Relationship between Properties of Pseudo-boehmite and its Synthetic Conditions

Lee, H.-W.,Park, B.-K.,Tian, M.-Y.,Lee, J.-M. THE KOREAN SOCIETY OF INDUSTRIAL AND ENGINEERING 2006 Journal of industrial and engineering chemistry Vol.12 No.2

Hyperosmotic Stimulus Down-regulates $1{\alpha}$, 25-dihydroxyvitamin $D_3$-induced Osteoclastogenesis by Suppressing the RANKL Expression in a Co-culture System

Tian, Yu-Shun,Jeong, Hyun-Joo,Lee, Sang-Do,Kong, Seok-Heui,Ohk, Seung-Ho,Yoo, Yun-Jung,Seo, Jeong-Taeg,Shin, Dong-Min,Sohn, Byung-Wha,Lee, Syng-Ill The Korean Society of Pharmacology 2010 The Korean Journal of Physiology & Pharmacology Vol.14 No.3

The hyperosmotic stimulus is regarded as a mechanical factor for bone remodeling. However, whether the hyperosmotic stimulus affects $1{\alpha}$, 25-dihydroxyvitamin $D_3$ ($1{\alpha},25(OH)_2D_3$)-induced osteoclastogenesis is not clear. In the present study, the effect of the hyperosmotic stimulus on $1{\alpha},25(OH)_2D_3$-induced osteoclastogenesis was investigated in an osteoblast-preosteoclast co-culture system. Serial doses of sucrose were applied as a mechanical force. These hyperosmotic stimuli significantly evoked a reduced number of $1{\alpha},25(OH)_2D_3$-induced tartrate-resistant acid phosphatase-positive multinucleated cells and $1{\alpha},25(OH)_2D_3$-induced bone-resorbing pit area in a co-culture system. In osteoblastic cells, receptor activator of nuclear factor ${\kappa}B$ ligand (RANKL) and Runx2 expressions were down-regulated in response to $1{\alpha},25(OH)_2D_3$. Knockdown of Runx2 inhibited $1{\alpha},25(OH)_2D_3$-induced RANKL expression in osteoblastic cells. Finally, the hyperosmotic stimulus induced the overexpression of TonEBP in osteoblastic cells. These results suggest that hyperosmolarity leads to the down-regulation of $1{\alpha},25(OH)_2D_3$-induced osteoclastogenesis, suppressing Runx2 and RANKL expression due to the TonEBP overexpression in osteoblastic cells.

Automated band annotation for RNA structure probing experiments with numerous capillary electrophoresis profiles

Lee, Seungmyung,Kim, Hanjoo,Tian, Siqi,Lee, Taehoon,Yoon, Sungroh,Das, Rhiju Oxford University Press 2015 Bioinformatics Vol.31 No.17

<P><B>Motivation:</B> Capillary electrophoresis (CE) is a powerful approach for structural analysis of nucleic acids, with recent high-throughput variants enabling three-dimensional RNA modeling and the discovery of new rules for RNA structure design. Among the steps composing CE analysis, the process of finding each band in an electrophoretic trace and mapping it to a position in the nucleic acid sequence has required significant manual inspection and remains the most time-consuming and error-prone step. The few available tools seeking to automate this band annotation have achieved limited accuracy and have not taken advantage of information across dozens of profiles routinely acquired in high-throughput measurements.</P><P><B>Results:</B> We present a dynamic-programming-based approach to automate band annotation for high-throughput capillary electrophoresis. The approach is uniquely able to define and optimize a robust target function that takes into account multiple CE profiles (sequencing ladders, different chemical probes, different mutants) collected for the RNA. Over a large benchmark of multi-profile datasets for biological RNAs and designed RNAs from the EteRNA project, the method outperforms prior tools (QuSHAPE and FAST) significantly in terms of accuracy compared with gold-standard manual annotations. The amount of computation required is reasonable at a few seconds per dataset. We also introduce an ‘<I>E</I>-score’ metric to automatically assess the reliability of the band annotation and show it to be practically useful in flagging uncertainties in band annotation for further inspection.</P><P><B>Availability and implementation:</B> The implementation of the proposed algorithm is included in the HiTRACE software, freely available as an online server and for download at http://hitrace.stanford.edu.</P><P><B>Contact:</B> sryoon@snu.ac.kr or rhiju@stanford.edu</P><P><B>Supplementary information:</B> Supplementary data are available at <I>Bioinformatics</I> online.</P>

Elk-3 Contributes to the Progression of Liver Fibrosis by Regulating the Epithelial-Mesenchymal Transition

