes, such as catalase, peroxiredoxin II and glutathione peroxidase I, were transiently induced by PPKO treatment. SOD II levels increased gradually, whereas the SOD I and III levels were biphasic during the experimental periods after PPKO treatment. Cellular senescence induced by PPKO was suppressed by chemical antioxidants, such as N‐acetylcysteine, 2,2,6,6‐tetramethylpiperidinyloxy, and L‐buthionine‐(<I>S</I>,<I>R</I>)‐sulfoximine. Furthermore, PPKO increased nitric oxide (NO) production via inducible NO synthase (iNOS) in HDFs. In the presence of NOS inhibitors, such as L‐NG‐nitroarginine methyl ester and L‐NG‐monomethylarginine, PPKO‐induced transient NO production and SA‐β‐gal staining were abrogated. Taken together, these results suggest that PPKO induces cellular senescence in association with transient ROS and NO production and the subsequent induction of senescence‐associated proteins<B>.</B></P>

THƠ VIẾT VỀ PHỤ NỮ TRONG BẮC HÀNH TẠP LỤC CỦA NGUYỄN DU

&#x110;inh Th&#x1ecb; Khang 조선대학교 국제문화연구원 2016 국제문화연구 Vol.9 No.2

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关于在情绪智力对工作满意度和情感承诺的关系中 : 积极情绪和消极情绪的调节效果的研究

董&#x73c8;含 · 羊米林 · &#x97e9;仁洙 朝鮮大學校 統一問題硏究所 2017 統一 問題 硏究 Vol.32 No.1

최근 조직구성원의 감성지능에 대한 관심이 고조되고 있다. 조직생활에 있어서는 지적지능 외에 감성지능이 구성원의 관계형성이나 직무수행에 더 영향이 크며 그 결 과 직무만족도나 조직에 대한 태도에도 영향을 미치는 것으로 인식되고 있기 때문이다. 본 연구는 조직에서 구성원의 감성지능이 그들의 직무만족이나 조직에 대한 정서적 몰입에 미치는 영향을 실증적으로 분석하고자 하였다. 동시에 그 과정에서 구성원의 긍정적 정서와 부정적 정서의 조절효과도 조사하였다. 실증적 조사 결과 구성원의 감성지능은 그들의 직무만족과 정서적 몰입에 정(+) 의 영향을 미치는 것으로 나타났다. 그리고 감성지능과 직무만족·정서적 몰입간의 관 계에서 긍정적 정서의 조절효과는 나타나지 않았으나 부정적 정서는 조절효과가 있는 것으로 밝혀졌다. 본 연구 결과는 조직에서 구성원의 감성지능을 높일 수 있는 실천적 방안 마련의 필요성과 함께 종업원 선발 시 선발요소로서 부정적 정서에 대한 특별한 고려가 필요 하다는 실천적 시사점을 제시해주고 있다. 주제어: 감성지능, 긍정적 정서, 부정적 정서, 직무만족, 정서적 몰입, 중국근로자 This study investigated the effect of emotional intelligence of employees on their job satisfaction and affective commitment. The moderating role of positive and negative affectivity at work was also analyzed in the relationships between them. Based on analysis of questionnaire survey obtained from 179 company employees, it was found that positive relationship between emotional intelligence and job satisfaction, and affective commitment. The moderating role of positive affectivity in the relationships between emotional intelligence and job satisfaction, affective commitment was not found, but negative affectivity moderated the relationships between emotional intelligence and job satisfaction, affective commitment such that the relationship was weaker in the employees with high negative affectivity. Finally, some practical recommendations for increasing emotional intelligence and decreasing negative affectivity of employees in organizations were suggested. Key words: Emotional intelligence, Positive and negative affectivity, Job satisfaction; Affective commitment, Chinese employees.

