Publications by authors named "Yangfan Lv"

8 Publications

  • Page 1 of 1

Spatio-temporal evolution and influencing mechanism of the COVID-19 epidemic in Shandong province, China.

Sci Rep 2021 04 9;11(1):7811. Epub 2021 Apr 9.

College of Urban and Environmental Sciences, Northwest University, Xi'an, 710127, China.

The novel coronavirus pneumonia (COVID-19) outbreak that emerged in late 2019 has posed a severe threat to human health and social and economic development, and thus has become a major public health crisis affecting the world. The spread of COVID-19 in population and regions is a typical geographical process, which is worth discussing from the geographical perspective. This paper focuses on Shandong province, which has a high incidence, though the first Chinese confirmed case was reported from Hubei province. Based on the data of reported confirmed cases and the detailed information of cases collected manually, we used text analysis, mathematical statistics and spatial analysis to reveal the demographic characteristics of confirmed cases and the spatio-temporal evolution process of the epidemic, and to explore the comprehensive mechanism of epidemic evolution and prevention and control. The results show that: (1) the incidence rate of COVID-19 in Shandong is 0.76/100,000. The majority of confirmed cases are old and middle-aged people who are infected by the intra-province diffusion, followed by young and middle-aged people who are infected outside the province. (2) Up to February 5, the number of daily confirmed cases shows a trend of "rapid increase before slowing down", among which, the changes of age and gender are closely related to population migration, epidemic characteristics and intervention measures. (3) Affected by the regional economy and population, the spatial distribution of the confirmed cases is obviously unbalanced, with the cluster pattern of "high-low" and "low-high". (4) The evolution of the migration pattern, affected by the geographical location of Wuhan and Chinese traditional culture, is dominated by "cross-provincial" and "intra-provincial" direct flow, and generally shows the trend of "southwest → northeast". Finally, combined with the targeted countermeasures of "source-flow-sink", the comprehensive mechanism of COVID-19 epidemic evolution and prevention and control in Shandong is revealed. External and internal prevention and control measures are also figured out.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41598-021-86188-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8035406PMC
April 2021

Gut microbiota and lipid metabolism alterations in mice induced by oral cadmium telluride quantum dots.

J Appl Toxicol 2020 08 13;40(8):1131-1140. Epub 2020 Mar 13.

Key Laboratory for Organic Electronics and Information Displays & Jiangsu Key Laboratory for Biosensors, Institute of Advanced Materials (IAM), Nanjing University of Posts and Telecommunications, Nanjing, China.

The potential toxicity of cadmium-containing quantum dots (QDs) has received much attention because of increasing biomedical applications. However, little has been known about how cadmium telluride (CdTe) QDs influence the gut microbiota and lipid metabolism. In this study, mice were exposed orally to CdTe QDs (200 μL of 0.2, 2, 20 or 200 μm; twice per week) for 4 weeks. The oral experiments showed CdTe QD exposure led to a decrease of the Firmicutes/Bacteroidetes (F/B) ratio of gut microbiota, which highly negatively correlated with the low-density lipoprotein (LDL), triglyceride (TG) and total cholesterol (TC) levels in serum. In addition, the low-dose (0.2 and 2 μm) CdTe QDs significantly increased the diversity of gut microbiota, and did not elevate the LDL, TG and TC levels in serum. The medium dose (20 μm) of CdTe QDs caused the biggest decrease of the F/B ratio, so it significantly increased the LDL, TG and TC levels compared with the control. Furthermore, high-dose (200 μm) CdTe QDs caused various toxicities in the histopathology of liver and intestine, liver function and intestinal immunity, but did not significantly lead to changes of the LDL, TG and TC levels in serum. This study demonstrates that high-dose oral CdTe QDs mainly lead to tissue damage of the liver and intestine, while the medium and low doses of oral CdTe QDs induce shifts of gut microbiota structure, which are associated with blood lipid levels.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/jat.3972DOI Listing
August 2020

CircMRPS35 suppresses gastric cancer progression via recruiting KAT7 to govern histone modification.

Mol Cancer 2020 03 12;19(1):56. Epub 2020 Mar 12.

Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.

Background: Aberrant expression of circular RNAs contributes to the initiation and progression of cancers, but the underlying mechanism remains elusive.

Methods: RNA-seq and qRT-PCR were performed to screen differential expressed circRNAs between gastric cancer tissues and adjacent normal tissues. Candidate circRNA (circMRPS35) was screened out and validated by qRT-PCR. Cell proliferation and invasion ability were determined by CCK-8 and cell invasion assays. RNA-seq, GO-pathway, RNA pull-down and ChIRP were further applied to search for detailed mechanism.

