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- 저자 : Abraham ZHANG (검색결과 4 건)
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Impacts of Global Manufacturing Trends on Port Development: The Case of Hong Kong
Abraham ZHANG,Hui Shan LOH,Vinh Van THAI 한국해운물류학회 2015 The Asian journal of shipping and Logistics Vol.31 No.1
Global manufacturing trends may have profound implications for regional port development. This paper studies Hong Kong port (HKP), which has been one of the world’s busiest container ports since the 1990s. In recent years, global manufacturers have started to move away from its primary cargo base, the Chinese Pearl River Delta. This study investigates impacts of the emerging global manufacturing trends on HKP development. It is found that relocation of manufacturing to Western Guangdong benefits HKP, while other relocation destinations make HKP less attractive or even irrelevant. Based on the findings, government policies are discussed that may be formulated to support the growth of the port and wider port-related economy.
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Extracellular ATP Acts on Jasmonate Signaling to Reinforce Plant Defense
Tripathi, Diwaker,Zhang, Tong,Koo, Abraham J.,Stacey, Gary,Tanaka, Kiwamu American Society of Plant Biologists 2018 Plant Physiology Vol.176 No.1
<P>Extracellular ATP signaling, mediated by the P2K1 receptor, directly changes the stability of JAZ1 protein in JA signaling to boost plant defense response.</P><P>Damaged cells send various signals to stimulate defense responses. Recent identification and genetic studies of the plant purinoceptor, P2K1 (also known as DORN1), have demonstrated that extracellular ATP is a signal involved in plant stress responses, including wounding, perhaps to evoke plant defense. However, it remains largely unknown how extracellular ATP induces plant defense responses. Here, we demonstrate that extracellular ATP induces plant defense mediated through activation of the intracellular signaling of jasmonate (JA), a well-characterized defense hormone. In Arabidopsis (<I>Arabidopsis thaliana</I>) leaves, ATP pretreatment induced resistance against the necrotrophic fungus, <I>Botrytis cinerea</I>. The induced resistance was enhanced in the P2K1 receptor overexpression line, but reduced in the receptor mutant, <I>dorn1</I>-<I>3</I>. Mining the transcriptome data revealed that ATP induces a set of JA-induced genes. In addition, the P2K1-associated coexpression network contains defense-related genes, including those encoding jasmonate ZIM-domain (JAZ) proteins, which play key roles as repressors of JA signaling. We examined whether extracellular ATP impacts the stability of JAZ1 in Arabidopsis. The results showed that the JAZ1 stability decreased in response to ATP addition in a proteasome-dependent manner. This reduction required intracellular signaling via second messengers—cytosolic calcium, reactive oxygen species, and nitric oxide. Interestingly, the ATP-induced JAZ1 degradation was attenuated in the JA receptor mutant, <I>coi1</I>, but not in the JA biosynthesis mutant, <I>aos</I>, or upon addition of JA biosynthesis inhibitors. Immunoprecipitation analysis demonstrated that ATP increases the interaction between COI1 and JAZ1, suggesting direct cross talk between extracellular ATP and JA in intracellular signaling events. Taken together, these results suggest that extracellular ATP signaling directly impacts the JA signaling pathway to maximize plant defense responses.</P>
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Di Pietro Caterina,Öz Hasan H.,Zhang Ping-xia,Cheng Ee-chun,Martis Valentino,Bonfield Tracey L.,Kelley Thomas J.,Jubin Ronald,Abuchowski Abraham,Krause Diane S.,Egan Marie E.,Murray Thomas S.,Bruscia 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Overwhelming neutrophilic inflammation is a leading cause of lung damage in many pulmonary diseases, including cystic fibrosis (CF). The heme oxygenase-1 (HO-1)/carbon monoxide (CO) pathway mediates the resolution of inflammation and is defective in CF-affected macrophages (MΦs). Here, we provide evidence that systemic administration of PP-007, a CO releasing/O2 transfer agent, induces the expression of HO-1 in a myeloid differentiation factor 88 (MyD88) and phosphatidylinositol 3-kinase (PI3K)/ protein kinase B (AKT)-dependent manner. It also rescues the reduced HO-1 levels in CF-affected cells induced in response to lipopolysaccharides (LPS) or Pseudomonas aeruginosa (PA). Treatment of CF and muco-obstructive lung disease mouse models with a single clinically relevant dose of PP-007 leads to effective resolution of lung neutrophilia and to decreased levels of proinflammatory cytokines in response to LPS. Using HO-1 conditional knockout mice, we show that the beneficial effect of PP-007 is due to the priming of circulating monocytes trafficking to the lungs in response to infection to express high levels of HO-1. Finally, we show that PP-007 does not compromise the clearance of PA in the setting of chronic airway infection. Overall, we reveal the mechanism of action of PP-007 responsible for the immunomodulatory function observed in clinical trials for a wide range of diseases and demonstrate the potential use of PP-007 in controlling neutrophilic pulmonary inflammation by promoting the expression of HO-1 in monocytes/macrophages.
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