[신간의 별자리x] 우리/미술, 그리고 ‘슬픔의 박물관’

https://backend.orbit.dtu.dk/ws/files/238108460/1_s2.0_S0092867420310084_main.pdf

Robust T Cell Immunity in Convalescent Individuals with Asymptomatic or Mild COVID-19.

BACKGROUND

There is disagreement about the level of asymptomatic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We conducted a living systematic review and meta-analysis to address three questions: (1) Amongst people who become infected with SARS-CoV-2, what proportion does not experience symptoms at all during their infection? (2) Amongst people with SARS-CoV-2 infection who are asymptomatic when diagnosed, what proportion will develop symptoms later? (3) What proportion of SARS-CoV-2 transmission is accounted for by people who are either asymptomatic throughout infection or presymptomatic?

METHODS AND FINDINGS

We searched PubMed, Embase, bioRxiv, and medRxiv using a database of SARS-CoV-2 literature that is updated daily, on 25 March 2020, 20 April 2020, and 10 June 2020. Studies of people with SARS-CoV-2 diagnosed by reverse transcriptase PCR (RT-PCR) that documented follow-up and symptom status at the beginning and end of follow-up or modelling studies were included. One reviewer extracted data and a second verified the extraction, with disagreement resolved by discussion or a third reviewer. Risk of bias in empirical studies was assessed with an adapted checklist for case series, and the relevance and credibility of modelling studies were assessed using a published checklist. We included a total of 94 studies. The overall estimate of the proportion of people who become infected with SARS-CoV-2 and remain asymptomatic throughout infection was 20% (95% confidence interval [CI] 17-25) with a prediction interval of 3%-67% in 79 studies that addressed this review question. There was some evidence that biases in the selection of participants influence the estimate. In seven studies of defined populations screened for SARS-CoV-2 and then followed, 31% (95% CI 26%-37%, prediction interval 24%-38%) remained asymptomatic. The proportion of people that is presymptomatic could not be summarised, owing to heterogeneity. The secondary attack rate was lower in contacts of people with asymptomatic infection than those with symptomatic infection (relative risk 0.35, 95% CI 0.10-1.27). Modelling studies fit to data found a higher proportion of all SARS-CoV-2 infections resulting from transmission from presymptomatic individuals than from asymptomatic individuals. Limitations of the review include that most included studies were not designed to estimate the proportion of asymptomatic SARS-CoV-2 infections and were at risk of selection biases; we did not consider the possible impact of false negative RT-PCR results, which would underestimate the proportion of asymptomatic infections; and the database does not include all sources.

CONCLUSIONS

The findings of this living systematic review suggest that most people who become infected with SARS-CoV-2 will not remain asymptomatic throughout the course of the infection. The contribution of presymptomatic and asymptomatic infections to overall SARS-CoV-2 transmission means that combination prevention measures, with enhanced hand hygiene, masks, testing tracing, and isolation strategies and social distancing, will continue to be needed.

/pdf/occurrence-and-transmission-potential-of-asymptomatic-and-27ou6uv041.pdf

Occurrence and transmission potential of asymptomatic and presymptomatic SARS-CoV-2 infections: A living systematic review and meta-analysis.

Mechanisms of SARS-CoV-2 Transmission and Pathogenesis.

South Australia is presently in the throes of major changes to its regulatory system governing land use, development of land and the development of planning policy against which development assessment decisions are to be made. Eventually the planning and development control system established under the Development Act 1993 (SA) will be replaced by a new system implemented by the Planning, Development and Infrastructure Act 2016 (SA) (the new Act).

COVID-19 Generated Changes to Planning and Development Controls in South Australia (preprint)

PM2.5-induced lung injury is attenuated in macrophage-specific NLRP3 deficient mice

Acute lung injury (ALI) induced by sepsis is characterized by an inflammatory process related to the up-regulation of inflammatory cytokines and chemokines. In the present study, we explored the role of circC3P1 in sepsis-induced ALI in vitro and in vivo. The caecal ligation and puncture (CLP)-induced sepsis model was established through CLP surgery. Forty adult male C57BL/6 mice were randomly assigned into sham, CLP, CLP + vector and CLP + circC3P1 (each n = 10). Primary murine pulmonary microvascular endothelial cells (MPVECs) were transfected with circC3P1 or empty vector 24 hours prior to LPS treatment via Lipofectamine 2000. The expressions of circC3P1, tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β were evaluated after 6-h LPS treatment. Cell apoptosis was evaluated via flow cytometry. The CLP group demonstrated pulmonary morphological abnormalities, increased concentrations of TNF-α, IL-6 and IL-1β in the lung tissue, compared with the sham group. MPVECs treated with LPS significantly elevated TNF-α, IL-6 and IL-1β levels and increased cell apoptosis than that in the control group. The circC3P1 overexpression in sepsis-induced ALI mice attenuated pulmonary injury, inflammation and apoptosis. Besides, circC3P1 revealed anti-inflammatory and anti-apoptotic effect in MPVEC-treated LPS. CircC3P1 overexpression reduced cell apoptosis and pro-inflammatory cytokines levels via down-regulating miR-21. CircC3P1 attenuated pro-inflammatory cytokine production and cell apoptosis in ALI induced by sepsis through modulating miR-21, indicating that circC3P1 is a promising therapeutic biomarker for sepsis-induced ALI.

