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The present work aims to investigate the negative effects of network latencies in immersive collaborative virtual environments. A user study was conducted to determine the impact of those delays on the performance of users. Participants of the study played a simple cooperative game designed for two players. The goal of the game was to correctly place bicolored cubes into their specific destinations. Since each player only saw the colors of the cubes of his or her partner, both players had to visually and verbally exchange information to complete the game. Each pair of participants played the game under four different latency conditions. The task performance was measured by the time needed to place one cube successfully. Besides, other subjectively observable variables were investigated. The results of the study show that a high end-to-end delay between two VR stations has an adverse effect on the users’ task performance, the amount of mutual understanding and the perceived workload. For the co-presence metric, i.e., the perceived amount of togetherness inside the virtual environment, no significant correlation to the network delay could be determined.

Distributed Virtual Reality systems enable globally dispersed users to interact with each other in a shared virtual environment. In such systems, different types of latencies occur. For a good VR experience, they need to be controlled. The time delay between the user's head motion and the corresponding display output of the VR system might lead to adverse effects such as a reduced sense of presence or motion sickness. Additionally, high network latency among worldwide locations makes collaboration between users more difficult and leads to misunderstandings. To evaluate the performance and optimize dispersed VR solutions it is therefore important to measure those delays. In this work, a novel, easy to set up, and inexpensive method to measure local and remote system latency will be described. The measuring setup consists of a microcontroller, a microphone, a piezo buzzer, a photosensor, and a potentiometer. With these components, it is possible to measure motion-to-photon and mouth-to-ear latency of various VR systems. By using GPS-receivers for timecode-synchronization it is also possible to obtain the end-to-end delays between different worldwide locations. The described system was used to measure local and remote latencies of two HMD based distributed VR systems.

After the enactment of the GDPR in 2018, many companies were forced to rethink their privacy management in order to comply with the new legal framework. These changes mostly affect the Controller to achieve GDPR-compliant privacy policies and management.However, measures to give users a better understanding of privacy, which is essential to generate legitimate interest in the Controller, are often skipped. We recommend addressing this issue by the usage of privacy preference languages, whereas users define rules regarding their preferences for privacy handling. In the literature, preference languages only work with their corresponding privacy language, which limits their applicability. In this paper, we propose the ConTra preference language, which we envision to support users during privacy policy negotiation while meeting current technical and legal requirements. Therefore, ConTra preferences are defined showing its expressiveness, extensibility, and applicability in resource-limited IoT scenarios. In addition, we introduce a generic approach which provides privacy language compatibility for unified preference matching.

Diamond is an attractive material for photonic quantum technologies because its colour centres have a number of outstanding properties, including bright single photon emission and long spin coherence times. To take advantage of these properties it is favourable to directly fabricate optical microcavities in high-quality diamond samples. Such microcavities could be used to control the photons emitted by the colour centres or to couple widely separated spins. Here, we present a method for the fabrication of one- and two-dimensional photonic crystal microcavities with quality factors of up to 700 in single crystal diamond. Using a post-processing etching technique, we tune the cavity modes into resonance with the zero phonon line of an ensemble of silicon-vacancy colour centres, and we measure an intensity enhancement factor of 2.8. The controlled coupling of colour centres to photonic crystal microcavities could pave the way to larger-scale photonic quantum devices based on single crystal diamond. Optical microcavities have been fabricated in single-crystal diamond and tuned into resonance with the zero phonon line of an ensemble of silicon-vacancy colour centres, which results in an enhancement of spontaneous emission.