( Tian Zhu Li ),( Sung Min Kim ),( Wonhee Hur ),( Jung Eun Choi ),( Jung-hee Kim ),( Sung Woo Hong ),( Eun Byul Lee ),( Joon Ho Lee ),( Seung Kew Yoon ) 대한소화기학회 2017 Gut and Liver Vol.11 No.1

Background/Aims: The role of Elk-3 in the epithelial-mesenchymal transition (EMT) during liver fibrogenesis remains unclear. Here, we determined the expression of Elk-3 in in vitro and in vivo models and in human liver fibrotic tissues. We also investigated the molecular relationships among Elk- 3, early growth response-1 (Egr-1), and the mitogen activated protein kinases (MAPK) pathway during EMT in hepatocytes. Methods: We established an in vitro EMT model in which normal mouse hepatocyte cell lines were treated with transforming growth factor (TGF)-β1 and a CCl₄-induced liver fibrosis model. Characteristics of EMT were determined by evaluating the expression levels of related markers. The expression of Elk-3 and its target Egr-1 were analyzed using Western blotting. Gene silencing of Elk-3 was performed using an siRNA knockdown system. Results: The expression levels of mesenchymal markers were increased during TGF-β1-induced EMT of hepatocytes. The expression levels of Elk-3 and Egr-1 were significantly (p<0.05) increased during the EMT of hepatocytes, in CCl₄-induced mouse liver fibrotic tissues, and in human liver cirrhotic tissues. Silencing of Elk-3 and inhibition of the Ras-Elk-3 pathway with an inhibitor suppressed the expression of EMT-related markers. Moreover, Elk-3 expression was regulated by p38 MAPK phosphorylation during EMT. Conclusions: Elk-3 contributes to the progression of liver fibrosis by modulating the EMT via the regulation of Egr- 1 under MAPK signaling. (Gut Liver 2017;11:102-111)

7-Nitroindazole, nitric oxide synthase inhibitor, attenuates physical dependence on butorphanol in rat

Tian, Yu-Hua,Lee, Kwang-Wook,You, In-Jee,Lee, Seok-Yong,Jang, Choon-Gon Wiley Subscription Services, Inc., A Wiley Company 2008 Synapse Vol.62 No.8

<P>Butorphanol is a synthetic opioid agonist/antagonist analgesic agent that mainly exerts its effects through κ-opioid receptors. It has been demonstrated that κ-opioid receptors preferentially mediate the development of physical dependence upon butorphanol and the associated withdrawal syndrome. However, it is not fully understood whether or not nNOS-containing neurons in the various brain regions play an important role in butorphanol withdrawal. Therefore, this study was conducted to determine whether the selective nNOS inhibitor, 7-NI, modifies the development of butorphanol withdrawal and changes of nNOS expressions in different brain regions in physically butorphanol-dependent rats. The first part of the study focused on withdrawal behaviors in male Sprague-Dawley rats. Physical dependence was induced by a 72-h i.c.v. infusion with butorphanol (26 nmol/μl/h) and withdrawal was subsequently precipitated by i.c.v. challenge with naloxone (48 nmol/5 μl/rat) 2 h after termination of the butorphanol infusion. The butorphanol/7-NI coadministration group showed a significant decrease in several signs of withdrawal such as teeth chattering, as compared with the butorphanol-treated group. In the second part of the study, immunohistochemical analysis was performed to determine the expression of nNOS in the various brain regions. In the butorphanol/7-NI coadministration group, the number of cells labeled for nNOS was significantly lower in the various brain regions (including the caudate putamen, nucleus accumbens, and hippocampus) than in the butorphanol group. Therefore, 7-NI decreased in butorphanol-induced physical dependence and nNOS expression. Taken together, these findings suggest that the nNOS system is involved in the development of butorphanol-induced physical dependence, and 7-NI has potential clinical application as a candidate for the treatment of opioid withdrawal syndrome. Synapse 62:582–589, 2008. © 2008 Wiley-Liss, Inc.</P>

SIRT3 deregulation is linked to mitochondrial dysfunction in Alzheimer's disease

Lee, Junghee,Kim, Yunha,Liu, Tian,Hwang, Yu Jin,Hyeon, Seung Jae,Im, Hyeonjoo,Lee, Kyungeun,Alvarez, Victor E.,McKee, Ann C.,Um, Soo‐,Jong,Hur, Manwook,Mook‐,Jung, Inhee,Kowall, Neil W.,Ry John Wiley and Sons Inc. 2018 Aging cell Vol.17 No.1

