Die Schweizerische Meteorologische Anstalt wird im Rahmen des Werkes «Klima der Schweiz» ein Kartenwerk in Form eines Kimaatlasses herausgeben. Es ist vorgesehen, sowohl kleinmaßstäbliche ...Klimaübersichtskarten im nationalen Raster als auch regionale Klimauntersuchungen für typische Räume unseres Landes in größeren Maßstäben darzustellen. Im vorliegenden Bericht wird das Projekt «Klimaatlas der Schweiz» vorgestellt. Dann folgt ein Überblick über grundsätzliche Fragen, wie sie bei der Bearbeitung langjähriger Meßreihen im Hinblick auf eine räumliche Darstellung auftreten. Die angeführten Sachfragen betreffend Messung, Aufbereitung und Darstellung von Klimadaten werden hernach am Beispiel der Lufttemperatur ausführlich dargelegt.
Abstract
Light-induced microbial electron transfer has potential for efficient production of value-added chemicals, biofuels and biodegradable materials owing to diversified metabolic pathways. ...However, most microbes lack photoactive proteins and require synthetic photosensitizers that suffer from photocorrosion, photodegradation, cytotoxicity, and generation of photoexcited radicals that are harmful to cells, thus severely limiting the catalytic performance. Therefore, there is a pressing need for biocompatible photoconductive materials for efficient electronic interface between microbes and electrodes. Here we show that living biofilms of
Geobacter sulfurreducens
use nanowires of cytochrome OmcS as intrinsic photoconductors. Photoconductive atomic force microscopy shows up to 100-fold increase in photocurrent in purified individual nanowires. Photocurrents respond rapidly (<100 ms) to the excitation and persist reversibly for hours. Femtosecond transient absorption spectroscopy and quantum dynamics simulations reveal ultrafast (~200 fs) electron transfer between nanowire hemes upon photoexcitation, enhancing carrier density and mobility. Our work reveals a new class of natural photoconductors for whole-cell catalysis.
Social support is a protective factor for siblings of children with neurodevelopmental disorders.
We reviewed studies on social support received by siblings of children with neurodevelopmental ...disorders.
We conducted a pre-registered systematic review (CRD42020207686), searching PsycINFO, MEDLINE, Web of Science, and Scopus.
Fifteen articles were eligible for the review, 13 of which used cross-sectional designs. Two studies investigated sibling social support after an intervention. Multiple variables were negatively related to social support (e.g., sibling depression, loneliness, stress). Variables that were positively related to social support included prosocial behavior, competence (academic, social, and activity-related), problem-focused coping, and family quality of life. Potential moderators of the relationship between social support and psychosocial adjustment included the type of disorder of the affected sibling and the type of social support provider. We conclude with an overview of the reliability and validity of the seven social support measurements used across the studies.
Lower levels of social support are associated with more negative psychosocial adjustment among siblings of children with neurodevelopmental disorders. We encourage future researchers to further investigate ways to increase social support for siblings to improve outcomes.
•Social support is an important protective factor for siblings of children with neurodevelopmental disorders.•Lower levels of social support have been linked to more negative psychosocial adjustment among these siblings.•Higher levels of social support were related to higher psychosocial functioning.•Siblings of children with autism reported lower social support compared to siblings of children with other disorders.•We found high heterogeneity in measures of social support in the selected studies.
Gut microbiota and their generated metabolites impact the host vascular phenotype. The metaorganismal metabolite trimethylamine N-oxide (TMAO) is both associated with adverse clinical thromboembolic ...events, and enhances platelet responsiveness in subjects. The impact of TMAO on vascular Tissue Factor (TF) in vivo is unknown. Here, we explore whether TMAO-enhanced thrombosis potential extends beyond TMAO effects on platelets, and is linked to TF. We also further explore the links between gut microbiota and vascular endothelial TF expression in vivo.
