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1.
Acta Microbiologica Sinica ; 2:672-685, 2022.
Article in Chinese | CAB Abstracts | ID: covidwho-1841702

ABSTRACT

[Objective] To explore whether porcine deltacoronavirus (PDCoV) can infect and proliferate in different animal species-derived cell lines. [Methods] The Sichuan isolate CHN-SC2015of PDCoV was inoculated in twelve cell lines derived from hamster,poultry,monkey, human and swine. After at least five blindly passages in each cell line, the virus was identified by RT-PCR,RT-q PCR, indirect immunofluorescence assay (IFA), and sequencing. [Results] PDCoV caused distinct cytopathic effect (CPE) in Vero,PAM,PK15,ST, and LLC-PK1 cells at the 1st passage (P1) and proliferated to various degrees in PAM,PK15,ST, and LLC-PK1 cells, while the CPE gradually disappeared during subsequent passages in Vero and PAM cells. Except that in the three susceptible cell lines (PK15,LLC-PK1, and ST), the viral copies of the infected cell lines gradually decreased with the increase in passages, and PDCoV could not be detected at P4 or P5 of DEF,Marc-145,HEK-293,ZYM-SIEC02, and PAM cells. PCR results showed that PDCoV could be detected only in CEF and Vero cells at P5. The IFA results showed that PDCoV could infect other cell lines except BHK-21 and ZYM-SIEC02, and specific immunofluorescence was observed in PK15,LLC-PK1, and ST cells at P1,P3, and P9. Therefore, only three cell lines (PK15,LLC-PK1, and ST) were suitable for serial passage, with the virus titers up to 107.11,107.00, and 107.37 TCID50/mL at P9,respectively. After passage in different cell lines,CHN-SC2015 accumulated 14 nucleotide mutations corresponding to 12 amino acid mutations. [Conclusion] This study indicates that PDCoV can infect a variety of cells in vitro, suggesting that it may have the potential of cross-species transmission.

2.
J Exp Med ; 219(6)2022 06 06.
Article in English | MEDLINE | ID: covidwho-1806201

ABSTRACT

Type I interferons (IFN-I) play a critical role in human antiviral immunity, as demonstrated by the exceptionally rare deleterious variants of IFNAR1 or IFNAR2. We investigated five children from Greenland, Canada, and Alaska presenting with viral diseases, including life-threatening COVID-19 or influenza, in addition to meningoencephalitis and/or hemophagocytic lymphohistiocytosis following live-attenuated viral vaccination. The affected individuals bore the same homozygous IFNAR2 c.157T>C, p.Ser53Pro missense variant. Although absent from reference databases, p.Ser53Pro occurred with a minor allele frequency of 0.034 in their Inuit ancestry. The serine to proline substitution prevented cell surface expression of IFNAR2 protein, small amounts of which persisted intracellularly in an aberrantly glycosylated state. Cells exclusively expressing the p.Ser53Pro variant lacked responses to recombinant IFN-I and displayed heightened vulnerability to multiple viruses in vitro-a phenotype rescued by wild-type IFNAR2 complementation. This novel form of autosomal recessive IFNAR2 deficiency reinforces the essential role of IFN-I in viral immunity. Further studies are warranted to assess the need for population screening.


Subject(s)
COVID-19 , Interferon Type I , Antiviral Agents/metabolism , Child , Humans , Inheritance Patterns , Interferon Type I/genetics , Interferon Type I/metabolism , Receptor, Interferon alpha-beta
3.
EuropePMC; 2022.
Preprint in English | EuropePMC | ID: ppcovidwho-334259

ABSTRACT

We found four striking differences in the COVID-19 case fatality rate (CFR) or the ratio of symptomatic COVID-19 cases versus asymptomatic infections. These striking differences all suggest that the risk for China to move away from its zero-COVID policy shall depend on China’s control measures. The CFR of COVID-19 in China can remain less than one tenth of influenza, namely that COVID-19 can be “tiny influenza”in China, if COVID-19 cases shall be well isolated in well disinfected environments (e.g., staying at well-disinfected home) with good maintenance treatment, to minimize their co-infections and maintain their body functions. Otherwise, the CFR of COVID-19 in China can be several times higher than influenza, namely that COVID-19 can be “giant influenza”in China. This analysis is also important to mitigate COVID-19 worldwide.

