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Knowing that the demand for advertising in a growing e-commerce market cannot be sufficiently addressed in a traditional advertising operation model, advertisers and e-commerce platforms apply arti...

In 2019, Premier Li Keqiang first raised the concept of "Internet + Sports" in the government work report, which means that the research, development and application of AI in sports are high on the agenda of the country and are of vital strategic significance for building China into a major sports power. The flexible combination of AI with the development of Chinese sports is urgent to every sports worker. This paper uses the literature review method and other research methods to discuss the significance and difficulties of adding AI to the efforts of building China into a major sports power, and analyze the status quo and characteristics of the development of sports industry in China, in the hope of providing constructive suggestions on the application of AI to China’s sports industry.

BACKGROUND Considerable research has been devoted to examining the mental health conditions of patients with COVID-19 and medical staff attending to these patients during the COVID-19 pandemic. However, there are few insights concerning how the pandemic may take a toll on the mental health of the general population, and especially of nonpatients (ie, individuals who have not contracted COVID-19). OBJECTIVE This study aimed to investigate the association between social media use and mental health conditions in the general population based on a national representative sample during the peak of the COVID-19 outbreak in China. METHODS We formed a national representative sample (N=2185) comprising participants from 30 provinces across China, who were the first to experience the COVID-19 outbreak in the world. We administered a web-based survey to these participants to analyze social media use, health information support received via social media, and possible psychiatric disorders, including secondary traumatic stress (STS) and vicarious trauma (VT). RESULTS Social media use did not cause mental health issues, but it mediated the levels of traumatic emotions among nonpatients. Participants received health information support via social media, but excessive social media use led to elevated levels of stress (β=.175; Pβ=.224; Pβ=.201; Pβ=.307; Pβ=.688; PP=.02). Furthermore, participants from small cities or towns were more anxious (P=.01), stressed (PP=.008) than those from rural areas. Obtaining more informational support (β=.165; Pβ=.144; Pβ=.332; Pβ=.130; PF2=3.549; P=.029) and the association between peer support and STS (F2=5.059; P=.006). Geolocation also interacted with health information support in predicting STS (F2=5.093; P=.006). CONCLUSIONS COVID-19 has taken a severe toll on the mental health of the general population, including individuals who have no history of psychiatric disorders or coronavirus infection. This study contributes to the literature by establishing the association between social media use and psychiatric disorders among the general public during the COVID-19 outbreak. The study findings suggest that the causes of such psychiatric disorders are complex and multifactorial, and social media use is a potential factor. The findings also highlight the experiences of people in China and can help global citizens and health policymakers to mitigate the effects of psychiatric disorders during this and other public health crises, which should be regarded as a key component of a global pandemic response.

