Digital common(s): the role of digital gamification in participatory design for the planning of high-density housing estates

“Digital Commons” explores the intersection between participatory design, digital gamification, and community engagement, contextualised in the planning of high-density housing estates in Hong Kong. The research project investigates how digital gamified participatory design can be applied in decision-making processes for the planning of public facilities in high-density housing estates. Focusing on community engagement methods, the project has engaged with residents of a case study housing estate, Jat Min Chuen in the Shatin Wai area of Hong Kong, to facilitate collective planning discussions about the past, present, and future of community facilities. Using a digital community game approach, it has collected opinions and needs from public housing residents, promoted collaborative design thinking processes, and provided a platform for participants to increase their understanding of the complexity of planning problems through 3D visualisation tools. The experiences documented in this study demonstrate how 3D interactivity, real-time engagement, and bottom-up perspectives may enhance the potential of using immersive digital twins during collective decision-making. The gaming outcomes show a high similarity across all teams in close relationship to users’ daily life routines, demonstrating a new powerful role for urban designers as a coordinator of interactive and collaborative planning processes

CCL4 participates in the reprogramming of glucose metabolism induced by ALV-J infection in chicken macrophages

Interferon and chemokine-mediated immune responses are two general antiviral programs of the innate immune system in response to viral infections and have recently emerged as important players in systemic metabolism. This study found that the chemokine CCL4 is negatively regulated by glucose metabolism and avian leukosis virus subgroup J (ALV-J) infection in chicken macrophages. Low expression levels of CCL4 define this immune response to high glucose treatment or ALV-J infection. Moreover, the ALV-J envelope protein is responsible for CCL4 inhibition. We confirmed that CCL4 could inhibit glucose metabolism and ALV-J replication in chicken macrophages. The present study provides novel insights into the antiviral defense mechanism and metabolic regulation of the chemokine CCL4 in chicken macrophages

Tuning intrinsic defects in γ-CuI by cation and anion doping

γ-CuI is a promising scintillator owing to the ultrafast decay time of 130 ps contributed by the near-band-edge emission. The luminescence properties of the γ-CuI are directly related to its intrinsic defects, such as Cu and I vacancies. In this context, tuning the intrinsic defects by cation and anion doping was proposed to improve the scintillation performance of γ-CuI. The structural properties of the dopants, including Li, Na, Mg, F, Cl and Br, were investigated by first-principles calculations. The Li, Na and Mg atoms were calculated to occupy the Cu site. The Cl and Br atoms turned out to replace the I atoms. Importantly, the Cu vacancies were created by Cl and Br dopants, and the I vacancies were eliminated through Li, Na, Mg, Cl and Br doping. These theoretical results were demonstrated by photoluminescence and X-ray excited luminescence spectra

TRIP13 Enhances Radioresistance of Lung Adenocarcinoma Cells through the Homologous Recombination Pathway

