Predictors of mortality for patients with COVID-19 pneumonia caused by SARS-CoV-2: a prospective cohort study.

The aim of this study was to identify factors associated with the death of patients with COVID-19 pneumonia caused by the novel coronavirus SARS-CoV-2.All clinical and laboratory parameters were collected prospectively from a cohort of patients with COVID-19 pneumonia who were hospitalised to Wuhan Pulmonary Hospital (Wuhan City, Hubei Province, China) between 25 December 2019 and 7 February 2020. Univariate and multivariate logistic regression analysis revealed that age ≥65 years (OR 3.765, 95% CI 1.146­17.394; p=0.023), pre-existing concurrent cardiovascular or cerebrovascular diseases (OR 2.464, 95% CI 0.755­8.044; p=0.007), CD3+CD8+ T-cells ≤75 cells·µL−1 (OR 3.982, 95% CI 1.132­14.006; p<0.001) and cardiac troponin I ≥0.05 ng·mL−1 (OR 4.077, 95% CI 1.166­14.253; p<0.001) were associated with an increase in risk of mortality from COVID-19 pneumonia." has been corrected to: "Univariate and multivariate logistic regression analysis revealed that age ≥65 years (OR 3.765, 95% CI 1.201−11.803; p=0.023), pre-existing concurrent cardiovascular or cerebrovascular diseases (OR 2.464, 95% CI 1.279−4.747; p=0.007), CD3+CD8+ T-cells ≤75 cells·µL−1 (OR 3.982, 95% CI 1.761­9.004; p<0.001) and cardiac troponin I ≥0.05 ng·mL−1 (OR 4.077, 95% CI 1.778­9.349; p<0.001) were associated with an increase in risk of mortality from COVID-19 pneumonia. In a sex-, age- and comorbid illness-matched case-control study, CD3+CD8+ T-cells ≤75 cells·µL-1 and cardiac troponin I ≥0.05 ng·mL-1 remained as predictors for high mortality from COVID-19 pneumonia.We identified four risk factors: age ≥65 years, pre-existing concurrent cardiovascular or cerebrovascular diseases, CD3+CD8+ T-cells ≤75 cells·µL-1 and cardiac troponin I ≥0.05 ng·mL-1 The latter two factors, especially, were predictors for mortality of COVID-19 pneumonia patients.

A fluorescent sensor to detect sodium dodecyl sulfate based on the glutathione-stabilized gold nanoclusters/poly diallyldimethylammonium chloride system.

A simple method for the detection of sodium dodecyl sulfate (SDS) was developed based on glutathione-stabilized gold nanoclusters (GSH-AuNCs) and poly(diallyldimethylammonium)chloride (PDDA) enhanced fluorescent system. Fluorescent Au NCs were synthesized by a one-step approach employing GSH as reducing/protecting reagent. The electrostatic group repulsions between GSH-Au NCs and PDDA resulted in strong fluorescence enhancement from the GSH-Au NCs. Moreover, the addition of SDS was able to cause a significant fluorescence recovery due to the strong affinity of PDDA and SDS. Thus the SDS can be detected. Under optimized conditions, the linear response to detect SDS ranges from 0.2 to 12 µg mL(-1) with a detection limit of 0.02 µg mL(-1).

Electrochemiluminescence of a nanoAg-carbon nanodot composite and its application to detect sulfide ions.

This work presents the enhanced electrochemiluminescence (ECL) of a newly prepared nanosilver-carbon nanodot (Ag-C-dot) composite and its application for the sensitive detection of sulfide (S(2-)) ions. The Ag-C-dot composite was easily prepared by adding silver nitrate into C-dot colloids through an alkaline reduction. The obtained Ag-C-dots were characterized by UV-vis spectra, fluorescence spectra and transmission electron microscopy. The electrochemical and ECL behaviors of the Ag-C-dot composite were investigated by cyclic voltammetry. Moreover, a simple label-free method to detect S(2-) ions with a high selectivity and sensitivity has been developed based on the ECL of the Ag-C-dot composite in aqueous media. The sensing mechanism could be due to the strong and specific interaction between the S(2-) ions and the Ag atoms/ions on the surface of the Ag-C-dot composite, which dramatically affects the resulting ECL of the Ag-C-dot composite. The linear response to detect S(2-) ions ranges from 0.05 to 100 µM with a detection limit of 0.027 µM (~1 ppb). This work indicates that the Ag-C-dot nanocomposite possesses potential applications for environment sensing.

Copper-aspirin complex inhibits cyclooxygenase-2 more selectively than aspirin.

The antiinflammatory effects of the copper-aspirin complex (Cu-Asp) were more potent than that of Asp in rats or mice with fewer classic adverse effects. The aim of this study was to determine the cause by evaluating Cu-Asp selective inhibition on cyclooxygenases (COX). COX-1 inhibition was evaluated based on 6-keto-prostaglandin F(1alpha) (6-keto-PGF(1alpha)) in an endothelial cell model, and COX-2 inhibition was based on prostaglandin E(2) (PGE(2)) in a macrophage model. Radioimmunoassay (RIA) was applied to determine 6-keto-PGF(1alpha) in resting human umbilical vein endothelial cell line (ECV304), and PGE(2) in activated macrophages. The results showed that the inhibition of 6-keto-PGF(1alpha) yield by Cu-Asp (3 to 0.01 mM) was markedly weaker than that by aspirin (Asp); while the inhibition of PGE(2) yield by Cu-Asp (10 to 0.1 mM) was significantly stronger than that by Asp. Based on the inhibition on 6-keto-PGF(1alpha) and PGE(2), the medium inhibitory concentration (IC(50)) of Cu-Asp on COX-1 and on COX-2 was 1.03+/-0.15 mM, and 0.32+/-0.04 mM, respectively. The selective inhibition index on COX-2, IC(50) (COX-1)/IC(50) (COX-2), of Cu-Asp was 3.33+/-0.89, while that of Asp was 0.42+/-0.12. The results suggest that, unlike Asp, Cu-Asp is a relatively selective inhibitor of COX-2 in the present models; the selectivity of Cu-Asp is about seven-fold greater than that of Asp.