<P><B>Summary</B></P><P>Alzheimer's disease (AD) is the leading cause of dementia in the elderly. Despite decades of study, effective treatments for AD are lacking. Mitochondrial dysfunction has been closely linked to the pathogenesis of AD, but the relationship between mitochondrial pathology and neuronal damage is poorly understood. Sirtuins (SIRT, silent mating type information regulation 2 homolog in yeast) are NAD‐dependent histone deacetylases involved in aging and longevity. The objective of this study was to investigate the relationship between SIRT3 and mitochondrial function and neuronal activity in AD. SIRT3 mRNA and protein levels were significantly decreased in AD cerebral cortex, and Ac‐p53 K320 was significantly increased in AD mitochondria. SIRT3 prevented p53‐induced mitochondrial dysfunction and neuronal damage in a deacetylase activity‐dependent manner. Notably, mitochondrially targeted p53 (mito‐p53) directly reduced mitochondria DNA‐encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption. ND2 and ND4 gene expressions were significantly decreased in patients with AD. p53‐ChIP analysis verified the presence of p53‐binding elements in the human mitochondrial genome and increased p53 occupancy of mitochondrial DNA in AD. SIRT3 overexpression restored the expression of ND2 and ND4 and improved mitochondrial oxygen consumption by repressing mito‐p53 activity. Our results indicate that SIRT3 dysfunction leads to p53‐mediated mitochondrial and neuronal damage in AD. Therapeutic modulation of SIRT3 activity may ameliorate mitochondrial pathology and neurodegeneration in AD.</P>

The effects of ENSO under negative AO phase on spring dust activity over northern China: an observational investigation

Lee, Yun Gon,Kim, Jhoon,Ho, Chang‐,Hoi,An, Soon‐,Il,Cho, Hi‐,Ku,Mao, Rui,Tian, Baijun,Wu, Dong,Lee, Jae N.,Kalashnikova, Olga,Choi, Yunsoo,Yeh, Sang‐,Wook John Wiley Sons, Ltd 2015 International journal of climatology Vol.35 No.6

<P><B>ABSTRACT</B></P><P>The effects of El Niño/Southern Oscillation (ENSO) under negative Arctic Oscillation (AO) phase on the Asian dust activity are investigated for springs of the period 1961–2002. The spring dust index (DI) describing the monthly frequencies of three types of dust events (e.g. dust storm, blowing dust, and floating dust) exhibits a significant increase in the years of negative AO phase (hereafter AO−) and El Niño, compared with that in the years of AO− and La Niña. Averaged over all observation stations, the spring DI (49.7) during the El Niño/AO− years is higher by 11.4% or 29.8% than that (38.3) during the La Niña/AO− years. We suggest possible physical mechanism that the anomalous large‐scale environments associated with AO− and El Niño are more effective to provide favourable conditions to enhance Asian dust activity. During the El Niño/AO− years, meridional gradients of pressure and temperature over the dust source regions are significantly enhanced by decreasing the geopotential height and warming air temperature that originated from the north and south of source regions, respectively, under the influence of AO− and El Niño. These also intensify the zonal wind shear and atmospheric baroclinicity, thereby producing enhanced cyclogenesis and dust occurrences over the major source regions. At the same time, dust transport paths with the stronger westerly winds are developed by the combined constraints of anomalous cyclone over the Siberia and the Mongolia and anomalous anticyclone over the western North Pacific, and thus strengthen dust transport to the downwind regions.</P>

The Anti-Stress Effect of <i>Mentha arvensis</i> in Immobilized Rats

Tian, Weishun,Akanda, Md Rashedunnabi,Islam, Anowarul,Yang, Hae-Dong,Lee, Sang-Cheon,Lee, Jeong-Ho,Kim, Sang-Ki,Choi, Yu-Jin,Im, So-Yeon,Park, Byung-Yong MDPI 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.2

<P>Stress can lead to inflammation, accelerated aging, and some chronic diseases condition. <I>Mentha arvensis</I> (MA) is a traditional medicine having antioxidant and anti-inflammatory activities. The present study investigated the anti-stress role of MA and fermented MA (FMA) extract in immobilized rats. We studied the lipopolysaccharide (LPS)-induced inflammation in RAW 264.7 cells and rats were immobilized for 2 h per day for 14 days using a restraining cage. MA (100 mg/kg) and FMA (100 mg/kg) were orally administered to rats 1 h prior to immobilization. Using high-performance liquid chromatography (HPLC) analysis, we determined the rosmarinic acid content of MA and FMA. The generation of malondialdehyde (MDA) and nitric oxide (NO) in RAW 246.7 cells were suppressed by both MA and FMA. In rats, MA and FMA notably improved the body weight, daily food intake, and duodenum histology. MDA and NO level were gradually decreased by MA and FMA treatment. MA and FMA significantly controlled the stress-related hormones by decreasing corticosterone and β-endorphin and increasing serotonin level. Moreover, protein expression levels of mitogen activated protein kinases (MAPK) and cyclooxygenase-2 (COX-2) were markedly downregulated by MA and FMA. Taken together, MA and FMA could ameliorate immobilized-stress by reducing oxidative stress, regulating stress-related hormones, and MAPK/COX-2 signaling pathways in rats. Particularly, FMA has shown greater anti-stress activities than MA. </P>

