Debate on appropriate triggers for transfusion of allogeneic blood products and their effects on short- and long-term survival in surgical and critically ill patients continue with no definitive evidence or decisive resolution. Although transfusion-related immune modulation (TRIM) is well established, its influence on immune competence in the recipient and its effects on cancer recurrence after a curative resection remains controversial. An association between perioperative transfusion of allogeneic blood products and risk for recurrence has been shown in colorectal cancer in randomized trials; whether the same is true for other types of cancer remains to be determined. This article focuses on the laboratory, animal, and clinical evidence to date on the mechanistic understanding of inflammatory and immune-modulatory effects of blood products and their significance for recurrence in the cancer surgical patient.

Neutrophil extracellular traps (NETs), released by polymorphonuclear neutrophils (PMNs), exert a robust antimicrobial function in infectious diseases such as sepsis. NETs also contribute to the pathogenesis and exacerbation of sepsis. Although the lung is highly vulnerable to infections, few studies have explored the role of NETs in sepsis‐induced acute lung injury (SI‐ALI). We demonstrate that NETs induce SI‐ALI via enhanced ferroptosis in alveolar epithelial cells. Our findings reveal that the excessive release of NETs in patients and mice with SI‐ALI is accompanied by upregulation of ferroptosis depending on METTL3‐induced m6A modification of hypoxia‐inducible factor‐1α (HIF‐1α) and subsequent mitochondrial metabolic reprogramming. In addition to conducting METTL3 overexpression and knockdown experiments in vitro, we also investigated the impact of ferroptosis on SI‐ALI caused by NETs in a caecum ligation and puncture (CLP)‐induced SI‐ALI model using METTL3 condition knockout (CKO) mice and wild‐type mice. Our results indicate the crucial role of NETs in the progression of SI‐ALI via NET‐activated METTL3 m6A‐IGF2BP2‐dependent m6A modification of HIF‐1α, which further contributes to metabolic reprogramming and ferroptosis in alveolar epithelial cells.

Acute pain after thoracic surgery is common and severe, and can lead to increased morbidity.^1,2 In the thorax, nociception travels primarily via the intercostal nerves.³ Therefore, blockade of the intercostal nerve is used to provide analgesia after thoracic surgery.⁴ Intercostal nerve blocks (ICNBs) are a common component of multimodal analgesia for thoracic surgery.⁵ Current guidelines suggest that continuous intercostal analgesia is similar to thoracic epidural analgesia (TEA).⁶ Aside from consideration of technical aspects and costs,⁷ the selection of any analgesic approach is typically based on its clinical benefits and disadvantages.^8,9

Preclinical studies have demonstrated that opioid receptor agonists increase the rate of non‐small cell lung cancer (NSCLC) growth and metastasis. Following institutional review board approval, we retrieved data on 901 patients who underwent surgery for NSCLC at MD Anderson Cancer Center. Comprehensive demographics, intraoperative data, and recurrence‐free survival (RFS) and overall survival (OS) at 3 and 5 years were obtained. Cox proportional analyses were conducted to assess the association between intraoperative opioid exposure and RFS and OS. The median intraoperative fentanyl equivalents dosage was 10.15 μg/kg. The multivariate analysis by stage indicated that a trend toward significance for opioid consumption as a risk factor in stage I patients (P = 0.053). No effect was found on RFS for stage II or III patients. Alternatively, opioid consumption was a risk factor for OS for stage I patients (P = 0.036), whereas no effect was noted for stage II or III patients. Intraoperative opioid use is associated with decreased OS in stage I but not stage II–III NSCLC patients. Until randomized controlled studies explore this association further, opioids should continue to be a key component of balanced anesthesia.

Patients with sepsis commonly suffer from coagulation dysfunction and lead to the formation of thrombus. During the development of sepsis, neutrophils migrate from the circulating blood to infected tissues and mediate the formation of neutrophil extracellular traps (NETs) that kill pathogens. However, the overactivation of neutrophils can promote the formation of immunothrombosis and even cause disseminated intravascular coagulation (DIC), which damages microcirculation. The outcome of sepsis depends on early recognition and intervention, so clinical evaluation of NETs function may be a valuable biomarker for early diagnosis of sepsis. The interaction of NETs with platelets, complement, and endothelium mediates the formation of immunothrombosis in sepsis. Inhibiting the formation of NETs is also considered to be one of the potential treatments for sepsis. In this review, we will discuss the key role of neutrophils and NETs in sepsis and septic thrombosis, in order to reveal new mechanisms for thrombosis treatment of sepsis.