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In the stability analysis of loess fill slope, the fissure nature of loess is often ignored, which makes the stability calculation of fill slope too conservative. Based on the upper limit theory of plastic limit analysis, the stability analysis model of loess-filled fissured slope supported by frame prestressed anchors was established. Considering the tensile strength cut-off yield property of soil, the stability coefficient of slope was calculated, and the influence of different factors on slope stability was analyzed. The results show that ignoring the fissures in loess will overestimate the stability of the fill slope, and the support structure can significantly improve the stability of the loess-filled fissure slope. The research results of this paper can further enrich the stability analysis theory of loess-filled fissured slope supported by frame prestressed anchors, which is of great significance to guide engineering practice.

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For lightweight steel frame structures consisting of steel H-beams and cold-formed steel columns filled with concrete, seismic performance comparison tests and numerical simulation analyses were performed for bare and infilled frames. The effects of the lightweight wall panels, the axial compression ratio and the wall thickness of the steel sections of the columns on the seismic properties of the structure were investigated. The failure of the bare frame was concentrated in the weld fractures at the beam-column joints. When the wall panels were embedded in the frame, the damage was concentrated at the corners and edges of the wall panels and the connectors. The wall panels significantly improved the initial stiffness of the frame, early energy dissipation and resistance, and the wall panel energy dissipation rate was initially as great as 91%. As the axial compression ratio increased, the resistance of the structure significantly decreased. Under monotonic loading, the resistance on the structure with an axial compression ratio of 0.4 was reduced by nearly 44% compared to the structure without axial compression. Increasing the wall thickness of the steel sections of the columns increased the load-bearing capacity of the structure, but the increase diminished with increasing wall thickness.

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To investigate the relationship between human immunodeficiency virus (HIV) infection and the risk of mortality among coronavirus disease 2019 (COVID-19) patients based on adjusted effect estimate by a quantitative meta-analysis. A random-effects model was used to estimate the pooled effect size (ES) with corresponding 95% confidence interval (CI). I2 statistic, sensitivity analysis, Begg's test, meta-regression and subgroup analyses were also conducted. This meta-analysis presented that HIV infection was associated with a significantly higher risk of COVID-19 mortality based on 40 studies reporting risk factors-adjusted effects with 131,907,981 cases (pooled ES 1.43, 95% CI 1.25-1.63). Subgroup analyses by male proportion and setting yielded consistent results on the significant association between HIV infection and the increased risk of COVID-19 mortality. Allowing for the existence of heterogeneity, further meta-regression and subgroup analyses were conducted to seek the possible source of heterogeneity. None of factors might be possible reasons for heterogeneity in the further analyses. Sensitivity analysis indicated the robustness of this meta-analysis. The Begg's test manifested that there was no publication bias (P = 0.2734). Our findings demonstrated that HIV infection was independently associated with a significantly increased risk of mortality in COVID-19 patients. Further well-designed studies based on prospective study estimates are warranted to confirm our findings.

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OBJECTIVE: To investigate the association between stroke and the risk for mortality among coronavirus disease 2019 (COVID-19) patients. METHODS: We performed systematic searches through electronic databases including PubMed, Embase, Scopus, and Web of Science to identify potential articles reporting adjusted effect estimates on the association of stroke with COVID-19-related mortality. To estimate pooled effects, the random-effects model was applied. Subgroup analyses and meta-regression were performed to explore the possible sources of heterogeneity. The stability of the results was assessed by sensitivity analysis. Publication bias was evaluated by Begg's test and Egger's test. RESULTS: This meta-analysis included 47 studies involving 7,267,055 patients. The stroke was associated with higher COVID-19 mortality (pooled effect = 1.30, 95% confidence interval (CI): 1.16-1.44; I2 = 89%, P < 0.01; random-effects model). Subgroup analyses yielded consistent results among area, age, proportion of males, setting, cases, effect type, and proportion of severe COVID-19 cases. Statistical heterogeneity might result from the different effect type according to the meta-regression (P = 0.0105). Sensitivity analysis suggested that our results were stable and robust. Both Begg's test and Egger's test indicated that potential publication bias did not exist. CONCLUSION: Stroke was independently associated with a significantly increased risk for mortality in COVID-19 patients.

