Clinical characteristics and risk factors for perioperative lung surgery patients with SARS‐CoV‐2 infection / 中国胸心血管外科临床杂志

@#Objective     To investigate the clinical characteristics and risk factors for perioperative lung surgery patients with SARS‐CoV‐2 Omicron variant infection. Methods     The clinical data of patients who underwent lung surgery at the Department of Thoracic Surgery, Renmin Hospital of Wuhan University from December 1, 2022 to January 9, 2023 were retrospectively analyzed. The patients were divided into an infection group and a non-infection group according to whether they were infected with SARS-CoV-2. And the clinical data of two groups were collected and compared. Multiple linear regression analysis was used to explore the risk factors affecting the time of hospitalization. Results     A total of 70 patients were enrolled in this study, including 36 (51.4%) males and 34 (48.6%) females at a median age of 61.0 (49.0, 66.8) years. There were 28 patients in the infection group and 42 patients in the non-infection group. The proportion of preoperative abnormal coagulation function and the risk of postoperative pulmonary infection in perioperative patients infected with SARS-CoV-2 were higher than those in the non-infection group (P<0.05). Subgroup analysis found that patients with preoperative SARS-CoV-2 infection were more likely to have pulmonary infection after surgery, but did not prolong the time of hospitalization or increase the risk of severe disease rate. The patients with postoperative SARS-CoV-2 infection had worse clinical prognosis, including longer time of hospitalization (P=0.004), higher ICU admission rate (P=0.000), higher lung infection rate (P=0.003) and respiratory failure rate (P=0.000). Multiple linear regression analysis showed that gender and extent of surgery were independent risk factors for prolonged hospitalization time. Conclusion     Preoperative infection with SARS-CoV-2 Omicron variant will increase the risk of pulmonary infection, but it will not affect the clinical prognosis. However, postoperative infection with SARS-CoV-2 Omicron variant will still prolong the time of hospitalization, increase the ICU rate, and the risk of pulmonary complications.

Interpretation of the NCCN clinical practice guidelines in oncology for non-small cell lung cancer (version 2.2023) / 中国胸心血管外科临床杂志

@#Lung cancer is the malignancy with the highest incidence and mortality rate in China. In recent years, the popular use of low-dose computed tomography in the population has led to an increase in the detection rate of pulmonary nodules. The National Comprehensive Cancer Network (NCCN) updated and released the NCCN clinical practice guidelines in oncology for non-small cell lung cancer (version 2.2023) on February 17, 2023. This article will interpret the main updates of the new guideline and compare it with the domestic lung cancer treatment guidelines, providing new ideas for the diagnosis and treatment of lung cancer for Chinese clinicians.

A novel mechanism for the protection against acute lung injury by melatonin: mitochondrial quality control of lung epithelial cells is preserved through SIRT3-dependent deacetylation of SOD2.

The mitochondrial quality control of lung epithelial cells is disturbed during sepsis, which contributes to abnormal mitochondrial function and acute lung injury. Melatonin is one of the primary hormones secreted by the pineal gland, displaying favorable antioxidative actions in sepsis and cardiopulmonary disease. However, the potential roles and molecular basis of melatonin in lipopolysaccharide (LPS)-treated lung epithelial cells have not been explored and reported. Herein, we investigated whether melatonin could protect against sepsis-induced acute lung injury (ALI) and LPS-treated lung epithelial cells through the mitochondrial quality control as well as its possible molecular targets. Wild type and Sirt3 knockout mice were intratracheally instilled with LPS for 12 h to construct an in vivo acute lung injury model. Both A549 lung epithelial cells and primary alveolar type II (AT-II) cells were used to explore the possible roles of melatonin in vitro by incubating with small interfering RNA against Sirt3. To determine the involvement of the melatonin receptor, cells and mice were treated with si Mtnr1b and luzindole. Melatonin pretreatment significantly inhibited pathological injury, inflammatory response, oxidative stress, and apoptosis in LPS-treated lung tissues and LPS-treated lung epithelial cells. Furthermore, melatonin also shifted the dynamic course of mitochondria from fission to fusion, inhibited mitophagy and fatty acid oxidation in LPS-treated lung epithelial cells in vitro and in vivo. However, SIRT3 inhibition abolished the protective roles of melatonin in acute lung injury. Mechanistically, we found that melatonin increased the activity and expression of SIRT3, which further promoted the deacetylation of SOD2 at K122 and K68. More importantly, melatonin exerted pulmonary protection by activating MTNR1B but not MTNR1A during ALI. Collectively, melatonin could preserve the mitochondrial quality control of lung epithelial cells through the deacetylation of SOD2 in a SIRT3-dependent manner, which eventually alleviated sepsis-induced injury, inflammation, oxidative stress, and apoptosis. Thus, melatonin may serve as a promising candidate against ALI in the future.