Periodontitis is associated with increased serum lipopolysaccharide (LPS) activity, which may be one mechanism linking periodontitis with the risk of cardiovascular diseases. As LPS-carrying proteins including lipoproteins modify LPS-activity, we investigated the determinants of serum LPS-neutralizing capacity (LPS-NC) in ischemic stroke. The association of LPS-NC and Aggregatibacter actinomycetemcomitans, a major microbial biomarker in periodontitis, was also investigated. The assay to measure LPS-NC was set up by spiking serum samples with E. coli LPS. The LPS-NC, LPS-binding protein (LBP), soluble CD14 (sCD14), lipoprotein profiles, apo(lipoprotein) A-I, apoB, and phospholipid transfer protein (PLTP) activity, were determined in 98 ischemic stroke patients and 100 age- and sex-matched controls. Serum and saliva immune response to A. actinomycetemcomitans, its concentration in saliva, and serotype-distribution were examined. LPS-NC values ranged between 51-83% in the whole population. Although several of the LPS-NC determinants differed significantly between cases and controls (PLTP, sCD14, apoA-I, HDL-cholesterol), the levels did not (p = 0.056). The main determinants of LPS-NC were i) triglycerides (β = -0.68, p<0.001), and ii) HDL cholesterol (0.260, <0.001), LDL cholesterol (-0.265, <0.001), PLTP (-0.196, 0.011), and IgG against A. actinomycetemcomitans (0.174, 0.011). Saliva A. actinomycetemcomitans concentration was higher [log mean (95% CI), 4.39 (2.35-8.19) vs. 10.7 (5.45-21) genomes/ml, p = 0.023) and serotype D more frequent (4 vs. 0%, p = 0.043) in cases than controls. Serotypeablity or serotypes did not, however, relate to the LPS-NC. Serum LPS-NC comprised low PLTP-activity, triglyceride and LDL cholesterol concentrations, as well as high HDL cholesterol and IgG against A. actinomycetemcomitans. The present findings let us to conclude that LPS-NC did not associate with stroke.

BackgroundA novel automated system for the control of the inspired fraction of oxygen, named LeoClac, has been implemented on a mechanical ventilator. The system uses a separate sensor for the measurement of peripheral oxygen saturation which is connected directly to the ventilator. We hypothesise that LeoClac will be superior to manual control in keeping critically ill and mechanically ventilated patients in a SpO2-target range (93–96%).MethodsThis is a randomised controlled, single-centre superiority study with two parallel groups including 40 patients. Mechanically ventilated patients treated on the intensive care unit (ICU) will be screened for eligibility and included in the study after written informed consent. Patients in the intervention group will be treated with LeoClac. In the control group, FiO2 will be controlled manually by the intensive care team. The primary endpoint of the study is the proportion of time in the target zone for peripheral oxygen saturation within the first 24 hours following randomisation. Secondary endpoints include the analysis of hyperoxia and hypoxia, number of changes in FiO2, number and reasons for self-aborts and manual overrides of the automated system, proportion of time in target zone for peripheral oxygen saturation in the subgroups of patients with hypoxemic respiratory failure and acute hypercapnic respiratory failure. Furthermore, ventilator-free days and ICU mortality at day 28 will be analysed.AnalysisThe precise control of FiO2 with the aim of avoiding both hyperoxia and hypoxia is a fundamental challenge in the highly technical field of mechanical ventilation. Incorporation of patient heterogeneity, the benefits of reduced manual intervention and the potential to optimise treatment outcomes underscore the importance of this research. By addressing the complexities of precise oxygen control in adults, this study contributes to the advancement of critical care practices and may improve patient outcomes.EthicsThe study protocol was approved by the ethics committee of the Christian-Albrechts-University Kiel, Germany, on 17 May 2023.Trial registration numberDRKS00032113.

Ventricular tachyarrhythmias are the main cause of sudden death in patients after myocardial infarction. Here we show that transplantation of embryonic cardiomyocytes (eCMs) in myocardial infarcts protects against the induction of ventricular tachycardia (VT) in mice. Engraftment of eCMs, but not skeletal myoblasts (SMs), bone marrow cells or cardiac myofibroblasts, markedly decreased the incidence of VT induced by in vivo pacing. eCM engraftment results in improved electrical coupling between the surrounding myocardium and the infarct region, and Ca 2+ signals from engrafted eCMs expressing a genetically encoded Ca 2+ indicator could be entrained during sinoatrial cardiac activation in vivo. eCM grafts also increased conduction velocity and decreased the incidence of conduction block within the infarct. VT protection is critically dependent on expression of the gap-junction protein connexin 43 (Cx43; also known as Gja1): SMs genetically engineered to express Cx43 conferred a similar protection to that of eCMs against induced VT. Thus, engraftment of Cx43-expressing myocytes has the potential to reduce life-threatening post-infarct arrhythmias through the augmentation of intercellular coupling, suggesting autologous strategies for cardiac cell-based therapy. Connexin 43 for the heart Cell-based therapies are thought to have great potential for the treatment of cardiovascular diseases. Current clinical trials aim to restore contractile force by the transplantation of autologous skeletal muscle or bone marrow cells in the failing heart, but this approach has so far met with only limited success. Work in mice with experimentally induced myocardial infarcts has now produced the finding that engraftment of fetal cardiomyocytes provides potent protection against ventricular arrhythmia, a common cause of death in patients following heart attack. The implanted cells are activated by the normal cardiac action potential and the engraftment of these electrically coupled cells establishes pathways of increased conduction into the infarct. In addition, connexin 43, a protein found at 'gap junctions' between neighbouring cells, has been implicated in this protection. Surprisingly, expressing this protein in skeletal muscle cells now confers properties similar to the fetal cardiomyocytes. These results suggest a new approach to cell-based therapy for cardiac dysfunction. Tachycardia can be prevented by engrafting embryonic cardiomyocytes into mice. A protein resident at 'gap junctions', connexin 43, is also identified as being important for this protection. Expression of this protein in skeletal myoblasts achieves similar levels of protection. These results suggest a new approach to cell-based therapy for cardiac dysfunction.

