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Thermal Aware Buffer Insertion in the Early Stage of Physical Designs
Kim, Jaehwan,Ahn, Byung-Gyu,Kim, Minbeom,Chong, Jongwha The Institute of Electronics and Information Engin 2012 Journal of semiconductor technology and science Vol.12 No.4
Thermal generation by power dissipation of the highly integrated System on Chip (SoC) device is irregularly distributed on the intra chip. It leads to thermal increment of the each thermally different region and effects on the propagation timing; consequently, the timing violation occurs due to the misestimated number of buffers. In this paper, the timing budgeting methodology considering thermal variation which contains buffer insertion with wire segmentation is proposed. Thermal aware LUT modeling for cell intrinsic delay is also proposed. Simulation results show the reduction of the worst delay after implementing thermal aware buffer insertion using by proposed wire segmentation up to 33% in contrast to the original buffer insertion. The error rates are measured by SPICE simulation results.
Thermal Aware Buffer Insertion in the Early Stage of Physical Designs
Jaehwan Kim,Byung-gyu Ahn,Minbeom Kim,Jongwha Chong 대한전자공학회 2012 Journal of semiconductor technology and science Vol.12 No.4
Thermal generation by power dissipation of the highly integrated System on Chip (SoC) device is irregularly distributed on the intra chip. It leads to thermal increment of the each thermally different region and effects on the propagation timing; consequently, the timing violation occurs due to the misestimated number of buffers. In this paper, the timing budgeting methodology considering thermal variation which contains buffer insertion with wire segmentation is proposed. Thermal aware LUT modeling for cell intrinsic delay is also proposed. Simulation results show the reduction of the worst delay after implementing thermal aware buffer insertion using by proposed wire segmentation up to 33% in contrast to the original buffer insertion. The error rates are measured by SPICE simulation results.
비아환(肥兒丸)이 난소적출로 유발된 흰쥐의 골다공증 모델에 미치는 영향
조창영 ( Chang-young Cho ),김은영 ( Eun-young Kim ),김동희 ( Dong Hee Kim ),김민범 ( Minbeom Kim ),김상배 ( Sang-bae Kim ),양규진 ( Kyujin Yang ),손영주 ( Youngjoo Sohn ),정혁상 ( Hyuk-sang Jung ) 대한한의학회 한방재활의학과학회 2017 한방재활의학과학회지 Vol.27 No.2
Objectives Osteoporosis is a common disease in adults with prevalence rate of more than 40%, and occurs more to female than to male. The purpose of this study is to identify the effect of Bia-hwan (Feier-wan) on the osteoporosis of ovariectomized rats. Methods 24 female rats were randomly assigned to a SHAM group, a control group, and a BAH group. Ovaries of the control group and the BAH group were extracted. After than, general animal feed were given to the SHAM group and the control group, animal feed contained BAH were given to the BAH group through mouths of them. After 8 weeks, rats were sacrificed and their weight, calcium, phosphorus, estradiol, total-cholesterol, triglyceride, ALP, albumin, AST, ALT, the weight of femur and tibia ash per body ratio, both area and thickness of trabecular bone, the area of osteoblast and the number of osteoclast were measured. Results The level of calcium, phosphorus, AST in the serum of the BAH group increased significantly compared to the control group. There was no significant difference between the control group and the BAH group in the level of estradiol, total-cholesterol, triglyceride, ALP, albumin, and ALT in the serum. There was no significant difference between the control group and the BAH group in the weight of femur and tibia ash per body ratio. The thickness of trabecular of the BAH group increased significantly compared to the control group, but there was no significant difference in the trabecular area. The area of osteoblast and the number of osteoclast of the BAH group decreased significantly compared to the control group. Conclusions From the results of the above study, oral intake of BAH can inhibit the decrease of calcium, phosphorus in blood and prevent the thinning process of the trabecular by suppressing activation of osteoclast. Thus, BAH may have effects on the treatment and prevention of osteoporosis. (J Korean Med Rehabil 2017;27(2):19-27)
Lee, Ji-Hyung,Jung, Su Myung,Yang, Kyung-Min,Bae, Eunjin,Ahn, Sung Gwe,Park, Jin Seok,Seo, Dongyeob,Kim, Minbeom,Ha, Jihoon,Lee, Jaewon,Kim, Jun-Hyeong,Kim, Jun Hwan,Ooshima, Akira,Park, Jinah,Shin, D Nature Publishing Group 2017 NATURE CELL BIOLOGY Vol. No.
Although the ubiquitin-editing enzyme A20 is a key player in inflammation and autoimmunity, its role in cancer metastasis remains unknown. Here we show that A20 monoubiquitylates Snail1 at three lysine residues and thereby promotes metastasis of aggressive basal-like breast cancers. A20 is significantly upregulated in human basal-like breast cancers and its expression level is inversely correlated with metastasis-free patient survival. A20 facilitates TGF-β1-induced epithelial–mesenchymal transition (EMT) of breast cancer cells through multi-monoubiquitylation of Snail1. Monoubiquitylated Snail1 has reduced affinity for glycogen synthase kinase 3β (GSK3β), and is thus stabilized in the nucleus through decreased phosphorylation. Knockdown of A20 or overexpression of Snail1 with mutation of the monoubiquitylated lysine residues into arginine abolishes lung metastasis in mouse xenograft and orthotopic breast cancer models, indicating that A20 and monoubiquitylated Snail1 are required for metastasis. Our findings uncover an essential role of the A20–Snail1 axis in TGF-β1-induced EMT and metastasis of basal-like breast cancers.
Lee Jaewon,Ha Jihoon,Kim Jun-Hyeong,Seo Dongyeob,Kim Minbeom,Lee Yerin,Park Seong Shil,Choi Dahee,Park Jin Seok,Lee Young Jae,Yang Siyoung,Yang Kyung-Min,Jung Su Myung,Hong Suntaek,Koo Seung-Hoi,Bae Y 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
The signaling pathways governing acetaminophen (APAP)-induced liver injury have been extensively studied. However, little is known about the ubiquitin-modifying enzymes needed for the regulation of APAP-induced liver injury. Here, we examined whether the Pellino3 protein, which has E3 ligase activity, is needed for APAP-induced liver injury and subsequently explored its molecular mechanism. Whole-body Peli3−/− knockout (KO) and adenovirus-mediated Peli3 knockdown (KD) mice showed reduced levels of centrilobular cell death, infiltration of immune cells, and biomarkers of liver injury, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), upon APAP treatment compared to wild-type (WT) mice. Peli3 deficiency in primary hepatocytes decreased mitochondrial and lysosomal damage and reduced the mitochondrial reactive oxygen species (ROS) levels. In addition, the levels of phosphorylation at serine 9 in the cytoplasm and mitochondrial translocation of GSK3β were decreased in primary hepatocytes obtained from Peli3−/− KO mice, and these reductions were accompanied by decreases in JNK phosphorylation and mitochondrial translocation. Pellino3 bound more strongly to GSK3β compared with JNK1 and JNK2 and induced the lysine 63 (K63)-mediated polyubiquitination of GSK3β. In rescue experiments, the ectopic expression of wild-type Pellino3 in Peli3−/− KO hepatocytes restored the mitochondrial translocation of GSK3β, but this restoration was not obtained with expression of a catalytically inactive mutant of Pellino3. These findings are the first to suggest a mechanistic link between Pellino3 and APAP-induced liver injury through the modulation of GSK3β polyubiquitination.