Results: Here, a novel circRNA named circMRPS35, was screened out by RNA-seq in gastric cancer tissues, whose expression is related to clinicopathological characteristics and prognosis in gastric cancer patients. Biologically, circMRPS35 suppresses the proliferation and invasion of gastric cancer cells in vitro and in vivo. Mechanistically, circMRPS35 acts as a modular scaffold to recruit histone acetyltransferase KAT7 to the promoters of FOXO1 and FOXO3a genes, which elicits acetylation of H4K5 in their promoters. Particularly, circMRPS35 specifically binds to FOXO1/3a promoter regions directly. Thus, it dramatically activates the transcription of FOXO1/3a and triggers subsequent response of their downstream target genes expression, including p21, p27, Twist1 and E-cadherin, resulting in the inhibition of cell proliferation and invasion. Moreover, circMRPS35 expression positively correlates with that of FOXO1/3a in gastric cancer tissues.

Conclusions: Our findings not only reveal the pivotal roles of circMRPS35 in governing histone modification in anticancer treatment, but also advocate for triggering circMRPS35/KAT7/FOXO1/3a pathway to combat gastric cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12943-020-01160-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066857PMC
March 2020

Anoikis‑resistant human osteosarcoma cells display significant angiogenesis by activating the Src kinase‑mediated MAPK pathway.

Oncol Rep 2019 Jan 29;41(1):235-245. Epub 2018 Oct 29.

Department of Pathology, Xinqiao Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, P.R. China.

Tumor cells must resist anoikis to metastasize. There is a key role of angiogenesis in the growth and metastasis of tumors. However, the relationship between anoikis resistance and angiogenesis has not been well explored in human osteosarcoma. In the present study, we reported the higher expression of vascular endothelial growth factor‑A (VEGF‑A) in osteosarcoma cells that were resistant to anoikis than in parental osteosarcoma cells, promoting the proliferation, tube formation, and migration of human umbilical vein endothelial cells (HUVECs). Src, JNK (Jun amino‑terminal kinase) and ERK (extracellular signal‑regulated kinase) signaling pathway phosphorylation was activated in anoikis‑resistant cells; Src inhibitor reduced the expression of VEGF‑A and angiogenesis and inhibited JNK and ERK pathway activity. Overexpression of phosphorylated (p)‑Src and VEGF‑A was positively correlated to the metastatic potential in human osteosarcoma tissues, as quantified by immunohistochemistry. In addition, p‑Src expression was directly correlated with VEGF‑A expression and microvessel density in vivo. Our findings revealed that anoikis resistance in osteosarcoma cells increased the expression of VEGF‑A and angiogenesis through the Src/JNK/ERK signaling pathways. Thus, Src may be a potential therapeutic alternative in osteosarcoma angiogenesis and metastasis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/or.2018.6827DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6278590PMC
January 2019

Acute kidney injury and inflammatory response of sepsis following cecal ligation and puncture in d-galactose-induced aging rats.

Clin Interv Aging 2017 29;12:593-602. Epub 2017 Mar 29.

Department of Critical Care Medicine, Chinese People's Liberation Army General Hospital, Beijing, People's Republic of China.

Background: Recently, the d-galactose (d-gal)-induced mimetic aging rat model has been widely used in studies of age-associated diseases, which have shown that chronic d-gal exposure induces premature aging similar to natural aging in rats. With the increasing rate of sepsis in the geriatric population, an easy-access animal model for preclinical studies of elderly sepsis is urgently needed. This study investigates whether a sepsis model that is established in d-gal-induced aging rats can serve as a suitable model for preclinical studies of elderly patients with sepsis.

Objective: To investigate the acute kidney injury (AKI) and inflammatory response of sepsis following cecal ligation and puncture (CLP) in d-gal-induced aging rats.

Methods: Twelve-week-old male Sprague Dawley rats were divided into low-dose d-gal (L d-gal, 125 mg/kg/d), high-dose d-gal (H d-gal, 500 mg/kg/d), and control groups. After daily subcutaneous injection of d-gal for 6 weeks, the CLP method was used to establish a sepsis model.

Results: The mortality was 73.3%, 40%, and 33.3% in the H d-gal, L d-gal, and control groups, respectively. Blood urea nitrogen, creatinine, plasma neutrophil gelatinase-associated lipocalin, interleukin-6, interleukin-10, and tumor necrosis factor-α were markedly increased in the H d-gal group after establishment of the sepsis model (H d-gal vs control, <0.05 at 12 h and 24 h post-CLP). The rate of severe AKI (RIFLE-F) at 24 h post-CLP was 43% for both the control and L d-gal groups and 80% for the H d-gal group.

Conclusion: High-dose- d-gal-induced aging rats are more likely to die from sepsis than are young rats, and probably this is associated with increased severity of septic AKI and an increased inflammatory response. Therefore, use of the high-dose- d-gal-induced aging rat model of sepsis for preclinical studies can provide more useful information for the treatment of sepsis in elderly patients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.2147/CIA.S132277DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384694PMC
July 2017

Preliminary screening of differentially expressed genes involved in methyl-CpG-binding protein 2 gene-mediated proliferation in human osteosarcoma cells.

Tumour Biol 2015 Apr 23;36(4):3009-15. Epub 2015 Jan 23.

Department of Pathology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.

