Sustainable development of Olympic sport participation legacy: A scoping review based on the PAGER framework

After the 2022 Beijing Winter Olympics, Chinese officials claimed that the goal of “driving 300 million people to participate in ice and snow sports” had been achieved. Historically, the London 2012 Olympic Games had a similar goal: to increase sports participation for all by hosting the Olympic Games. Given these goals, the impact of the Olympic Games on sports participation has clearly become significant. These impacts can be referred to as the Olympic sport participation legacy, an intangible Olympic legacy. The Olympic sport participation legacy has attracted a lot of researchers’ interest in the academic field in recent years. This paper aims to conduct a scoping review of Olympic sport participation legacy studies between 2000 and 2021 to identify the progress of studies on the sustainability of Olympic sport participation legacies. Unlike previous scoping reviews on sport participation legacies, this review adopts a Patterns, Advances, Gaps, Evidence of Practice, and Research Recommendations (PAGER) framework at the results analysis stage to improve the quality of the findings. The results from the scoping review contained 54 peer-reviewed articles on three levels of research: the population level, social level, and intervention processes. Many studies indicate that achieving a sustainable Olympic sport participation legacy requires joint collaboration and long-term planning between governments, community organisations, and other stakeholders.</p

Low concentrations of metformin inhibited Erk and mTOR phosphorylation and increased Akt phosphorylation of CD133⁺ pancreatic cancer cells.

<p>Pancreatic cancer cells were treated with metformin for 4 h (0.2 mM for AsPC-1, 0.1 mM for SW1990) and CD133⁺ cells were sorted by flow cytometry. Expression of AMPKα, Akt, Erk1/2, and mTOR and phosphorylation of CD133⁺ cells were evaluated by western blotting and the results were quantified using ImageJ V.1.46r (National Institutes of Health). Significant decreases of phospho-ERK1/2 and phospho-mTOR expression and a significant increase of phospho-Akt expression were observed in the metformin treated cells. Error bars represent the standard deviation. ^*<i>P</i><0.05.</p

A novel underwater dam crack detection and classification approach based on sonar images

<div><p>Underwater dam crack detection and classification based on sonar images is a challenging task because underwater environments are complex and because cracks are quite random and diverse in nature. Furthermore, obtainable sonar images are of low resolution. To address these problems, a novel underwater dam crack detection and classification approach based on sonar imagery is proposed. First, the sonar images are divided into image blocks. Second, a clustering analysis of a 3-D feature space is used to obtain the crack fragments. Third, the crack fragments are connected using an improved tensor voting method. Fourth, a minimum spanning tree is used to obtain the crack curve. Finally, an improved evidence theory combined with fuzzy rule reasoning is proposed to classify the cracks. Experimental results show that the proposed approach is able to detect underwater dam cracks and classify them accurately and effectively under complex underwater environments.</p></div

Low concentrations of metformin induced cell cycle arrest but not apoptosis in CD133⁺ pancreatic cancer cells.

<p>A, Effect of low concentrations of metformin on apoptosis in pancreatic cancer. AsPC-1 and SW1990 cells were incubated with 0.2 mM or 0.1 mM metformin, respectively, for 72 h and the proportions of apoptotic cells were determined by flow cytometry. No significant differences were observed between the treated cells and controls. B, Effect of low concentrations of metformin on the cell cycle in pancreatic cancer. AsPC-1 and SW1990 cells were incubated with 0.2 mM or 0.1 mM metformin, respectively, for 72 h and the proportions of cells in each stage of the cell cycle were determined by flow cytometry. A decrease of total S phase cells and an increase of G0/G1 phase suggest G1/S arrest in CD133⁺ cells. Error bars represent the standard deviation. ^*<i>P</i><0.05.</p

Low concentrations of metformin did not inhibit the proliferation of pancreatic cancer cells.

