Objective Scavenger receptor A (SRA), a pattern recognition molecule, is implicated in immune response after acute brain injury. We strived to identify serum soluble SRA (sSRA) as a potential biomarker of prognosis after aneurysmal subarachnoid hemorrhage (aSAH). Methods In this prospective observational study, we quantified serum sSRA levels of 131 aSAH patients and 131 healthy controls. A poor outcome was defined as extended Glasgow outcome scale (GOSE) scores of 1–4 at 90 days after injury. Relations of serum sSRA levels to severity, delayed cerebral ischemia (DCI) and poor outcome were assessed using multivariate analysis. Predictive efficiency was determined via area under receiver operating characteristic curve (AUC). Results Serum sSRA levels were markedly higher in aSAH patients than in controls (median, 2.9 ng/mL versus 1.0 ng/mL; P < 0.001). Serum sSRA levels were independently correlated with Hunt-Hess scores (beta, 0.569; 95% confidence interval (CI), 0.244–0.894; P = 0.001), modified Fisher scores (beta, 0.664; 95% CI, 0.254–1.074; P = 0.002) and 90-day GOSE scores (beta, −0.275; 95% CI, −0.440–0.110; P = 0.005). Serum sSRA levels independently predicted DCI (odds ratio, 1.305; 95% CI, 1.012–1.687; P = 0.040) and a poor outcome (odds ratio, 2.444; 95% CI, 1.264–4.726; P = 0.008), as well as showed significant accuracy for the discrimination of DCI (AUC, 0.753; 95% CI, 0.649–0.857; P < 0.001) and a poor outcome (AUC, 0.800; 95% CI, 0.721–0.880; P < 0.001). Its combination with Hunt-Hess scores and modified Fisher scores displayed significantly improved AUCs for predicting DCI and poor outcome, as compared to any of them (all P < 0.05). Conclusion There is a significant elevation of serum sSRA levels after aSAH, which in close correlation with illness severity, are independently associated with DCI and poor clinical outcome after aSAH. Hypothetically, SRA may regulate immune response in acute brain injury after aSAH and serum sSRA is presumed to be a potential prognostic biomarker of aSAH.

In this report, silver nanowires (NWs) with different sizes have been obtained by using the poly process synthesis method. As-synthesized samples 1, 2, and 3 with high purity and different sizes have been obtained by changing the amount and kind of inorganic agent in the synthesis procedure. Three samples have been characterized by the scanning electron microscopy (SEM) and powder X-ray diffraction (PXRD). The SEM images of Ag NW 1 (74 nm in diameter, 20–30 μm in length), Ag NW 2 with (60 nm in diameter, 30–40 μm in length), and Ag NWs 3 with (46 nm in diameter, 30–40 μm in length) are obtained. The PXRD results for Ag NWs 1–3 show four typical diffraction peaks at 38.2°, 44.5°, 64.5°, and 77.4°, matching the face-centered cubic lattice for Ag substance and confirming the purity of the Ag NWs sample. In addition, the relative expression of the PTEN and mTOR was determined with real-time RT-PCR at the mRNA level. The content of inflammatory cytokines during stoke was measured with indicated ELISA assay.

ObjectiveHypoxia-inducible factor 1alpha (HIF-1α) functions as a crucial transcriptional mediator in hypoxic and ischemic brain response. We endeavored to assess the prognostic significance of serum HIF-1α in human aneurysmal subarachnoid hemorrhage (aSAH).MethodsIn this prospective, longitudinal, multicenter, and observational study of 257 patients with aSAH and 100 healthy controls, serum HIF-1α levels were quantified. Univariate analyses, followed by multivariate analyses, were performed to discern the relationship between serum HIF-1α levels and severity and delayed cerebral ischemia (DCI) plus poststroke 6-month poor outcome [extended Glasgow outcome scale (GOSE) scores of 1–4]. Predictive efficiency was determined under the receiver operating characteristic (ROC) curve.ResultsThere were significantly increased serum HIF-lα levels after aSAH, in comparison to controls (median, 288.0 vs. 102.6 pg/ml; P &lt; 0.001). Serum HIF-lα levels were independently correlated with Hunt–Hess scores [β, 78.376; 95% confidence interval (CI): 56.446–100.305; P = 0.001] and modified Fisher scores (β, 52.037; 95% CI: 23.461–80.614; P = 0.002). Serum HIF-lα levels displayed significant efficiency for discriminating DCI risk [area under ROC curve (AUC), 0.751; 95% CI: 0.687–0.815; P &lt; 0.001] and poor outcome (AUC, 0.791; 95% CI: 0.736–0.846; P &lt; 0.001). Using the Youden method, serum HIF-1α levels &gt;229.3 pg/ml predicted the development of DCI with 92.3% sensitivity and 48.4% specificity and serum HIF-1α levels &gt;384.0 pg/ml differentiated the risk of a poor prognosis with 71.4% sensitivity and 81.1% specificity. Serum HIF-1α levels &gt;229.3 pg/ml were independently predictive of DCI [odds ratio (OR), 3.061; 95% CI: 1.045–8.965; P = 0.041] and serum HIF-1α levels &gt;384.0 pg/ml were independently associated with a poor outcome (OR, 2.907; 95% CI: 1.403–6.024; P = 0.004). The DCI predictive ability of their combination was significantly superior to those of Hunt–Hess scores (AUC, 0.800; 95% CI: 0.745–0.855; P = 0.039) and modified Fisher scores (AUC, 0.784; 95% CI: 0.726–0.843; P = 0.004). The prognostic predictive ability of their combination substantially exceeded those of Hunt–Hess scores (AUC, 0.839; 95% CI: 0.791–0.886; P &lt; 0.001) and modified Fisher scores (AUC, 0.844; 95% CI: 0.799–0.890; P &lt; 0.001).ConclusionElevated serum HIF-lα levels after aSAH, in independent correlation with stroke severity, were independently associated with DCI and 6-month poor outcome, substantializing serum HIF-lα as a potential prognostic biomarker of aSAH.