Daily Ards Research Analysis

BACKGROUND: Neonatal acute respiratory distress syndrome (NARDS) can cause respiratory failure in newborns and even pose a threat to their lives, causing a heavy financial burden on families. AIM: This study aims to explore the potential role of miR-155 as a diagnostic marker and prognostic predictor for NARDS. METHODS: This study included 100 non-NARDS newborns and 100 NARDS newborns. The plasma miR-155 expression was measured by RT-qPCR. The ROC curve was used to analyze the diagnostic efficacy of miR-155 alone and the combined diagnostic efficacy of PT, APTT, FIB, and CRP. The correlation between clinical indicators and miR-155 expression was analyzed by the chi-square test. The general clinical information of NARDS neonates with different severity degrees and prognosis was compared. Multivariate logistic regression was used to identify the risk factors for NARDS. RESULTS: The plasma miR-155 level was elevated in NARDS newborns. miR-155 may serve as a promising biomarker in the diagnosis of NARDS. The value of the multi-factor combined diagnosis was significantly improved. 1-minute Apgar score, PT, APTT, and CRP level were statistically related to the miR-155 expression. Abnormal FIB level and the miR-155 expression were independent risk factors for NARDS. The more severe NARDS newborns have poorer coagulation function, stronger inflammatory response, and higher miR-155 level. A higher level of miR-155 was observed in NARDS newborns with a poorer prognosis. CONCLUSION: The plasma miR-155 level is upregulated in NARDS, and miR-155 may be a potential diagnostic marker for NARDS. NARDS newborns with miR-155 high expression have a poor prognosis.

BACKGROUND: Coronaviruses such as SARS-CoV and SARS-CoV-2 have caused severe respiratory syndromes and prominent global health crises over the past two decades. Despite vaccines and antiviral therapies, treatment limitations persist, particularly in preventing viral entry and addressing emerging variants. ACE2, the primary receptor for SARS-CoV-2, represents a critical target for intervention. Cell-based approaches, including mesenchymal stromal cell therapies, have shown safety and promise in clinical trials. Building on our prior success with IL-27 gene therapy for acute respiratory distress syndrome, we explored ACE2-targeted IL-27 delivery as a potential strategy to reduce SARS-CoV-2 entry. METHODS AND RESULTS: We developed an in vitro model using SARS-CoV-2 spike pseudotyped lentivirus to mimic viral entry. Human adipose-derived stromal cells were electroporated with plasmid DNA encoding either ACE2-targeted or non-targeted IL-27, and conditioned media were collected. Two regimens were tested: "prevention," where cells were pre-treated with conditioned media before viral exposure, and "treatment," where conditioned media and pseudotyped virus were added simultaneously. Viral entry was quantified using luciferase reporter activity and genome copy units in HEK293-ACE2 and A549-ACE2 cells. ACE2-targeted IL-27 showed a concentration-dependent trend toward reduced lentiviral entry, particularly in A549-ACE2 cells, although differences were not statistically significant. CONCLUSIONS: These findings provide proof-of-concept that ACE2-targeted IL-27 stromal cell-based gene therapy may help inhibit SARS-CoV-2 entry. Further optimization of dosing, delivery platforms, and testing in models that assess viral replication and inflammation, as well as evaluation against spike variants, are warranted to explore its potential as an adjunct to COVID-19 treatments.

Clinically suspected invasive meningococcal disease can deteriorate rapidly in previously well children. Prompt recognition of the petechial-purpuric rash with shock, early empirical antibiotics, and aggressive supportive pediatric intensive care are cornerstones of management as multiorgan dysfunction and Acute Respiratory Distress Syndrome may occur, but they are reversible with appropriate care.