Analysis of the Role of Tariff Concessions in East Asia

While there are many studies focusing on the impacts of various trade policy agreements across the world in the recent years, there is not much focus in the literature on the extent to which these agreements are implemented later, in terms of the aspects agreed upon therein. In this paper, we firstly identify the past achievements of the Economic Partnership Agreements (EPAs) in East Asian regions in terms of tariff removals and suggest future rooms for further economic benefits from trade liberalization in the region. Secondly, we provide the tariff concession dataset in the GTAP Data Base, which distinguishes the tariff removals agreed in these EPAs in East Asia but not implemented yet, from the existing overall tariffs in the benchmark year. As the standard GTAP Data Base only incorporates enforced tariff reductions through the base year applied tariffs, to analyse future trade integration, it might be worth it to integer commitments that are not yet implemented. We do that at the HS6 levels for East Asian EPAs that allows us to compare the economic impacts of partial versus complete implementation of the trade liberalization agreed in East Asian EPAs. Our results suggest that taking those commitments into account economically matters and that such satellite dataset might be taken as actual baseline for future policy simulations.JEL Classification Codes: D58, F13, F14, F15, F17The earlier version of this study was presented at the 18th Annual Conference on Global Economic Analysis on 17-19 June, 2015 in Melbourne

East Asia tariff concession: A CGE analysis

While there are many studies focusing on the impacts of various trade policy agreements across the world in the recent years, there is not much focus in the literature on the extent to which these agreements are implemented later, in terms of the aspects agreed upon therein. In this paper, we identify the past achievements of the Economic Partnership Agreements (EPAs) in the East Asian regions in terms of tariff removals and suggest future rooms for further economic benefits from trade liberalization in the region. Secondly, we provide the tariff concession dataset in the GTAP database, which distinguishes the tariff removals agreed in these EPAs in East Asia but not implemented yet, from the existing overall tariffs in the benchmark year. The standard GTAP Data Base incorporates all tariff reductions that have been included in the agreements that are in force; however not all of them are implemented in reality. We have quantified the actual tariff removals in the East Asia EPAs at HS6 levels. These will be aggregated to GTAP sectoral level, to arrive at a GTAP-consistent tariff dataset that contains actually implemented tariffs in East Asia. This is suggested to be taken as the actual baseline for policy simulations in the future. Based on this dataset, we compare the economic impacts of partial versus complete implementation of the trade liberalization agreed in the East Asia EPAs. This is accomplished in two steps: firstly, we prepare simulations (using the Altertax tool, documented in Malcolm (1998), GTAP Technical Paper No: 12) to switch from the GTAP tariffs to the levels implied by our new tariff dataset; secondly, we evaluate the impacts of reducing the tariffs from the modified levels to those included in the standard GTAP Data Base. The second step gives the difference between completely implementing all tariff reductions included in the agreements and partial implementation that has been done in reality...

Nuclear translocation of MLKL enhances necroptosis by a RIP1/RIP3-independent mechanism in H9c2 cardiomyoblasts

Accumulating evidence suggests that necroptosis of cardiomyocytes contributes to cardiovascular diseases. Lethal disruption of the plasma membrane in necroptosis is induced by oligomers of mixed lineage kinase domain-like (MLKL) that is translocated to the membrane from the cytosol. However, the role played by cytoplasmic-nuclear shuttling of MLKL is unclear. Here, we tested the hypothesis that translocation of MLKL to the nucleus promotes the necroptosis of cardiomyocytes. Activation of the canonical necroptotic signaling pathway by a combination of TNF-α and zVAD (TNF/zVAD) increased nuclear MLKL levels in a RIP1-activity-dependent manner in H9c2 cells, a rat cardiomyoblast cell line. By use of site-directed mutagenesis, we found a nuclear export signal sequence in MLKL and prepared its mutant (MLKL-L280/283/284A), though a search for a nuclear import signal was unsuccessful. MLKL-L280/283/284A localized to both the cytosol and the nucleus. Expression of MLKL-L280/283/284A induced necroptotic cell death, which was attenuated by GppNHp, an inhibitor of Ran-mediated nuclear import, but not by inhibition of RIP1 activity or knockdown of RIP3 expression. GppNHp partly suppressed H9c2 cell death induced by TNF/zVAD treatment. These results suggest that MLKL that is translocated to the nucleus via RIP1-mediated necroptotic signaling enhances the necroptosis of cardiomyocytes through a RIP1-/RIP3-independent mechanism

Downregulation of extramitochondrial BCKDH and its uncoupling from AMP deaminase in type 2 diabetic OLETF rat hearts

Abstract Systemic branched‐chain amino acid (BCAA) metabolism is dysregulated in cardiometabolic diseases. We previously demonstrated that upregulated AMP deaminase 3 (AMPD3) impairs cardiac energetics in a rat model of obese type 2 diabetes, Otsuka Long‐Evans‐Tokushima fatty (OLETF). Here, we hypothesized that the cardiac BCAA levels and the activity of branched‐chain α‐keto acid dehydrogenase (BCKDH), a rate‐limiting enzyme in BCAA metabolism, are altered by type 2 diabetes (T2DM), and that upregulated AMPD3 expression is involved in the alteration. Performing proteomic analysis combined with immunoblotting, we discovered that BCKDH localizes not only to mitochondria but also to the endoplasmic reticulum (ER), where it interacts with AMPD3. Knocking down AMPD3 in neonatal rat cardiomyocytes (NRCMs) increased BCKDH activity, suggesting that AMPD3 negatively regulates BCKDH. Compared with control rats (Long‐Evans Tokushima Otsuka [LETO] rats), OLETF rats exhibited 49% higher cardiac BCAA levels and 49% lower BCKDH activity. In the cardiac ER of the OLETF rats, BCKDH‐E1α subunit expression was downregulated, while AMPD3 expression was upregulated, resulting in an 80% lower AMPD3‐E1α interaction compared to LETO rats. Knocking down E1α expression in NRCMs upregulated AMPD3 expression and recapitulated the imbalanced AMPD3‐BCKDH expressions observed in OLETF rat hearts. E1α knockdown in NRCMs inhibited glucose oxidation in response to insulin, palmitate oxidation, and lipid droplet biogenesis under oleate loading. Collectively, these data revealed previously unrecognized extramitochondrial localization of BCKDH in the heart and its reciprocal regulation with AMPD3 and imbalanced AMPD3‐BCKDH interactions in OLETF. Downregulation of BCKDH in cardiomyocytes induced profound metabolic changes that are observed in OLETF hearts, providing insight into mechanisms contributing to the development of diabetic cardiomyopathy