6 research outputs found

    Prefetching Method for Low-Latency Web AR in the WMN Edge Server

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    Recently, low-latency services for large-capacity data have been studied given the development of edge servers and wireless mesh networks. The 3D data provided for augmented reality (AR) services have a larger capacity than general 2D data. In the conventional WebAR method, a variety of data such as HTML, JavaScript, and service data are downloaded when they are first connected. The method employed to fetch all AR data when the client connects for the first time causes initial latency. In this study, we proposed a prefetching method for low-latency AR services. Markov model-based prediction via the partial matching (PPM) algorithm was applied for the proposed method. Prefetched AR data were predicted during AR services. An experiment was conducted at the Nowon Career Center for Youth and Future in Seoul, Republic of Korea from 1 June 2022 to 31 August 2022, and a total of 350 access data points were collected over three months; the prefetching method reduced the average total latency of the client by 81.5% compared to the conventional method

    Synthesis and biological evaluation of flavonoid-based IP6K2 inhibitors

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    AbstractInositol polyphosphates (IPs) are a group of inositol metabolites that act as secondary messengers for external signalling cues. They play various physiological roles such as insulin release, telomere length maintenance, cell metabolism, and aging. Inositol hexakisphosphate kinase 2 (IP6K2) is a key enzyme that produces 5-diphosphoinositol 1,2,3,4,6-pentakisphosphate (5-IP7), which influences the early stages of glucose-induced exocytosis. Therefore, regulation of IP6Ks may serve as a promising strategy for treating diseases such as diabetes and obesity. In this study, we designed, synthesised, and evaluated flavonoid-based compounds as new inhibitors of IP6K2. Structure-activity relationship studies identified compound 20s as the most potent IP6K2 inhibitor with an IC50 value of 0.55 μM, making it 5-fold more potent than quercetin, the reported flavonoid-based IP6K2 inhibitor. Compound 20s showed higher inhibitory potency against IP6K2 than IP6K1 and IP6K3. Compound 20s can be utilised as a hit compound for further structural modifications of IP6K2 inhibitors

    Hypothalamic Macrophage Inducible Nitric Oxide Synthase Mediates Obesity-Associated Hypothalamic Inflammation

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    Summary: Obesity-associated metabolic alterations are closely linked to low-grade inflammation in peripheral organs, in which macrophages play a central role. Using genetic labeling of myeloid lineage cells, we show that hypothalamic macrophages normally reside in the perivascular area and circumventricular organ median eminence. Chronic consumption of a high-fat diet (HFD) induces expansion of the monocyte-derived macrophage pool in the hypothalamic arcuate nucleus (ARC), which is significantly attributed to enhanced proliferation of macrophages. Notably, inducible nitric oxide synthase (iNOS) is robustly activated in ARC macrophages of HFD-fed obese mice. Hypothalamic macrophage iNOS inhibition completely abrogates macrophage accumulation and activation, proinflammatory cytokine overproduction, reactive astrogliosis, blood-brain-barrier permeability, and lipid accumulation in the ARC of obese mice. Moreover, central iNOS inhibition improves obesity-induced alterations in systemic glucose metabolism without affecting adiposity. Our findings suggest a critical role for hypothalamic macrophage-expressed iNOS in hypothalamic inflammation and abnormal glucose metabolism in cases of overnutrition-induced obesity. : Lee et al. demonstrate in mice that, upon prolonged high-fat diet feeding, hypothalamic macrophages proliferate, expand their pool, and sustain hypothalamic inflammation. Moreover, they show that hypothalamic macrophage iNOS inhibition diminishes macrophage activation, astrogliosis, blood-brain-barrier permeability, and impaired glucose metabolism in diet-induced obese mice. Keywords: obesity, inflammation, hypothalamus, macrophage, iNOS, microglia, diet, glucose, metabolis
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