4.
Int J Mol Sci ; 23(6)2022 Mar 18.
Article in English | MEDLINE | ID: covidwho-1760651

ABSTRACT

PDCoV is an emerging enteropathogenic coronavirus that mainly causes acute diarrhea in piglets, seriously affecting pig breeding industries worldwide. To date, the molecular mechanisms of PDCoV-induced immune and inflammatory responses or host responses in LLC-PK cells in vitro are not well understood. HSP90 plays important roles in various viral infections. In this study, HSP90AB1 knockout cells (HSP90AB1KO) were constructed and a comparative transcriptomic analysis between PDCoV-infected HSP90AB1WT and HSP90AB1KO cells was conducted using RNA sequencing to explore the effect of HSP90AB1 on PDCoV infection. A total of 1295 and 3746 differentially expressed genes (DEGs) were identified in PDCoV-infected HSP90AB1WT and HSP90AB1KO cells, respectively. Moreover, most of the significantly enriched pathways were related to immune and inflammatory response-associated pathways upon PDCoV infection. The DEGs enriched in NF-κB pathways were specifically detected in HSP90AB1WT cells, and NF-κB inhibitors JSH-23, SC75741 and QNZ treatment reduced PDCoV infection. Further research revealed most cytokines associated with immune and inflammatory responses were upregulated during PDCoV infection. Knockout of HSP90AB1 altered the upregulated levels of some cytokines. Taken together, our findings provide new insights into the host response to PDCoV infection from the transcriptome perspective, which will contribute to illustrating the molecular basis of the interaction between PDCoV and HSP90AB1.


Subject(s)
Coronavirus Infections/veterinary , Deltacoronavirus , Gene Expression Profiling , HSP90 Heat-Shock Proteins/genetics , Immunity/genetics , Swine Diseases/etiology , Transcriptome , Animals , Computational Biology/methods , Disease Susceptibility , Gene Knockdown Techniques , Gene Ontology , Host-Pathogen Interactions/genetics , Host-Pathogen Interactions/immunology , NF-kappa B/metabolism , Swine
5.
J Virol ; 96(5): e0208621, 2022 03 09.
Article in English | MEDLINE | ID: covidwho-1736026

ABSTRACT

Coronavirus infections induce the expression of multiple proinflammatory cytokines and chemokines. We have previously shown that in cells infected with gammacoronavirus infectious bronchitis virus (IBV), interleukin 6 (IL-6), and IL-8 were drastically upregulated, and the MAP kinase p38 and the integrated stress response pathways were implicated in this process. In this study, we report that coronavirus infection activates a negative regulatory loop that restricts the upregulation of a number of proinflammatory genes. As revealed by the initial transcriptomic and subsequent validation analyses, the anti-inflammatory adenine-uridine (AU)-rich element (ARE)-binding protein, zinc finger protein 36 (ZFP36), and its related family members were upregulated in cells infected with IBV and three other coronaviruses, alphacoronaviruses porcine epidemic diarrhea virus (PEDV), human coronavirus 229E (HCoV-229E), and betacoronavirus HCoV-OC43, respectively. Characterization of the functional roles of ZFP36 during IBV infection demonstrated that ZFP36 promoted the degradation of transcripts coding for IL-6, IL-8, dual-specificity phosphatase 1 (DUSP1), prostaglandin-endoperoxide synthase 2 (PTGS2) and TNF-α-induced protein 3 (TNFAIP3), through binding to AREs in these transcripts. Consistently, knockdown and inhibition of JNK and p38 kinase activities reduced the expression of ZFP36, as well as the expression of IL-6 and IL-8. On the contrary, overexpression of mitogen-activated protein kinase kinase 3 (MKK3) and MAPKAP kinase-2 (MK2), the upstream and downstream kinases of p38, respectively, increased the expression of ZFP36 and decreased the expression of IL-8. Taken together, this study reveals an important regulatory role of the MKK3-p38-MK2-ZFP36 axis in coronavirus infection-induced proinflammatory response. IMPORTANCE Excessive and uncontrolled induction and release of proinflammatory cytokines and chemokines, the so-called cytokine release syndrome (CRS), would cause life-threatening complications and multiple organ failure in severe coronavirus infections, including severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS) and COVID-19. This study reveals that coronavirus infection also induces the expression of ZFP36, an anti-inflammatory ARE-binding protein, promoting the degradation of ARE-containing transcripts coding for IL-6 and IL-8 as well as a number of other proteins related to inflammatory response. Furthermore, the p38 MAP kinase, its upstream kinase MKK3 and downstream kinase MK2 were shown to play a regulatory role in upregulation of ZFP36 during coronavirus infection cycles. This MKK3-p38-MK2-ZFP36 axis would constitute a potential therapeutic target for severe coronavirus infections.


