[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)

Eriocitrin attenuates sepsis-induced acute lung injury in mice by regulating MKP1/MAPK pathway mediated-glycolysis.

Sepsis is one common cause of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), which is closely associated with high mortality in intensive care units (ICU). Histone deacetylase 3 (HDAC3) serves as an important epigenetic modifying enzyme which could affect chromatin structure and transcriptional regulation. Here, we explored the effects of HDAC3 in type II alveolar epithelial cells (AT2) on lipopolysaccharide (LPS)-induced ALI and shed light on potential molecular mechanisms. We generated ALI mouse model with HDAC3 conditional knockout mice (Sftpc-cre; Hdac3f/f) in AT2 and the roles of HDAC3 in ALI and epithelial barrier integrity were investigated in LPS-treated AT2. The levels of HDAC3 were significantly upregulated in lung tissues from mice with sepsis and in LPS-treated AT2. HDAC3 deficiency in AT2 not only decreased inflammation, apoptosis, and oxidative stress, but also maintained epithelial barrier integrity. Meanwhile, HDAC3 deficiency in LPS-treated AT2 preserved mitochondrial quality control (MQC), evidenced by the shift of mitochondria from fission into fusion, decreased mitophagy, and improved fatty acid oxidation (FAO). Mechanically, HDAC3 promoted the transcription of Rho-associated protein kinase 1 (ROCK1) in AT2. In the context of LPS stimulation, the upregulated ROCK1 elicited by HDAC3 could be phosphorylated by Rho-associated (RhoA), thus disturbing MQC and triggering ALI. Furthermore, we found that forkhead box O1 (FOXO1) was one of transcription factors of ROCK1. HDAC3 directly decreased the acetylation of FOXO1 and promoted its nuclear translocation in LPS-treated AT2. Finally, HDAC3 inhibitor RGFP966 alleviated epithelial damage and improved MQC in LPS-treated AT2. Altogether, HDAC3 deficiency in AT2 alleviated sepsis-induced ALI by preserving mitochondrial quality control via FOXO1-ROCK1 axis, which provided a potential strategy for the treatment of sepsis and ALI. 

https://doi.org/10.1016/j.redox.2023.102746

HDAC3 deficiency protects against acute lung injury by maintaining epithelial barrier integrity through preserving mitochondrial quality control

PM2.5 contributed to pulmonary epithelial senescence and ferroptosis by regulating USP3-SIRT3-P53 axis.

https://doi.org/10.1016/j.isci.2023.107158

Rui Xiong

Papers

Eriocitrin attenuates sepsis-induced acute lung injury in mice by regulating MKP1/MAPK pathway mediated-glycolysis.

HDAC3 deficiency protects against acute lung injury by maintaining epithelial barrier integrity through preserving mitochondrial quality control

PM2.5 contributed to pulmonary epithelial senescence and ferroptosis by regulating USP3-SIRT3-P53 axis.

HDAC3 promotes macrophage pyroptosis via regulating histone deacetylation in acute lung injury