High intensities of population movement were associated with high incidence of COVID-19 during the pandemic.

Increased population movements and increased mobility made it possible for severe acute respiratory syndrome coronavirus 2, which is mainly spread by respiratory droplets, to spread faster and more easily. This study tracked and analysed the development of the coronavirus 2019 (COVID-19) outbreak in the top 100 cities that were destinations for people who left Wuhan before the city entered lockdown. Data were collected from the top 100 destination cities for people who travelled from Wuhan before the lockdown, the proportion of people travelling into each city, the intensity of intracity travel and the daily reports of COVID-19. The proportion of the population that travelled from Wuhan to each city from 10 January 2020 to 24 January 2020, was positively correlated with and had a significant linear relationship with the cumulative number of confirmed cases of COVID-19 in each city after 24 January (all P < 0.01). After the State Council launched a multidepartment joint prevention and control effort on 22 January 2020 and compared with data collected on 18 February, the average intracity travel intensity of the aforementioned 100 cities decreased by 60-70% (all P < 0.001). The average intensity of intracity travel on the nth day in these cities during the development of the outbreak was positively related to the growth rate of the number of confirmed COVID-19 cases on the n + 5th day in these cities and had a significant linear relationship (P < 0.01). Higher intensities of population movement were associated with a higher incidence of COVID-19 during the pandemic. Restrictions on population movement can effectively curb the development of an outbreak.

Analysis of the Clinical Diagnostic Value of GMFB in Cerebral Infarction.

BACKGROUND: Glial Maturation Factor Beta (GMFB) is a highly conserved brain-enriched protein implicated in immunoregulation, neuroplasticity and apoptosis, processes central to neural injury and repair following cerebral ischaemia. Therefore, we examined if changes in neurocellular GMFB expression and release can be used to assess brain injury following ischaemia. METHODS AND RESULTS: Immunofluorescence staining, Western blotting, immunohistochemistry and ELISA were used to measure GMFB in cultured neurons and astrocytes, rat brain tissues and plasma samples from stroke model rats and stroke patients, while cell viability assays, TTC staining and micro- PET were used to assess neural cell death and infarct severity. Immunofluorescence and immunohistochemistry revealed GMFB expression mainly in astrocyte and neuronal nuclei but also in neuronal axons and dendrites. Free GMFB concentration increased progressively in the culture medium during hypoxia-hypoglycaemia treatment. Plasma GMFB concentration increased in rats subjected to middle cerebral artery occlusion (MCAO, a model of stroke-reperfusion) and in stroke patients. Plasma GMFB in MCAO model rats was strongly correlated with infarct size (R2=0.9582). Plasma GMFB concentration was also markedly elevated in stroke patients within 24 h of onset and remained elevated for more than one week. Conversely, plasma GMFB elevations were not significant in myocardial infarct patients and stroke patients without infarction. CONCLUSION: GMFB has the prerequisite stability, expression specificity and response dynamics to serve as a reliable indicator of ischaemic injury in animal models and stroke patients. Plasma GMFB may be a convenient non-invasive adjunct to neuroimaging for stroke diagnosis and prognosis.

[Effect of 2Me, DTT, ZAAP and Enzyme on JMH Antigen on the Surface of Human Erythrocytes].