paṃsukūlaについて

&#x9752;野道彦 불교학연구회 2016 불교학연구 Vol.46 No.-

초기 불교의 출가유행자들은 “분소의(糞掃衣)”라는 초라한 옷을 입고 있었다고 한다. 본 논문은 그 원어의 하나인 빨리어 paṃsukūla의 의미를 빨리율을 중심으로 한 빨리문헌의 관련 용례를 조사함으로써 고찰한다. paṃsukūla는 아베지온 (阿部慈園) 에 따르면 “오물 또는 쓰레기나 먼지처럼 불필요하고 가치없는 곳곳에 버려진 천 조각을 기어서 만든 옷”이라고 한다. 또한 J. Dantinne에 따르면 “쓰레기 더미, 길거리, 묘지에서 찾은 버려진 천 조각으로 만든 옷”이라고한다. 여기에서 볼 수 있는 것처럼 paṃsukūla는 일반적으로 “불필요한 천 조각으로 만든 옷” 으로 이해되는 경우가 많다. 그런데 paṃsukūla와 그 파생어인 paṃsukūlika의 용례를 살펴보면 이러한 일반적인 이해는 충분하지 않다. paṃsukūla는 “불필요한 천 조각으로 만든 옷”이 아니라 그소재인 “불필요한 천 조각”의 의미로 사용되는 경우가 있기 때문이다. 또한 paṃsukūla는 옷뿐만 아니라 다양한 것을 가리켜 사용되기 때문에, 원래의 의미를 감안하여 “주인없는 버려진 것”이라는 뜻으로 이해하는 것이 더 적절한 경우가 있기 때문이다. 본 논문은 이러한 paṃsukūla의 의미를 설명하기 위해 paṃsukūla와 paṃsukūlika의 용례를 빨리문헌에서 인용하고 제시한다. This paper examines the meaning of the term paṃsukūla as found in the Theravāda Tipiṭaka, especially the Vinayapiṭaka. It is thought that the early Buddhist monks wore paṃsukūla, described by Jion Abe as a “robe made of rags which were discarded here and there as useless and worthless things like filth.” This description is commonly accepted in foreign countries as well as in Japan. Jean Dantinne views it as “un vêtement fait de haillons, trouvés sur un tas d’ordures, en rue, dans un cimetière,” while Reginald A. Ray calls them/it “clothes made from cast-off rags.” The popular definition of paṃsukūla in the Theravāda Tipiṭaka, is accurate in many cases, but the term does not always mean “robe made of rags.” It can also mean “refuse rags,” which are materials of robe. In addition, it is used to describe an ownerless “lump of refuse” or “heap of waste,” which is an original meaning of the term. This article provides examples of paṃsukūla and its derivative, paṃsukūlika, from the Theragāthā and the Vinayapiṭaka to validate the meanings described above.

Increased plasma levels of retinol‐binding protein 4 with visceral obesity is associated with cardiovascular risk factors

Won, Jong Chul,Park, Cheol&#x2010,Young,Oh, Sang Woo,Park, Sung Woo Blackwell Publishing Ltd 2012 Journal of diabetes investigation Vol.3 No.5

<P><B>Abstract</B></P><P><B>Aims/Introduction: </B> Visceral obesity has been suggested to be an independent risk factor for cardiovascular disease (CVD); the role of adipokines in the risk for CVD is less clear. Aim of this study was to investigate the relationship between parameters of visceral obesity and index of CVD risk factors.</P><P><B>Materials and Methods: </B> A cross‐sectional analysis of healthy males (<I>n</I> = 116) and females (<I>n</I> = 175) for evaluation of clinical, laboratory and anthropometric parameters were undertaken. Abdominal subcutaneous (SAT) and visceral adipose tissues (VAT) were measured by computed tomography. Adipokines, including retinol‐binding protein 4 (RBP4) and adiponectin, were determined. The risk for CVD was estimated using the 10‐year Framingham Coronary Heart Disease Risk Point scale (Framingham score).</P><P><B>Results: </B> The Framingham score was increased in subjects with metabolic syndrome, and significantly increased with various indices of obesity, traditional risk factors of CVD, C‐reactive protein (CRP) and RBP4, but decreased with adiponectin. With multiple linear regression analysis, the Framingham score independently associated with age, smoking status, body mass index, triglyceride and RBP4. The magnitude of the Framingham score showed a linear trend of increase with CRP, VAT and RBP4 (all <I>P</I> < 0.001), but of decrease with SAT and adiponectin (all <I>P</I> < 0.05) at stratified levels of obesity.</P><P><B>Conclusions: </B> RBP4 is increased with visceral fat accumulation and associated with CVD risk factors independent of obesity or traditional risk factors. <B>(J Diabetes Invest, doi: </B>10.1111/j.2040‐1124.2012.00213.x<B>, 2012)</B></P>

2′‐Hydroxycinnamaldehyde inhibits proliferation and induces apoptosis via signal transducer and activator of transcription 3 inactivation and reactive oxygen species generation

Yoon, Yae Jin,Kim, Young&#x2010,Hwan,Lee, Yu&#x2010,Jin,Choi, Jiyeon,Kim, Cheol&#x2010,Hee,Han, Dong Cho,Kwon, Byoung&#x2010,Mog John Wiley and Sons Inc. 2019 CANCER SCIENCE Vol.110 No.1