Hyperhomocysteinemia (HHcy) is an established and potent independent risk factor for degenerative diseases, including cardiovascular disease (CVD), Alzheimer disease, type II diabetes mellitus, and chronic kidney disease. HHcy has been shown to inhibit proliferation and promote inflammatory responses in endothelial cells (EC), and impair endothelial function, a hallmark for vascular injury. However, metabolic processes and molecular mechanisms mediating HHcy-induced endothelial injury remains to be elucidated. This study examined the effects of HHcy on the expression of microRNA (miRNA) and mRNA in human aortic EC treated with a pathophysiologically relevant concentration of homocysteine (Hcy 500 μM). We performed a set of extensive bioinformatics analyses to identify HHcy-altered metabolic and molecular processes. The global functional implications and molecular network were determined by Gene Set Enrichment Analysis (GSEA) followed by Cytoscape analysis. We identified 244 significantly differentially expressed (SDE) mRNA, their relevant functional pathways, and 45 SDE miRNA. HHcy-altered SDE inversely correlated miRNA-mRNA pairs (45 induced/14 reduced mRNA) were discovered and applied to network construction using an experimentally verified database. We established a hypothetical model to describe the biochemical and molecular network with these specified miRNA/mRNA axes, finding: 1) HHcy causes metabolic reprogramming by increasing glucose uptake and oxidation, by glycogen debranching and NAD+/CoA synthesis, and by stimulating mitochondrial reactive oxygen species production via NNT/IDH2 suppression-induced NAD+/NADP-NADPH/NADP+ metabolism disruption; 2) HHcy activates inflammatory responses by activating inflammasome-pyroptosis mainly through ↓miR193b→↑CASP-9 signaling and by inducing IL-1β and adhesion molecules through the ↓miR29c→↑NEDD9 and the ↓miR1256→↑ICAM-1 axes, as well as GPCR and interferon α/β signaling; 3) HHcy promotes cell degradation by the activation of lysosome autophagy and ubiquitin proteasome systems; 4) HHcy causes cell cycle arrest at G1/S and S/G2 transitions, suppresses spindle checkpoint complex and cytokinetic abscission, and suppresses proliferation through ↓miRNA335/↑VASH1 and other axes. These findings are in accordance with our previous studies and add a wealth of heretofore-unexplored molecular and metabolic mechanisms underlying HHcy-induced endothelial injury. This is the first study to consider the effects of HHcy on both global mRNA and miRNA expression changes for mechanism identification. Molecular axes and biochemical processes identified in this study are useful not only for the understanding of mechanisms underlying HHcy-induced endothelial injury, but also for discovering therapeutic targets for CVD in general., Graphical abstract Image 1, Highlights • Identified multiple HHcy-altered metabolic and molecular processes potentially responsible for HHcy-induced endothelial injury via examining global mRNA/miRNA expression changes in Hcy-treated EC and performing comprehensive bioinformatic studies. • HHcy may activate glucose uptake signaling via the ↓miR148b→↑SLC2A axis. • HHcy may induce glucose oxidation signaling by switching pyruvate metabolism from lactate synthesis to mitochondrial oxidation via expression changes of ↑MPC1 & ↓LDHB. • HHcy may disrupt redox homeostasis mostly by suppressing NNT/IDH2-related mt-NADPH/mt-NAD+ signaling. • HHcy may increase FA β-oxidation, glutamine, TCA cycle and OXPHOS signaling. • HHcy may activate inflammatory signaling via the ↓miR29c→↑NEDD9 and the ↓miR1256→↑ICAM-1 axes. • HHcy may activate inflammasome/pyroptosis-related signaling by the ↓miR137→↑TLR3, the ↓miR574→↑TRAF5, and the ↓miR193b→↑CASP-9 axes, and induce IL1α/β and CASP-10/7. • HHcy may induce inflammation signaling via GPCR activation through the ↓miRNA335→↑CXCR4/↑GNA14 axes. • HHcy may activate molecular degradation process signaling through the ↓miRNA335→↑ASAH1/↑ABCB9 axes. • HHcy may suppress cell cycle and proliferation through the miR491→↓HMGA2→↓CCNA2/CCNB2, the ↓miR335→↑VASH1, the ↓miR181a→↑PHLDA1, the miR6045→↓CENPH, the miR22→↓PRR11/↓BRCA2, and the miR605/miR497/miR514a→CEP55 axes

Background Considerable research has been devoted to examining the mental health conditions of patients with COVID-19 and medical staff attending to these patients during the COVID-19 pandemic. However, there are few insights concerning how the pandemic may take a toll on the mental health of the general population, and especially of nonpatients (ie, individuals who have not contracted COVID-19). Objective This study aimed to investigate the association between social media use and mental health conditions in the general population based on a national representative sample during the peak of the COVID-19 outbreak in China. Methods We formed a national representative sample (N=2185) comprising participants from 30 provinces across China, who were the first to experience the COVID-19 outbreak in the world. We administered a web-based survey to these participants to analyze social media use, health information support received via social media, and possible psychiatric disorders, including secondary traumatic stress (STS) and vicarious trauma (VT). Results Social media use did not cause mental health issues, but it mediated the levels of traumatic emotions among nonpatients. Participants received health information support via social media, but excessive social media use led to elevated levels of stress (β=.175; P Conclusions COVID-19 has taken a severe toll on the mental health of the general population, including individuals who have no history of psychiatric disorders or coronavirus infection. This study contributes to the literature by establishing the association between social media use and psychiatric disorders among the general public during the COVID-19 outbreak. The study findings suggest that the causes of such psychiatric disorders are complex and multifactorial, and social media use is a potential factor. The findings also highlight the experiences of people in China and can help global citizens and health policymakers to mitigate the effects of psychiatric disorders during this and other public health crises, which should be regarded as a key component of a global pandemic response.