Subject(s)
Coronavirus Infections/metabolism , Interleukin-6/metabolism , Interleukin-8/metabolism , Tristetraprolin/metabolism , p38 Mitogen-Activated Protein Kinases/metabolism , Adenine/metabolism , Animals , Cell Line , Chlorocebus aethiops , Coronavirus Infections/genetics , Gene Expression Regulation , Humans , Infectious bronchitis virus/metabolism , Infectious bronchitis virus/pathogenicity , Interleukin-6/genetics , Interleukin-8/genetics , Intracellular Signaling Peptides and Proteins/metabolism , Phosphorylation , Transcriptional Activation , Up-Regulation , Uridine/metabolism , Vero Cells
6.
Transbound Emerg Dis ; 2022 Mar 03.
Article in English | MEDLINE | ID: covidwho-1731242

ABSTRACT

From 2003 onwards, three pandemics have been caused by coronaviruses: severe acute respiratory syndrome coronavirus (SARS-CoV); middle east respiratory syndrome coronavirus (MERS-CoV); and, most recently, SARS-CoV-2. Notably, all three were transmitted from animals to humans. This would suggest that animals are potential sources of epidemics for humans. The emerging porcine delta-coronavirus was reported to infect children. This is a red flag that marks the ability of PDCoV to break barriers of cross-species transmission to humans. Therefore, we conducted molecular genetic analysis of global clade PDCoV to characterize spatiotemporal patterns of viral diffusion and genetic diversity. PDCoV was classified into three major lineages, according to distribution and phylogenetic analysis of PDCoV. It can be inferred based on the analysis results of the currently known PDCoV strains that PDCoV might originate in Asia. We also selected six special spike amino acid sequences to align and analyze to find seven significant mutation sites. The accumulation of these mutations may enhance dynamic movements, accelerating spike protein membrane fusion events and transmission. Altogether, our study offers a novel insight into the diversification, evolution, and interspecies transmission and origin of PDCoV and emphasizes the need to study the zoonotic potential of the PDCoV and comprehensive surveillance and enhanced biosecurity precautions for PDCoV.

7.
Current Issues in Tourism ; 25(3):490-507, 2022.
Article in English | CAB Abstracts | ID: covidwho-1722015

ABSTRACT

The COVID-19 pandemic is greatly affecting the hospitality industry worldwide. Lodging demand is severely reduced as people's fear of coronavirus spreading risk in hotels. This research makes a timely contribution to the hospitality literature by proposing the mixed data sampling models (MIDAS) to monitor and forecast latest hotel occupancy rates with high-frequency big data sources, such as daily visitor arrivals and search query data. Quantitative evidence from Macau from January to July 2020 confirms that MIDAS models can measure the dynamic impacts of the COVID-19 pandemic on hotel occupancy and have a better prediction accuracy and explanation ability than competitive models. Industry practitioners can adopt this big data analytical framework to make daily or monthly updates of lodging demand, conduct scenario analysis, plan and trace the recovery schedule during and post COVID-19 phases. Finally, managerial implications and future work are highlighted.

8.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-323885

ABSTRACT

Objective: To conduct a meta-analysis of current studies that examined sex differences in severity and mortality in patients with COVID-19, and identify potential mechanisms underpinning these differences. Methods: We performed a systematic review to collate data from observational studies examining associations of sex differences with clinical outcomes of COVID-19. PubMed, Web of Science and four preprint servers were searched for relevant studies. Data were extracted and analyzed using meta-analysis where possible, with summary data presented otherwise. Publicly available bulk RNA sequencing (RNA-seq), single-cell RNA sequencing (scRNA-seq), and chromatin immunoprecipitation sequencing (ChIP-seq) data were analyzed to explore the potential mechanisms underlying the observed association. Results: 39 studies met inclusion criteria, representing 77932 patients, of which 41510 (53.3%) were males. Men were at a markedly increased risk of developing severe cases compared with women. Furthermore, the pooled odds ratio (OR) of mortality for male group compared with the female group indicated significant higher mortality rate for male. Data from scRNA-seq suggest that men have a higher amount of ACE2-expressing pulmonary alveolar type II cells than women. Sex-based immunological differences exist. The expression of androgen receptor (AR) is positively correlated with ACE2, and there is evidence that AR may directly regulate the expression of ACE2. Conclusions: This meta-analysis detected an increased severity and mortality rate in the male populations with COVID-19, which might be attributable to the sex-based differences in cellular compositions and immunological microenvironments of the lung. The host cell receptor ACE2 is likely regulated by AR signaling pathway, which is identified as a potential target for prevention and treatment of SARS-Cov-2 infections in men.

