Promoting health knowledge and improving the public's health literacy is an inherent requirement of the Healthy China Initiative.In the era of deepening implementation of the Healthy China strategy and rapid development of all media,large public hospitals play an irreplaceable and important role in leading the popularization of health knowledge and impro-ving the quality of information.However,in the process of carrying out health popularization work,many hospitals still face prob-lems such as lack of a regular working mechanism,lack of comprehensive team building,and lack of differentiated operation strategies.In response to these problems,the First Affiliated Hospital of Sun Yat-sen University has established a health populari-zation working mechanism led by the Party organization and coordinated at all levels,and has innovated in terms of personnel team,platform construction,content creation,and expression form,exploring a new model of health popularization work to pro-vide reference for other hospitals.

Objective To explore the mechanism of action of curcumin in the treatment of silicosis by network pharmacology combined with molecular docking technology. Methods The targets prediction network of curcumin in treating silicosis was established based on the collection of targets of curcumin and silicosis in multiple databases, cross-targets were submitted to the STRING database, and their connectivity was analyzed by Cytoscape software. Gene ontology (GO) function analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed on the top 20 genes. The molecular docking was performed on the key targets to study the mechanism of action of curcumin in treating silicosis. Results A total of 311 targets related to curcumin, 270 targets related to silicosis, and 74 cross-targets were obtained from the databases. GO function analysis revealed 2 665 related pathways, and KEGG pathway enrichment analysis revealed 188 related pathways. Molecular docking results showed that curcumin had good binding ability with the targets of mitogen-activated protein kinase 3 (MAPK3), interleukin (IL) 6, serine/threonine kinase 1 (AKT1), vascular endothelial growth factor A (VEGFA), signal transducer and activator of transcription 3, albumin, Jun proto-oncogene, tumor necrosis factor (TNF), IL1B, tumor protein p53, C-C motif chemokine ligand 2 and fibronectin 1. Conclusion The therapeutical effects of curcumin on silicosis were implemented through multi-targets and multi-pathways. Curcumin may play a role in the treatment of silicosis by binding to the core targets MAPK3, IL6, AKT1, VEGFA and TNF and regulating the MAPK, IL6, TNF, phosphatidylinositol 3-kinase/protein kinase B and VEGF signaling pathways.

ObjectiveTo determine the complications of hypertension among local residents in Minhang district of Shanghai， and provide scientific evidence for key preventive intervention. MethodsWe retrieved the data from the electronic health records， in which hypertensive patients were included for community-based management， in Minhang district of Shanghai from January 1st， 2014 to December 31st， 2018. A total of 38 599 hypertensive patients who had not had hypertension related clinical symptom when included in the electronic health records were enrolled in our study. Chi-square test and Cochran-Mantel-Haenszel test were used to determine the complications of hypertension. ResultsThe incidence proportion of complications was 10.77%， of which cerebrovascular damage was the highest （7.44%）， followed by cardiac damage （3.55%） and peripheral vascular damage （0.81%）. The incidence proportions in patients aged 18‒59， 60‒69， 70 and above were 5.53%， 9.61% and 16.19%， respectively. There was significant difference in the incidence proportions of complications among age groups （χ²=668.670， P<0.05）. Cochran-Mantel-Haenszel test showed that in the hypertensive patients aged 60‒69， the incidence proportion of complications in females was lower than that in males （χ²=5.937， P<0.05）. However， in those aged above 70， the incidence proportion of complications in females was higher than that in males （χ²=11.619， P<0.05）. ConclusionIn patients with hypertension， the incidence proportions of cardiovascular and cerebrovascular diseases remains relatively high in Minhang district of Shanghai. Additionally， both age and gender have influence on the incidence of complications.

