To evaluate if the unruptured intracranial aneurysm treatment score (UIATS) is a sensitive tool to detect aneurysms at risk of rupture, we conducted an a posteriori retrospective study on ruptured intracranial aneurysms. We performed a retrospective analysis of adult patients admitted to our center from January 2010 to April 2016 with aneurysmal subarachnoid hemorrhage. The UIATS was applied to all ruptured aneurysms. Patients for whom the UIATS recommended treatment were labeled as “true positives,” whereas patients for whom the UIATS recommended observation were labeled as “false negatives.” Patients for whom the UIATS was inconclusive were excluded from the final analysis. Based on the UIATS recommendation, a sensitivity analysis was performed. A total of 262 patients with aneurysmal subarachnoid hemorrhage were screened. Of these, 212 were included in our analysis. Median age was 53 years (23–90). Most patients were females (n = 134, 63%), with an equal distribution between low-grade and high-grade hemorrhages (Hunt & Hess ≥ 3 n = 107, 50%). UIATS recommended treatment in n = 52, 25% cases (TP), was inconclusive in n = 93, 44% (excluded), and recommended observation in n = 67, 32% (FN). Based on these data, the UIATS showed a sensitivity of 44% (CI 35–53%). The UIATS exhibits rather low sensitivity for detecting aneurysms at risk of rupture.

There is a lack of information regarding electrical properties of white matter and brain tumors. To investigate the feasibility of in-vivo measurement of electrical resistivity during brain surgery and establish a better understanding of the resistivity patterns of brain tumors in correlation to the white matter. A bipolar probe was used to measure electrical resistivity during surgery in a prospective cohort of patients with brain tumors. For impedance measurement, the probe applied a constant current of 0.7 μA with a frequency of 140 Hz. The measurement was performed in the white matter within and outside peritumoral edema as well as in non-enhancing, enhancing and necrotic tumor areas. Resistivity values expressed in ohmmeter (Ω∗m) were compared between different intracranial tissues and brain tumors. Ninety-two patients (gliomas WHO II:16, WHO III:10, WHO IV:33, metastasis:33) were included. White matter outside peritumoral edema had higher resistivity values (13.3 ± 1.7 Ω∗m) than within peritumoral edema (8.5 ± 1.6 Ω∗m), and both had higher values than brain tumors including non-enhancing (WHO II:6.4 ± 1.3 Ω∗m, WHO III:6.3 ± 0.9 Ω∗m), enhancing (WHO IV:5 ± 1 Ω∗m, metastasis:5.4 ± 1.3 Ω∗m) and necrotic tumor areas (WHO IV:3.9 ± 1.1 Ω∗m, metastasis:4.3 ± 1.3 Ω∗m), p=<0.001. No difference was found between low-grade and anaplastic gliomas, p = 0.808, while resistivity values in both were higher than the highest values found in glioblastomas, p = 0.003 and p = 0.004, respectively. The technique we applied enabled us to measure electrical resistivity of white matter and brain tumors in-vivo presumably with a significant effect with regard to dielectric polarization. Our results suggest that there are significant differences within different areas and subtypes of brain tumors and that white matter exhibits higher electrical resistivity than brain tumors.

Purpose: Interactions with tumor-associated microglia and macrophages (TAM) are critical for glioblastoma progression. Polysialic acid (polySia) is a tumor-associated glycan, but its frequency of occurrence and its prognostic value in glioblastoma are disputed. Through interactions with the opposing immune receptors Siglec-11 and Siglec-16, polySia is implicated in the regulation of microglia and macrophage activity. However, due to a nonfunctional SIGLEC16P allele, SIGLEC16 penetrance is less than 40%. Here, we explored possible consequences of SIGLEC16 status and tumor cell–associated polySia on glioblastoma outcome. Experimental Design: Formalin-fixed paraffin-embedded specimens of two independent cohorts with 70 and 100 patients with newly diagnosed glioblastoma were retrospectively analyzed for SIGLEC16 and polySia status in relation to overall survival. Inflammatory TAM activation was assessed in tumors, in heterotypic tumor spheroids consisting of polySia-positive glioblastoma cells and Siglec-16–positive or Siglec-16–negative macrophages, and by exposing Siglec-16–positive or Siglec-16–negative macrophages to glioblastoma cell–derived membrane fractions. Results: Overall survival of SIGLEC16 carriers with polySia-positive tumors was increased. Consistent with proinflammatory Siglec-16 signaling, levels of TAM positive for the M2 marker CD163 were reduced, whereas the M1 marker CD74 and TNF expression were increased, and CD8+ T cells enhanced in SIGLEC16/polySia double-positive tumors. Correspondingly, TNF production was elevated in heterotypic spheroid cultures with Siglec-16–expressing macrophages. Furthermore, a higher, mainly M1-like cytokine release and activating immune signaling was observed in SIGLEC16-positive as compared with SIGLEC16-negative macrophages confronted with glioblastoma cell–derived membranes. Conclusions: Collectively, these results strongly suggest that proinflammatory TAM activation causes the better outcome in patients with glioblastoma with a functional polySia-Siglec-16 axis.