Background Plasma S100A1 protein is a novel inflammatory biomarker associated with acute myocardial infarction and neurodegenerative disease’s pathophysiological mechanisms. This study aimed to determine the levels of this protein in patients with acute ischemic stroke early in the disease progression and to investigate its role in the pathogenesis of acute ischemic stroke. Methods A total of 192 participants from hospital stroke centers were collected for the study. Clinically pertinent data were recorded. The volume of the cerebral infarction was calculated according to the Pullicino formula. Multivariate logistic regression analysis was used to select independent influences. ROC curve was used to analyze the diagnostic value of AIS and TIA. The correlation between S100A1, NF-κB p65, and IL-6 levels and cerebral infarction volume was detected by Pearson correlation analysis. Results There were statistically significant differences in S100A1, NF-κB p65, and IL-6 among the AIS,TIA, and PE groups (S100A1, [230.96 ± 39.37] vs [185.85 ± 43.24] vs [181.47 ± 27.39], P < 0.001; NF-κB p65, [3.99 ± 0.65] vs [3.58 ± 0.74] vs [3.51 ± 0.99], P = 0.001; IL-6, [13.32 ± 1.57] vs [11.61 ± 1.67] vs [11.42 ± 2.34], P < 0.001). Multivariate logistic regression analysis showed that S100A1 might be an independent predictive factor for the diagnosis of disease (P < 0.001). The AUC of S100A1 for diagnosis of AIS was 0.818 (P < 0.001, 95% CI [0.749–0.887], cut off 181.03, Jmax 0.578, Se 95.0%, Sp 62.7%). The AUC of S100A1 for diagnosis of TIA was 0.720 (P = 0.001, 95% CI [0.592–0.848], cut off 150.14, Jmax 0.442, Se 50.0%, Sp 94.2%). There were statistically significant differences in S100A1, NF-κB p65, and IL-6 among the SCI,MCI, and LCI groups (S100A1, [223.98 ± 40.21] vs [225.42 ± 30.92] vs [254.25 ± 37.07], P = 0.001; NF-κB p65, [3.88 ± 0.66] vs [3.85 ± 0.64] vs [4.41 ± 0.45], P < 0.001; IL-6, [13.27 ± 1.65] vs [12.77 ± 1.31] vs [14.00 ± 1.40], P = 0.007). Plasma S100A1, NF-κB p65, and IL-6 were significantly different from cerebral infarction volume (S100A1, r = 0.259, P = 0.002; NF-κB p65, r = 0.316, P < 0.001; IL-6, r = 0.177, P = 0.036). There was a positive correlation between plasma S100A1 and IL-6 with statistical significance (R = 0.353, P < 0.001). There was no significant positive correlation between plasma S100A1 and NF-κB p65 (R < 0.3), but there was statistical significance (R = 0.290, P < 0.001). There was a positive correlation between IL-6 and NF-κB p65 with statistical significance (R = 0.313, P < 0.001). Conclusion S100A1 might have a better diagnostic efficacy for AIS and TIA. S100A1 was associated with infarct volume in AIS, and its level reflected the severity of acute cerebral infarction to a certain extent. There was a correlation between S100A1 and IL-6 and NF-κB p65, and it was reasonable to speculate that this protein might mediate the inflammatory response through the NF-κB pathway during the pathophysiology of AIS.

Posterior reversible encephalopathy syndrome (PRES) is a rare, reversible neurological disease that is frequently associated with the use of targeted therapy agents. In this case study, we examine the development of posterior reversible encephalopathy syndrome (PRES) in a 44-year-old woman with metastatic colon cancer following 1 month of treatment with the vascular endothelial growth factor receptor (VEGFR) inhibitor, fruquintinib. The occurrence of PRES after 1 month of VEGFR inhibitor administration is a common phenomenon. However, it is noteworthy that this is the first reported case of PRES associated with fruquintinib. The patient’s neurological function improved upon discontinuing the drug for a week, but worsening was observed following a lower-dose fruquintinib treatment. This patient’s experience highlights the potential for neurological deterioration in those treated with fruquintinib, prompting physicians to consider the possibility of PRES. Notably, this may be the first reported case linking fruquintinib to the syndrome, underscoring the importance of recognizing the association between PRES and fruquintinib.

Background It has been reported in previous studies that blood selenium is associated with Parkinson’s disease (PD), however, this association is still controversial. The purpose of this cross-sectional study was to assess the association between blood selenium and PD in U.S. adults. Methods A cross-sectional study of 54,674 adults aged over 40 years old was conducted using the 2010–2022 NHANES data. To analyze the association between blood selenium and PD, logistic regression, and multivariate logistic regression were used. The restricted cubic spline (RCS) model was additionally utilized to check the dose-response relationships between blood selenium and PD. Results A total of 15,660 participants were included in this study, and we found that blood selenium was negatively associated with the occurrence of PD [OR: 0.38(0.17, 0.85)] (P < 0.05). We observed consistent results between blood selenium and PD in three statistical models. Conclusion PD patients have lower blood selenium than non-PD patients. Higher levels of blood selenium may be a protective factor for PD. Further prospective studies are warranted to investigate the effect of blood selenium in patients with PD.