The regulator of expression of virion(Rev)protein binds specifically to the Rev-responsive element(RRE)RNA in order to regulate the expression of the human immunodeficiency virus(HIV)-1 genes.Fluores-cence indicator displacement assays have been used to identify ligands that can inhibit the Rev-RRE interaction;however,the small fluorescence indicators cannot fully replace the Rev peptide or protein.As a result,a single rhodamine B labeled Rev(RB-Rev)model peptide was utilized in this study to develop a direct and efficient Rev-RRE inhibitor screening model.Due to photon-induced electron transfer quenching of the tryptophan residue on the RB fluorophore,the fluorescence of RB in Rev was weakened and could be dramatically reactivated by interaction with RRE RNA in ammonium acetate buffer(approximately six times).The interaction could reduce the electron transfer between tryptophan and RB,and RRE could also increase RB fluorescence.The inhibitor screening model was evaluated using three known positive Rev-RRE inhibitors,namely,proflavin,6-chloro-9-[3-(2-chloroethylamino)pro-pylamino]-2-methoxyacridine(ICR 191),and neomycin,as well as a negative drug,arginine.With the addition of the positive drugs,the fluorescence of the Rev-RRE decreased,indicating the displacement of RB-Rev.This was confirmed using atomic force microscopy(AFM)and the fluorescence was essentially unaffected by the addition of arginine.The results demonstrated that RB-Rev can be used as a fluorescent probe for recognizing small ligands that target RRE RNA.The Rev-RRE inhibitor screening model offers a novel approach to evaluating and identifying long-acting Rev inhibitors.

Objective To investigate the role and the mechanism of ppk1 gene (coding for polyphosphate kinase 1) in oxidative stress resistance in uropathogenic Escherichia coli (UPEC).MethodsMutant strains with ppk1-deletion (△pk1) and complemented strains (△pk1-C) were constructed based on the UPEC strain CFT073.A comparative analysis was conducted to analyze survival rates of CFT073, △pk1 and △pk1-C strains at different time points while they were under oxidative stress.Differences in protein expression between CFT073 and △pk1 strains were analyzed using mass spectrometric analysis.Differences between CFT073 and △pk1 strains in expression of katG and katE genes were analyzed using real-time quantitative RT-PCR.Results The survival rate of △pk1 strains was lower than that of CFT073 strains at every time point, while the survival rate of △pk1-C strains was basically the same as that of CFT073 strains.Gel image analysis and mass spectrometric analysis revealed that six proteins were down-regulated and one was up-regulated in △pk1 strains as compared with those in CFT073 strains.Expression of the catalase-coding genes katG and katE in △pk1 strains were respectively (20.5±8.2)% and (20.9±6.9)% of those in CFT073 strains (P<0.05).Conclusion The ppk1 gene plays an important role in oxidative stress resistance in UPEC by modulating the expression of catalase-coding genes katG and katE.

Objective To explore the role of ppk1 gene in E.coli CFT073 strain during urinary tract infection (UTI). Methods C57BL/6 mouse models of acute UTI with the wild-type(CFT073) and ppk1 mutant (△pk1) infected, were used to compare the bacteria colonization and inflammation induction abilities of bladder tissues. Results In the mouse models, the △pk1 strain showed a significantly lower infection rate (73.3% vs 93.3%) and lower adhesion frequency of bladder (0.01%vs 0.5%) than those of the CFT073 strain. The expression of IL-6 and TNF-αwere reduced in the bladder of △pk1 infected group (P<0.05). Hematoxylin-Eosin tissue staining showed that the damage degree of bladders in △pk1 infected mice were less serious than the CFT073 infected mice. Conclusion ppk1 gene plays an important role in E.coli colonization to bladder and the inflammation induction ability.

OBJECTIVETo study the changes in biological behaviors of meningitis E. coli K1 strain E44 after deletion of polyphosphate kinase 1 (ppk1) gene and explore the role of ppk1 in the pathogenesis of E. coli K1-induced meningitis.

METHODSThe wild-type strain E. coli K1 and ppk1 deletion mutant were exposed to heat at 56 degrees celsius; for 6 min, and their survival rates were determined. The adhesion and invasion of the bacteria to human brain microvascular endothelial cells (HBMECs) were observed using electron microscopy and quantitative tests. HBMECs were co-incubated with wild-type strain or ppk1 deletion mutant, and the cytoskeleton rearrangement was observed under laser scanning confocal microscope.

