Halide Superionic Conductors with Non-Close-Packed Anion Frameworks.

Halide superionic conductors (SICs) are drawing significant research attention for their potential applications in all-solid-state batteries. A key challenge in developing such SICs is to explore and design halide structural frameworks that enable rapid ion movement. In this work, we show that the close-packed anion frameworks shared by traditional halide ionic conductors face intrinsic limitations in fast ion conduction, regardless of structural regulation. Beyond the close-packed anion frameworks, we identify that the non-close-packed anion frameworks have great potential to achieve superionic conductivity. Notably, we unravel that the non-close-packed UCl3-type framework exhibit superionic conductivity for a diverse range of carrier ions, including Li+, Na+, K+, and Ag+, which are validated through both ab initio molecular dynamics simulations and experimental measurements. We elucidate that the remarkable ionic conductivity observed in the UCl3-type framework structure stems from its significantly more distorted site and larger diffusion channel than its close-packed counterparts. By employing the non-close-packed anion framework as the key feature for high-throughput computational screening, we also identify LiGaCl3 as a promising candidate for halide SICs. These discoveries provide crucial insights for the exploration and design of novel halide SICs.

Nimodipine Improves Cognitive Impairment After Subarachnoid Hemorrhage in Rats Through IncRNA NEAT1/miR-27a/MAPT Axis.

BACKGROUND: Subarachnoid hemorrhage (SAH) is a cerebral hemorrhage disease that severely damages the brain and causes cognitive impairment (CI). Therefore, accurate and appropriate treatment strategies are urgently needed. The application of nimodipine can not only improve blood circulation in patients with SAH but also repair ischemic neuron injury. PURPOSE: To investigate the effects of nimodipine and lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1)/miR-27a/microtubule-associated protein tau (MAPT) axis on CI after SAH. METHODS: One hundred and twenty healthy male rats were selected and equally divided into control group, sham operation group, model group, PBS group, nimodipine group (drug group), NC siRNA group, NC mimics group, NEAT1 siRNA, miR-27a mimics, MAPT siRNA, drug + NEAT1-ad, and drug + NC-ad groups by random number table. Rats in the model group were constructed by double-hemorrhage model, and expression vectors were injected into the tail to regulate the expression of lncRNA NEAT1, miR-27a and MAPT. In addition, Western blot was employed to detect brain tissue protein, flow cytometry was applied to measure brain tissue apoptosis, and MTT was utilized to determine cell activity, so as to evaluate brain damage and cognitive function in each group. RESULTS: Nimodipine, down-regulated lncRNA NEAT1, up-regulated miR-27a and down-regulated MAPT all improved brain damage and CI, inhibited brain tissue cell apoptosis, and enhanced brain cell activity. The common binding sites of lncRNA NEAT1 and MAPT were found on the miR-27a sequence fragment, and miR-27a could be paired with the former two. Nimodipine was found to cause the down-regulation of lncRNA NEAT1 and MAPT, as well as the up-regulation of miR-27a. CONCLUSION: Nimodipine can improve CI after SAH in rats through the lncRNA NEAT1/miR-27a/MAPT axis.

Hyperhomocysteinemia as a Risk Factor for Saccular Intracranial Aneurysm: A Cohort Study in a Chinese Han Population.

BACKGROUND: We evaluated the possible relationships between serum total homocysteine and folate and Vitamin B12 in patients with intracranial aneurysm. METHODS: We enrolled consecutive patients with intracranial aneurysm from the Han population who were admitted to the hospital, as well as control subjects who received medical examination on an outpatient basis. The serum total homocysteine, folate, and Vitamin B12 levels were measured in patients with intracranial aneurysm and the control group, and the associations between those factors were analyzed using multivariate logistic analysis. RESULTS: A total of 140 patients with intracranial aneurysm and 140 control subjects were enrolled from July 2014 to December 2015. The mean serum total homocysteine level in the patient group (19.98 ± 10.84 µmol/L) was significantly higher than that in the control group (15.13 ± 5.55 µmol/L, P < .001). The serum total homocysteine level was negatively correlated with folate and Vitamin B12 levels (r = -.349, P < .001; r = -.531, P < .001, respectively) in the patient group. Homocysteine had an adjusted odds ratio of 2.196 (95% confidence interval: 1.188-4.057, P = .012) for the development of intracranial aneurysm. CONCLUSIONS: The present study provides evidence regarding the association between serum total homocysteine and folate and Vitamin B12 in patients with intracranial aneurysm. Hyperhomocysteinemia is an independent risk factor for intracranial aneurysm, and folate and Vitamin B12 are protective against intracranial aneurysm due to their roles in regulating the metabolism of homocysteine.

