Although the neurovascular unit was originally developed as a conceptual framework for stroke, it is now recognized that these cell-cell interactions play critical roles in many other CNS disorders as well. In brain trauma, perturbations within the neurovascular unit may be especially important. Changes in neurovascular coupling may disrupt blood flow and metabolic regulation. Disruption of transmitter release-reuptake kinetics in neurons and astrocytes may augment excitotoxicity. Alterations in gliovascular signaling may underlie blood-brain barrier disruptions and traumatic edema. Perturbations in cell-cell signaling between all neuronal, glial, and vascular compartments may increase susceptibility to cell death. Finally, repairing the brain after trauma requires the integrated restoration of all neural, glial, and vascular connectivity for effective functional recovery. Just as in stroke, saving neurons alone may also be insufficient for treating brain trauma. In this minireview, we attempt to briefly highlight some of these pathways to underscore the importance of rescuing the entire neurovascular unit in brain trauma.

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The objective of this study is to evaluate the diagnostic accuracy of the first generation dual-source computed tomography (DSCT) in the diagnosis of coronary artery disease (CAD). We selected articles from four databases (Pubmed, Embase, the Cochrane central register of controlled trials (CENTRAL) and Chinese biomedical literature database. The strict study selection was made, and two reviewers independently extracted data back-to-back from included studies. Meta-Disc version 1.4 was used to obtain the pooled results. 24 studies were included in meta-analysis. A cut off point of ≥50% stenosis was used in all the studies to define significant coronary artery stenosis. In patient-based analysis (n = 801), pooled sensitivity was 0.980 [95% confidence interval (CI):0.970-0.990], specificity 0.870 (95% CI: 0.830-0.900), median positive predictive value (PPV) across studies 0.876 (range from 0.741 to 0.943) and negative predictive value (NPV) 0.964 (range from 0.900 to 1.000). In vessel-based analysis (n = 3,620) DSCT pooled sensitivity was 0.957 (95% CI: 0.943-0.969), specificity 0.930 (95% CI: 0.910-0.940), median PPV across studies 0.838 (range from 0.534 to 0.964) and NPV 0.973 (range from 0.885 to 0.996). In segment-based analysis (n = 6,177) DSCT pooled sensitivity was 0.915 (95% CI: 0.901-0.928), specificity 0.959 (95% CI: 0.956-0.963), median PPV 0.782 (range from 0.320 to 0.927) and NPV 0.985 (range from 0.929 to 0.999). In subgroups analysis, pooled sensitivity and specificity in segment based analysis were 93.1 and 92.3% when heart rate (HR) is beyond 70 bpm; when HR was below 70 bpm, the sensitivity was similar (93%), but specificity increased a little from 92.3 to 94%. When analysed based on segment with a cut-off calcium score of 400, the sensitivity was slightly higher in the subgroup with a score over 400 than in the subgroup with a score below 400 (94 vs. 91%), while the specificity was much lower in the subgroup with the high calcium score than the subgroup with the low calcium score (85 vs. 96%). For subgroups with heart rate beyond and below 65 bpm in patient-based analysis, sensitivities were 0.95 (95% CI: 0.86-0.99) and 0.98 (95% CI 0.91-1.00), respectively, while the specificities were 0.88 (95% CI 0.81-0.94) and 0.85 (95% CI 0.77-0.91), respectively. The area under the receiver operating characteristic curve (AUC) in the two subgroups were 0.9608 and 0.9786, respectively. DSCT is highly sensitive for patient-based analysis of CAD and has high specificity and NPV for segment-based analysis of CAD. First generation DSCT may have a role in the evaluation of patients with chest pain as a simple non-invasive examination because of its ability to diagnose or exclude significant CAD.