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RailChain
(2023)
The RailChain project designed, implemented, and experimentally evaluated a juridical recorder that is based on a distributed consensus protocol. That juridical blockchain recorder has been realized as distributed ledger on board the advanced TrainLab (ICE-TD 605 017) of Deutsche Bahn.
For the project, a consortium consisting of DB Systel, Siemens, Siemens Mobility, the Hasso Plattner Institute for Digital Engineering, Technische Universität Braunschweig, TÜV Rheinland InterTraffic, and Spherity has been formed. These partners not only concentrated competencies in railway operation, computer science, regulation, and approval, but also combined experiences from industry, research from academia, and enthusiasm from startups.
Distributed ledger technologies (DLTs) define distributed databases and express a digital protocol for transactions between business partners without the need for a trusted intermediary. The implementation of a blockchain with real-time requirements for the local network of a railway system (e.g., interlocking or train) allows to log data in the distributed system verifiably in real-time. For this, railway-specific assumptions can be leveraged to make modifications to standard blockchains protocols.
EULYNX and OCORA (Open CCS On-board Reference Architecture) are parts of a future European reference architecture for control command and signalling (CCS, Reference CCS Architecture – RCA). Both architectural concepts outline heterogeneous IT systems with components from multiple manufacturers. Such systems introduce novel challenges for the approved and safety-relevant CCS of railways which were considered neither for road-side nor for on-board systems so far. Logging implementations, such as the common juridical recorder on vehicles, can no longer be realized as a central component of a single manufacturer. All centralized approaches are in question.
The research project RailChain is funded by the mFUND program and gives practical evidence that distributed consensus protocols are a proper means to immutably (for legal purposes) store state information of many system components from multiple manufacturers. The results of RailChain have been published, prototypically implemented, and experimentally evaluated in large-scale field tests on the advanced TrainLab. At the same time, the project showed how RailChain can be integrated into the road-side and on-board architecture given by OCORA and EULYNX.
Logged data can now be analysed sooner and also their trustworthiness is being increased. This enables, e.g., auditable predictive maintenance, because it is ensured that data is authentic and unmodified at any point in time.
Arsenic-containing hydrocarbons (AsHCs), a subgroup of arsenolipids found in fish and algae, elicit substantial toxic effects in various human cell lines and have a considerable impact on cellular energy levels. The underlying mode of action, however, is still unknown. The present study analyzes the effects of two AsHCs (AsHC 332 and AsHC 360) on the expression of 44 genes covering DNA repair, stress response, cell death, autophagy, and epigenetics via RT-qPCR in human liver (HepG2) cells. Both AsHCs affected the gene expression, but to different extents. After treatment with AsHC 360, flap structure-specific endonuclease 1 (FEN1) as well as xeroderma pigmentosum group A complementing protein (XPA) and (cytosine-5)-methyltransferase 3A (DNMT3A) showed time- and concentration-dependent alterations in gene expression, thereby indicating an impact on genomic stability. In the subsequent analysis of epigenetic markers, within 72 h, neither AsHC 332 nor AsHC 360 showed an impact on the global DNA methylation level, whereas incubation with AsHC 360 increased the global DNA hydroxymethylation level. Analysis of cell extracts and cell media by HPLC-mass spectrometry revealed that both AsHCs were considerably biotransformed. The identified metabolites include not only the respective thioxo-analogs of the two AsHCs, but also several arsenic-containing fatty acids and fatty alcohols, contributing to our knowledge of biotransformation mechanisms of arsenolipids.
Major depressive disorder (MDD) is a common and severe disease characterized by mood changes, somatic alterations, and often suicide. MDD is treated with antidepressants, but the molecular mechanism of their action is unknown. We found that widely used antidepressants such as amitriptyline and fluoxetine induce autophagy in hippocampal neurons via the slow accumulation of sphingomyelin in lysosomes and Golgi membranes and of ceramide in the endoplasmic reticulum (ER). ER ceramide stimulates phosphatase 2A and thereby the autophagy proteins Ulk, Beclin, Vps34/Phosphatidylinositol 3-kinase, p62, and Lc3B. Although treatment with amitriptyline or fluoxetine requires at least 12 days to achieve sphingomyelin accumulation and the subsequent biochemical and cellular changes, direct inhibition of sphingomyelin synthases with tricyclodecan-9-yl-xanthogenate (D609) results in rapid (within 3 days) accumulation of ceramide in the ER, activation of autophagy, and reversal of biochemical and behavioral signs of stress-induced MDD. Inhibition of Beclin blocks the antidepressive effects of amitriptyline and D609 and induces cellular and behavioral changes typical of MDD. These findings identify sphingolipid-controlled autophagy as an important target for antidepressive treatment methods and provide a rationale for the development of novel antidepressants that act within a few days.
Objective:
Brain-derived neurotrophic factor (BDNF) supports neurogenesis, angiogenesis, and promotes the survival of various cell types in the brain and the coronary system. Moreover, BDNF is associated with both coronary heart disease (CHD) and depression. The current study aims to investigate whether serum BDNF levels are associated with the course of depressive symptoms in CHD patients.
Methods:
At baseline, N = 225 CHD patients were enrolled while hospitalized. Of these, N = 190 (84%) could be followed up 6 months later. Depressive symptoms were assessed both at baseline and at the 6-months follow-up using the Patient Health Questionnaire (PHQ-9). Serum BDNF concentrations were measured using fluorometric Enzyme-linked immunosorbent assays (ELISA).