Pirfenidone has been widely used in the treatment of idiopathic pulmonary fibrosis (IPF). However, the role of pirfenidone in LPS-induced acute lung injury (ALI) remains unclear. This study aims to investigate the protective effects of pirfenidone in ALI and to explore its underlying mechanism. Pirfenidone clearly reduces LPS-triggered ALI as indicated by significant pathological alterations, reduced oxidative stress and inflammatory responses in vivo. Furthermore, pirfenidone also blocks apoptosis of LPS-induced alveolar epithelial type II (ATII) cells through inhibition of endoplasmic reticulum (ER) stress and mitochondrial injury in vivo and in vitro. A lower expression level of BAP31, an ER transmembrane protein, was found to be associated with ALI followed LPS challenge. The reintroduction of BAP31 blunted LPS induced ER stress and mitochondrial damage and therefore alleviated ATII cell apoptosis, which correlated with pirfenidone treatment. Knockdown of BAP31 expression in pirfenidone treated ATII cells re-activated ER stress, mitochondrial damage and followed cellular apoptosis. In summary, this study confirms the beneficial effect of pirfenidone on ER stress and mitochondrial dysfunction mediated apoptosis via upregulation of BAP31. Our results demonstrated that pirfenidone may be considered as a potential agent for the treatment of ALI in the future.

We used 335 Mycobacterium tuberculosis strains from 2010 National Epidemiologic Survey for TB in China and performed comparative sequence analysis of 38 kDa gene after amplification. From the results, we found that there were 5.07% M.tuberculosis strains that demonstrated genetic diversity of 38 kDa in China, and 2.99% strains showed polymorphism of the 38 kDa antigen, and this may be the reason for changes in the antigen produced, which may in turn cause alterations of related functions, thereby allowing immune evasion.

Many studies have reported the association between the matrix metalloproteinase (MMP) polymorphisms and lung cancer susceptibility, but the results were inconclusive. We conducted a meta-analysis, using a comprehensive strategy based on the logistic regression and a model-free approach, to derive a more precise estimation of the relationship between MMP1, MMP2, MMP9 and MMP13 polymorphisms with lung cancer risk. A total of 22 case-control studies including 8202 cases and 7578 controls were included in this meta-analysis. For MMP1-1607 1G/2G, increased lung cancer risk was found among Asians in additive model(OR = 1.34, 95%CI:1.18-1.53) and with model-free approach(ORG = 1.41, 95%CI:1.21-1.65). For MMP2-1306 C/T and -735 C/T, based on the model-free approach, a significantly reduced risk was found in Asians(MMP2-1306 C/T:ORG = 0.49,95%CI:0.42-0.57; MMP2-735 C/T: ORG = 0.71, 95%CI:0.61-0.84). For MMP9-1562 C/T, a significantly increased risk was found among Asians(OR = 2.73, 95%CI:1.74-4.27) with model-free approach. For MMP13-77A/G, there was no association between this polymorphism and lung cancer risk in the recessive model(OR = 1.02, 95%CI:0.83-1.26) and with the model-free approach(ORG = 0.95, 95%CI:0.76-1.17). Therefore, this meta-analysis suggests that the MMP1-1607 1G/2G, MMP2-1306 C/T, MMP2-735 C/T, MMP9 -1562 C/T polymorphisms were risk factors for lung cancer among Asians, while MMP13 -77A/G polymorphism was not associated with lung cancer risk.