OBJECTIVE: To explore the the effects of 2-Me, DTT, papain, pineapple protease and ZZAP on the antigenicity of JMH antigen of human red blood cells (RBC) surface. METHODS: Firstly, human RBC were treated with 2-Me, DTT, pineapple protease, papain and ZZAP reagents, respectively. The antigenicity of JMH antigen on human RBC surface was detected and analyzed by flow cytometry. RESULTS: Flow cytometric analysis found that compared with level before treatment, the antigenicity of JMH antigen on RBC surface was significantly reduced after 2-Me treatment, the positive rate of JMH antigen: 69.5%±4.5% vs 56.5%±3.4% (t=12.44, P＜0.01); fluorescence intensity: 4906±317 vs 3003±165 (t=11.84, P＜0.01). The antigenicity of JMH antigen on RBC surface significantly increased after DTT treatment, showing the positive rate of JMH antigen: 61.7%±3.8% vs 75.5±4.9% (t=16.57, P＜0.01), fluorescence intensity: 4044±294 vs 4854±319 (t=15.46, P＜0.01). However, both bromelain and papain could significantly reduce the antigenicity of JMH antigen on the RBC surface, Bromelain: the positive rate of JMH antigen: 62.2%±3.8% vs 8.8%±1.2% (t=26.44, P＜0.01), fluorescence intensity: 4263±273 vs 1444±212 (t=19.27, P＜0.01); Papain: the positive rate of JMH antigen: 62.8%±3.6% vs 8.8%±1.5% (t=21.38, P＜0.01), fluorescence intensity: 4389±284 vs 1458±230 (t=17.49, P＜0.01). The flow cytometric analysis revealed that ZZAP treatment significantly reduced the antigenicity of JMH antigen on the RBC surface, the positive rate of JMH antigen: 62.2%±4.4% vs 48.2%±4.1% (t=14.87, P＜0.01), fluorescence intensity: 4106±263 vs 2063±175 (t=17.49, P＜0.01). CONCLUSION: The treatment with 2-Me can reduce the antigenicity of JMH antigen on human RBC surface. The antigenicity of JMH antigen on human RBC surface increased after DTT treatment. The antigenicity of JMH antigen on human RBC surface significantly reduces after the treatment with pineapple protease or papain. ZZAP treatment can reduce the antigenicity of JMH antigen on the RBC surface.

Combined induction with anti-PD-1 and anti-CTLA-4 antibodies provides synergistic antitumor effects in DC-CIK cells in renal carcinoma cell lines.

Immune escape of cancer cells has become the main challenge in the immunocytotherapy field. In this study, we analyzed the cytotoxicity of DC-CIK cells induced by anti-PD-1 and anti-CTLA-4 antibodies in RCC cell lines. Flow cytometry analysis was performed to analyze the immune phenotypes of DC-CIK cells. Click-iT EdU assay was performed to analyze the proliferation of DC-CIK cells. ELISA analysis was performed to detect the expression of cytokines in DC-CIK cells. Compared with DC-CIK cells without any treatment, the growth inhibition rate was significantly higher in the other three groups. Moreover, combined induction with anti-PD-1 plus anti-CTLA-4 antibodies provides synergistic antitumor effects of DC-CIK cells in renal carcinoma cell lines. The combined treatment promoted DC-CIK cell proliferation and differentiation into CD3+CD56+ NKT cells and CD3+CD8+ CTL cells. Compared with the control group, combined treatment significantly up-regulated the secretion of immune-stimulatory cytokines, such as IFN-γ and TNF-α, and down-regulated the secretion of the immunosuppressive cytokine IL-10. Furthermore, the co-induction promoted the early activation of DC-CIK cells. These results indicated the co-induction with anti-PD-1 plus anti-CTLA-4 antibodies improved antitumor effects of DC-CIK cells by promoting proliferation, differentiation, and early activation and regulating the secretion of immune-stimulatory and suppressive cytokines in renal carcinoma cell lines.

MgONPs Can Boost Plant Growth: Evidence from Increased Seedling Growth, Morpho-Physiological Activities, and Mg Uptake in Tobacco (Nicotiana tabacum L.).