<p>AsPC-1 and SW1990 cells were incubated with different concentrations of metformin for 72 h and numbers of viable cells were determined by CCK-8 assay. The results are presented as the proportion of viable cells relative to the control. No difference in viable cells was observed between cells treated with low concentrations of metformin (≤0.5 mM) and controls. Error bars represent the standard deviation.</p

Multicompartment Nanoparticles of Poly(4-vinylpyridine) Graft Block Terpolymer: Synthesis and Application as Scaffold for Efficient Au Nanocatalyst

Multicompartment nanoparticles (MCBNs) constructed with the brush block terpolymer of [poly­(<i>p</i>-chloromethylstyrene)-<i>graft</i>-poly­(4-vinylpyridine)]-<i>block</i>-polystyrene (PCMS-<i>g</i>-P4VP)-<i>b</i>-PS are prepared through dispersion polymerization of styrene in the methanol/water mixture mediated by the brush macro-RAFT agent of poly­(<i>p</i>-chloromethylstyrene)-<i>graft</i>-poly­(4-vinylpyridine) trithiocarbonate. During the dispersion RAFT polymerization, the molecular weight of the brush (PCMS-<i>g</i>-P4VP)-<i>b</i>-PS block terpolymer linearly increases with the monomer conversion. Ascribed to the brush (PCMS-<i>g</i>-P4VP) block, MCBNs including a PS core and discrete subdomains of (PCMS-<i>g</i>-P4VP) on the PS core dispersed in water are formed. The reasons leading to formation of MCBNs are discussed, and the immiscibility of the brush (PCMS-<i>g</i>-P4VP) block with the PS core, the low number density of the brush (PCMS-<i>g</i>-P4VP₂₅)₂₁ chains tethered on per surface area of the PS core, and the high molecular weight but the low polymerization degree of the brush (PCMS-<i>g</i>-P4VP) block are ascribed. Au nanoparticles are immobilized on the bulgy PCMS-<i>g</i>-P4VP subdomains on MCBNs and show high catalytic efficiency in the aerobic alcohol oxidation

Oral administration of metformin inhibited pancreatic cancer xenograft growth.

<p>A, Xenograft at sacrifice. Eight hundred milligrams per liter of metformin was diluted in the drinking water of <i>nu</i>/<i>nu</i> mice 72 h before injection of pancreatic cancer cells. Mice were sacrificed 18 or 24 days after the implantation. Xenografts from mice treated with oral metformin were much smaller than those from untreated mice. B, Effect of oral administration of metformin on growth of xenografts. Eight hundred milligrams per liter of metformin was diluted in the drinking water of <i>nu</i>/<i>nu</i> mice 72 h before injection of pancreatic cancer cells. Tumors were measured every 3 days after the injection and tumor volume (V) was calculated according to V =  (length × width²)/2. Xenograft growth was significantly inhibited by oral administration of metformin. Error bars represent the standard deviation. ^*<i>P</i><0.05.</p

Low concentrations of metformin inhibited the invasion of pancreatic cancer cells.

<p>Effect of low concentrations of metformin on invasion in pancreatic cancer. AsPC-1 and SW1990 cells were incubated with 0.2 mM or 0.1 mM metformin, respectively, for 72 h and cell invasion was determined by Transwell assay. Low concentrations of metformin reduced the invasion of pancreatic cancer cells. Error bars represent the standard deviation. ^*<i>P</i><0.05.</p

Low concentrations of metformin selectively inhibited the proliferation of CD133⁺ pancreatic cancer cells.

<p>A, Growth curves for pancreatic cancer cells treated with low concentrations of metformin. AsPC-1 and SW1990 cells were incubated with 0.2 mM or 0.1 mM metformin, respectively, and their numbers counted at each time point. The results are presented as the fold increase relative to 0 h. B, Effect of low concentrations of metformin on the proportion of CD133⁺ cells. AsPC-1 and SW1990 cells were incubated with 0.2 mM or 0.1 mM metformin, respectively, and the proportion of CD133⁺ cells was determined at each time point. The proportion of CD133⁺ cells decreased gradually. C, Growth curves for CD133⁺ and CD133^– pancreatic cancer cells treated with low concentrations of metformin. The total number of pancreatic cancer cells and the proportions of CD133⁺ and CD133^– cells were determined at each time point. The results are presented as the fold increase relative to 0 h. The proliferation of CD133⁺ cells was selectively inhibited. Error bars represent the standard deviation.</p

Panc-1 CSCs inhibited lymphocyte proliferation.

<p>Lymphocytes were stimulated to proliferate with PHA or anti-CD3 monoclonal antibodies. Panc-1 CSCs were co-cultured with lymphocyte at a ratio of 1∶10 in the presence of PHA or anti-CD3 monoclonal antibodies. Lymphocytes stimulated with PHA or anti-CD3 monoclonal antibodies solely were set as control. MTT assay indicated that lymphocyte proliferation promoted by PHA or anti-CD3 monoclonal antibodies was inhibited in the presence of Panc-1 CSCs.</p