9.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-323702

ABSTRACT

Importance: Since December 2019, a novel coronavirus (SARS-CoV-2) causing COVID-19 has spread across the world in a global pandemic. Tens of thousands of people were infected, several thousand patients died. However, key risk factors for predicting mortality remain unclear. Objective: To identify the key risk factors for COVID-19 mortality. Design: , Setting, Participants: Retrospective, randomly selected eight family clusters consisting of 21 individual cases who had been confirmed positive for SARS-CoV-2 and admitted to the Wuhan Union Hospital, Wuhan, China, from February 6 to March 3 2020. This study aims to analyze the differences in mortal risk factors between fatal and non-fatal cases within each family.

10.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-323595

ABSTRACT

Background: Cigarette smoking (CS) is a global public health problem and a high-risk factor for various diseases. In December 2019, a novel coronavirus (HCoV-19) was identified in Wuhan, China. Because ACE2 has been identified as a receptor for HCoV-19, we hypothesize that CS affects the expression pattern of ACE2 in respiratory tract, causing differences in susceptibility to the virus. Methods: Three datasets (GSE994, GSE17913, and GSE18344), were downloaded from the Gene Expression Omnibus (GEO) database. Correlation and enrichment analysis were used to evaluate the function of ACE2. Also, the different expression of ACE2 in different groups of three datasets were analyzed. Results: Genes associated with ACE2 were enriched in important biological processes such as viral processes and immune response. Elevated ACE2 were found in intrapulmonary airways (GSE994) and oral epithelial cells (GSE17913) of smokers but not those of non-smokers or former smokers. Significant dose- and time-dependent relationships between CS and ACE2 expression were observed in mouse lung tissues, and long periods without smoking were found to significantly reduce ACE2 expression. Conclusions: Both human and rat data confirmed that CS could induce increased ACE2 in the respiratory tract, indicating that smokers have a higher susceptibility to HCoV-19.

12.
Arthritis Res Ther ; 24(1): 6, 2022 01 03.
Article in English | MEDLINE | ID: covidwho-1590005

ABSTRACT

BACKGROUND: Hydroxychloroquine (HCQ) has been recommended as a basic treatment for lupus nephritis (LN) during this decade based on its ability to improve LN-related renal immune-mediated inflammatory lesions. As a classical lysosomal inhibitor, HCQ may inhibit lysosomal degradation and disrupt protective autophagy in proximal tubular epithelial cells (PTECs). Therefore, the final renal effects of HCQ on LN need to be clarified. METHOD: HCQ was administered on spontaneous female MRL/lpr LN mice with severe proteinuria daily for 4 weeks. Moreover, the MRL/lpr mice with proteinuric LN were subjected to cisplatin-induced or unilateral ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) after 2 weeks of HCQ preadministration. RESULTS: As expected, HCQ treatment increased the survival ratio and downregulated the levels of serum creatinine in the mice with LN, ameliorated renal lesions, and inhibited renal interstitial inflammation. Unexpectedly, HCQ preadministration significantly increased susceptibility to and delayed the recovery of AKI complicated by LN, as demonstrated by an increase in PTEC apoptosis and expression of the tubular injury marker KIM-1 as well as the retardation of PTEC replenishment. HCQ preadministration suppressed the proliferation of PTECs by arresting cells in G1/S phase and upregulated the expression of cell cycle inhibitors. Furthermore, HCQ preadministration disrupted the PTEC autophagy-lysosomal pathway and accelerated PTEC senescence. CONCLUSION: HCQ treatment may increase susceptibility and delay the recovery of AKI complicated by LN despite its ability to improve LN-related renal immune-mediated inflammatory lesions. The probable mechanism involves accelerated apoptosis and inhibited proliferation of PTECs via autophagy-lysosomal pathway disruption and senescence promotion.