Anti-stress effects of Mentha arvensis inimmobilized rats

Weishun Tian,Rashedunnabi Aka,Anowarul Islam,Hae Dong Yang,Sang Cheon Lee,Jeong Ho Lee,Sang Ki Kim,Yu Jin Choi,So Yeon Im,Byung Yong Park 대한수의학회 2017 대한수의학회 학술대회발표집 Vol.2017 No.-

미세분진이 흰쥐의 폐포대식세포에서 TNF-α와 IL-1β의 형성에 미치는 효과

리천주 ( Tian Zhu Li ),이수진 ( Soo Jin Lee ),박세종 ( Se Jong Park ),장병준 ( Byung Joon Chang ),이종환 ( Jong Hwan Lee ),김길수 ( Kil Soo Kim ),이명헌 ( Myoung Heon Lee ),최농훈 ( Nong Hoon Choe ) 대한결핵 및 호흡기학회 2006 Tuberculosis and Respiratory Diseases Vol.60 No.5

연구배경: 대도시의 대기오염은 점차 악화되어 시민의 건강을 위협하고 심,폐 질환의 발병률과 이로 인한 사망률을 증가시키고 있다. 서울시 도로가의 PM이 TNF-α와 IL-1β의 생성에 직접적으로 어떠한 영향을 미치는지와 PM의 노출이 LPS의 TNF-α와 IL-1β의 생성효과에는 어떠한 영향을 미치는지를 평가하고자 하였다. 방법: 폐렴이 있는 흰쥐와 SPF 흰쥐의 폐포대식 세포 각각에 PM을 농도별로 처리하여 분비되는 TNF-α와 IL-1β의 농도를 측정하였다. 측정 방법으로는 western blot, ELISA 및 세포면역화학염색법을 이용하였다. 또한 동일 PM 농도에서 배양시간을 달리하여 위와 같이 측정하였다. 결과: SPF인 흰쥐에서 분리된 폐포대식세포에 PM을 단독으로 투여하였을 때 대조군에 비해서 TNF-α와 IL-1β의 생성도가 모든 투여군에서 유의하게 증가하였으나, 투여용량의 증가에 따른 유의성은 없었다. 그러나 염증성인 쥐에서 분리된 폐포대식세포에서는 모든 투여군에서 대조군에 비하여 통계 학적으로 유의하게 증가하였으며, PM 투여농도의 증가에 따른 생성량도 유의하게 증가하였다. 결론: PM을 장기간 혹은 일정 농도 이상으로 흡입할 경우 폐포대식세포의 TNF-α와 IL-1β의 분비에 영향을 미쳐 새로운 폐질환을 유발할 수 있다. 그러므로 기존에 염증성 폐질환이나 기관지천식이 있는 환자가 미세먼지를 흡입할 경우에는 TNF-α와 IL-1β의 생성에 커다란 영향을 미쳐 호흡기 질환을 더욱 악화시킬 가능성이 있을 것으로 추정된다. Background: PM is known to induce various pulmonary diseases, including asthma, cancer, fibrosis and chronic bronchitis. Despite the epidemiological evidence the pathogenesis of PM-related pulmonary diseases is unclear. Methods: This study examined the effects of PM exposure on the secretion of TNF-α and IL-1β in the cultured alveolar macrophages. The cultured primary alveolar macrophages were treated with the medium, PM (5~20㎍/㎠), LPS (5ng/ml), and PM with LPS for 24h and 48h respectively. ELISA was used to assay the secreted TNF-α and IL-β in the culture medium. Western blotting was used to identify and determine the level of proteins isolated from the culture cells. The cells cultured in the Lab-Tek(R) chamber slides were stained with immunocytochemical stains. Results: PM induced TNF-α and IL-1β secretion in the culturing alveolar macrophages, collected from the SPF and inflammatory rats. However, the effects were only dose-dependent in the inflammatory macrophages. When the cells were co-treated with PM and LPS, there was a significant synergistic effect compared with the LPS in the both cell types. Conclusion: PM might be play an important role in the induction and/or potentiation of various lung diseases by oversecretion of TNF-α and IL-1β. (Tuberc Respir Dis 2006; 60: 554-563)