Predictive values of bilirubin for in-hospital adverse events in patients with ST-segment elevation myocardial infarction after primary percutaneous coronary intervention

Abstract Purpose To investigate the association between serum bilirubin levels and in-hospital Major Adverse Cardiac Events (MACE) in patients with ST-segment Elevation Myocardial Infarction (STEMI) undergoing primary Percutaneous Coronary Intervention (PCI). Methods A total of 418 patients with STEMI who underwent primary PCI were enrolled from October 1st, 2021 to October 31st 2022. The average age of enrolled participants was 59.23 years, and 328 patients (78.50%) were male patients. Patients were divided into MACE (patients with angina pectoris after infarction, recurrent myocardial infarction, acute heart failure, cardiogenic shock, malignant arrhythmias, or death after primary PCI) (n = 98) and non-MACE (n = 320) groups. Univariate and multivariate logistic regression analyses were performed to estimate the association between different bilirubin levels including Total Bilirubin (TB), Direct Bilirubin (DB), Indirect Bilirubin (IDB), and risk of in-hospital MACE. The area under the Receiver Operating Characteristic (ROC) curve was used to determine the accuracy of bilirubin levels in predicting in-hospital MACE. Results The incidence of MACE in STEMI patients increased from the lowest to the highest bilirubin tertiles. Multivariate logistic regression analysis showed that increased total bilirubin level was an independent predictor of in-hospital MACE in patients with STEMI (p for trend = 0.02). Compared to the first TB group, the ORs for risk of MACE were 1.58 (95% CI 0.77‒3.26) and 2.28 (95% CI 1.13‒4.59) in the second and third TB groups, respectively. The ROC curve analysis showed that the areas under the curve for TB, DB and IDB in predicting in-hospital MACE were 0.642 (95% CI 0.578‒0.705, p < 0.001), 0.676 (95% CI 0.614‒0.738, p < 0.001), and 0.619 (95% CI 0.554‒0.683, p < 0.001), respectively. Conclusions The current study showed that elevated TB, DB, and IDB levels are independent predictors of in-hospital MACE in patients with STEMI after primary PCI, and that DB has a better predictive value than TB and IDB.

Lipocalin 2 in the Paraventricular Thalamic Nucleus Contributes to DSS-Induced Depressive-Like Behaviors / 神经科学通报·英文版

The incidence rate of anxiety and depression is significantly higher in patients with inflammatory bowel diseases (IBD) than in the general population. The mechanisms underlying dextran sulfate sodium (DSS)-induced depressive-like behaviors are still unclear. We clarified that IBD mice induced by repeated administration of DSS presented depressive-like behaviors. The paraventricular thalamic nucleus (PVT) was regarded as the activated brain region by the number of c-fos-labeled neurons. RNA-sequencing analysis showed that lipocalin 2 (Lcn2) was upregulated in the PVT of mice with DSS-induced depressive behaviors. Upregulating Lcn2 from neuronal activity induced dendritic spine loss and the secreted protein induced chemokine expression and subsequently contributed to microglial activation leading to blood-brain barrier permeability. Moreover, Lcn2 silencing in the PVT alleviated the DSS-induced depressive-like behaviors. The present study demonstrated that elevated Lcn2 in the PVT is a critical factor for DSS-induced depressive behaviors.

Effect of sevoflurane preconditioning on expression of metabotropic glutamate receptor typeⅡ dur-ing focal cerebral ischemia-reperfusion in rats / 中华麻醉学杂志

Objective To evaluate the effect of sevoflurane preconditioning on the expression of metabotropic glutamate receptor type Ⅱ( mGluRⅡ) during focal cerebral ischemia-reperfusion ( I∕R) in rats. Methods Forty-eight clean-grade healthy male Sprague-Dawley rats were divided into 3 groups (n＝16 each) using a random number table method: sham operation group ( group S), cerebral I∕R group (group I∕R) and sevoflurane preconditioning group (group Sev). Rats were anesthetized with 10% chloral hydrate 3 ml∕kg. Focal cerebral I∕R was produced by occlusion of the right middle cerebral artery for 2 h fol-lowed by 24 h reperfusion. In group Sev, 2. 7% sevoflurane was inhaled for 1 h and 24 h later focal cerebral I∕R was produced. At 24 h after reperfusion, neurological deficit was scored, the cerebral infarct size was determined by TTC staining, the cell apoptosis in ischemic penumbra was observed by TUNEL, IκB-α ex-pression was detected by Western blot, and mGluRⅡexpression was determined by immunofluorescent stai-ning. The apoptosis rate was calculated. Results Compared with group S, the neurological deficit score, cerebral infarct size and apoptosis rate were significantly increased, the expression of mGluRⅡwas up-regu-lated, and the expression of IκB-α was down-regulated in I∕R and Sev groups ( P＜0. 05). Compared with group I∕R, the neurological deficit score, cerebral infarct size and apoptosis rate were significantly de-creased, the expression of mGluRⅡwas down-regulated, and the expression of IκB-α was up-regulated in group Sev (P＜0. 05). Conclusion Sevoflurane preconditioning reduces focal cerebral I∕R injury through inhibiting the expression of mGluRⅡ in rats.