Subject(s)
Acute Kidney Injury , Lupus Nephritis , Acute Kidney Injury/chemically induced , Animals , Female , Hydroxychloroquine/pharmacology , Kidney/pathology , Mice , Mice, Inbred MRL lpr
13.
Vet Microbiol ; 266: 109333, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1629002

ABSTRACT

Porcine deltacoronavirus (PDCoV) is an enteropathogen found in many pig producing countries. It can cause acute diarrhea, vomiting, dehydration, and death in newborn piglets, seriously affecting the development of pig breeding industries. To date, our knowledge of the pathogenesis of PDCoV and its interactions with host cell factors remains incomplete. Using Co-IP coupled with LC/MS-MS, we identified 67 proteins that potentially interact with PDCoV in LLC-PK1 cells; five of the identified proteins were chosen for further evaluation (IMMT, STAT1, XPO5, PIK3AP1, and TMPRSS11E). Five LLC-PK1 cell lines, each with one of the genes of interest knocked down, were constructed using CRISPR/cas9. In these knockdown cells lines, only STAT1KD resulted in a significantly greater virus yield. Knockdown of the remaining four genes resulted, to varying degrees, in a lower virus yield that wild-type LLC-PK1 cells. The absence of STAT1 did not significantly affect the attachment of PDCoV to cells, but did result in increased viral internalization. Additionally, PDCoV infection stimulated expression of interferon stimulated genes (ISGs) downstream of STAT1 (IFIT1, IFIT2, RADS2, ISG15, MX1, and OAS1) while knockdown of STAT1 resulted in a greater than 80 % decrease in the expression of all six ISGs. Our findings show that STAT1 interacts with PDCoV, and plays a negative regulatory role in PDCoV infection.


Subject(s)
Coronavirus Infections , Swine Diseases , Animals , Coronavirus Infections/veterinary , Interferons , LLC-PK1 Cells , Swine , Virus Internalization
14.
EuropePMC; 2021.
Preprint in English | EuropePMC | ID: ppcovidwho-297084

ABSTRACT

RNA replication and transcription machinery is an important drug target for fighting against coronavirus. Non-structure protein nsp8 was proposed harboring primase activity. However, the RNA primer synthesis mechanism of nsp8 is still largely unknown. Here, we purified dimer and tetramer forms of SARS-CoV-2 nsp8. Combined with DLS, SANS and thermo-stability analysis, we found that both dimer and tetramer become loosened and destabilized with decreasing salt concentration, and the dimer form is more stable than the tetramer form. Further investigation showed that nsp8 dimer and tetramer can undergo phase separation but exhibit different phase separation behaviors. nsp8 dimer can form liquid-like droplets in the buffer with a low concentration of NaCl;phase separation of nsp8 tetramer depends on the assistance of RNA. Our findings on different phase separation behaviors of nsp8 dimer and tetramer could provide novel insight into the primer synthesis mechanism in coronavirus and facilitate developing novel therapeutic agents against SARS-CoV-2.

16.
Current Issues in Tourism ; : 1-18, 2021.
Article in English | Taylor & Francis | ID: covidwho-1488103
17.
Evid Based Complement Alternat Med ; 2021: 4303380, 2021.
Article in English | MEDLINE | ID: covidwho-1455773

ABSTRACT

BACKGROUND: In view of the global efforts to develop effective treatments for the current worldwide coronavirus 2019 (COVID-19) pandemic, Qingfei Paidu decoction (QPD), a novel traditional Chinese medicine (TCM) prescription, was formulated as an optimized combination of constituents of classic prescriptions used to treat numerous febrile and respiratory-related diseases. This prescription has been used to treat patients with COVID-19 pneumonia in Wuhan, China. Hypothesis/Purpose. We hypothesized that QPD would have beneficial effects on patients with COVID-19. We aimed to prove this hypothesis by evaluating the efficacy of QPD in patients with COVID-19 pneumonia. METHODS: In this single-center, retrospective, observational study, we identified eligible participants who received a laboratory diagnosis of COVID-19 between January 15 and March 15, 2020, in the west campus of Union Hospital in Wuhan, China. QPD was supplied as an oral liquid packaged in 200-mL containers, and patients were orally administered one package twice daily 40 minutes after a meal. The primary outcome was death, which was compared between patients who did and did not receive QPD (QPD and NoQPD groups, respectively). Propensity score matching (PSM) was used to identify cohorts. RESULTS: In total, 239 and 522 participants were enrolled in the QPD and NoQPD groups, respectively. After PSM at a 1 : 1 ratio, 446 patients meeting the criteria were included in the analysis with 223 in each arm. In the QPD and NoQPD groups, 7 (3.2%) and 29 (13.0%) patients died, and those in the QPD group had a significantly lower risk of death (hazard ratio (HR) 0.29, 95% CI: 0.13-0.67) than those in the NoQPD group (p = 0.004). Furthermore, the survival time was significantly longer in the QPD group than in the NoQPD group (p < 0.001). CONCLUSION: The use of QPD may reduce the risk of death in patients with COVID-19 pneumonia.

