Hardware-Software Implementation of MPEG-4 Video Codec

김성민,서기범,엄낙웅,김경숙,Ju-HyunPark,Seong-MoPark,Bon-TaeKoo,Kyoung-SeonShin,Ig-KyunKim 한국전자통신연구원 2003 ETRI Journal Vol.25 No.6

This paper presents an MPEG-4 video codec, called MoVa, for video coding applications that adopts 3G-324M. We designed MoVa to be optimal by embedding a costeffective ARM7TDMI core and partitioning it into hardwired blocks and firmware blocks to provide a reasonable tradeoff between computational requirements, power consumption, and programmability. Typical hardwired blocks are motion estimation and motion compensation, discrete cosine transform and quantization, and variable length coding and decoding, while intra refresh, rate control, error resilience, error concealment, etc. are implemented by software. MoVa has a pipeline structure and its operation is performed in four stages at encoding and in three stages at decoding. It meets the requirements of MPEG-4 SP@L2 and can perform either 30 frames/s (fps) of QCIF or SQCIF, or 7.5 fps (in codec mode) to 15 fps (in encode/decode mode) of CIF at a maximum clock rate of 27 MHz for 128 kbps or 144 kbps. MoVa can be applied to many video systems requiring a high bit rate and various video formats, such as videophone, videoconferencing, surveillance, news, and entertainment.

Quinic acid inhibits vascular inflammation in TNF-α-stimulated vascular smooth muscle cells

Jang, Seon-A,Park, Dae Won,Kwon, Jeong Eun,Song, Hae Seong,Park, Bongkyun,Jeon, Hyelin,Sohn, Eun-Hwa,Koo, Hyun Jung,Kang, Se Chan EDITIONS SCIENTIFIQUES ELSEVIER 2017 BIOMEDICINE AND PHARMACOTHERAPY Vol.96 No.-

<P> Atherosclerosis is a chronic inflammatory disease, and the increased expression of adhesion molecules on vascular smooth muscle cells contributes to the progression of vascular disease. Quinic acid (QA) has been shown to possess radioprotection, anti-neuroinflammatory, and anti-oxidant activities; however, an anti-vascular inflammatory effect has not been reported. This study investigated the effect of QA on the expression of vascular cell adhesion molecule-1 (VCAM-1) stimulated by TNF-α in MOVAS cells. Pre-incubation of MOVAS cells, the mouse vascular smooth muscle cell line for 2 h with QA (0.1, 1 and 10 μg/mL) dose-dependently inhibits TNF-α-induced mRNA and protein expression of VCAM-1 and monocyte adhesion. QA inhibits TNF-α-stimulated phosphorylation of MAP kinase and NK-κB activation. Our results indicate that QA inhibits the TNF-α-stimulated induction of VCAM-1 in VSMC by inhibiting the MAP kinase and NF-κB signaling pathways and the adhesion capacity of VSMC, which may explain the ability of QA to inhibit vascular inflammation such as atherosclerosis. </P>

중세 동슬라브의 문학어 형성에 관한 연구

김용화 한국러시아문학회 2011 러시아어문학 연구논집 Vol.36 No.-

Мы рассмотрели в данной статье образование и развитие средневосточнославянских литературных языков(далее ЛЯ), сравнивая Юго-западную Русь и Московскую Русь, и пришли к следующим выводам: (1) После ‘Второго южнославянского влияния’ в Юго-западной Руси оформлена ‘проста мова’(далее ПМ), возникшая на основе делового языка Юго-западной Руси, и она функционировала как ЛЯ в 16-17 вв. наряду с церковнослвянским(лалее ц-сл.) языком, а в Московской Руси внутри ц-сл. языка произошла дифференция на две стилистические разновидности, одна из которых перешла в ‘простой русский язык(далее ПЯ)’ в 18 в. (2) ПМ и ПЯ ориентированы на ‘простоту’ языка и игнорирование нормы ц-сл. языка. (3) На ПМ оказывали большое влияние польский язык и польские текстовые образцы, а они в свою очередь трансплантировались просто в ПМ и с ней не сливались, что обусловило неустойчивость системы ПМ. В отличие от ПМ, в ПЯ огранически соединились ц-сл., деловой и разговорный языки, употреблявшиеся в Московской Руси, что могло гарантировать в некоторой степени устойчивость системы ПЯ. (4) Принадлежащие Юго-западной Руси территории изменялись в зависимости от политических перемен несколько раз, а Московская Русь сохранила свою политическую и государственную идентичность. (5) ПМ изчезла в истории, не оставив никакого следа в современном украинском и белорусском ЛЯ, а ПЯ является ростком русского национального ЛЯ 2-ой половины 18 в., который через период поиска нормы утвержден как современный русский ЛЯ. (6) Исчезновение ПМ и сохранение ПЯ зависят, прежде всего, от факторов (3)-(5), т.е. неустойчивости /устойчивости системы ПМ и ПЯ и нестабильности/стабильности политических обстоятельств Юго-западной Руси и Москвоской Руси.

