23 research outputs found

    ‘Help for trauma from the app stores?’ A systematic review and standardised rating of apps for Post-Traumatic Stress Disorder (PTSD)

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    Background: Mobile health applications (apps) are considered to complement traditional psychological treatments for Post-Traumatic Stress Disorder (PTSD). However, the use for clinical practice and quality of available apps is unknown. Objective: To assess the general characteristics, therapeutic background, content, and quality of apps for PTSD and to examine their concordance with established PTSD treatment and self-help methods. Method: A web crawler systematically searched for apps targeting PTSD in the British Google Play and Apple iTunes stores. Two independent researchers rated the apps using the Mobile App Rating Scale (MARS). The content of high-quality apps was checked for concordance with psychological treatment and self-help methods extracted from current literature on PTSD treatment. Results: Out of 555 identified apps, 69 met the inclusion criteria. The overall app quality based on the MARS was medium (M = 3.36, SD = 0.65). Most apps (50.7%) were based on cognitive behavioural therapy and offered a wide range of content, including established psychological PTSD treatment methods such as processing of trauma-related emotions and beliefs, relaxation exercises, and psychoeducation. Notably, data protection and privacy standards were poor in most apps and only one app (1.4%) was scientifically evaluated in a randomized controlled trial. Conclusions: High-quality apps based on established psychological treatment techniques for PTSD are available in commercial app stores. However, users are confronted with great difficulties in identifying useful high-quality apps and most apps lack an evidence-base. Commercial distribution channels do not exploit the potential of apps to complement the psychological treatment of PTSD

    No Evidence of Persisting Unrepaired Nuclear DNA Single Strand Breaks in Distinct Types of Cells in the Brain, Kidney, and Liver of Adult Mice after Continuous Eight-Week 50 Hz Magnetic Field Exposure with Flux Density of 0.1 mT or 1.0 mT

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    BACKGROUND: It has been hypothesized in the literature that exposure to extremely low frequency electromagnetic fields (50 or 60 Hz) may lead to human health effects such as childhood leukemia or brain tumors. In a previous study investigating multiple types of cells from brain and kidney of the mouse (Acta Neuropathologica 2004; 107: 257-264), we found increased unrepaired nuclear DNA single strand breaks (nDNA SSB) only in epithelial cells of the choroid plexus in the brain using autoradiographic methods after a continuous eight-week 50 Hz magnetic field (MF) exposure of adult mice with flux density of 1.5 mT. METHODS: In the present study we tested the hypothesis that MF exposure with lower flux densities (0.1 mT, i.e., the actual exposure limit for the population in most European countries, and 1.0 mT) shows similar results to those in the previous study. Experiments and data analysis were carried out in a similar way as in our previous study. RESULTS: Continuous eight-week 50 Hz MF exposure with 0.1 mT or 1.0 mT did not result in increased persisting unrepaired nDNA SSB in distinct types of cells in the brain, kidney, and liver of adult mice. MF exposure with 1.0 mT led to reduced unscheduled DNA synthesis (UDS) in epithelial cells in the choroid plexus of the fourth ventricle in the brain (EC-CP) and epithelial cells of the cortical collecting duct in the kidney, as well as to reduced mtDNA synthesis in neurons of the caudate nucleus in the brain and in EC-CP. CONCLUSION: No evidence was found for increased persisting unrepaired nDNA SSB in distinct types of cells in the brain, kidney, and liver of adult mice after continuous eight-week 50 Hz magnetic field exposure with flux density of 0.1 mT or 1.0 mT

    The European Reference Genome Atlas: piloting a decentralised approach to equitable biodiversity genomics.