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Staphylococcus aureus is a serious threat to public health. S. aureus infection can cause acute or long-term persistent infections that are often resistant to antibiotics and are associated with high morbidity and death. Understanding the defensive systems of S. aureus can help clinicians make the best use of antimicrobial drugs and can also help with antimicrobial stewardship. The mechanisms and clinical implications of S. aureus defense systems, as well as potential response systems, were discussed in this study. Because resistance to all currently available antibiotics is unavoidable, new medicines are always being developed. Alternative techniques, such as anti-virulence and bacteriophage therapies, are being researched and may become major tools in the fight against staphylococcal infections in the future, in addition to the development of new small compounds that affect cell viability.

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OBJECTIVE: The aim of this study was to investigate the impact of asthma on the risk for mortality among coronavirus disease 2019 (COVID-19) patients in the United States by a quantitative meta-analysis. METHODS: A random-effects model was used to estimate the pooled odds ratio (OR) with corresponding 95% confidence interval (CI). I2 statistic, sensitivity analysis, Begg's test, meta-regression and subgroup analyses were also performed. RESULTS: The data based on 56 studies with 426,261 COVID-19 patients showed that there was a statistically significant association between pre-existing asthma and the reduced risk for COVID-19 mortality in the United States (OR: 0.82, 95% CI: 0.74-0.91). Subgroup analyses by age, male proportion, sample size, study design and setting demonstrated that pre-existing asthma was associated with a significantly reduced risk for COVID-19 mortality among studies with age ≥ 60 years old (OR: 0.79, 95% CI: 0.72-0.87), male proportion ≥ 55% (OR: 0.79, 95% CI: 0.72-0.87), male proportion ＜ 55% (OR: 0.81, 95% CI: 0.69-0.95), sample sizes ≥ 700 cases (OR: 0.80, 95% CI: 0.71-0.91), retrospective study/case series (OR: 0.82, 95% CI: 0.75-0.89), prospective study (OR: 0.83, 95% CI: 0.70-0.98) and hospitalized patients (OR: 0.82, 95% CI: 0.74-0.91). Meta-regression did reveal none of factors mentioned above were possible reasons of heterogeneity. Sensitivity analysis indicated the robustness of our findings. No publication bias was detected in Begg's test (P = 0.4538). CONCLUSION: Our findings demonstrated pre-existing asthma was significantly associated with a reduced risk for COVID-19 mortality in the United States.

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BACKGROUND: The association of asthma with the risk for mortality among coronavirus disease 2019 (COVID-19) patients is not clear. OBJECTIVE: To investigate the association between asthma and the risk for mortality among COVID-19 patients. METHODS: We performed systematic searches through electronic databases including PubMed, EMBASE, and Web of Science to identify potential articles reporting adjusted effect estimates on the association of asthma with fatal COVID-19. A random-effects model was conducted to estimate pooled effects. Sensitivity analysis, subgroup analysis, meta-regression, Begg's test and Egger's test were also performed. RESULTS: Based on 62 studies with 2,457,205 cases reporting adjusted effect estimates, COVID-19 patients with asthma had a significantly reduced risk for mortality compared with those without it (15 cohort studies: 829,670 patients, pooled hazard ratio [HR] = 0.88, 95% confidence interval [CI], 0.82-0.95, I2 = 65.9%, P < .001; 34 cohort studies: 1,008,015 patients, pooled odds ratio [OR] = 0.88, 95% CI, 0.82-0.94, I2 = 39.4%, P = .011; and 11 cross-sectional studies: 1,134,738 patients, pooled OR = 0.87, 95% CI, 0.78-0.97, I2 = 41.1%, P = .075). Subgroup analysis based on types of adjusted factors indicated that COVID-19 patients with asthma had a significantly reduced risk for mortality among studies adjusting for demographic, clinical, and epidemiologic variables (pooled OR = 0.87, 95% CI, 0.83-0.92, I2 = 36.3%, P = .013; pooled HR = 0.90, 95% CI, 0.83-0.97, I2 = 69.2%, P < .001), but not among studies adjusting only for demographic variables (pooled OR = 0.88, 95% CI, 0.70-1.12, I2 = 40.5%, P = .097; pooled HR = 0.82, 95% CI, 0.64-1.06, I2 = 0%, P = .495). Sensitivity analysis proved that our results were stable and robust. Both Begg's test and Egger's test indicated that potential publication bias did not exist. CONCLUSIONS: Our data based on adjusted effect estimates indicated that asthma was significantly related to a reduced risk for COVID-19 mortality.

