Predictors and Dynamic Nomogram to Determine the Individual Risk of Malignant Brain Edema After Endovascular Thrombectomy in Acute Ischemic Stroke

Background@#and Purpose This study aimed to construct an optimal dynamic nomogram for predicting malignant brain edema (MBE) in acute ischemic stroke (AIS) patients after endovascular thrombectomy (ET). @*Methods@#We enrolled AIS patients after ET from May 2017 to April 2021. MBE was defined as a midline shift of >5 mm at the septum pellucidum or pineal gland based on follow-up computed tomography within 5 days after ET. Multivariate logistic regression and LASSO (least absolute shrinkage and selection operator) regression were used to construct the nomogram. The area under the receiver operating characteristic curve (AUC) and decisioncurve analysis were used to compare our nomogram with two previous risk models for predicting brain edema after ET. @*Results@#MBE developed in 72 (21.9%) of the 329 eligible patients. Our dynamic web-based nomogram (https://successful.shinyapps.io/DynNomapp/) consisted of five parameters: basal cistern effacement, postoperative National Institutes of Health Stroke Scale (NIHSS) score, brain atrophy, hypoattenuation area, and stroke etiology. The nomogram showed good discrimination ability, with a C-index (Harrell’s concordance index) of 0.925 (95% confidence interval=0.890–0.961), and good calibration (Hosmer-Lemeshow test, p=0.386). All variables had variance inflation factors of 0.7, suggesting no significant collinearity among them. The AUC of our nomogram (0.925) was superior to those of Xiang-liang Chen and colleagues (0.843) and Ming-yang Du and colleagues (0.728). @*Conclusions@#Our web-based dynamic nomogram reliably predicted the risk of MBE in AIS patients after ET, and hence is worthy of further evaluation.

The effect of edaravone on the inflammasome NLRP3 and blood brain barrier associated protein after embolic stroke in rat / 医学研究生学报

ObjectiveIn cerebral ischemia, free radicals form in large quantities and activate the inflammasome nod-like recepter protein 3(NLRP3), thereby exacerbating brain damage. Edaravone has the effect of scavenging free radicals, but the relationgship between its neuroprotective effect and inflammasome NLRP3 has not been reported. To study the neuroprotective effects of edaravone on inflammasome NLRP3 and associated protein of the blood-brain barrier against cerebral ischemia injury.Methods60 male Sprague-Dawley rats were randomly divided into Sham group, cerebral embolism group and edaravone group, respectively. Rat thromboembolic MCAO models were established and edaravone (3mg/kg) was intravenous injected immediately after occlusion and 4 hours after occlusion. In the sham group, cervical blood vessels were separated only, and no embolus was injected. At 24 hours after thrombi injected, mNSS score was used to evaluate neurological function deficits. Brain infarct volume was estimated by TTC staining. The expression of inflammasome NLRP3, occludin and ZO-1 was detected by Western blot. Immunohistochemistry was used to measure IgG leakage.ResultsThe mNSS score and infarct volume of cerebral embolism group at 24 hours after stroke were significantly higher than Sham group (P<0.05). The expression of inflammasome NLRP3 in the brain increased (P<0.05), occludin and ZO-1 blood brain barrier associated protein decreased (P<0.05), and IgG leakage increased. But compared with cerebral embolism group, the mNSS score（4.50±2.12 vs 6.50±1.35, P<0.05）and infarct volume （19.29±11.92 vs 29.99±7.56, P<0.05）decreased when treated with edaravone. Edaravone treatment significantly attenuated inflammasome NLRP3 expression in cerebral ischemic area (0.97±0.47 vs 1.58±0.86, P<0.05), degradation of BBB components (occludin, ZO-1) (1.04±0.19 vs 0.53±0.09, 0.66±0.05 vs 0.30±0.04,P<0.05) and IgG leakage decreased.ConclusionInflammasome NLRP3 play an important role in acute cerebral ischemia injury. Edaravone may provide neuroprotection by inhibiting expression of inflammasome NLRP3 and degradation of associated protein of blood brain barrier.

Effect of substance K on the contractility of cardiomyocytes / 中国应用生理学杂志

<p><b>AIM</b>To investigate the influence and the mechanism of SK on the contractility of cultured cardiomyocytes of rats.</p><p><b>METHODS</b>The primary cultured single myocardial cell was treated with SK and the contraction frequency and size of cardiomyocyte were determined by a computer image analysis system. At the same time the effects of propranolol (a beta receptor antagonist), phentolamine (a alpha receptor antagonist), DSP (a tachykinin receptor antagonist) on the action of SK were investigated.</p><p><b>RESULTS</b>SK increased contractive extend of the cardiomyocyte, in which a dose-response relationship of SK at 1.78 x 10(-8) - 1.78 x 10(-5) mol/L exists. But the frequency of contraction did not change, pretreatment with propranolol, phentolamine had no action on the effect of SK, but DSP markedly attenuated the effects of SK.</p><p><b>CONCLUSION</b>SK may directly enhance the contractility of single cardiomyocyte, which may be related with the tachykinin receptor.</p>