RESULTSThe survival rate of the ppk1 deletion mutant was significantly lower than that of the wild-type strain after heat exposure. The ppk1 deletion mutant also showed lowered cell adhesion and invasion abilities and weakened ability to induce cytoskeleton rearrangement in HBMECs.

CONCLUSIONSppk1 gene is important for E.coli K1 for heat resistance, cell adhesion and invasion, and for inducing cytoskeletal rearrangement in HBMECs.

Brain ; cytology ; Cells, Cultured ; Cytoskeleton ; Endothelial Cells ; cytology ; microbiology ; Escherichia coli ; genetics ; physiology ; Escherichia coli Proteins ; genetics ; Gene Deletion ; Humans ; Phosphotransferases (Phosphate Group Acceptor) ; genetics

Objective To study the changes in biological behaviors of meningitis E. coli K1 strain E44 after deletion of polyphosphate kinase 1 (ppk1) gene and explore the role of ppk1 in the pathogenesis of E. coli K1-induced meningitis. Methods The wild-type strain E. coli K1 and ppk1 deletion mutant were exposed to heat at 56℃for 6 min, and their survival rates were determined. The adhesion and invasion of the bacteria to human brain microvascular endothelial cells (HBMECs) were observed using electron microscopy and quantitative tests. HBMECs were co-incubated with wild-type strain or ppk1 deletion mutant, and the cytoskeleton rearrangement was observed under laser scanning confocal microscope. Results The survival rate of the ppk1 deletion mutant was significantly lower than that of the wild-type strain after heat exposure. The ppk1 deletion mutant also showed lowered cell adhesion and invasion abilities and weakened ability to induce cytoskeleton rearrangement in HBMECs. Conclusion ppk1 gene is important for E.coli K1 for heat resistance, cell adhesion and invasion, and for inducing cytoskeletal rearrangement in HBMECs.

Objective To study the changes in biological behaviors of meningitis E. coli K1 strain E44 after deletion of polyphosphate kinase 1 (ppk1) gene and explore the role of ppk1 in the pathogenesis of E. coli K1-induced meningitis. Methods The wild-type strain E. coli K1 and ppk1 deletion mutant were exposed to heat at 56℃for 6 min, and their survival rates were determined. The adhesion and invasion of the bacteria to human brain microvascular endothelial cells (HBMECs) were observed using electron microscopy and quantitative tests. HBMECs were co-incubated with wild-type strain or ppk1 deletion mutant, and the cytoskeleton rearrangement was observed under laser scanning confocal microscope. Results The survival rate of the ppk1 deletion mutant was significantly lower than that of the wild-type strain after heat exposure. The ppk1 deletion mutant also showed lowered cell adhesion and invasion abilities and weakened ability to induce cytoskeleton rearrangement in HBMECs. Conclusion ppk1 gene is important for E.coli K1 for heat resistance, cell adhesion and invasion, and for inducing cytoskeletal rearrangement in HBMECs.

Objective To construct a Polyphosphate kinase 1 ( ppk1) gene deletion mutant of uro-pathogenic Escherichia coli (E.coli) CFT073, and to explore the biological properties of the mutant strain . Methods The ppk1 gene deletion strain (△pk1) was constructed based on CFT073 E.coli strain by usingλRed homologous recombination technology .A comparison analysis was conducted on adhesive and invasive abilities between CFT073 wild type strain and △pk1 strain in in vitro model of human bladder cancer epithe-lial cell 5637 .Crystal violet staining method was used to evaluate the influences of ppk1 gene deletion on biofilm formation.Results The CFT073 ppk1 deletion mutant strain was successfully constructed .Com-pared with the wild type strain ,△pk1 strain showed impaired adhesive and invasive abilities to 5637 cells. Moreover , the absorbance values of crystal violet at 570 nm at each time point of the mutant strain group were also lower than those of the wild-type strain group .Conclusion The ppk1 gene deletion mutant of uro-pathogenic E.coli CFT073 could be successfully constructed by Red homologous recombination technology and its biological properties indicates that ppk1 gene plays an important role in the pathogenesis of uropatho-genic E.coli infection through regulating the abilities of adhesion , invasion and biofilm formation .