Results:
Logistic regression models showed that lower BDNF levels were associated with persistent depressive symptoms, even after adjustment for age, sex, smoking and potential medical confounders. The incidence of depressive symptoms was not related to lower BDNF levels. However, somatic comorbidity (as measured by the Charlson Comorbidity Index) was significantly associated with the incidence of depressive symptoms.
Conclusions:
Our findings suggest a role of BDNF in the link between CHD and depressive symptoms. Particularly, low serum BDNF levels could be considered as a valuable biomarker for the persistence of depressive symptoms among depressed CHD patients.
Objective:
Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF).
Methods:
The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment.
Results:
Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS.
Conclusion:
Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.
Objective:
Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF).
Methods:
The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment.
Results:
Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS.
Conclusion:
Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.
Self-assembly of plasmonic nanoantenna-waveguide structures for subdiffractional chiral sensing
(2021)
Spin-momentum locking is a peculiar effect in the near-field of guided optical or plasmonic modes. It can be utilized to map the spinning or handedness of electromagnetic fields onto the propagation direction. This motivates a method to probe the circular dichroism of an illuminated chiral object. In this work, we demonstrate local, subdiffraction limited chiral coupling of light and propagating surface plasmon polaritons in a self-assembled system of a gold nanoantenna and a silver nanowire. A thin silica shell around the nanowire provides precise distance control and also serves as a host for fluorescent molecules, which indicate the direction of plasmon propagation. We characterize our nanoantenna-nanowire systems comprehensively through correlated electron microscopy, energy-dispersive X-ray spectroscopy, dark-field, and fluorescence imaging. Three-dimensional numerical simulations support the experimental findings. Besides our measurement of far-field polarization, we estimate sensing capabilities and derive not only a sensitivity of 1 mdeg for the ellipticity of the light field, but also find 10(3) deg cm(2)/dmol for the circular dichroism of an analyte locally introduced in the hot spot of the antenna-wire system. Thorough modeling of a prototypical design predicts on-chip sensing of chiral analytes. This introduces our system as an ultracompact sensor for chiral response far below the diffraction limit.
Land-use intensification is a major driver of biodiversity loss(1,2). Alongside reductions in local species diversity, biotic homogenization at larger spatial scales is of great concern for conservation. Biotic homogenization means a decrease in beta-diversity (the compositional dissimilarity between sites). Most studies have investigated losses in local (alpha)-diversity(1,3) and neglected biodiversity loss at larger spatial scales. Studies addressing beta-diversity have focused on single or a few organism groups (for example, ref. 4), and it is thus unknown whether land-use intensification homogenizes communities at different trophic levels, above-and belowground. Here we show that even moderate increases in local land-use intensity (LUI) cause biotic homogenization across microbial, plant and animal groups, both above- and belowground, and that this is largely independent of changes in alpha-diversity. We analysed a unique grassland biodiversity dataset, with abundances of more than 4,000 species belonging to 12 trophic groups. LUI, and, in particular, high mowing intensity, had consistent effects on beta-diversity across groups, causing a homogenization of soil microbial, fungal pathogen, plant and arthropod communities. These effects were nonlinear and the strongest declines in beta-diversity occurred in the transition from extensively managed to intermediate intensity grassland. LUI tended to reduce local alpha-diversity in aboveground groups, whereas the alpha-diversity increased in belowground groups. Correlations between the alpha-diversity of different groups, particularly between plants and their consumers, became weaker at high LUI. This suggests a loss of specialist species and is further evidence for biotic homogenization. The consistently negative effects of LUI on landscape-scale biodiversity underscore the high value of extensively managed grasslands for conserving multitrophic biodiversity and ecosystem service provision. Indeed, biotic homogenization rather than local diversity loss could prove to be the most substantial consequence of land-use intensification.
Maturation of fleshy fruits such as tomato (Solanum lycopersicum) is subject to tight genetic control. Here we describe the development of a quantitative real-time PCR platform that allows accurate quantification of the expression level of approximately 1000 tomato transcription factors. In addition to utilizing this novel approach, we performed cDNA microarray analysis and metabolite profiling of primary and secondary metabolites using GC-MS and LC-MS, respectively. We applied these platforms to pericarp material harvested throughout fruit development, studying both wild-type Solanum lycopersicum cv. Ailsa Craig and the hp1 mutant. This mutant is functionally deficient in the tomato homologue of the negative regulator of the light signal transduction gene DDB1 from Arabidopsis, and is furthermore characterized by dramatically increased pigment and phenolic contents. We choose this particular mutant as it had previously been shown to have dramatic alterations in the content of several important fruit metabolites but relatively little impact on other ripening phenotypes. The combined dataset was mined in order to identify metabolites that were under the control of these transcription factors, and, where possible, the respective transcriptional regulation underlying this control. The results are discussed in terms of both programmed fruit ripening and development and the transcriptional and metabolic shifts that occur in parallel during these processes.
Ziel Vergleich der Erkennungsgüte von drei Depressions-Screeninginstrumenten bei Patienten mit koronarer Herzerkrankung (KHK).
Methodik 1019 KHK-Patienten erhielten den Patient Health Questionnaire (PHQ-9 und PHQ-2) und die Hospital Anxiety and Depression Scale (HADS-D) sowie ein klinisches Interview (Composite International Diagnostic Interview) als Referenzstandard.
Ergebnisse Bezüglich der Erkennungsgüte waren PHQ-9 und HADS-D dem PHQ-2 überlegen. Optimale Cut-off-Werte waren 7 (PHQ-9 und HADS-D) und 2 (PHQ-2).
Schlussfolgerung PHQ-9 und HADS-D haben eine vergleichbare Diskriminationsfähigkeit für depressive Störungen bei KHK-Patienten.