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    ABSTRACT: A global genome database of all of Earth’s species diversity could be a treasure trove of scientific discoveries. However, regardless of the major advances in genome sequencing technologies, only a tiny fraction of species have genomic information available. To contribute to a more complete planetary genomic database, scientists and institutions across the world have united under the Earth BioGenome Project (EBP), which plans to sequence and assemble high-quality reference genomes for all ∼1.5 million recognized eukaryotic species through a stepwise phased approach. As the initiative transitions into Phase II, where 150,000 species are to be sequenced in just four years, worldwide participation in the project will be fundamental to success. As the European node of the EBP, the European Reference Genome Atlas (ERGA) seeks to implement a new decentralised, accessible, equitable and inclusive model for producing high-quality reference genomes, which will inform EBP as it scales. To embark on this mission, ERGA launched a Pilot Project to establish a network across Europe to develop and test the first infrastructure of its kind for the coordinated and distributed reference genome production on 98 European eukaryotic species from sample providers across 33 European countries. Here we outline the process and challenges faced during the development of a pilot infrastructure for the production of reference genome resources, and explore the effectiveness of this approach in terms of high-quality reference genome production, considering also equity and inclusion. The outcomes and lessons learned during this pilot provide a solid foundation for ERGA while offering key learnings to other transnational and national genomic resource projects.info:eu-repo/semantics/publishedVersio

    Einfluss einer achtwöchigen 50-Hz-Magnetfeld-Exposition auf DNA-Reparatur und mitochondriale DNA-Synthese von Sammelrohr-Epithelzellen der Niere

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    1) Currently no generally accepted scientific model on the long-term effects of weak electromagnetic fields exists. Therefore, there is a considerable demand for a better analysis of the impact of electromagnetic fields on living organisms. To do this, a mouse model was used to elucidate the question whether a nuclear exposure to a 50 Hz magnetic field over a period of eight weeks causes DNA-damage and influences mitochondrial mtDNS-synthesis.2) Altogether, 81 male, seven months old mice were exposed over a period of eight weeks to a magnetic field (MF) of 50 Hz with a magnetic flux density of 0,1 and 1 mT, or they were sham-exposed. Following the exposure to the magnetic field, 3H-thymidine (3H-TdR) was injected. Depending on the subgroup, this was either done five minutes, 24 hours or seven days after the end of MF exposure. This way, a) the nuclear (n) DNA repair synthetic rate (so-called unscheduled DNA-synthesis, UDS) for measuring MF-induced nDNA damage as well as b) the mtDNA synthetic rate as an indicator of metabolic cell activity was examined cell-type specifically in situ. After considering the background labelling, normalization to nuclear DNA content as well as determination of the cytoplasmatic grain densities the measured data of different cell types were directly comparable. 115 minutes after the injection of 3H-TdR the mice were narcotized and subsequently sacrifized through perfusion fixation. Autoradiograms were prepared from paraffin sections of the kidneys and afterwards microscopically evaluated with the help of the computer program „Discus“. For that, 100 successive kidney collecting tubule cells and their adjacent cytoplasm in medulla and cortex were analyzed in view of grain counts and the nuclear as well as cytoplasmatic profile areas. Finally, cumulative frequency distributions of the grain counts were drawn. On the basis of these graphs, mice that were suspected to be affected by artifacts were taken out of the assessment. 3) Univariance analysis showed a statistically significant result only for nDNA-repair of epithelial cells of the cortical collecting tubule regarding the applied MF dose. However, this could not be substantiated when considering a Bonferroni correction. This means that one has to expect nDNA damage in these cell types after exposure to a magnetic field. As there is no indication for MF induced nDNA damage after 24 hours and seven days after the end of MF exposure, one can assume that existing damage is repaired within a short period of time (< 24 hours). 4) Regarding mtDNA synthesis measurements and the corresponding metabolic cell activity, only the univariance analysis generated significant results for the variables “dose” and “time of 3H-TdR-injection” of cortical collecting tubule cells. These results could not be confirmed with post-hoc t-tests. A linear regression analysis including the data of Freuding (2004), which were generated using the same method for a dose of 1,5 mT, showed a dose-dependant significant raise of the metabolic cell activity for the range between 0,1 and 1,5 mT five minutes after the end of MF exposure. This coincides with Freuding’s (2004) data that showed 5 minutes after ending the magnetic exposure a significant difference between the mice that were exposed to a 1,5 mT magnetic field and the controls. No evidence for a longer lasting effect could be found. 5) The range of the obtained data within the test groups was remarkably higher than it was in the previous analysis of Freuding (2004) after a MF exposure of 1,5 mT. This might contribute to the fact that no significant correlations could be found

    Einfluss einer achtwöchigen 50-Hz-Magnetfeld-Exposition auf DNA-Reparatur und mitochondriale DNA-Synthese von Sammelrohr-Epithelzellen der Niere