Background and objective Radiation therapy is one of the most common treatments for non-small cell lung cancer (NSCLC). However, the insensitivity of some tumor cells to radiation is one of the major reasons for the poor efficacy of radiotherapy and the poor prognosis of patients, and exploring the underlying mechanisms behind radioresistance is the key to solving this clinical challenge. This study aimed to identify the molecules associated with radioresistance in lung adenocarcinoma (LUAD), identified thyroid hormone receptor interactor 13 (TRIP13) as the main target initially, and explored whether TRIP13 is related to radioresistance in LUAD and the specific mechanism, with the aim of providing theoretical basis and potential targets for the combination therapy of LUAD patients receiving radiotherapy in the clinic. Methods Three datasets, GSE18842, GSE19188 and GSE33532, were selected from the Gene Expression Omnibus (GEO) database and screened for differentially expressed genes (|log FC|>1.5, P<0.05) in each of the three datasets using the R 4.1.3 software, and then Venn diagram was used to find out the differentially expressed genes common to the three datasets. The screened differential genes were then subjected to protein-protein interaction (PPI) analysis and module analysis with the help of STRING online tool and Cytoscape software, and survival prognosis analysis was performed for each gene with the help of Kaplan-Meier Plotter database, and the TRIP13 gene was identified as the main molecule for subsequent studies. Subsequently, the human LUAD cell line H292 was irradiated with multiple X-rays using a sub-lethal dose irradiation method to construct a radioresistant cell line, H292DR. The radioresistance of H292DR cells was verified using cell counting kit-8 (CCK-8) assay and clone formation assay. The expression levels of TRIP13 in H292 and H292DR cells were measured by Western blot. Small interfering RNA (siRNA) was used to silence the expression of TRIP13 in H292DR cells and Western blot assay was performed. The clone formation ability and migration ability of H292DR cells were observed after TRIP13 silencing, followed by the detection of changes in the expression levels of proteins closely related to homologous recombination, such as ataxia telangiectasia mutated (ATM) protein. Results Screening of multiple GEO datasets, validation of external datasets and survival analysis revealed that TRIP13 was highly expressed in LUAD and was associated with poor prognosis in LUAD patients who had received radiation therapy. And the results of gene set enrichment analysis (GSEA) of TRIP13 suggested that TRIP13 might be closely associated with LUAD radioresistance by promoting homologous recombination repair after radiation therapy. Experimentally, TRIP13 expression was found to be upregulated in H292DR, and silencing of TRIP13 was able to increase the sensitivity of H292DR cells to radiation. Conclusion TRIP13 is associated with poor prognosis in LUAD patients treated with radiation, possibly by promoting a homologous recombination repair pathway to mediate resistance of LUAD cells to radiation

Interactive Cognitive Motor Training: A Promising Approach for Sustainable Improvement of Balance in Older Adults

Physical exercise has been shown to improve balance, gait, and cognitive function in older adults. Interactive cognitive-motor training (ICMT) combines physical exercise and cognitive stimulation, but few studies have focused on the effect of ICMT on static and dynamic balance in older adults. This study aims to improve the balance of older adults to reduce fall-related injuries for sustainable development goals. We randomly assigned 38 older adults to either the ICMT group (n = 22) or the control group (n = 16). The ICMT group participated in 60-min exercise sessions three times a week for 12 weeks, while the control group maintained their regular activities. The static and dynamic balances were assessed before and after the intervention. The results indicated the ICMT group demonstrated significant improvements in static balance, specifically in swing path and velocity (V) in the medial-lateral (M-L) direction with eyes open (p p p < 0.05). In conclusion, ICMT effectively enhances static balance and maintains dynamic balance in older adults

PI3K/Akt-independent negative regulation of JNK signaling by MKP-7 after cerebral ischemia in rat hippocampus

Abstract Background The inactivation of c-Jun N-terminal kinase (JNK) is associated with anti-apoptotic and anti-inflammatory effects in cerebral ischemia, which can be induced by an imbalance between upstream phosphatases and kinases. Result Mitogen-activated protein kinase phosphatase 7 (MKP-7) was upregulated significantly at 4 h of reperfusion postischemia in rat hippocampi. By administration of cycloheximide or siRNA against mitogen-activated protein kinase phosphatase 7 (MKP-7) in a rat model of ischemia/reperfusion, an obvious enhancement of JNK activity was observed in 4 h of reperfusion following ischemia, suggesting MKP-7 was involved in JNK inactivation after ischemia. The subcellular localization of MKP-7 altered after ischemia, and the inhibition of MKP-7 nuclear export by Leptomycin B up-regulated JNK activity. Although PI3K/Akt inhibition could block downregulation of JNK activity through SEK1 and MKK-7 activation, PI3K/Akt activity was not associated with the regulation of JNK by MKP-7. Conclusions MKP-7, independently of PI3K/Akt pathway, played a key role in downregulation of JNK activity after ischemia in the rat hippocampus, and the export of MKP-7 from the nucleus was involved in downregulation of cytoplasmic JNK activity in response to ischemic stimuli.</p