In initial exploratory clinical studies, we observed that among sequential stable subjects (n = 2989) on anti-platelet therapy undergoing elective diagnostic cardiovascular evaluation at a single-site referral centre, TMAO levels were associated with an increased incident (3 years) risk for major adverse cardiovascular events (MACE) (myocardial infarction, stroke, or death) 4th quartile (Q4) vs. Q1 adjusted hazard ratio (HR) 95% confidence interval (95% CI), 1.73 (1.25-2.38). Similar results were observed within subjects on aspirin mono-therapy during follow-up adjusted HR (95% CI) 1.75 (1.25-2.44), n = 2793. Leveraging access to a second higher risk cohort with previously reported TMAO data and monitoring of anti-platelet medication use, we also observed a strong association between TMAO and incident (1 year) MACE risk in the multi-site Swiss Acute Coronary Syndromes Cohort, focusing on the subset (n = 1469) on chronic dual anti-platelet therapy during follow-up adjusted HR (95% CI) 1.70 (1.08-2.69). These collective clinical data suggest that the thrombosis-associated effects of TMAO may be mediated by cells/factors that are not inhibited by anti-platelet therapy. To test this, we first observed in human microvascular endothelial cells that TMAO dose-dependently induced expression of TF and vascular cell adhesion molecule (VCAM)1. In mouse studies, we observed that TMAO-enhanced aortic TF and VCAM1 mRNA and protein expression, which upon immunolocalization studies, was shown to co-localize with vascular endothelial cells. Finally, in arterial injury mouse models, TMAO-dependent enhancement of in vivo TF expression and thrombogenicity were abrogated by either a TF-inhibitory antibody or a mechanism-based microbial choline TMA-lyase inhibitor (fluoromethylcholine).
Endothelial TF contributes to TMAO-related arterial thrombosis potential, and can be specifically blocked by targeted non-lethal inhibition of gut microbial choline TMA-lyase.
The photobioelectrochemical impact of a series of conjugated oligoelectrolytes (COEs) with a systematic progression of chemical structures was elucidated by their direct incorporation into thylakoid ...bioanodes. In both three-electrode electrochemical cells and bio-solar cell devices, significant anodic performance enhancements (p< 0.1) were observed when anodes were modified with certain COEs. Amperometric photocurrent densities increased by up to 2.3-fold for the best COE. In bio-solar cell devices, short-circuit photocurrent increased by up to 1.7-fold and short-circuit dark current increased by up to 1.4-fold, indicating that the best COEs enhance both photocurrent generation and interfacial electron transfer. Trends in these results indicate that the molecular length and pendant charge of COEs differentially contribute to photobioelectrochemical enhancements, and the optimal combination of these features is revealed. Control experiments indicate that COEs augment native thylakoid functionality, as COEs do not have redox activity or undergo chemical degradation.
An excess of free heme is present in the blood during many types of hemolytic anemia. This has been linked to organ damage caused by heme-mediated oxidative stress and vascular inflammation. We ...investigated the mechanism of heme-induced coagulation activation in vivo. Heme caused coagulation activation in wild-type mice that was attenuated by an anti-tissue factor antibody and in mice expressing low levels of tissue factor. In contrast, neither factor XI deletion nor inhibition of factor XIIa-mediated factor XI activation reduced heme-induced coagulation activation, suggesting that the intrinsic coagulation pathway is not involved. We investigated the source of tissue factor in heme-induced coagulation activation. Heme increased the procoagulant activity of mouse macrophages and human PBMCs. Tissue factor-positive staining was observed on leukocytes isolated from the blood of heme-treated mice but not on endothelial cells in the lungs. Furthermore, heme increased vascular permeability in the mouse lungs, kidney and heart. Deletion of tissue factor from either myeloid cells, hematopoietic or endothelial cells, or inhibition of tissue factor expressed by non-hematopoietic cells did not reduce heme-induced coagulation activation. However, heme-induced activation of coagulation was abolished when both non-hematopoietic and hematopoietic cell tissue factor was inhibited. Finally, we demonstrated that coagulation activation was partially attenuated in sickle cell mice treated with recombinant hemopexin to neutralize free heme. Our results indicate that heme promotes tissue factor-dependent coagulation activation and induces tissue factor expression on leukocytes in vivo. We also demonstrated that free heme may contribute to thrombin generation in a mouse model of sickle cell disease.
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