Smart Digital Signage With Eye Tracking System

Digital signage is a more effective advertising solution compared to the traditional sign board since it is able to show multimedia contents and the advertising information can be easily updated. Current digital signage system has limited user interactive capability. Besides that, current system also lacks a way to collect viewer’s behaviour for analytic purposes. With the advancement of information technology, smart signage system allows some interactions between the viewer and the signage. In this project, a smart digital signage system which is capable of interaction between a user’s mobile device and the signage system is proposed. The user’s application on the mobile device provides a convenience way for navigating and storing the digital advertisements shown on the signage system instead of having paper brochure. Besides interactive capability, the proposed system is also able to detect faces and eyes to count the users viewing duration for each advertisement shown on the display. The faces and eyes detection were implemented using Haar Cascaded classifier available in the OpenCV library. A sanity checking algorithm is proposed to filter out the wrong detected eyes and improve the overall detection rate. Test results showed that the implemented face and eyes detection function can achieve 82.5% of true positive rate and 17.5% of false negative rate. Test on the complete system showed that the proposed smart signage system is able to work as expected. It is able to collect the users’ viewing duration for each advertisement with an average error of less than 12%

Angiopoietin-like 4 induces a β-catenin-mediated upregulation of ID3 in fibroblasts to reduce scar collagen expression

In adult skin wounds, collagen expression rapidly re-establishes the skin barrier, although the resultant scar is aesthetically and functionally inferior to unwounded tissue. Although TGFβ signaling and fibroblasts are known to be responsible for scar-associated collagen production, there are currently no prophylactic treatments for scar management. Fibroblasts in crosstalk with wound keratinocytes orchestrate collagen expression, although the precise paracrine pathways involved remain poorly understood. Herein, we showed that the matricellular protein, angiopoietin-like 4 (ANGPTL4), accelerated wound closure and reduced collagen expression in diabetic and ANGPTL4-knockout mice. Similar observations were made in wild-type rat wounds. Using human fibroblasts as a preclinical model for mechanistic studies, we systematically elucidated that ANGPTL4 binds to cadherin-11, releasing membrane-bound β-catenin which translocate to the nucleus and transcriptionally upregulate the expression of Inhibitor of DNA-binding/differentiation protein 3 (ID3). ID3 interacts with scleraxis, a basic helix-loop-helix transcription factor, to inhibit scar-associated collagen types 1α2 and 3α1 production by fibroblasts. We also showed ANGPTL4 interaction with cadherin-11 in human scar tissue. Our findings highlight a central role for matricellular proteins such as ANGPTL4 in the attenuation of collagen expression and may have a broader implication for other fibrotic pathologies.ASTAR (Agency for Sci., Tech. and Research, S’pore)Published versio

Structural basis for distinct inflammasome complex assembly by human NLRP1 and CARD8

Nod-like receptor (NLR) proteins activate pyroptotic cell death and IL-1 driven inflammation by assembling and activating the inflammasome complex. Closely related sensor proteins NLRP1 and CARD8 undergo unique auto-proteolysis-dependent activation and are implicated in auto-inflammatory diseases; however, their mechanisms of activation are not understood. Here we report the structural basis of how the activating domains (FIINDUPA-CARD) of NLRP1 and CARD8 self-oligomerize to assemble distinct inflammasome complexes. Recombinant FIINDUPA-CARD of NLRP1 forms a two-layered filament, with an inner core of oligomerized CARD surrounded by an outer ring of FIINDUPA. Biochemically, self-assembled NLRP1-CARD filaments are sufficient to drive ASC speck formation in cultured human cells—a process that is greatly enhanced by NLRP1-FIINDUPA which forms oligomers in vitro. The cryo-EM structures of NLRP1-CARD and CARD8-CARD filaments, solved here at 3.7 Å, uncover unique structural features that enable NLRP1 and CARD8 to discriminate between ASC and pro-caspase-1. In summary, our findings provide structural insight into the mechanisms of activation for human NLRP1 and CARD8 and reveal how highly specific signaling can be achieved by heterotypic CARD interactions within the inflammasome complexes

Overview of the Observing System and Initial Scientific Accomplishments of the East Asian VLBI Network (EAVN)

The East Asian VLBI Network (EAVN) is an international VLBI facility in East Asia and is operated under mutual collaboration between East Asian countries, as well as part of Southeast Asian and European countries. EAVN currently consists of 16 radio telescopes and three correlators located in China, Japan, and Korea, and is operated mainly at three frequency bands, 6.7, 22, and 43 GHz with the longest baseline length of 5078 km, resulting in the highest angular resolution of 0.28 milliarcseconds at 43 GHz. One of distinct capabilities of EAVN is multi-frequency simultaneous data reception at nine telescopes, which enable us to employ the frequency phase transfer technique to obtain better sensitivity at higher observing frequencies. EAVN started its open-use program in the second half of 2018, providing a total observing time of more than 1100 h in a year. EAVN fills geographical gap in global VLBI array, resulting in enabling us to conduct contiguous high-resolution VLBI observations. EAVN has produced various scientific accomplishments especially in observations toward active galactic nuclei, evolved stars, and star-forming regions. These activities motivate us to initiate launch of the ’Global VLBI Alliance’ to provide an opportunity of VLBI observation with the longest baselines on the earth

Empagliflozin in Patients with Chronic Kidney Disease

Background The effects of empagliflozin in patients with chronic kidney disease who are at risk for disease progression are not well understood. The EMPA-KIDNEY trial was designed to assess the effects of treatment with empagliflozin in a broad range of such patients. Methods We enrolled patients with chronic kidney disease who had an estimated glomerular filtration rate (eGFR) of at least 20 but less than 45 ml per minute per 1.73 m(2) of body-surface area, or who had an eGFR of at least 45 but less than 90 ml per minute per 1.73 m(2) with a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of at least 200. Patients were randomly assigned to receive empagliflozin (10 mg once daily) or matching placebo. The primary outcome was a composite of progression of kidney disease (defined as end-stage kidney disease, a sustained decrease in eGFR to < 10 ml per minute per 1.73 m(2), a sustained decrease in eGFR of & GE;40% from baseline, or death from renal causes) or death from cardiovascular causes. Results A total of 6609 patients underwent randomization. During a median of 2.0 years of follow-up, progression of kidney disease or death from cardiovascular causes occurred in 432 of 3304 patients (13.1%) in the empagliflozin group and in 558 of 3305 patients (16.9%) in the placebo group (hazard ratio, 0.72; 95% confidence interval [CI], 0.64 to 0.82; P < 0.001). Results were consistent among patients with or without diabetes and across subgroups defined according to eGFR ranges. The rate of hospitalization from any cause was lower in the empagliflozin group than in the placebo group (hazard ratio, 0.86; 95% CI, 0.78 to 0.95; P=0.003), but there were no significant between-group differences with respect to the composite outcome of hospitalization for heart failure or death from cardiovascular causes (which occurred in 4.0% in the empagliflozin group and 4.6% in the placebo group) or death from any cause (in 4.5% and 5.1%, respectively). The rates of serious adverse events were similar in the two groups. Conclusions Among a wide range of patients with chronic kidney disease who were at risk for disease progression, empagliflozin therapy led to a lower risk of progression of kidney disease or death from cardiovascular causes than placebo