Early elevated levels of soluble triggering receptor expressed on myeloid cells-1 in subarachnoid hemorrhage patients.

Early brain injury (EBI) contributes to poor prognosis of subarachnoid hemorrhage (SAH). This study aimed to clarify whether triggering receptor expressed on myeloid cells-1 (TREM-1) was implicated in the inflammatory mechanisms of EBI. The cerebrospinal fluid (CSF) levels of soluble TREM-1 (sTREM-1), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) as well as plasma levels of white blood cells (WBC) count and C-reactive protein in 17 SAH patients at early stage (within the EBI period) and 9 volunteers were observed. Also World Federation of Neurosurgical Societies (WFNS) scale of SAH patients was calculated on admission. Compared to controls, increased CSF levels of sTREM-1 (t = 5.66, P < 0.001), TNF-α (t = 5.41, P < 0.001) and IL-6 (t = 2.98, P = 0.007) as well as elevated plasma WBC counts (t = 7.61, P < 0.001) and C-reactive protein levels (t = 3.91, P = 0.001) were found in SAH patients. Considering the increased WBC counts in SAH group, covariate analysis was also performed when comparing patients' sTREM-1 levels with respect to controls and no obvious difference was found (F = 0.982, P = 0.332). For SAH group, early CSF concentrations of sTREM-1 were correlated with those of both TNF-α (r = 0.582, P = 0.014) and IL-6 (r = 0.593, P = 0.012). Also the CSF sTREM-1 levels were positively correlated with WBC counts (r = 0.629, P = 0.007) and C-reactive protein levels (r = 0.804, P < 0.001) as well as WFNS scale (r = 0.835, P < 0.001). This study showed an early increased sTREM-1 CSF level in SAH patients, which correlated with inflammation intensity post-SAH and clinical severity, indicating that TREM-1 may participate in the inflammatory mechanisms of EBI.

Increased levels of soluble triggering receptor expressed on myeloid cells-1 in cerebrospinal fluid of subarachnoid hemorrhage patients.

Triggering receptor expressed on myeloid cells-1 (TREM-1) has been highlighted as a key amplifier of inflammatory response in various diseases. To determine the contribution of TREM-1 in the inflammatory cascade after subarachnoid hemorrhage (SAH), concentrations of soluble TREM-1 (sTREM-1) in cerebrospinal fluid (CSF) from 30 SAH patients and 9 healthy volunteers were measured by enzyme-linked immunosorbent assay. It was shown that the CSF sTREM-1 levels of SAH patients increased significantly than that of the volunteers (P<0.05). Interestingly, the levels were up-regulated dynamically over time with an early increase within 2days and a late peak at day 6 after SAH onset. In addition, it was found that the early sTREM-1 levels (within 3days post-SAH) were negatively correlated with Glasgow Coma Scale (r=-0.550, P=0.022) and positively correlated with the Hunt and Hess scale (r=0.603, P=0.010) respectively conducted on admission, also the early sTREM-1 levels were negatively correlated with Glasgow Outcome Scale (r=-0.505, P=0.039) and positively correlated with modified Rankin Scale (r=0.557, P=0.020) respectively conducted one month after SAH. Altogether, this is the first study showing CSF sTREM-1 dynamics in SAH patients, and exploring the correlations of early CSF sTREM-1 levels to patients' severity and prognosis, which suggests that TREM-1 may play an important role in the inflammatory cascade after SAH and act as a monitoring biomarker facilitated to assess the severity and prognosis of SAH patients.