In patients with heart failure and reduced ejection fraction who were receiving guideline-directed medical therapy, digitoxin lowered the risk of death or hospitalization for heart failure as compared with placebo.

Background Physical activity (PA) is associated with lower risk of stroke. We tested the hypothesis that lack of pre-stroke PA is an independent predictor of poor outcome after first-ever ischemic stroke. Methods We assessed recent self-reported PA and other potential predictors for loss of functional independence - modified Rankin Scale (mRS) > 2 - one year after first-ever ischemic stroke in 1370 patients registered between 2006 and 2010 in the Ludwigshafen Stroke Study, a population-based stroke registry. Results After 1 year, 717 (52.3%) of patients lost their independence including 251 patients (18.3%) who had died. In multivariate logistic regression analysis lack of regular PA prior to stroke (Odds Ratio (OR) 1.7, Confidence Interval (CI) 1.1–2.5), independently predicted poor outcome together with higher age (65–74: OR 1.7; CI 1.1–2.8, 75–84 years: OR 3.3; CI 2.1–5.3; ≥85 years OR 14.5; CI 7.4–28.5), female sex (OR 1.5; CI 1.1–2.1), diabetes mellitus (OR 1.8; CI 1.3–2.5), stroke severity (OR 1.2; CI 1.1–1.2), probable atherothrombotic stroke etiology (OR 1.8; CI 1.1–2.8) and high leukocyte count (> 9.000/mm 3 ; OR 1.4; CI 1.0–1.9) at admission. Subclassifying unknown stroke etiology, embolic stroke of unknown source (ESUS; n  = 40, OR 2.2; CI 0.9–5.5) tended to be associated with loss of independence. Conclusion In addition to previously reported factors, lack of PA prior to stroke as potential indicator of worse physical condition, high leukocyte count at admission as indicator of the inflammatory response and probable atherothrombotic stroke etiology might be independent predictors for non-functional independence in first-ever ischemic stroke.

Background Risk diseases and risk factors for stroke include atrial fibrillation, hypertension, diabetes mellitus, smoking, and elevated LDL-cholesterol. Due to modern treatment options, the impact of these risk diseases on subsequent cardiovascular events or death after a first stroke is less clear and needs to be elucidated. We therefore aimed to get insights into the persistence of adverse prognostic effects of these risk diseases and risk factors on subsequent stroke or death events 1 year after the first stroke by using the new weighted all-cause hazard ratio. Methods This study evaluates the 1 year follow-up of 470 first ever stroke cases identified in the area of Ludwigshafen, Germany, with 23 deaths and 34 subsequent stroke events. For this purpose, the recently introduced “weighted all-cause hazard ratio” was used, which allows a weighting of the competing endpoints within a composite endpoint. Moreover, we extended this approach to allow an adjustment for covariates. Results None of these risk factors and risk diseases, most probably being treated after the first stroke, remained to be associated with a subsequent death or stroke [weighted hazard ratios (95% confidence interval) for diabetes mellitus, atrial fibrillation, high cholesterol, hypertension, and smoking are 0.4 (0.2–0.9), 0.8 (0.4–2.2), 1.3 (0.5–2.5), 1.2 (0.3–2.7), 1.6 (0.8–3.6), respectively]. However, when analyzed separately in terms of death and stroke, the risk factors and risk diseases under investigation affect the subsequent event rate to a variable degree. Conclusions Using the new weighted hazard ratio, established risk factors and risk diseases for the occurrence of a first stroke do not remain to be significant predictors for subsequent events like death or recurrent stroke. It has been demonstrated that the new weighted hazard ratio can be used for a more adequate analysis of cardiovascular risk and disease progress. The results have to be confirmed within a larger study with more events.