CircC3P1 attenuated pro-inflammatory cytokine production and cell apoptosis in acute lung injury induced by sepsis through modulating miR-21.

Scope Mangiferin (MF) is a natural phytopolyphenol, which displays potential pharmacological properties involving antibacterial, anti-inflammation, antioxidant and anti-tumor. However, little is known about the roles of MF in lung injury. The aim of this study is to demonstrate the modulatory effects and molecular mechanisms by which MF operates in sepsis-induced lung injury. Methods and results To examine the protective properties of MF, an in vivo model of lipopolysaccharide (LPS)-induced lung injury in mice and an in vitro model of LPS-treated J774A.1 cells were established, respectively. The results revealed that MF treatment significantly relieved LPS-induced pathological injury and inflammatory response in murine lung tissues. Meanwhile, MF treatment also inhibited nucleotide-binding oligomerization domain (NOD)-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome activation and pyroptosis induced by LPS. In macrophage-specific NLRP3 deficiency mice treated with LPS, MF showed little protective effects. NLRP3 overexpression by adenovirus could also offset the beneficial effects of MF in LPS-treated J774A.1 cells. Furthermore, we found that MF could suppress the expression of NLPR3 and pyroptosis of macrophages by inhibiting the nuclear translocation of the nuclear factor-κB (NF-κB) subunits P50 and P65. Conclusion MF protects against lung injury and inflammatory response by inhibiting NLRP3 inflammasome activation in a NF-κB-dependent manner in macrophages, which provides a promising therapeutic candidate for the treatment of lung injury.

/pdf/mangiferin-mitigates-lipopolysaccharide-induced-lung-injury-57zz7jazwb.pdf

Mangiferin Mitigates Lipopolysaccharide-Induced Lung Injury by Inhibiting NLRP3 Inflammasome Activation

Ferroptosis is a new type of regulatory cell death that differs from autophagy, apoptosis, necrosis, and pyroptosis; it is caused primarily by the accumulation of iron and lipid peroxides in the cell. Studies have shown that many classical signaling pathways and biological processes are involved in the process of ferroptosis. In recent years, investigations have revealed that ferroptosis plays a crucial role in the progression of tumors, especially lung cancer. In particular, inducing ferroptosis in cells can inhibit the growth of tumor cells, thereby reversing tumorigenesis. In this review, we summarize the characteristics of ferroptosis from its underlying basis and role in lung cancer and provide possible applications for it in lung cancer therapies.

/pdf/ferroptosis-a-new-promising-target-for-lung-cancer-therapy-3j085fx5u7.pdf

Ferroptosis: A New Promising Target for Lung Cancer Therapy.

The number of corona virus disease 2019 cases is increasing rapidly. However, the comparison of clinical characteristics between patients ≥ 70 and those < 70 has not been implemented yet. To achieve that, we collected clinical data of consecutive 222 patients in Renmin Hospital of Wuhan University diagnosed between January 13, 2020 and February 4, 2020. We divided them into an under-70 group and an over-70 group according to their ages, comparing their clinical characteristics. Meanwhile, univariate and multivariate Cox regression analyses were performed to identify the prognostic factors. Among the patients enrolled, 37 (16.67%) were 70 or older and 185 (83.33%) were younger than 70. Higher proportions of dyspnoea, expectoration, chronic cardiovascular disease, diabetes, organ complications, severe-to-critical cases, a higher death rate, a longer hospital stay and decreased immune status were observed in the over-70 group patients compared with their younger counterparts. The risk factors for death included dyspnoea, muscle ache, elevated myocardial enzymes, elevated C3 in over-70 patients and dyspnoea, pharyngalgia, chronic cardiac disease, increased C-reactive protein, IgA, decreased platelets in under-70 patients. Overall, our research compared the clinical characteristics of the two populations with different immune status and illustrated differentiated risk factors for death in them.

Rui Xiong

Papers

PM2.5-induced lung injury is attenuated in macrophage-specific NLRP3 deficient mice

CircC3P1 attenuated pro-inflammatory cytokine production and cell apoptosis in acute lung injury induced by sepsis through modulating miR-21.

Mangiferin Mitigates Lipopolysaccharide-Induced Lung Injury by Inhibiting NLRP3 Inflammasome Activation

Ferroptosis: A New Promising Target for Lung Cancer Therapy.

Comparison of clinical characteristics of COVID-19 between elderly patients and young patients: a study based on a 28-day follow-up.