In this study, we documented the impact of magnesium oxide nanoparticles (MgONPs) on the various morpho-physiological changes by root irrigation in tobacco plants in the matrix media, as well as the uptake and accumulation of the NPs over a range of concentrations (50⁻250 µg/mL). Our results showed that the seed germination rate was not affected following exposure to MgONPs for 5 days. Enhanced plant growth together with increased peroxidase activity (39.63 U mg-1 protein in the 250 µg/mL MgONPs treatment, 36.63 U mg-1 protein in the control), superoxide dismutase activity (30.15 U mg-1 protein compared to 26.95 U mg-1 protein in the control), and chlorophyll content (the chlorophyll a and b contents in 0 and 250 µg/mL of MgONPs were 0.21, 0.12 µg/g to 1.21, 0.67 µg/g, respectively) were observed after 30 days of MgONP treatment. However, the malondialdehyde, protein, and relative water contents did not differ significantly, indicating that the NPs in the test concentrations had no phytotoxicity and even promoted plant growth. Scanning electron microscopy and paraffin section observations indicated that the MgONPs did not affect the plant tissue structures and cells. In addition, an elevated Mg content was detected in the plant tissues exposed to MgONPs, suggesting that the Mg was taken up by the tobacco roots and translocated to the shoots and leaves, which were probably the most important tools to cause an increase in the chlorophyll content and stimulate growth. In particular, compared with the controls, a substantially higher Mg content was observed in the leaves (12.93 mg/g in the MgONPs treatment, 9.30 mg/g in the control) exposed to 250 µg/mL MgONPs, especially in the lower and middle leaves. This result confirmed that the contents of plant Mg-element in the old leaves were increased by MgONPs. In summary, this study investigated increased Mg uptake and growth stimulation, as well as the induction of various positive morpho-physiological changes to tobacco plants when exposed to MgONPs. Results elucidate the promotional impact of the NPs on plant health and their implications for agricultural safety and security.

Magnesium Oxide Nanoparticles: Effective Agricultural Antibacterial Agent Against Ralstonia solanacearum.

Magnesium (Mg) is an essential mineral element for plants and is nontoxic to organisms. In this study, we took advantage of nanotechnologies to systematically investigate the antibacterial mechanisms of magnesium oxide nanoparticles (MgONPs) against the phytopathogen Ralstonia solanacearum (R. solanacearum) in vitro and in vivo for the first time. R. solanacearum has contributed to catastrophic bacterial wilt, which has resulted in the world-wide reduction of tobacco production. The results demonstrated that MgONPs possessed statistically significant concentration-dependent antibacterial activity, and the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) were measured as 200 and 250 µg/mL, respectively. Additional studies, aimed at understanding the toxicity mechanism of MgONPs, indicated that physical injury occurred to the cell membranes, along with decreased motility and biofilm formation ability of R. solanacearum, due to the direct attachment of MgONPs to the surfaces of the bacterial cells, which was observed by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Reactive oxygen species (ROS) accumulation could also be an important reason for the antibacterial action, inducing DNA damage. The toxicity assessment assay under greenhouse conditions demonstrated that the MgONPs had exerted a large effect on tobacco bacterial wilt, reducing the bacterial wilt index. Altogether, the results suggest that the development of MgONPs as alternative antibacterial agents will become a new research subject.

Overexpression of trefoil factor 3 (TFF3) contributes to the malignant progression in cervical cancer cells.

BACKGROUND: There remains a great need for effective therapies for cervical cancers, the majority of which are aggressive leaving patients with poor prognosis. METHODS AND RESULTS: Here, we identify a novel candidate therapeutic target, trefoil factor 3 (TFF3) which overexpressed in cervical cancer cells and was associated with reduced postoperative survival. Functional studies demonstrated that TFF3 overexpression promoted the proliferation and invasion of cervical cancer cells, and inhibited the apoptosis by inducing the mRNA changes in SiHa and Hela cell lines. Conversely, TFF3 silencing disrupted the proliferation and invasion of cervical cancer cells, and induced the apoptosis via Click-iT EdU test, flow cytometry analysis and two-dimensional Matrigel Transwell analysis. Western blot analysis showed that overexpression of TFF3 repressed E-cadherin (CDH1) expression to promote the invasion of cervical cancer cells. Furthermore, down-regulated CDH1 via overexpression of TFF3 was significantly up-regulated by virtue of inhibitor of p-STAT3. CONCLUSIONS: These results suggested that TFF3 stimulated the invasion of cervical cancer cells probably by activating the STAT3/CDH1 signaling pathway. Furthermore, overexpression of TFF3 decreased the sensitivity of cervical cancer cells to etoposide by increasing P-glycoprotein (P-gp) functional activity. Overall, our work provides a preclinical proof that TFF3 not only contributes to the malignant progression of cervical cancers and but also is a potential therapeutic target.