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INTRODUCTION: Smoking can cause mucociliary clearing dysfunction and poor pulmonary immunity, leading to more severe infection. We performed this study to explore the association between smoking and mortality of coronavirus disease 2019 (COVID-19) patients utilizing a quantitative meta-analysis on the basis of adjusted effect estimates. AIMS AND METHODS: We conducted a systematic search of the online databases including PubMed, Web of Science, Scopus, and Embase. Only articles reporting adjusted effect estimates on the association between smoking and the risk of mortality among COVID-19 patients in English were included. Newcastle-Ottawa scale was fitted to assess the risk of bias. A random-effects model was applied to calculate the pooled effect with the corresponding 95% confidence interval (CI). RESULTS: A total of 73 articles with 863 313 COVID-19 patients were included in this meta-analysis. Our results indicated that smoking was significantly associated with an increased risk for death in patients with COVID-19 (pooled relative risk = 1.19, 95% CI = 1.12-1.27). Sensitivity analysis indicated that our results were stable and robust. CONCLUSIONS: Smoking was independently associated with an increased risk for mortality in COVID-19 patients. IMPLICATIONS: This present study may contribute to summarizing the association between smoking and the risk of COVID-19 mortality based on adjusted effect estimates. More detailed and complete data on smoking status should be collected to more accurately estimate the effect of smoking on COVID-19 mortality.

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BACKGROUND: Cancer is one of the major threats to human health and current cancer therapies have been unsuccessful in eradicating it. Ferroptosis is characterized by iron-dependence and lipid hydroperoxides accumulation, and its primary mechanism involves the suppression of system Xc--GSH (glutathione)-GPX4 (glutathione peroxidase 4) axis. Co-incidentally, cancer cells are also metabolically characterized by iron addiction and ROS tolerance, which makes them vulnerable to ferroptosis. This may provide a new tactic for cancer therapy. SCOPE OF REVIEW: The general features and mechanisms of ferroptosis, and the basis that makes cancer cells vulnerable to ferroptosis are described. Further, we emphatically discussed that disrupting GSH may not be ideal for triggering ferroptosis of cancer cells in vivo, but directly inhibiting GPX4 and its compensatory members could be more effective. Finally, the various approaches to directly inhibit GPX4 without disturbing GSH were described. MAJOR CONCLUSIONS: Targeting system Xc- or GSH may not effectively trigger cancer cells' ferroptosis in vivo the existence of other compensatory pathways. However, directly targeting GPX4 and its compensatory members without disrupting GSH may be more effective to induce ferroptosis in cancer cells in vivo, as GPX4 is essential in preventing ferroptosis. GENERAL SIGNIFICANCE: Cancer is a severe threat to human health. Ferroptosis-based cancer therapy strategies are promising, but how to effectively induce ferroptosis in cancer cells in vivo is still a question without clear answers. Thus, the viewpoints raised in this review may provide some references and different perspectives for researchers working on ferroptosis-based cancer therapy.

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