<P>Inhibition of the signal transducer and activator of transcription 3 (STAT3) signaling pathway is a novel therapeutic strategy to treat human cancers with constitutively active STAT3. During the screening of natural products to find STAT3 inhibitors, we identified 2′‐hydroxycinnamaldehyde (HCA) as a STAT3 inhibitor, which was isolated from the stem bark of <I>Cinnamomum cassia</I>. In this study, we found that HCA inhibited constitutive and inducible STAT3 activation in STAT3‐activated DU145 prostate cancer cells. HCA selectively inhibited the STAT3 activity by direct binding to STAT3, which was confirmed by biochemical methods, including a pull‐down assay with biotin‐conjugated HCA, a drug affinity responsive target stability (DARTS) experiment and a cellular thermal shift assay (CETSA). HCA inhibited STAT3 phosphorylation at the tyrosine 705 residue, dimer formation, and nuclear translocation in DU145 cells, which led to a downregulation of STAT3 target genes. The downregulation of cell cycle progression and antiapoptosis‐related gene expression by HCA induced the accumulation of cells in the G0/G1 phase of the cell cycle and then induced apoptosis. We also found that reactive oxygen species (ROS) were involved in the HCA‐induced inhibition of STAT3 activation and cell proliferation because the suppressed p‐STAT3 level was rescued by glutathione or N‐acetyl‐L‐cysteine treatment, which are general ROS inhibitors. These results suggest that HCA could be a potent anticancer agent targeting STAT3‐activated tumor cells.</P>

Anti‐inflammatory mechanism of ginsenoside Rh1 in lipopolysaccharide‐stimulated microglia: critical role of the protein kinase A pathway and hemeoxygenase‐1 expression

Jung, Ji&#x2010,Sun,Shin, Jin A.,Park, Eun&#x2010,Mi,Lee, Jung&#x2010,Eun,Kang, Young&#x2010,Sook,Min, Sung&#x2010,Won,Kim, Dong&#x2010,Hyun,Hyun, Jin&#x2010,Won,Shin, Chan&#x2010,Young,Kim, Hee&#x201 Blackwell Publishing Ltd 2010 Journal of Neurochemistry Vol.115 No.6

<P> <I>J. Neurochem.</I> (2010) <B>115,</B> 1668–1680.</P><P><B>Abstract</B></P><P>Microglia activation plays a pivotal role in neurodegenerative diseases, and thus controlling microglial activation has been suggested as a promising therapeutic strategy for neurodegenerative diseases. In the present study, we showed that ginsenoside Rh1 inhibited inducible nitric oxide synthase, cyclooxygenase‐2, and pro‐inflammatory cytokine expression in lipopolysaccharide (LPS)‐stimulated microglia, while Rh1 increased anti‐inflammatory IL‐10 and hemeoxygenase‐1 (HO‐1) expression. Suppression of microglial activation by Rh1 was also observed in the mouse brain following treatment with LPS. Subsequent mechanistic studies revealed that Rh1 inhibited LPS‐induced MAPK phosphorylation and nuclear factor‐κB (NF‐κB)‐mediated transcription without affecting NF‐κB DNA binding. As the increase of pCREB (cAMP responsive element‐binding protein) is known to result in suppression of NF‐κB‐mediated transcription, we examined whether Rh1 increased pCREB levels. As expected, Rh1 increased pCREB, which was shown to be related to the anti‐inflammatory effect of Rh1 because pre‐treatment with protein kinase A inhibitors attenuated the Rh1‐mediated inhibition of nitric oxide production and the up‐regulation of IL‐10 and HO‐1. Furthermore, treatment of HO‐1 shRNA attenuated Rh1‐mediated inhibition of nitric oxide and reactive oxygen species production. Through this study, we have demonstrated that protein kinase A and its downstream effector, HO‐1, play a critical role in the anti‐inflammatory mechanism of Rh1 by modulating pro‐ and anti‐inflammatory molecules in activated microglia.</P>

Long‐term efficacy and safety of bosutinib in patients with advanced leukemia following resistance/intolerance to imatinib and other tyrosine kinase inhibitors

Gambacorti&#x2010,Passerini, Carlo,Kantarjian, Hagop M.,Kim, Dong&#x2010,Wook,Khoury, Hanna J.,Turkina, Anna G.,Brü,mmendorf, Tim H.,Matczak, Ewa,Bardy&#x2010,Bouxin, Nathalie,Shapiro, Mark,Turnbu John Wiley and Sons Inc. 2015 American journal of hematology Vol.90 No.9

