Endogenous sulfur dioxide (SO₂) used to be perceived as a notorious, toxic pollutant of the atmosphere. However, recently several studies revealed that in vivo generated mainly from sulfur-containing amino acids, SO₂ serves as an essential novel gasotransmitter involved in the regulation of extensive biological activities. Several studies indicate that endogenous SO₂ protects against inflammation by inhibiting the production of inflammatory mediators via different molecular pathways. The present review, therefore, summarized the anti-inflammatory effect of endogenous SO₂ and its molecular mechanisms.

During assisted mechanical ventilation, the respiratory system is exposed to the positive pressure from the ventilator and the negative pressure generated by the respiratory muscles. Both excessively high and low respiratory drive and effort can injure the respiratory muscles and lungs resulting in worse patient's outcomes. Monitoring respiratory drive and inspiratory effort are key to prevent harm by adjusting sedation and ventilation to meet safe targets of respiratory drive and inspiratory effort. Based on physiological studies and observational data, it is currently recommended to target an intermediate range of drive and effort in most patients, however, these targets need to be validated prospective and adjusted for different patient populations. The gold standard for measuring inspiratory effort requires the insertion of an esophageal catheter and additional equipment. However, recently, several noninvasive techniques using end-expiratory or end-inspiratory occlusions on the ventilator have been validated to estimate respiratory drive and effort allowing clinicians to monitor drive and effort easily at the bedside. In this narrative review, we discuss potential beneficial and deleterious consequences of breathing effort during assisted ventilation, available monitoring techniques, and propose a structured approach for bedside implementation.

Objective: The objective of the study is to describe the clinical characteristics, risk factors, and prognosis for acute kidney injury (AKI) among patients with coronavirus disease (COVID-19). Methods: Retrospective study of 456 consecutive patients with confirmed COVID-19 infection at the whole hospital from January 1 to March 1, 2020 was enrolled. Demographic, clinical characteristics, the risk factors, and prognosis were collected and analyzed. Results: Of 456 patients with COVID-19, 38 patients developed AKI. Patients with AKI were older and predominantly male sex and were more likely to have comorbidities such as hypertension, cardiovascular, and cerebrovascular diseases. Among patients with AKI, the white blood cell count, neutrophil count, neutrophil-to-lymphocyte ratio, alanine aminotransferase, and C-reaction protein were increased, and lymphocyte and platelet count were decreased. Multivariate analysis showed that age, hypertension, and lymphocyte count were independent risk factors for AKI. The overall mortality rate of 456 patients was 9.9%, and the mortality rate of patients with AKI was 23.7%. In particular, increasing AKI severity was associated with increased risk. Conclusions: The risk of AKI was high in patients with COVID-19. Older age, hypertension, and lower lymphocyte count were independent risk factors for AKI. COVID-19-associated AKI was associated with higher risk of death in patients with COVID-19.