The Urban fabric: upcycling textile waste into raw material for urban ground surface design

Landscape surface materials have the opportunity to ground us in our experience and use of materials in the built environment. Surface materials describe the physical textures of the urban areas and include soft and hard landscape solutions, streetscapes, and roads. In modern landscape design, turf, concrete, asphalt, brick or rubber are the most common materials for urban parks or playgrounds. However, the unlimited use of, and lack of awareness about urban landscape surface materials has become a common trend. This “take-make-discard” culture has negatively impacted our environment ecologically, economically, and socially. This thesis study focuses on upcycling textile waste into a recyclable, degradable, and decomposable material for public pavements, especially in public parks and playgrounds. It aims to understand the larger landscape and ecological impacts of existing materials in comparison to a new set of proposed materials, while also revealing the potential opportunities of utilizing circular second-hand material strategies. The material exploration combines research and critique of existing surface materials with an investigation of recycling strategies of textile materials. It then proposes new types of hybrid surface materials that embrace weathering by adding the degradable characteristic of textiles as a new standpoint for thinking about ground surfaces. Ultimately, this research studies the benefits and negative impacts on the environment of public parks from the perspectives offered by this new set of proposed materials, as well as their social interactions and economic conditions

Graph-Driven Generative Models for Heterogeneous Multi-Task Learning

We propose a novel graph-driven generative model, that unifies multiple heterogeneous learning tasks into the same framework. The proposed model is based on the fact that heterogeneous learning tasks, which correspond to different generative processes, often rely on data with a shared graph structure. Accordingly, our model combines a graph convolutional network (GCN) with multiple variational autoencoders, thus embedding the nodes of the graph i.e., samples for the tasks) in a uniform manner while specializing their organization and usage to different tasks. With a focus on healthcare applications (tasks), including clinical topic modeling, procedure recommendation and admission-type prediction, we demonstrate that our method successfully leverages information across different tasks, boosting performance in all tasks and outperforming existing state-of-the-art approaches.Comment: Accepted by AAAI-202

IKKbeta Deficiency in Myeloid Cells Ameliorates Alzheimer's Disease-Related Symptoms and Pathology

Alzheimer's disease (AD) is characterized by extracellular amyloid-beta (Abeta) deposits and microglia-dominated inflammatory activation. Innate immune signaling controls microglial inflammatory activities and Abeta clearance. However, studies examining innate immunity in Abeta pathology and neuronal degeneration have produced conflicting results. In this study, we investigated the pathogenic role of innate immunity in AD by ablating a key signaling molecule, IKKbeta, specifically in the myeloid cells of TgCRND8 APP-transgenic mice. Deficiency of IKKbeta in myeloid cells, especially microglia, simultaneously reduced inflammatory activation and Abeta load in the brain and these effects were associated with reduction of cognitive deficits and preservation of synaptic structure proteins. IKKbeta deficiency enhanced microglial recruitment to Abeta deposits and facilitated Abeta internalization, perhaps by inhibiting TGF-beta-SMAD2/3 signaling, but did not affect Abeta production and efflux. Therefore, inhibition of IKKbeta signaling in myeloid cells improves cognitive functions in AD mice by reducing inflammatory activation and enhancing Abeta clearance. These results contribute to a better understanding of AD pathogenesis and could offer a new therapeutic option for delaying AD progression

Characterization of Different Kinds of Silicon Dioxide and Their Application in Low-Temperature Adsorption Refining of Fragrant Rapeseed Oil

Three kinds of silicon dioxide including S655, R92 and R40F were characterized, and their application in low-temperature adsorption refining of fragrant rapeseed oil was studied. The results showed that all three kinds of silicon dioxide had a loose porous structure, but the particle size distribution, specific surface area, pore volume and pore size were obviously different. After being treated with 1.0% silicon dioxide at 45 ℃ for 30 min, the dephosphorization rates of rapeseed oil by S655, R92 and R40F were 90.3%, 99.6% and 88.5%, the lightness increased by 49.9%, 52.5% and 53.9%, the redness decreased by 31.5%, 23.4% and 37.8%, the yellowness increased by 17.3%, 20.0% and 20.6%, respectively. Meanwhile, the retention rate of sterols (above 97.1%) was high, and there were no significant differences in deacidification rate, fatty acid composition or tocopherol retention rate among the three treatment groups. The highest retention rates of total phenol and canolol (98.1% and 99.4%) were found in the samples treated with R92. The contents of glucosinolate degradation products, pyrazines, aldehydes and ketones in fragrant rapeseed oil all increased significantly after refining with the three kinds of silicon dioxide