Fano-Like Resonance of Heat-Reconfigurable Silicon Grating Metasurface Tuned by Laser-Induced Graphene

We propose a heat-reconfigurable metasurface composed of the silicon-based gold grating. The asymmetric Fano-like line shape is formed due to the mutual coupling of the local surface plasmon (LSP) in the gap between the two layers of Au gratings and the surface propagating plasmon (SPP) on the surface of the Au gratings. Then, we effectively regulate the Fano resonance by applying a bias voltage to laser-induced graphene (LIG), to generate Joule heat, so that the resonant dip of one mode of the Fano resonance can shift up to 28.5 nm. In contrast, the resonant dip of the other mode barely changes. This effectively regulates the coupling between two resonant modes in Fano resonance. Our study presents a simple and efficient method for regulating Fano-like interference in the near-infrared band

Effects of 1-Methylcyclopropene Treatment on the Quality and Malic Acid Metabolism of ‘Xiangjiao’ Plum under Low-Temperature Storage

‘Xiangjiao’ plum (Prunus salicina Lindl.) is a stone fruit that is vulnerable to the chilling injury (CI) that is caused by low-temperature stress. The effects of 1-methylcyclopropene (1-MCP) and ethylene absorbent (EA) treatments on the fruit quality and malic acid metabolism of ‘Xiangjiao’ plum stored at 4 °C were compared in this study. Compared with the control check (CK) and EA treatment, fumigation with 1.0 mg·L−1 of 1-MCP for 24 h could more significantly maintain the sensory and physiological quality of the fruit, increase the activity of antioxidant enzymes, and prolong the storage time of plums. Furthermore, 1-MCP treatment can regulate the high expression of the tonoplast dicarboxylate transporter (tDT) and phosphoenolpyruvate carboxylase (PEPC) gene, regulate the high expression of the NAD-malate dehydrogenase (NAD-MDH) gene at the end of storage, and inhibit the expression of the NADP-malic enzyme (NADP-ME) gene. These changes resulted in increased NAD-MDH enzyme activity and decreased NADP-ME enzyme activity, which inhibited the degradation of malic acid that is caused by CI. As a result, 1-MCP can effectively maintain the storage quality of ‘Xiangjiao’ plum, reduce the loss of pleasant sour taste, and improve the edible flavor and commercial value of the fruit

Batf3-dependent CD8α+ Dendritic Cells Aggravates Atherosclerosis via Th1 Cell Induction and Enhanced CCL5 Expression in Plaque Macrophages

Dendritic cells (DCs) play an important role in controlling T cell-mediated adaptive immunity in atherogenesis. However, the role of the basic leucine zipper transcription factor, ATF-like 3 (Batf3)-dependent CD8α+ DC subset in atherogenesis remains unclear. Here we show that Batf3−/−Apoe−/− mice, lacking CD8α+ DCs, exhibited a significant reduction in atherogenesis and T help 1 (Th1) cells compared with Apoe−/− controls. Then, we found that CD8α+ DCs preferentially induce Th1 cells via secreting interleukin-12 (IL-12), and that the expression of interferon-gamma (IFN-γ)or chemokine (C-C motif) ligand 5 (CCL5) in aorta were significantly decreased in Batf3−/−Apoe−/− mice. We further demonstrated that macrophages were the major CCL5-expressing cells in the plaque, which was significantly reduced in Batf3−/−Apoe−/− mice. Furthermore, we found CCL5 expression in macrophages was promoted by IFN-γ. Finally, we showed that Batf3−/−Apoe−/− mice displayed decreased infiltration of leukocytes in the plaque. Thus, CD8α+ DCs aggravated atherosclerosis, likely by inducing Th1 cell response, which promoted CCL5 expression in macrophages and increased infiltration of leukocytes and lesion inflammation