Methyl-CpG-binding protein 2 (MeCP2) is essential in human brain development and has been linked to several cancer types and neuro-developmental disorders. This study aims to screen the MeCP2 related differentially expressed genes and discover the therapeutic targets for osteosarcoma. CCK8 assay was used to detect the proliferation and SaOS2 and U2OS cells. Apoptosis of cells was detected by flow cytometry analysis that monitored Annexin V-APC/7-DD binding and 7-ADD uptake simultaneously. Denaturing formaldehyde agarose gel electrophoresis was employed to examine the quality of total RNA 18S and 28S units. Gene chip technique was utilized to discover the differentially expressed genes correlated with MeCP2 gene. Differential gene screening criteria were used to screen the changed genes. The gene up-regulation or down-regulation more than 1.5 times was regarded as significant differential expression genes. The CCK8 results indicated that the cell proliferation of MeCP2 silencing cells (LV-MeCP2-RNAi) was significantly decreased compared to non-silenced cells (LV-MeCP2-RNAi-CN) (P < 0.05). MeCP2 silencing could also induce significant apoptosis compared to non-silenced cells (P < 0.05); 107 expression changed genes were screened from a total of 49,395 transcripts. Among the total 107 transcripts, 34 transcripts were up-regulated and 73 transcripts were down-regulated. There were five significant differentially expressed genes, including IGFBP4, HOXC8, LMO4, MDK, and CTGF, which correlated with the MeCP2 gene. The methylation frequency of CpG in IGFBP4 gene could achieve 55%. In conclusion, the differentially expressed IGFBP4, HOXC8, LMO4, MDK, and CTGF genes may be involved in MeCP2 gene-mediated proliferation and apoptosis in osteosarcoma cells.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s13277-014-2935-4DOI Listing
April 2015

Epigenetic silencing of methyl-CpG-binding protein 2 gene affects proliferation, invasion, migration, and apoptosis of human osteosarcoma cells.

Tumour Biol 2014 Dec 17;35(12):11819-27. Epub 2014 Sep 17.

Department of Pathology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.

Methyl-CpG-binding protein 2 (MeCP2) is a DNA methylation-related gene of the methyl-CpG-binding protein family. Here, we investigated the epigenetic function of the MeCP2 in SaOS2 and U2OS cell lines, and explored the antitumor effects of the gene silencing for osteosarcoma. In this study, chromatin immunoprecipitation assay was used to detect MeCP2 binding activity with TSSC3 gene. RT-PCR and western blot assay were used to analyze the MeCP2 expression in osteosarcoma cell lines after transfection with LV-MECP2-RNAi. Transwell invasion and migration assays were used to detect the cell invasion and migration. The cell apoptosis was examined by using the flow cytometry assay. The tumor size was also assessed to determine the therapeutic effects of gene silencing. The results indicated that MeCP2 indicated the highest combining power with TSSC3 gene. LV-MECP2-RNAi could decrease MeCP2 level in tumor cells compared with the untreated cells (P < 0.05). LV-MECP2-RNAi inhibited the U2OS and SaOS2 cells invasion and migration compared with the control cells (P < 0.05). LV-MECP2-RNAi triggered the U2OS and SaOS2 cell apoptosis, and inhibited the cell proliferation significantly compared with the control cells (P < 0.05). The gene silencing of RNAi could also decreased the tumor size significantly compared with untreated cells (P < 0.05). In conclusion, silencing the MeCP2 gene could block the MeCP2 expression and inhibit the tumor cell migration, invasion, and proliferation, and decreases the tumor size by inducing the apoptosis of the tumor cells.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s13277-014-2336-8DOI Listing
December 2014

Epigenetic regulation of the pro-apoptosis gene TSSC3 in human osteosarcoma cells.

Biomed Pharmacother 2014 Feb 18;68(1):45-50. Epub 2013 Oct 18.

Department of Pathology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China. Electronic address:

Promoter hypermethylation can lead to a loss of genetic imprinting in carcinogenesis. The mechanism for the loss of expression of the imprinted gene TSSC3 has not been investigated in cases of osteosarcoma. In this study, we treated osteosarcoma cell lines with 5-Aza-CdR, which is a widely-used DNA methyltransferase inhibitor, and found dose-dependent reduction in cell growth, conversion of cell morphology to a non-motile phenotype, and obvious increase in apoptosis. In addition, we also found that 5-Aza-CdR reactivated TSSC3 expression through demethylation of the promoter regions. These findings indicate that the TSSC3 gene is silenced through hypermethylation of the promoter regions, a mechanism commonly associated with gene silencing in cancer. Finally, we examined the role of TSSC3 in human osteosarcoma SaOS2 cells. We showed that TSSC3 overexpression suppressed SaOS2 cell growth and increased apoptosis through caspase-3 upregulation, thereby, suggesting that TSSC3 may play a pro-apoptosis role to maintain the normal balance of growth. Taken together, these observations suggest that the epigenetic regulation of TSSC3, a pro-apoptosis gene, provides valuable insights into possible osteosarcoma therapies.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.biopha.2013.10.006DOI Listing
February 2014