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Purpose: To evaluate the clinical applicability of a prototype virtual non-contrast (VNC) reconstruction algorithm based on coronary CT angiography (cCTA) to assess calcified coronary plaques by calcium scoring (CACS).Methods: Eighty consecutive patients suspected of coronary artery disease were retrospectively included. All patients underwent a cardiac CT using a dual-layer spectral-detector CT system. The standardized acquisition protocol included unenhanced CACS and cCTA. Datasets were acquired using 120 keV. VNC-reconstructions were calculated from the cCTA images at 2.5 mm (VNC group 1), 2.5 of 0.9 mm (group 2), and 0.9 mm (group 3) slice thickness. We compared the Agatston score and Coronary Artery Calcium Data and Reporting System (CAC-DRS) of all VNC reconstructions with the true non-contrast (TNC)-dataset as the gold standard. Results: In total, 73 patients were evaluated. Fifty patients (68.5 %) had a CACS > 0 based on TNC. We found a significant difference in the Agatston score comparing all VNC-reconstructions (1: 1.35, 2: 3.7, 3: 10.4) with the TNC dataset (3.8) (p < 0.001). Correlation analysis of the datasets showed an excellent correlation of the TNC results with the different VNC-reconstructions (r = 0.904-0.974, p < 0.001) with a slope of 1.89-2.53. Mean differences and limits of agreement by Bland-Altman analysis between TNC and group 1 were 83 and -196 to 362, respectively. By using the VNC-reconstructions, in group 1 23 patients (31.5 %), in group 2 10 (13.7 %), and in group 3 23 (31.5 %) were reclassified according to CAC-DRS compared to TNC. Classification according to CAC-DRS revealed a significant difference between TNC and group 1 (p = 0.024) and no significance compared to groups 2 and 3 (p = 0.670 and 0.273).Conclusion: The investigated VNC reconstruction algorithm of routine cCTA allows the detection and evaluation of coronary calcium burden without the requirement for an additional acquisition of an unenhanced CT scan for CACS and, ther

Objectives There is broad evidence that sleep as opposed to waking facilitates the consolidation of both declarative and procedural memory. The current study addressed the question whether different extents of sleep restriction after learning would impair long-term memory consolidation in adolescents. Methods Eighty-eight healthy adolescents were randomized to five different sleep protocols with 9, 8, 7, 6 or 5 h of time in bed for four consecutive nights under controlled conditions that excluded daytime sleep. Declarative (word-pair task) and procedural memory (mirror tracing task) encoding was assessed prior to the sleep restriction protocol. Recall was assessed after two recovery nights following the sleep protocol and 4 weeks later. Results Sleep diaries and actigraphy data demonstrated that the participants closely followed the sleep protocols. There were no differences in demographic parameters or memory encoding at baseline. In contrast to the initial prediction, restriction of nocturnal sleep over four consecutive nights had no significant impact on declarative or procedural memory consolidation. Polysomnographic monitoring after sleep restriction demonstrated a high preservation of the amount of slow wave sleep in the restricted conditions. Conclusions The results suggest that adolescents show a high resilience of memory consolidation to substantial sleep curtailment across four nights that might be promoted by increased sleep intensity under conditions of sleep restriction.

Neutralizing the interaction of the platelet receptor gpIb with VWF is an attractive strategy to treat and prevent thrombotic complications. ALX-0081 is a bivalent Nanobody which specifically targets the gpIb-binding site of VWF and interacts avidly with VWF. Nanobodies are therapeutic proteins derived from naturally occurring heavy-chain - only Abs and combine a small molecular size with a high inherent stability. ALX-0081 exerts potent activity in vitro and in vivo. Perfusion experiments with blood from patients with acute coronary syndrome on standard antithrombotics demonstrated complete inhibition of platelet adhesion after addition of ALX-0081, while in the absence of ALX-0081 residual adhesion was observed. In a baboon efficacy and safety model measuring acute thrombosis and surgical bleeding, ALX-0081 showed a superior therapeutic window compared with marketed antithrombotics. Pharmacokinetic and biodistribution experiments demonstrated target-mediated clearance of ALX-0081, which leads to a self-regulating disposition behavior. In conclusion, these preclinical data demonstrate that ALX-0081 combines a high efficacy with an improved safety profile compared with currently marketed antithrombotics. ALX-0081 has entered clinical development.