The Education Bureau and the Agriculture, Fisheries & Conservation Department (AFCD) today announced their latest arrangements on public services starting May 4.

All Regional Education Offices, the Joint Office for Kindergartens & Child Care Centres, the School Places Allocation Section, the Qualifications Framework Secretariat and other service units will resume normal opening hours from May 4.

However, the Hong Kong Teachers' Centre, Special Education Resource Centre, Central Resources Centre and Young Achievers' Gallery located at Kowloon Tong Education Services Centre, as well as the Arts & Technology Education Centre will remain closed until further notice.

The AFCD’s licensing services and reception counters at Cheung Sha Wan Government Offices and the Marine Parks Office at CDW Building in Tsuen Wan will resume normal services Monday to Friday from 8.30am to 12.30pm and 1.30pm to 5.45pm.

The anti-rabies dog inoculation and dog licensing services at the animal management centres will also resume as normal from May 4.

Meanwhile, the Hong Kong Wetland Park (except some indoor facilities and play areas), eight Country Park Visitor/Education Centres, seven Hong Kong Geopark Park Visitor Centres and the Endangered Species Resources Centre will reopen from May 4.

However, school and public programmes will remain suspended until further notice.

The barbecue sites and campsites in country parks will also continue to be closed until May 7.

Click here for the latest public service arrangements.

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Taewook Kang
Apr 7, 2020; 0:RA119.001882v1-mcp.RA119.001882
Research

The onset of obesity-linked type 2 diabetes (T2D) is marked by an eventual failure in pancreatic β-cell function and mass that is no longer able to compensate for the inherent insulin resistance and increased metabolic load intrinsic to obesity. However, in a commonly used model of T2D, the db/db mouse, β-cells have an inbuilt adaptive flexibility enabling them to effectively adjust insulin production rates relative to the metabolic demand. Pancreatic β-cells from these animals have markedly reduced intracellular insulin stores, yet high rates of (pro)insulin secretion, together with a substantial increase in proinsulin biosynthesis highlighted by expanded rough endoplasmic reticulum and Golgi apparatus. However, when the metabolic overload and/or hyperglycemia is normalized, β-cells from db/db mice quickly restore their insulin stores and normalize secretory function. This demonstrates the β-cell’s adaptive flexibility and indicates that therapeutic approaches applied to encourage β-cell rest are capable of restoring endogenous β-cell function. However, mechanisms that regulate β-cell adaptive flexibility are essentially unknown. To gain deeper mechanistic insight into the molecular events underlying β-cell adaptive flexibility in db/db β-cells, we conducted a combined proteomic and post-translational modification specific proteomic (PTMomics) approach on islets from db/db mice and wild-type controls (WT) with or without prior exposure to normal glucose levels. We identified differential modifications of proteins involved in redox homeostasis, protein refolding, K48-linked deubiquitination, mRNA/protein export, focal adhesion, ERK1/2 signaling, and renin-angiotensin-aldosterone signaling, as well as sialyltransferase activity, associated with β-cell adaptive flexibility. These proteins are all related to proinsulin biosynthesis and processing, maturation of insulin secretory granules, and vesicular trafficking—core pathways involved in the adaptation of insulin production to meet metabolic demand. Collectively, this study outlines a novel and comprehensive global PTMome signaling map that highlights important molecular mechanisms related to the adaptive flexibility of β-cell function, providing improved insight into disease pathogenesis of T2D.

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