Mixed reality entertainment systems for social and physical human interaction

Master'sMASTER OF ENGINEERIN

Mixed Reality Human Media for Social and Physical Interaction

Abstract: This paper outlines new facilities within ubiquitous human media spaces supporting embodied interaction between humans and computation both socially and physically. We believe that the current approach to developing electronic based design environments is lacking with regard to support for multi-person multi-modal design interactions. In this paper, we present an alternative ubiquitous computing environment based on an integrated design of real and virtual worlds. We implement three different research prototype systems: the Virtual Kyoto Garden, Touchy Internet, and the Human Pacman. The functional capabilities implemented in these systems include spatially-aware 3D navigation, tangible interaction, and ubiquitous human media spaces. Some of its details, benefits, and issues regarding design support are discussed

HNF4A Haploinsufficiency in MODY1 Abrogates Liver and Pancreas Differentiation from Patient-Derived Induced Pluripotent Stem Cells.

Maturity-onset diabetes of the young 1 (MODY1) is a monogenic diabetes condition caused by heterozygous HNF4A mutations. We investigate how HNF4A haploinsufficiency from a MODY1/HNF4A mutation influences the development of foregut-derived liver and pancreatic cells through differentiation of human induced pluripotent stem cells from a MODY1 family down the foregut lineage. In MODY1-derived hepatopancreatic progenitors, which expressed reduced HNF4A levels and mislocalized HNF4A, foregut genes were downregulated, whereas hindgut-specifying HOX genes were upregulated. MODY1-derived hepatocyte-like cells were found to exhibit altered morphology. Hepatic and β cell gene signatures were also perturbed in MODY1-derived hepatocyte-like and β-like cells, respectively. As mutant HNF4A (p.Ile271fs) did not undergo complete nonsense-mediated decay or exert dominant negativity, HNF4A-mediated loss of function is likely due to impaired transcriptional activation of target genes. Our results suggest that in MODY1, liver and pancreas development is perturbed early on, contributing to altered hepatic proteins and β cell defects in patients

HNF4A haploinsufficiency in MODY1 abrogates liver and pancreas differentiation from patient-derived induced pluripotent stem cells

Maturity-onset diabetes of the young 1 (MODY1) is a monogenic diabetes condition caused by heterozygous HNF4A mutations. We investigate how HNF4A haploinsufficiency from a MODY1/HNF4A mutation influences the development of foregut-derived liver and pancreatic cells through differentiation of human induced pluripotent stem cells from a MODY1 family down the foregut lineage. In MODY1-derived hepatopancreatic progenitors, which expressed reduced HNF4A levels and mislocalized HNF4A, foregut genes were downregulated, whereas hindgut-specifying HOX genes were upregulated. MODY1-derived hepatocyte-like cells were found to exhibit altered morphology. Hepatic and β cell gene signatures were also perturbed in MODY1-derived hepatocyte-like and β-like cells, respectively. As mutant HNF4A (p.Ile271fs) did not undergo complete nonsense-mediated decay or exert dominant negativity, HNF4A-mediated loss of function is likely due to impaired transcriptional activation of target genes. Our results suggest that in MODY1, liver and pancreas development is perturbed early on, contributing to altered hepatic proteins and β cell defects in patients.publishedVersio

Benchmarking the competitiveness of Singapore as a manufacturing location

107 p.In the wake of economic liberalization in the Asia-Pacific region, competition from emerging economies is intensifying and Singapore must compete for direct investment from multinational companies (MNCs). In the past, these investments have contributed significantly to Singapore's economic growth, and for Singapore to continue to sustain its high economic growth, a reassessment of Singapore's competitive position as a manufacturing base for MNCs is crucial.ACCOUNTANC

