The Hong Kong construction industry has been a powerful engine behind the city's rapid urban development. It serves to improve the living environment and standards, create a connected society, promote Hong Kong's sustainable development, and enhance Hong Kong's long-term competitiveness. To tackle manpower shortfall and to enhance its efficiency, the industry also strives to become a leading techno-construction industry in the region. Being the coordinating body of the industry, the Construction Industry Council (CIC) is taking the lead in pushing the boundaries and bringing the industry's competitiveness to the next level. We ride the waves of change to anticipate and meet evolving challenges by promoting new initiatives such as modular design and fabrication, Building Information Modelling (BIM), renewable energy technologies, construction automation and robotisation. More initiatives like the above are needed to spur the industry to re-invent our construction processes and ensure that stakeholders in the value chain work in an integrated manner. This paper presents state-of-the-art R&D and technologies adopted in the Hong Kong construction industry, and highlights the challenges ahead of driving innovations in the industry. More importantly, an overarching vision of the construction industry is set to better serve the changing needs of the community. Innovative technologies and ideas are explored and exhibited to achieve the vision.

Background & AimsIdentification and validation of new functionally relevant and pharmacologically actionable targets for pancreatic ductal adenocarcinoma (PDAC) remains a great challenge. Premalignant acinar cell reprogramming (acinar-to-ductal metaplasia [ADM]) is a precursor of pancreatic intraepithelial neoplasia (PanIN) lesions that can progress to PDAC. This study investigated the role of proline-rich tyrosine kinase 2 (PYK2) in mutant Kras-induced and pancreatitis-associated ADM and PanIN formation, as well as in PDAC maintenance.MethodsGenetically engineered mouse models of mutant Kras (glycine 12 to aspartic acid) and Pyk2 deletion were used for investigating the role of PYK2 in PDAC genesis in mice. In vitro ADM assays were conducted using primary pancreatic acinar cells isolated from mice. Immunohistochemistry, immunofluorescence, and a series of biochemical experiments were used to investigate upstream regulators/downstream targets of PYK2 in pancreatic carcinogenesis. PDAC cell line xenograft experiments were performed to study the role of PYK2 and its downstream target in PDAC maintenance.ResultsPYK2 was increased substantially in ADM lesions induced by mutant Kras or inflammatory injury. Pyk2 deletion remarkably suppressed ADM and PanIN formation in a mutant Kras-driven and pancreatitis-associated PDAC model, whereas PYK2 knockdown substantially inhibited PDAC cell growth in vitro and in nude mice. This study uncovered a novel yes-associated protein 1/transcriptional co-activator with PDZ binding motif/signal transducer and activator of transcription 3/PYK2/β-catenin regulation axis in PDAC. Our results suggest that PYK2 contributes to PDAC genesis and maintenance by activating the Wnt/β-catenin pathway through directly phosphorylating β-cateninY654.ConclusionsThe current study uncovers PYK2 as a novel downstream effector of mutant KRAS signaling, a previously unrecognized mediator of pancreatitis-induced ADM and a novel intervention target for PDAC.

Inherited genetic variations in the melanocortin-1 receptor (MC1R) responsible for human red hair color (RHC-variants) are associated with impaired DNA damage repair and increased melanoma risk. MC1R signaling is critically dependent on palmitoylation, primarily mediated by the protein acyltransferase ZDHHC13. A better understanding of how ZDHHC13 is physiologically activated could help identify approaches to prevent melanomagenesis in red-heads. Here we report that AMPK phosphorylates ZDHHC13 at S208 to strengthen the interaction between ZDHHC13 and MC1R-RHC, leading to enhanced MC1R palmitoylation in red-heads. Consequently, phosphorylation of ZDHHC13 by AMPK increased MC1R-RHC downstream signaling. AMPK activation and MC1R palmitoylation repressed UVB-induced transformation of human melanocytes in vitro and delayed melanomagenesis in vivo in C57BL/6J-MC1R-RHC mice. The importance of AMPK to MC1R signaling was validated in human melanomas where AMPK upregulation correlated with expression of factors downstream from MC1R signaling and with prolonged patient survival. These findings suggest AMPK activation as a promising strategy to reduce melanoma risk, especially for individuals with red hair.