BackgroundEosinophils contribute to antibacterial defense by releasing mitochondrial DNA, which are decreased in patients with acute ischemic stroke (AIS). However, the impact of eosinophils on stroke-associated pneumonia (SAP) among patients with AIS remains unclear. Moreover, whether SAP is in the path of the association between eosinophils and clinical outcomes also remains unclear. We aimed to assess the relationships between eosinophils, SAP, and clinical outcome after mechanical thrombectomy in patients with AIS.MethodsA total of 328 consecutive patients with AIS who underwent mechanical thrombectomy between May 2017 and March 2021 were analyzed. Their baseline data and peripheral eosinophil counts were recorded on admission. Regression analysis was used to assess the effect of eosinophils on SAP, and its effect on poor outcome is defined as a modified Rankin Scale score of 3–6 at month 3 after admission. Mediation analysis was utilized to assess the proportion of the total effect of SAP on the association between eosinophils and poor outcomes.ResultsMultivariate analysis revealed that eosinophils was independently associated with SAP after adjusting for potential confounders (odds ratio, 0.00; 95% CI, 0.00–0.38; P = 0.0267), which are consistent with the result of eosinophils (dichotomous) as a categorical variable (odds ratio, 0.54; 95% CI, 0.31–0.96; P = 0.0342). A non-linear relationship was detected between eosinophils and SAP, whose inflection point was 0.06. Subgroup analyses further confirmed these associations. Eosinophils were also associated with poor outcomes (odds ratio, 0.00; 95% CI, 0.00–0.14; P = 0.0124). Additionally, mediation analysis found that SAP partially mediated the negative relationship between eosinophils and poor outcome (indirect effect = −0.169; 95% CI:−0.339 –−0.040, P < 0.001).ConclusionOur findings suggested that a lower eosinophil level was associated with higher SAP and poorer outcome, and SAP might play an important effect in the association between eosinophils and poor outcomes.

A B S T R A C T We have shown that two unrelated prostaglandin antagonists block both thyrotropin (TSH) and prostaglandins E (PGE1, PGE2) stimulation of thyroidal adenyl cyclase activation and cyclic 3',5'-adenosine monophosphate (cAMP) formation, suggesting that prostaglandins play an important role in regulating thyroid function. To further explore this postulate, we measured prostaglandin content by radioimmunoassay in homogeneous bovine thyroid cell preparations in the presence and absence of TSH. Antibodies to albuminconjugated PGE1 and PGF2. showed specificity for prostaglandins E and F, respectively, but reacted, albeit far less effectively, with heterologous prostaglandins. A double antibody system was used to separate free from antibody-bound PGE1-'H and PGF2.-'H. Thyroid cells were extracted with ethanol/ethyl acetate and the various prostaglandins separated on silicic acid columns. Recoveries of added PGE1-'H and PGF2a-3H through the extraction and separation procedures ranged from 50-80%. The sensitivity of the method was 10-50 pg. Basal thyroid cell content of PGE1 and PGF2a "equivalents" varied between cell preparations (range = 2-6 ng/ 0.2 ml cell suspension) but, in each instance, remained constant during 5-30-min incubations at 370C. TSH, 10-100 mU/ml, increased the levels of cell PGEi and PGF2a "equivalents" 30-80% above basal during 5-15-min incubations. The stimulatory effect was specific for TSH, no increase in PGE, or PGF2a "equivalent" levels being seen with luteinizing hormone (LH), human growth hormone (HGH), adrenocorticotropic hormone (ACTH), or glucagon. These data support the thesis that prostaglandins may mediate TSH effects on thyroid.

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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 decision-curve 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 <1.5 and tolerances 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.