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    1) Currently no generally accepted scientific model on the long-term effects of weak electromagnetic fields exists. Therefore, there is a considerable demand for a better analysis of the impact of electromagnetic fields on living organisms. To do this, a mouse model was used to elucidate the question whether a nuclear exposure to a 50 Hz magnetic field over a period of eight weeks causes DNA-damage and influences mitochondrial mtDNS-synthesis.2) Altogether, 81 male, seven months old mice were exposed over a period of eight weeks to a magnetic field (MF) of 50 Hz with a magnetic flux density of 0,1 and 1 mT, or they were sham-exposed. Following the exposure to the magnetic field, 3H-thymidine (3H-TdR) was injected. Depending on the subgroup, this was either done five minutes, 24 hours or seven days after the end of MF exposure. This way, a) the nuclear (n) DNA repair synthetic rate (so-called unscheduled DNA-synthesis, UDS) for measuring MF-induced nDNA damage as well as b) the mtDNA synthetic rate as an indicator of metabolic cell activity was examined cell-type specifically in situ. After considering the background labelling, normalization to nuclear DNA content as well as determination of the cytoplasmatic grain densities the measured data of different cell types were directly comparable. 115 minutes after the injection of 3H-TdR the mice were narcotized and subsequently sacrifized through perfusion fixation. Autoradiograms were prepared from paraffin sections of the kidneys and afterwards microscopically evaluated with the help of the computer program „Discus“. For that, 100 successive kidney collecting tubule cells and their adjacent cytoplasm in medulla and cortex were analyzed in view of grain counts and the nuclear as well as cytoplasmatic profile areas. Finally, cumulative frequency distributions of the grain counts were drawn. On the basis of these graphs, mice that were suspected to be affected by artifacts were taken out of the assessment. 3) Univariance analysis showed a statistically significant result only for nDNA-repair of epithelial cells of the cortical collecting tubule regarding the applied MF dose. However, this could not be substantiated when considering a Bonferroni correction. This means that one has to expect nDNA damage in these cell types after exposure to a magnetic field. As there is no indication for MF induced nDNA damage after 24 hours and seven days after the end of MF exposure, one can assume that existing damage is repaired within a short period of time (< 24 hours). 4) Regarding mtDNA synthesis measurements and the corresponding metabolic cell activity, only the univariance analysis generated significant results for the variables “dose” and “time of 3H-TdR-injection” of cortical collecting tubule cells. These results could not be confirmed with post-hoc t-tests. A linear regression analysis including the data of Freuding (2004), which were generated using the same method for a dose of 1,5 mT, showed a dose-dependant significant raise of the metabolic cell activity for the range between 0,1 and 1,5 mT five minutes after the end of MF exposure. This coincides with Freuding’s (2004) data that showed 5 minutes after ending the magnetic exposure a significant difference between the mice that were exposed to a 1,5 mT magnetic field and the controls. No evidence for a longer lasting effect could be found. 5) The range of the obtained data within the test groups was remarkably higher than it was in the previous analysis of Freuding (2004) after a MF exposure of 1,5 mT. This might contribute to the fact that no significant correlations could be found

    Supplemental screening ultrasound increases cancer detection yield in BRCA1 and BRCA2 mutation carriers

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    This study aimed at evaluating the efficacy of ultrasound for the early detection of breast cancers in BRCA1/2 mutation carriers. Between 01/1997 and 10/2008 221 BRCA1/2 mutation carriers participated in a breast cancer screening program which included semi-annual ultrasound in combination with annual mammography and magnetic resonance imaging (MRI). Women underwent on average (median) five semi-annual screening rounds with a range of one to 22 appointments, totaling 1,855 rounds of screening. All three imaging modalities were coded according to the American College of Radiology (BI-RADS classification). In total, we detected 27 BRCA-associated breast cancers in 25 patients. The sensitivity was 77 % for ultrasound, 27 % for mammography, and 100 % for MRI. Three tumors were detected directly as a result of only the semi-annual ultrasound screen. Due to the specific tumor morphology and the considerably elevated tumor doubling time, mutation carriers benefit from the addition of semi-annual ultrasound screening as a sensitive and cost-effective method
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