Objective: Sepsis-associated encephalopathy (SAE) is a severe and common complication of sepsis and can induce cognitive dysfunction and apoptosis of neurons and neuroinflammation. Emodin has been confirmed to have anti-inflammatory effects. Thus, we sought to investigate the role of Emodin in SAE. Methods: The cecal ligation and puncture (CLP) method was used for the establishment of SAE in mice model. For treatment of Emodin, intraperitoneal injection of 20 mg/kg Emodin was performed before the surgery. The Morris water maze and open field tests were carried for measurement of cognitive dysfunction. Hematoxylin and eosin staining was for histological analysis of hippocampus. Cell apoptosis of hippocampus neurons was measured by TUNEL staining. Pro-inflammatory and anti-inflammatory cytokines in hippocampus tissue homogenate were evaluated by ELISA. BDNF/TrkB signaling-related proteins (TrkB, p-TrkB, and BDNF), autophagy-related proteins (LC3 II/I and Beclin-1), and apoptosis-related proteins (Bax, Bcl-2, and cleaved caspase-3) were detected by Western blotting. Results: Emodin significantly inhibited apoptosis and induced autophagy in hippocampal neurons of CLP-treated mice. In addition, Emodin significantly ameliorated CLP-induced cognitive dysfunction and pathological injury in mice. Meanwhile, Emodin notably inhibited CLP-induced inflammatory responses in mice via upregulation of BDNF/TrkB signaling, while the effect of Emodin was partially reversed in the presence of K252a (BDNF/TrkB signaling inhibitor). Conclusion: Emodin significantly inhibited the progression of SAE via mediation of BDNF/TrkB signaling. Thus, Emodin might serve as a new agent for SAE treatment.

Sepsis-associated encephalopathy (SAE) is a common complication of sepsis. It is imperative to recognize, diagnose, and effectively manage SAE at the early stages. The aim of this study was to evaluate the potential of using the serum tau protein level in the diagnosis of SAE and the prediction of SAE outcomes. This was a retrospective and observational study. The patients included in this study were diagnosed with severe sepsis or septic shock. The serum tau protein level was measured using a commercial enzyme-linked immunosorbent assay. The association between the level of serum tau protein and SAE was assessed by multiple logistic regression analysis. One hundred nine patients with severe sepsis were enrolled during a period of two years. Of the 109 enrolled patients, 27 developed SAE. The serum tau protein level was significantly higher in the patients with SAE than that of the non-SAE group. The serum tau protein level and the sequential organ failure assessment (SOFA) score were independent factors that were associated with SAE. The combined use of the serum tau protein level with the SOFA score improved the accuracy in distinguishing SAE from non-SAE patients. A cutoff value serum tau protein level of 75.92 pg/mL had 81.1% sensitivity and 86.1% specificity in predicting the 28-day mortality in patients with severe sepsis. We identified a close association between the serum tau protein level with the appearance of SAE in patients with severe sepsis. The serum tau protein level can be useful in the prediction of poor outcomes in patients with sepsis.

Objective To develop a convenient nomogram for the bedside evaluation of patients with acute organophosphorus poisoning (AOPP). Design This was a retrospective study. Setting Two independent hospitals in northern China, the First Hospital of Jilin University and the Lequn Hospital of the First Hospital of Jilin University. Participants A total of 1657 consecutive patients admitted for the deliberate oral intake of AOPP within 24 hours from exposure and aged >18 years were enrolled between 1 January 2013 and 31 December 2018. The exclusion criteria were: normal range of plasma cholinesterase, exposure to any other type of poisonous drug(s), severe chronic comorbidities including symptomatic heart failure (New York Heart Association III or IV) or any other kidney, liver and pulmonary diseases. Eight hundred and thirty-four patients were included. Primary outcome measure The existence of severely poisoned cases, defined as patients with any of the following complications: cardiac arrest, respiratory failure requiring ventilator support, hypotension or in-hospital death. Results 440 patients from one hospital were included in the study to develop a nomogram of severe AOPP, whereas 394 patients from the other hospital were used for the validation. Associated risk factors were identified by multivariate logistic regression. The nomogram was validated by the area under the receiver operating characteristic curve (AUC). A nomogram was developed with age, white cells, albumin, cholinesterase, blood pH and lactic acid levels. The AUC was 0.875 (95% CI 0.837 to 0.913) and 0.855 (95% CI 0.81 to 0.9) in the derivation and validation cohorts, respectively. The calibration plot for the probability of severe AOPP showed an optimal agreement between the prediction by nomogram and actual observation in both derivation and validation cohorts. Conclusion A convenient severity evaluation nomogram for patients with AOPP was developed, which could be used by physicians in making clinical decisions and predicting patients’ prognosis.