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SARS-CoV-2 rapidly spreads among humans via social networks, with social mixing and network characteristics potentially facilitating transmission. However, limited data on topological structural features has hindered in-depth studies. Existing research is based on snapshot analyses, preventing temporal investigations of network changes. Comparing network characteristics over time offers additional insights into transmission dynamics. We examined confirmed COVID-19 patients from an eastern Chinese province, analyzing social mixing and network characteristics using transmission network topology before and after widespread interventions. Between the two time periods, the percentage of singleton networks increased from 38.9$ \% $ to 62.8$ \% $$ (p<0.001) $; the average shortest path length decreased from 1.53 to 1.14 $ (p<0.001) $; the average betweenness reduced from 0.65 to 0.11$ (p<0.001) $; the average cluster size dropped from 4.05 to 2.72 $ (p=0.004) $; and the out-degree had a slight but nonsignificant decline from 0.75 to 0.63 $ (p=0.099). $ Results show that nonpharmaceutical interventions effectively disrupted transmission networks, preventing further disease spread. Additionally, we found that the networks’ dynamic structure provided more information than solely examining infection curves after applying descriptive and agent-based modeling approaches. In summary, we investigated social mixing and network characteristics of COVID-19 patients during different pandemic stages, revealing transmission network heterogeneities.
The current epidemic of type 2 diabetes mellitus (T2DM) significantly affects human health worldwide. Activation of brown adipocytes and browning of white adipocytes are considered as a promising molecular target for T2DM treatment. Mulberry leaf, a traditional Chinese medicine, has been demonstrated to have multi-biological activities, including anti-diabetic and anti-inflammatory effects. Our experimental results showed that mulberry leaf significantly alleviated the disorder of glucose and lipid metabolism in T2DM rats. In addition, mulberry leaf induced browning of inguinal white adipose tissue (IWAT) by enhancing the expressions of brown-mark genes as well as beige-specific genes, including uncoupling protein-1 (UCP1), peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), peroxisome proliferator-activated receptor alpha (PPARα), PRD1-BF-1-RIZ1 homologous domain containing protein 16 (PRDM16), cell death inducing DFFA-like effector A (Cidea), CD137 and transmembrane protein 26 (TMEM26). Mulberry leaf also activated brown adipose tissue (BAT) by increasing the expressions of brown-mark genes including UCP1, PGC-1α, PPARα, PRDM16 and Cidea. Moreover, mulberry leaf enhanced the expression of nuclear respiratory factor 1 (NRF-1) and mitochondrial transcription factor A (TFAM) genes that are responsible for mitochondrial biogenesis in IWAT and BAT. Importantly, mulberry leaf also increased the expression of UCP1 and carnitine palmitoyl transferase 1 (CPT-1) proteins in both IWAT and BAT via a mechanism involving AMP-activated protein kinase (AMPK) and PGC-1α pathway. In conclusion, our findings identify the role of mulberry leaf in inducing adipose browning, indicating that mulberry leaf may be used as a candidate browning agent for the treatment of T2DM.
Annexin A2 (ANXA2) is reported to be associated with cancer development. To investigate the roles ANXA2 plays during the development of cancer, the RNAi method was used to inhibit the ANXA2 expression in caco2 (human colorectal cancer cell line) and SMMC7721 (human hepatocarcinoma cell line) cells. The results showed that when the expression of ANXA2 was efficiently inhibited, the growth and motility of both cell lines were significantly decreased, and the development of the motility relevant microstructures, such as pseudopodia, filopodia, and the polymerization of microfilaments and microtubules were obviously inhibited. The cancer cell apoptosis was enhanced without obvious significance. The possible regulating pathway in the process was also predicted and discussed. Our results suggested that ANXA2 plays important roles in maintaining the malignancy of colorectal and hepatic cancer by enhancing the cell proliferation, motility, and development of the motility associated microstructures of cancer cells based on a possible complicated signal pathway.
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