Lobaric Acid Inhibits VCAM-1 Expression in TNF-α-Stimulated Vascular Smooth Muscle Cells via Modulation of NF-κB and MAPK Signaling Pathways

Kwon, Ii-Seul,Yim, Joung-Han,Lee, Hong-Kum,Pyo, Suhkneung The Korean Society of Applied Pharmacology 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.1

Lichens have been known to possess multiple biological activities, including anti-proliferative and anti-inflammatory activities. Vascular cell adhesion molecule-1 (VCAM-1) may play a role in the development of atherosclerosis. Hence, VCAM-1 is a possible therapeutic target in the treatment of the inflammatory disease. However, the effect of lobaric acid on VCAM-1 has not yet been investigated and characterized. For this study, we examined the effect of lobaric acid on the inhibition of VCAM-1 in tumor necrosis factor-alpha (TNF-${\alpha}$)-stimulated mouse vascular smooth muscle cells. Western blot and ELISA showed that the increased expression of VCAM-1 by TNF-${\alpha}$ was significantly suppressed by the pre-treatment of lobaric acid ($0.1-10{\mu}g/ml$) for 2 h. Lobaric acid abrogated TNF-${\alpha}$-induced NF-${\kappa}B$ activity through preventing the degradation of $I{\kappa}B$ and phosphorylation of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK), and p38 mitogen activated protein (MAP) kinase. Lobaric acid also inhibited the expression of TNF-${\alpha}$ receptor 1 (TNF-R1). Overall, our results suggest that lobaric acid inhibited VCAM-1 expression through the inhibition of p38, ERK, JNK and NF-${\kappa}B$ signaling pathways, and downregulation of TNF-R1 expression. Therefore, it is implicated that lobaric acid may suppress inflammation by altering the physiology of the atherosclerotic lesion.

Lobaric Acid Inhibits VCAM-1 Expression in TNF-α-Stimulated Vascular Smooth Muscle Cells via Modulation of NF-kB and MAPK Signaling Pathways

권이슬,임정한,이홍금,표석능 한국응용약물학회 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.1

Lichens have been known to possess multiple biological activities, including anti-proliferative and anti-inflammatory activities. Vascular cell adhesion molecule-1 (VCAM-1) may play a role in the development of atherosclerosis. Hence, VCAM-1 is a possible therapeutic target in the treatment of the inflammatory disease. However, the effect of lobaric acid on VCAM-1 has not yet been investigated and characterized. For this study, we examined the effect of lobaric acid on the inhibition of VCAM-1 in tumor necrosis factor-alpha (TNF-α)-stimulated mouse vascular smooth muscle cells. Western blot and ELISA showed that the increased expression of VCAM-1 by TNF-α was significantly suppressed by the pre-treatment of lobaric acid (0.1-10 μg/ml) for 2 h. Lobaric acid abrogated TNF-α-induced NF-κB activity through preventing the degradation of IκB and phosphorylation of extracellular signalregulated kinases (ERK), c-Jun N-terminal kinases (JNK), and p38 mitogen activated protein (MAP) kinase. Lobaric acid also inhibited the expression of TNF-α receptor 1 (TNF-R1). Overall, our results suggest that lobaric acid inhibited VCAM-1 expression through the inhibition of p38, ERK, JNK and NF-κB signaling pathways, and downregulation of TNF-R1 expression. Therefore, it is implicated that lobaric acid may suppress inflammation by altering the physiology of the atherosclerotic lesion.

Lobaric Acid Inhibits VCAM-1 Expression in TNF-α-Stimulated Vascular Smooth Muscle Cells via Modulation of NF-kB and MAPK Signaling Pathways

( Ii Seul Kwon ),( Joung Han Yim ),( Hong Kum Lee ),( Suhkneung Pyo ) 한국응용약물학회 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.1

Lichens have been known to possess multiple biological activities, including anti-proliferative and anti-inflammatory activities. Vascular cell adhesion molecule-1 (VCAM-1) may play a role in the development of atherosclerosis. Hence, VCAM-1 is a possible therapeutic target in the treatment of the inflammatory disease. However, the effect of lobaric acid on VCAM-1 has not yet been investigated and characterized. For this study, we examined the effect of lobaric acid on the inhibition of VCAM-1 in tumor necrosis factor-alpha (TNF-α)-stimulated mouse vascular smooth muscle cells. Western blot and ELISA showed that the increased expression of VCAM-1 by TNF-α was significantly suppressed by the pre-treatment of lobaric acid (0.1-10 μg/ml) for 2 h. Lobaric acid abrogated TNF-α-induced NF-κB activity through preventing the degradation of IκB and phosphorylation of extracellular signalregulated kinases (ERK), c-Jun N-terminal kinases (JNK), and p38 mitogen activated protein (MAP) kinase. Lobaric acid also inhibited the expression of TNF-α receptor 1 (TNF-R1). Overall, our results suggest that lobaric acid inhibited VCAM-1 expression through the inhibition of p38, ERK, JNK and NF-κB signaling pathways, and downregulation of TNF-R1 expression. Therefore, it is implicated that lobaric acid may suppress inflammation by altering the physiology of the atherosclerotic lesion.

중세 동슬라브의 문학어 형성에 관한 연구

김용화 한국러시아문학회 2011 러시아어문학 연구논집 Vol.36 No.-