18.
Mil Med Res ; 8(1): 51, 2021 09 13.
Article in English | MEDLINE | ID: covidwho-1416822

ABSTRACT

To determine the prevalence and clinical features of olfactory and taste disorders among coronavirus disease 2019 (COVID-19) patients in China. A cross-sectional study was performed in Wuhan from April 3, 2020 to April 15, 2020. A total of 187 patients with confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) completed face-to-face interviews or telephone follow-ups. We found that the prevalence of olfactory and taste disorders was significantly lower in the Chinese cohort than in foreign COVID-19 cohorts. Females were more prone to olfactory and taste disorders. In some patients, olfactory and taste disorders precede other symptoms and can be used as early screening and warning signs.


Subject(s)
COVID-19/complications , Olfaction Disorders/etiology , Smell , Taste Disorders/etiology , Taste , Adolescent , Adult , Aged , Aged, 80 and over , China/epidemiology , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Olfaction Disorders/epidemiology , Prevalence , SARS-CoV-2 , Sex Factors , Taste Disorders/epidemiology , Young Adult
19.
J Cell Mol Med ; 25(17): 8558-8566, 2021 09.
Article in English | MEDLINE | ID: covidwho-1393908

ABSTRACT

Mesenchymal stem cells (MSCs) have been shown as an effective medicinal means to treat bronchopulmonary dysplasia (BPD). The widely used MSCs were from Wharton's jelly of umbilical cord (UC-MSCs) and bone marrow (BM-MSCs). Amniotic fluid MSCs (AF-MSCs) may be produced before an individual is born to treat foetal diseases by autoplastic transplantation. We evaluated intratracheal (IT) MSCs as an approach to treat an hyperoxia-induced BPD animal model and compared the therapeutic effects between AF-, UC- and BM-MSCs. A BPD animal model was generated by exposing newborn rats to 95% O2 . The continued stress lasted 21 days, and the treatment of IT MSCs was conducted for 4 days. The therapeutic effects were analysed, including lung histology, level of inflammatory cytokines, cell death ratio and state of angiogenesis, by sacrificing the experimental animal at day 21. The lasting hyperoxia stress induced BPD similar to the biological phenotype. The treatment of IT MSCs was safe without deaths and normal organ histopathology. Specifically, the treatment was effective by inhibiting the alveolar dilatation, reducing inflammatory cytokines, inducing angiogenesis and lowering the cell death ratio. AF-MSCs had better therapeutic effects compared with UC-MSCs in relieving the pulmonary alveoli histological changes and promoting neovascularization, and UC-MSCs had the best immunosuppressive effect in plasma and lung lysis compared with AF-MSCs and BM-MSCs. This study demonstrated the therapeutic effects of AF-, UC- and BM-MSCs in BPD model. Superior treatment effect was provided by antenatal MSCs compared to BM-MSC in a statistical comparison.


Subject(s)
Bronchopulmonary Dysplasia/therapy , Hyperoxia/therapy , Mesenchymal Stem Cell Transplantation/methods , Animals , Animals, Newborn , Cells, Cultured , Humans , Mesenchymal Stem Cells , Neovascularization, Physiologic , Rats , Rats, Sprague-Dawley , Umbilical Cord
20.
Int J Disaster Risk Reduct ; 65: 102524, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1364079

ABSTRACT

BACKGROUND: The characteristics of COVID-19, such as the long incubation period, the fast transmission speed, the high demand for treatment, and the lack of prior treatment experience, have brought tremendous psychological stress to the medical staff involved in the epidemic prevention and control, seriously affecting the mental health of medical staff. Therefore, this paper conducts a discussion on the psychological stress and mental health of medical staff. METHODS: (1)Interview 28 medical staff fighting against COVID-19 from Wuhan Central Hospital and Hubei Provincial Hospital of Traditional Chinese medicine. They have worked as doctors in mental health departments, surgery departments and emergency departments, nurses and management staffs; (2)Based on interviews and literature, the questionnaire survey is conducted among 528 medical personnel from all over the country who have participated in the fight against COVID-19 in Wuhan; (3)Use the structural equation modeling to explore the influence mechanism of medical staff's psychological stress and mental health in the prevention and control of COVID-19. Results: The epidemic severity in hospital and the work intensity are the important psychological stressors for the front-line medical staff. Self-risk perception has a mediating effect on the severity of epidemic in hospitals and mental health of medical staff. Social identification has no moderating effect between the self-risk perception and the mental health.

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