Aims: This study aimed to determine the sensitivity and specificity of ultrasound for the diagnosis of acute pulmonary edema by meta-analysis.Materials and methods: A systematic search was conducted through the following databases: Cochrane, PubMed, EMBASE and Ovid MEDLINE. Prospective cohort and prospective case-control studies that reported sensitivity and specificity of lung ultrasound in diagnosis of acute pulmonary edema were selected. An independent review of citations was carried out for inclusion and data extraction. Quality assessment was conducted using the QUADAS-2 tool. Sensitivity and specificity were taken from the studied articles and then calculated with the contingency tables. A total of 984 articles were identified but only eight studies (1301 patients) were included in this meta-analysis. One study was a case-control study and seven studies were prospective cohort study.Results: The overall sensitivity of ultrasound for the diagnosis of acute pulmonary edema is 97% (95% CI: 96%–98%) and the overall specificity was 98% (95% CI: 97%–99%).Conclusion: The diagnostic test accuracy suggests that lung ultrasound using B-lines is a useful and reliable diagnostic tool for critically illpatients with acute pulmonary edema.
Acetaminophen (APAP) overdose is one of the most common causes of acute liver failure. The study aimed to investigate the protective effect of carnosic acid (CA) on APAP-induced acute hepatotoxicity and its underlying mechanism in mice. To induce hepatotoxicity, APAP solution (400 mg/kg) was administered into mice by intraperitoneal injection. Histological analysis revealed that CA treatment significantly ameliorated APAP-induced hepatic necrosis. The levels of both alanine aminotransferase (ALT) and aspartate transaminase (AST) in serum were reduced by CA treatment. Moreover, CA treatment significantly inhibited APAP-induced hepatocytes necrosis and lactate dehydrogenase (LDH) releasing. Western blot analysis showed that CA abrogated APAP-induced cleaved caspase-3, Bax and phosphorylated JNK protein expression. Further results showed that CA treatment markedly inhibited APAP-induced pro-inflammatory cytokines TNF-α, IL-1β, IL-6 and MCP-1 mRNA expression and the levels of phosphorylated IκBα and p65 protein in the liver. In addition, CA treatment reduced APAP- induced hepatic malondialdehyde (MDA) contents and reactive oxygen species (ROS) accumulation. Conversely, hepatic glutathione (GSH) level was increased by administration of CA in APAP-treated mice. Mechanistically, CA facilitated Nrf2 translocation into nuclear through blocking the interaction between Nrf2 and Keap1, which, in turn, upregulated anti-oxidant genes mRNA expression. Taken together, our results indicate that CA facilitates Nrf2 nuclear translocation, causing induction of Nrf2-dependent genes, which contributes to protection from acetaminophen hepatotoxicity.
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