Children gain a valuable insight into Hong Kong’s waterworks by directing the flow of water at an attraction designed to emulate the water cycle at the Water Supplies Department’s brand new H2OPE Centre.

They learn how rain passes through catchwaters in mountains and is filtered and distributed to people’s homes at the attraction, one of the 54 games or displays at the water education centre.

Kids can also try their hand at a fishing simulator to learn about tips and advice on fishing in reservoirs and discover ways to recycle and save water at other exhibits of the 720-sq m centre, which opened in December.

“It is extremely fun. We do not have this at school. I know how to save water now,” student Kim Lam said.

“Usually, we sit in a classroom and answer questions. But now we can learn about water in Hong Kong by playing games. It is excellent,” fellow student Alan Zeng added.

Children can also watch immersive videos at the centre’s 3D dome theatre.

Deeper understanding

The department hopes the centre will raise public awareness about water conservation.

“Its exhibits, live demonstrations and interactive games help visitors gain more insight into Hong Kong’s water resources,” Water Supplies Department Senior Engineer Irene Tong explained.

People can also visit the city’s important waterworks facilities such as the Waterworks Heritage Trails and the High Island Reservoir in Sai Kung, by joining the department’s Excursion with Water Save Dave. 

Water Save Dave is the department’s mascot to help promote a water conservation culture in the community.

Water Supplies Department Engineer Fion Chan said: “Water Save Dave is blue and shaped like a water drop to encourage us to cherish every single drop of water.

“We hope that guided tours of waterworks facilities will raise the public’s awareness about water resources and conservation.”

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There is no special announcement (19:45 HKT on 03.05.2020)

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Like many of his classmates, Dr. Faheem Ahmed started the spring semester, primed to put the finishing touches on his MBA. But after COVID-19 began to spread, he relocated to his home in London to complete his degree remotely and work on the frontline of the crisis.

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Rt Hon Jeremy Wright QC MP, Attorney General, UK
Chair: Elizabeth Wilmshurst CMG, Distinguished Fellow, Chatham House

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Priorities, practices and principles in a digital age

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The canonical pathway of eicosanoid production in most mammalian cells is initiated by phospholipase A2-mediated release of arachidonic acid, followed by its enzymatic oxidation resulting in a vast array of eicosanoid products. However, recent work has demonstrated that the major phospholipase in mitochondria, iPLA2γ (patatin-like phospholipase domain containing 8 (PNPLA8)), possesses sn-1 specificity, with polyunsaturated fatty acids at the sn-2 position generating polyunsaturated sn-2-acyl lysophospholipids. Through strategic chemical derivatization, chiral chromatographic separation, and multistage tandem MS, here we first demonstrate that human platelet-type 12-lipoxygenase (12-LOX) can directly catalyze the regioselective and stereospecific oxidation of 2-arachidonoyl-lysophosphatidylcholine (2-AA-LPC) and 2-arachidonoyl-lysophosphatidylethanolamine (2-AA-LPE). Next, we identified these two eicosanoid-lysophospholipids in murine myocardium and in isolated platelets. Moreover, we observed robust increases in 2-AA-LPC, 2-AA-LPE, and their downstream 12-LOX oxidation products, 12(S)-HETE-LPC and 12(S)-HETE-LPE, in calcium ionophore (A23187)-stimulated murine platelets. Mechanistically, genetic ablation of iPLA2γ markedly decreased the calcium-stimulated production of 2-AA-LPC, 2-AA-LPE, and 12-HETE-lysophospholipids in mouse platelets. Importantly, a potent and selective 12-LOX inhibitor, ML355, significantly inhibited the production of 12-HETE-LPC and 12-HETE-LPE in activated platelets. Furthermore, we found that aging is accompanied by significant changes in 12-HETE-LPC in murine serum that were also markedly attenuated by iPLA2γ genetic ablation. Collectively, these results identify previously unknown iPLA2γ-initiated signaling pathways mediated by direct 12-LOX oxidation of 2-AA-LPC and 2-AA-LPE. This oxidation generates previously unrecognized eicosanoid-lysophospholipids that may serve as biomarkers for age-related diseases and could potentially be used as targets in therapeutic interventions.

Fatty acid transport protein 2 (FATP2) is highly expressed in the liver, small intestine, and kidney, where it functions in both the transport of exogenous long-chain fatty acids and the activation of very-long-chain fatty acids. Here, using a murine model, we investigated the phenotypic impacts of deleting FATP2, followed by a transcriptomic analysis using unbiased RNA-Seq to identify concomitant changes in the liver transcriptome. WT and FATP2-null (Fatp2−/−) mice (5 weeks) were maintained on a standard chow diet for 6 weeks. The Fatp2−/− mice had reduced weight gain, lowered serum triglyceride, and increased serum cholesterol levels and attenuated dietary fatty acid absorption. Transcriptomic analysis of the liver revealed 258 differentially expressed genes in male Fatp2−/− mice and a total of 91 in female Fatp2−/− mice. These genes mapped to the following gene ontology categories: fatty acid degradation, peroxisome biogenesis, fatty acid synthesis, and retinol and arachidonic acid metabolism. Targeted RT-quantitative PCR verified the altered expression of selected genes. Of note, most of the genes with increased expression were known to be regulated by peroxisome proliferator–activated receptor α (PPARα), suggesting that FATP2 activity is linked to a PPARα-specific proximal ligand. Targeted metabolomic experiments in the Fatp2−/− liver revealed increases of total C16:0, C16:1, and C18:1 fatty acids; increases in lipoxin A4 and prostaglandin J2; and a decrease in 20-hydroxyeicosatetraenoic acid. We conclude that the expression of FATP2 in the liver broadly affects the metabolic landscape through PPARα, indicating that FATP2 provides an important role in liver lipid metabolism through its transport or activation activities.