Increased life expectancy coupled with declining birth rates leads to an aging population structure. Agingcaused changes, such as physical or cognitive decline, could affect people's quality of life, resulting in injuries, mental health or the lack of physical activity. Sensor-based human activity recognition (HAR) is one of the most promising assistive technologies to support older people's daily life, which has enabled enormous potential in human-centred applications. Recent surveys either focus on the deep learning approaches or one specific sensor modality in HAR. This survey aims to provide a comprehensive introduction for newcomers to HAR, including the conventional approaches and the deep learning methods. It specifically puts more emphasis on wearable sensor-based HAR systems. We first describe the state-of-art sensor modalities. We then detail each step of the wearable sensor-based HAR. In the feature learning section, we concentrate both hand-crafted features and deep learned features in HAR. We also present the ambient-sensor-based HAR, including camera-based systems, and the systems which combine the wearable and ambient sensors. Finally, we identify certain challenges in HAR to pose research problems for further improvement in HAR.

Epidemiological and experimental studies provide supportive evidence that lycopene (LY), a major carotenoid from tomatoes and tomato products, may act as a chemopreventive agent against certain types of cancers. We recently showed that high-fat diet (HFD)-induced nonalcoholic steatohepatitis (NASH) promoted diethylnitrosamine (DEN)-initiated hepatocarcinogenesis in a rat model. Using this model, we investigated the efficacy of an equivalent dosage of dietary LY from either a pure compound or a tomato extract (TE) against NASH-promoted hepatocarcinogenesis. Six groups of rats were injected with DEN and then fed either Lieber-DeCarli control diet or HFD with or without LY or TE for 6 weeks. Results showed that both LY and TE supplementations significantly decreased the number of altered hepatic foci expressing the placental form of glutathione Stransferase in the livers of HFD-fed rats. This was associated with significantly lower proliferating cell nuclear antigen positive hepatocytes and cyclinD1 protein, as well as decreased activation of extracellular signal-regulated kinase and nuclear NF-jB. Although both LY and TE supplementations reduced HFD-induced lipid peroxidation in the livers, we observed significantly decreased cytochrome P450 2E1, inflammatory foci and mRNA expression of proinflammatory cytokines (TNF-a, IL-1b and IL-12) in the HFD1TE fed group but increased nuclear NF-E2-related factor-2 and heme oxygenase-1 proteins in the HFD1LY fed group, relative to HFD feeding alone. These data indicate that LY and TE can inhibit NASH-promoted hepatocarcinogenesis mainly as a result of reduced oxidative stress, which could be fulfilled through different mechanisms.Primary liver cancer has become the 5th commonest malignancy worldwide, accounting for 5.6% of all human cancers. 1Although surgical resection is the major therapeutic option, the lack of early detection or screening biomarkers usually leads to its diagnosis at an advanced stage. Thus, the identification of potential risk factors for early hepatocarcinogenesis and the exploration of preventive or protective measures against them at an early stage are immensely needed. Over the past decade, growing evidence has revealed a close association between hepatocellular carcinoma and nonalcoholic steatohepatitis (NASH), a chronic and progressive liver disease characterized by the concurrence of fat accumulation and infiltration of inflammatory cells in the liver.2-4 Moreover, patients with NASH have a high risk for proceeding to cirrhosis 5 and eventually hepatocellular carcinoma. Recently, we provided experimental evidence that the altered hepatic foci (AHF) expressing placental form of glutathione S-transferase (P-GST), as initiated by hepatic carcinogen diethylnitrosamine (DEN), were significantly increased in the context of high-fat diet (HFD) induced NASH,6 in which increased oxidative stress could act as a key component contributing to this preneoplastic process. Since NASH has become one of the most common causes of advanced liver diseases in both dev...

Background. The aim of this study is to investigate whether (-)-epigallocatechin-3-gallate (EGCG) can prevent the UA-induced inflammatory effect of human umbilical vein endothelial cells (HUVEC) and the involved mechanisms in vitro. Methods. HUVEC were subjected to uric acid (UA) with or without EGCG treatment. RT-PCR and western blots were performed to determine the level of inflammation marker. The antioxidant activity was evaluated by measuring scavenged reactive oxygen species (ROS). Functional studies of the role of Notch-1 in HUVEC lines were performed using RNA interference analyses. Results. UA significantly increased the expressions of IL-6, ICAM-1, TNF-α, and MCP-1 and the production of ROS in HUVEC. Meanwhile, the expression of Notch-1 and its downstream effects significantly increased. Using siRNA, inhibition of Notch-1 signaling significantly impeded the expressions of inflammatory cytokines under UA treatment. Interestingly, EGCG suppressed the expressions of inflammatory cytokines and the generation of ROS. Western blot analysis of Notch-1 showed that EGCG significantly decreased the expressions of inflammatory cytokines through Notch-1 signaling pathways. Conclusions. In summary, our findings indicated that Notch-1 plays an important role in the UA-induced inflammatory response, and the downregulation of Notch-1 by EGCG could be an effective approach to decrease inflammation and oxidative stress induced by UA.