Deficiency of IKKβ in neurons ameliorates Alzheimer's disease pathology in APP- and tau-transgenic mice

In Alzheimer's disease (AD) brain, inflammatory activation regulates protein levels of amyloid-β-peptide (Aβ) and phosphorylated tau (p-tau), as well as neurodegeneration; however, the regulatory mechanisms remain unclear. We constructed APP- and tau-transgenic AD mice with deletion of IKKβ specifically in neurons, and observed that IKKβ deficiency reduced cerebral Aβ and p-tau, and modified inflammatory activation in both AD mice. However, neuronal deficiency of IKKβ decreased apoptosis and maintained synaptic proteins (e.g., PSD-95 and Munc18-1) in the brain and improved cognitive function only in APP-transgenic mice, but not in tau-transgenic mice. Additionally, IKKβ deficiency decreased BACE1 protein and activity in APP-transgenic mouse brain and cultured SH-SY5Y cells. IKKβ deficiency increased expression of PP2A catalytic subunit isoform A, an enzyme dephosphorylating cerebral p-tau, in the brain of tau-transgenic mice. Interestingly, deficiency of IKKβ in neurons enhanced autophagy as indicated by the increased ratio of LC3B-II/I in brains of both APP- and tau-transgenic mice. Thus, IKKβ deficiency in neurons ameliorates AD-associated pathology in APPand tau-transgenic mice, perhaps by decreasing Aβ production, increasing p-tau dephosphorylation, and promoting autophagy-mediated degradation of BACE1 and p-tau aggregates in the brain. However, IKKβ deficiency differently protects neurons in APP- and tau-transgenic mice. Further studies are needed, particularly in the context of interaction between Aβ and p-tau, before IKKβ/NF-κB can be targeted for AD therapies

Haploinsufficiency of microglial MyD88 ameliorates Alzheimer's pathology and vascular disorders in APP/PS1-transgenic mice

Growing evidence indicates that innate immune molecules regulate microglial activation in Alzheimer's disease (AD); however, their effects on amyloid pathology and neurodegeneration remain inconclusive. Here, we conditionally deleted one allele of myd88 gene specifically in microglia in APP/PS1-transgenic mice by 6 months and analyzed AD-associated pathologies by 9 months. We observed that heterozygous deletion of myd88 gene in microglia decreased cerebral amyloid β (Aβ) load and improved cognitive function of AD mice, which was correlated with reduced number of microglia in the brain and inhibited transcription of inflammatory genes, for example, tnf-α and il-1β, in both brain tissues and individual microglia. To investigate mechanisms underlying the pathological improvement, we observed that haploinsufficiency of MyD88 increased microglial recruitment toward Aβ deposits, which might facilitate Aβ clearance. Microglia with haploinsufficient expression of MyD88 also increased vasculature in the brain of APP/PS1-transgenic mice, which was associated with up-regulated transcription of osteopontin and insulin-like growth factor genes in microglia. Moreover, MyD88-haploinsufficient microglia elevated protein levels of LRP1 in cerebral capillaries of APP/PS1-transgenic mice. Cell culture experiments further showed that treatments with interleukin-1β decreased LRP1 expression in pericytes. In summary, haploinsufficiency of MyD88 in microglia at a late disease stage attenuates pro-inflammatory activation and amyloid pathology, prevents the impairment of microvasculature and perhaps also protects LRP1-mediated Aβ clearance in the brain of APP/PS1-transgenic mice, all of which improves neuronal function of AD mice