<P>Long‐term efficacy and safety of bosutinib (≥4 years follow‐up from last enrolled patient) were evaluated in an ongoing phase 1/2 study in the advanced leukemia cohort with prior treatment failure (accelerated‐phase [AP, <I>n =</I> 79] chronic myeloid leukemia [CML], blast‐phase [BP, <I>n =</I> 64] CML, acute lymphoblastic leukemia [ALL, <I>n =</I> 24]). Fourteen AP, 2 BP, and 1 ALL patient remained on bosutinib at 4 years (vs. 38, 8, 1 at 1 year); median (range) treatment durations: 10.2 (0.1–88.6), 2.8 (0.03–55.9), 0.97 (0.3–89.2) months. Among AP and BP patients, 57% and 28% newly attained or maintained baseline overall hematologic response (OHR); 40% and 37% attained/maintained major cytogenetic response (MCyR) by 4 years (most by 12 months). In responders at 1 versus 4 years, Kaplan‐Meier (KM) probabilities of maintaining OHR were 78% versus 49% (AP) and 28% versus 19% (BP); KM probabilities of maintaining MCyR were 65% versus 49% (AP) and 21% versus 21% (BP). Most common AEs (AP, BP) were gastrointestinal (96%; 83%), primarily diarrhea (85%; 64%), which was typically low grade (maximum grade 1/2: 81%; 59%) and transient; no patient discontinued due to diarrhea. Serious AEs occurred in 44 (56%) AP and 37 (58%) BP patients, most commonly pneumonia (<I>n =</I> 9) for AP and pyrexia (<I>n =</I> 6) for BP; 11 and 13 died within 30 days of last dose (2 considered bosutinib‐related [AP] per investigator). Responses were durable in ∼50% AP responders at 4 years (∼25% BP patients responded at year 1, suggesting possible bridge‐to‐transplant role in BP patients); toxicity was manageable.Am. J. Hematol. 90:755–768, 2015. © 2015 The Authors. American Journal of Hematology Published by Wiley Periodicals, Inc.</P>

HOẠT ĐỘNG KINH TẾ TRUYỀN THỐNG CỦA CÁC TỘC NGƯỜI THIỂU SỐ TẠI CHỖ Ở ĐÔNG NAM BỘ - VIỆT NAM VÀ NHỮNG THAY

Hu&#x1ef3;nh Ng&#x1ecd;c Thu 조선대학교 국제문화연구원 2016 국제문화연구 Vol.9 No.2

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Development of real‐time motion verification system using in‐room optical images for respiratory‐gated radiotherapy

Park, Yang&#x2010,Kyun,Son, Tae&#x2010,geun,Kim, Hwiyoung,Lee, Jaegi,Sung, Wonmo,Kim, Il Han,Lee, Kunwoo,Bang, Young&#x2010,bong,Ye, Sung&#x2010,Joon John Wiley and Sons Inc. 2013 Journal of applied clinical medical physics Vol.14 No.5

<P>Phase‐based respiratory‐gated radiotherapy relies on the reproducibility of patient breathing during the treatment. To monitor the positional reproducibility of patient breathing against a 4D CT simulation, we developed a real‐time motion verification system (RMVS) using an optical tracking technology. The system in the treatment room was integrated with a real‐time position management system. To test the system, an anthropomorphic phantom that was mounted on a motion platform moved on a programmed breathing pattern and then underwent a 4D CT simulation with RPM. The phase‐resolved anterior surface lines were extracted from the 4D CT data to constitute 4D reference lines. In the treatment room, three infrared reflective markers were attached on the superior, middle, and inferior parts of the phantom along with the body midline and then RMVS could track those markers using an optical camera system. The real‐time phase information extracted from RPM was delivered to RMVS via in‐house network software. Thus, the real‐time anterior‐posterior positions of the markers were simultaneously compared with the 4D reference lines. The technical feasibility of RMVS was evaluated by repeating the above procedure under several scenarios such as ideal case (with identical motion parameters between simulation and treatment), cycle change, baseline shift, displacement change, and breathing type changes (abdominal or chest breathing). The system capability for operating under irregular breathing was also investigated using real patient data. The evaluation results showed that RMVS has a competence to detect phase‐matching errors between patient's motion during the treatment and 4D CT simulation. Thus, we concluded that RMVS could be used as an online quality assurance tool for phase‐based gating treatments.</P><P>PACS number: 87.55.Qr</P>