LIPID MICROEMULSION-BASED HYDROGELS FOR EFFECTIVE TOPICAL DELIVERY OF PHENYTOIN

Objective: Microemulsion is a promising drug delivery vehicle for lipophilic drugs but its acceptability for topical application is limited to its very low viscosity. The aim of the present study was to develop and characterize lipid microemulsion hydrogel as a topical drug carrier for phenytoin.Methods: Lipid oil-in-water (O/W) emulsions were formulated from palm kernel oil (PKO), coconut kernel oil (CKO) and soybean oil (SBO), and their blends using phase inversion temperature method. Stable nano-sized microemulsions were identified and formulated into phenytoin loaded hydrogels. The physicochemical properties of the formulations were evaluated in term of emulsion stability index, droplet size, zeta potential, pH, and rheological properties. The efficacy of in vitro drug release of phenytoin was further evaluated using Franz diffusion cells.Results: Stability study revealed that ten lipid emulsions mixing with surfactant Tween 80 at an oil-to-surfactant ratio of 1:9 having 100% emulsion stability indices. Among these, two emulsions (F6 and F21) were identified as the most stable nano-sized microemulsions with clear and transparent appearances; mean droplet size maintained within 100 nm (11–16 nm) as per stability study. Rheological data showed that all phenytoin is loaded hydrogels exhibited non-Newtonian and shear-thinning flow behavior, with high yield stress of a 10.3–18.8 Pa. The in vitro release profiles followed the first-order kinetic model, with R2>0.95, where F21 demonstrated the highest release rate, with 93.12% drug released in 12 h.Conclusion: These findings concluded that CKO/SBO blend microemulsion hydrogel has the highest potential for topical phenytoin delivery

Adapting perturbation voltage in PV array with power point tracking and differential evolution

The power output of photovoltaic array may reduce as the photovoltaic panels’ connection close to each other and lead to the occurrence of partials shading. Under partial shading condition, the unshaded modules of PV array receive solar irradiation at higher level, while the shaded module of PV array receives lower irradiation. Thus, multiple maximum power point also will occur under the partial shading condition. The proposed modelling in this paper is 4x4 PV array and tested two different conditions in partial shading condition (PSC) where there are random irradiance values that had been set. Therefore, this paper aim to model more than one PV array and the platform modelling for this paper is 4x4 PV array. Besides that, explore the conventional method which is Perturb and Observe (P&O) based MPPT controller in optimizing the efficiency of the PV array. Unfortunately, the conventional method only can trap the power at the local maximum power under partial shading conditions. Thus, the proposed algorithm that used to track the maximum power is differential evolution (DE) in order to improve the power output of the PV array. The simulation results shows the proposed DE able to track the global MPP

Single-cell analyses of human islet cells reveal de-differentiation signatures

Abstract Human pancreatic islets containing insulin-secreting β-cells are notoriously heterogeneous in cell composition. Since β-cell failure is the root cause of diabetes, understanding this heterogeneity is of paramount importance. Recent reports have cataloged human islet transcriptome but not compared single β-cells in detail. Here, we scrutinized ex vivo human islet cells from healthy donors and show that they exhibit de-differentiation signatures. Using single-cell gene expression and immunostaining analyses, we found healthy islet cells to contain polyhormonal transcripts, and INS+ cells to express decreased levels of β-cell genes but high levels of progenitor markers. Rare cells that are doubly positive for progenitor markers/exocrine signatures, and endocrine/exocrine hormones were also present. We conclude that ex vivo human islet cells are plastic and can possibly de-/trans-differentiate across pancreatic cell fates, partly accounting for β-cell functional decline once isolated. Therefore, stabilizing β-cell identity upon isolation may improve its functionality

HNF4A haploinsufficiency in MODY1 abrogates liver and pancreas differentiation from patient-derived induced pluripotent stem cells

Maturity-onset diabetes of the young 1 (MODY1) is a monogenic diabetes condition caused by heterozygous HNF4A mutations. We investigate how HNF4A haploinsufficiency from a MODY1/HNF4A mutation influences the development of foregut-derived liver and pancreatic cells through differentiation of human induced pluripotent stem cells from a MODY1 family down the foregut lineage. In MODY1-derived hepatopancreatic progenitors, which expressed reduced HNF4A levels and mislocalized HNF4A, foregut genes were downregulated, whereas hindgut-specifying HOX genes were upregulated. MODY1-derived hepatocyte-like cells were found to exhibit altered morphology. Hepatic and β cell gene signatures were also perturbed in MODY1-derived hepatocyte-like and β-like cells, respectively. As mutant HNF4A (p.Ile271fs) did not undergo complete nonsense-mediated decay or exert dominant negativity, HNF4A-mediated loss of function is likely due to impaired transcriptional activation of target genes. Our results suggest that in MODY1, liver and pancreas development is perturbed early on, contributing to altered hepatic proteins and β cell defects in patients