Worldwide, 80% of patients who undergo surgery receive opioid analgesics as the fundamental agent for pain relief. However, the irrational use of opioids leads to excessive drug dependence and drug abuse, resulting in an increased mortality rate and huge economic loss. The crisis of opioid overuse remains a great challenge. In this review, we summarize several key factors in opioid abuse, including race, region, income, genetic factors, age and gender, smoking and alcohol abuse, history of chronic pain and analgesic drug abuse, surgery, neuropsychiatric illness, depression and antidepressant use, human factors, national policies, hospital regulations, and health insurance under treatment of pain. Furthermore, we present several prevention strategies, such as perioperative measures, opioid substitutes, treatment of the primary illness, emotional regulation, use of opioid antagonists, efforts of the state, hospitals, doctors and pharmacy benefit managers, gene therapy, and vaccines. Greater understanding and better assessment are required of the risks associated with opioid abuse to ensure the safety and analgesic effects of pain treatment after surgery.

Over the past 10 years, the crisis of sepsis has remained a great challenge. According to data from 2016, the sepsis-related mortality rate remains high. In addition, sepsis consumes extensive medical resources in intensive care units, and anti-inflammatory agents fail to improve sepsis-associated hyperinflammation and symptoms of immunosuppression. The specific immune mechanism of sepsis remains to be elucidated. Reactive oxygen species (ROS) are triggered by energy metabolism and respiratory dysfunction in sepsis, which not only cause oxidative damage to tissues and organelles, but also directly and indirectly promote NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation. NLRP3 inflammasomes enlarge the inflammatory response and trigger apoptosis of immune cells to exacerbate sepsis progression. Inhibiting the negative effects of ROS and NLRP3 inflammasomes therefore provides the possibility of reversing the excessive inflammation during sepsis. In this review, we describe the interaction of ROS and NLRP3 inflammasomes during sepsis, provide prevention strategies, and identify fields that need further study.

Objective:To investigate the effect of smoking cessation before surgery on postoperative pain and analgesic consumption after thoracoscopic radical resection of lung cancer in elderly patients with high nicotine dependence.Methods:A total of 107 male patients, ages 60 to 70 years, undergoing elective thoracoscopic radical lung cancer surgery from July 2017 to July 2018 were enrolled into 3 groups: group A (highly nicotine-dependent and discontinued smoking <3 weeks before surgery, n = 36), group B (highly nicotine-dependent and discontinued smoking >3 weeks before surgery, n = 38), and group C (nonsmokers, n = 33). Postoperative sufentanil consumption, visual analog scale (VAS) pain scores at rest and during cough, rescue analgesia, opioid-related adverse events, and patient satisfaction were assessed from 0 to 48 h postoperatively.Results:Patient characteristics were comparable among the 3 groups. Sufentanil consumption and VAS pain scores from postoperative 0 to 48 h were significantly higher in groups A and B than in group C. In addition, group B had lower sufentanil consumption and pain scores than group A. No differences in the need for rescue analgesia, patient satisfaction, or occurrence of postoperative adverse events, including nausea, vomiting, respiratory depression, and oversedation, were observed among the 3 groups.Conclusion:Compared with nonsmokers, highly nicotine-dependent male patients who were deprived of cigarettes experienced more severe pain and required treatment with more sufentanil after thoracoscopic radical lung cancer surgery. Moreover, preoperative smoking cessation at least 3 weeks before surgery led to better postoperative pain outcomes than smoking cessation within 3 weeks of surgery.

No abstract

Global spread of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is still ongoing. Before an effective vaccine is available, the development of potential treatments for resultant coronavirus disease 2019 (COVID‐19) is crucial. One of the disease hallmarks is hyper‐inflammatory responses, which usually leads to a severe lung disease. Patients with COVID‐19 also frequently suffer from neurological symptoms such as acute diffuse encephalomyelitis, brain injury and psychiatric complications. The metabolic pathway of sphingosine‐1‐phosphate (S1P) is a dynamic regulator of various cell types and disease processes, including the nervous system. It has been demonstrated that S1P and its metabolic enzymes, regulating neuroinflammation and neurogenesis, exhibit important functions during viral infection. S1P receptor 1 (S1PR1) analogues including AAL‐R and RP‐002 inhibit pathophysiological responses at the early stage of H1N1 virus infection and then play a protective role. Fingolimod (FTY720) is an S1P receptor modulator and is being tested for treating COVID‐19. Our review provides an overview of SARS‐CoV‐2 infection and critical role of the SphK‐S1P‐SIPR pathway in invasion of SARS‐CoV‐2 infection, particularly in the central nervous system (CNS). This may help design therapeutic strategies based on the S1P‐mediated signal transduction, and the adjuvant therapeutic effects of S1P analogues to limit or prevent the interaction between the host and SARS‐CoV‐2, block the spread of the SARS‐CoV‐2, and consequently treat related complications in the CNS.