87 research outputs found

    General knowledge about climate change, factors influencing risk perception and willingness to insure

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    In two empirical surveys in Germany the link between the information respondents have about climate change and their risk perception of the phenomenon was analysed. We found that a better understanding of the effects of climate change might lead to a decrease of the perceived hazard. In contrast, a high self-declared knowledge about climate change might correspond with higher risk perception. Further factors affecting the risk perception of climate change are gender, experience of extreme weather events and trust in external aid. Surprisingly, information campaigns based on scientific facts are not effective for increasing risk perception and willingness to insure. Higher risk perception might induce higher interest in precautionary measures like insurance. --Climate Change,Knowledge Illusion,Insurance,Risk Perception,Information,Psychometric paradigm

    General knowledge about climate change, factors influencing risk perception and willingness to insure

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    In two empirical surveys in Germany the link between the information respondents have about climate change and their risk perception of the phenomenon was analysed. We found that a better understanding of the effects of climate change might lead to a decrease of the perceived hazard. In contrast, a high self-declared knowledge about climate change might correspond with higher risk perception. Further factors affecting the risk perception of climate change are gender, experience of extreme weather events and trust in external aid. Surprisingly, information campaigns based on scientific facts are not effective for increasing risk perception and willingness to insure. Higher risk perception might induce higher interest in precautionary measures like insurance

    Rathke's Cleft Cyst Abscess with a Very Unusual Course

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    Infected Rathke's cleft cysts (RCC) are extremely rare with only a few published cases. We report the case of a 31-year-old man who presented with headaches, visual disturbance, and hypopituitarism secondary to an infected RCC with extension of abscesses along the optic tract. Magnetic resonance imaging showed ring enhancing cystic lesions within an expanded sella with suprasellar and intraparenchymal extension. The radiological appearance suggested a high-grade optic glioma, but an endoscopic transsphenoidal biopsy revealed frank pus in the pituitary fossa, which subsequently grew Staphylococcus aureus . Pathological examination of the cyst wall showed an inflamed RCC. Following a prolonged course of intravenous antibiotics, the infection resolved and vision improved. RCC abscesses are rare and the intracranial extension of the infection in our case makes it unique

    Characterization of coatings for straylight and photoluminescence suppression in the Raman Spectrometer for MMX (RAX)

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    The Martian Moons eXploration (MMX) mission led by JAXA to Mars moons Phobos and Deimos involves a small rover developed by DLR/CNES that will be operating on Phobos’ surface. Aboard it is the Raman Spectrometer for MMX (RAX), whose main scientific objectives address Phobos surface mineralogy, its heterogeneity and relation to the Mars mineralogy. Raman spectrometers require strong suppression of straylight, since this technique operates with few nano-Watt signals that should have significant contrast to all other sources of light inside the instrument. The mission requirements involving RAX call for a compact and sophisticated optical design, precluding space for straylight suppressive elements. To optimize straylight suppression in RAX, Raman scattering, Photoluminescence and reflection were characterized for candidate coatings representing different absorbing materials and fabrication technologies over spectral ranges between 530 nm and 680 nm. This was complimented by mechanical testing to aid selection of the coatings for parts inside the RAX flight model

    Adults with RRM2B-related mitochondrial disease have distinct clinical and molecular characteristics.

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    Mutations in the nuclear-encoded mitochondrial maintenance gene RRM2B are an important cause of familial mitochondrial disease in both adults and children and represent the third most common cause of multiple mitochondrial DNA deletions in adults, following POLG [polymerase (DNA directed), gamma] and PEO1 (now called C10ORF2, encoding the Twinkle helicase) mutations. However, the clinico-pathological and molecular features of adults with RRM2B-related disease have not been clearly defined. In this multicentre study of 26 adult patients from 22 independent families, including five additional cases published in the literature, we show that extra-ocular neurological complications are common in adults with genetically confirmed RRM2B mutations. We also demonstrate a clear correlation between the clinical phenotype and the underlying genetic defect. Myopathy was a prominent manifestation, followed by bulbar dysfunction and fatigue. Sensorineural hearing loss and gastrointestinal disturbance were also important findings. Severe multisystem neurological disease was associated with recessively inherited compound heterozygous mutations with a mean age of disease onset at 7 years. Dominantly inherited heterozygous mutations were associated with a milder predominantly myopathic phenotype with a later mean age of disease onset at 46 years. Skeletal muscle biopsies revealed subsarcolemmal accumulation of mitochondria and/or cytochrome c oxidase-deficient fibres. Multiple mitochondrial DNA deletions were universally present in patients who underwent a muscle biopsy. We identified 18 different heterozygous RRM2B mutations within our cohort of patients, including five novel mutations that have not previously been reported. Despite marked clinical overlap between the mitochondrial maintenance genes, key clinical features such as bulbar dysfunction, hearing loss and gastrointestinal disturbance should help prioritize genetic testing towards RRM2B analysis, and sequencing of the gene may preclude performance of a muscle biopsy

    Oligosarcomas, IDH‑mutant are distinct and aggressive

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    Oligodendrogliomas are defined at the molecular level by the presence of an IDH mutation and codeletion of chromosomal arms 1p and 19q. In the past, case reports and small studies described gliomas with sarcomatous features arising from oligodendrogliomas, so called oligosarcomas. Here, we report a series of 24 IDH-mutant oligosarcomas from 23 patients forming a distinct methylation class. The tumors were recurrences from prior oligodendrogliomas or developed de novo. Precursor tumors of 12 oligosarcomas were histologically and molecularly indistinguishable from conventional oligodendrogliomas. Oligosarcoma tumor cells were embedded in a dense network of reticulin fibers, frequently showing p53 accumulation, positivity for SMA and CALD1, loss of OLIG2 and gain of H3K27 trimethylation (H3K27me3) as compared to primary lesions. In 5 oligosarcomas no 1p/19q codeletion was detectable, although it was present in the primary lesions. Copy number neutral LOH was determined as underlying mechanism. Oligosarcomas harbored an increased chromosomal copy number variation load with frequent CDKN2A/B deletions. Proteomic profiling demonstrated oligosarcomas to be highly distinct from conventional CNS WHO grade 3 oligodendrogliomas with consistent evidence for a smooth muscle differentiation. Expression of several tumor suppressors was reduced with NF1 being lost frequently. In contrast, oncogenic YAP1 was aberrantly overexpressed in oligosarcomas. Panel sequencing revealed mutations in NF1 and TP53 along with IDH1/2 and TERT promoter mutations. Survival of patients was significantly poorer for oligosarcomas as first recurrence than for grade 3 oligodendrogliomas as first recurrence. These results establish oligosarcomas as a distinct group of IDH-mutant gliomas differing from conventional oligodendrogliomas on the histologic, epigenetic, proteomic, molecular and clinical level. The diagnosis can be based on the combined presence of (a) sarcomatous histology, (b) IDH-mutation and (c) TERT promoter mutation and/or 1p/19q codeletion, or, in unresolved cases, on its characteristic DNA methylation profile
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