64 research outputs found
An Observational Overview of Solar Flares
We present an overview of solar flares and associated phenomena, drawing upon
a wide range of observational data primarily from the RHESSI era. Following an
introductory discussion and overview of the status of observational
capabilities, the article is split into topical sections which deal with
different areas of flare phenomena (footpoints and ribbons, coronal sources,
relationship to coronal mass ejections) and their interconnections. We also
discuss flare soft X-ray spectroscopy and the energetics of the process. The
emphasis is to describe the observations from multiple points of view, while
bearing in mind the models that link them to each other and to theory. The
present theoretical and observational understanding of solar flares is far from
complete, so we conclude with a brief discussion of models, and a list of
missing but important observations.Comment: This is an article for a monograph on the physics of solar flares,
inspired by RHESSI observations. The individual articles are to appear in
Space Science Reviews (2011
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Target Organs in Chronic Bioassays fo 533 Chemical Carcinogens
Recommended from our members
Target Organs in Chronic Bioassays fo 533 Chemical Carcinogens
INCREASE OF DNA POLYMERASE ACTIVITY FIRMLY BOUND TO NUCLEI DURING THE DNA SYNTHETIC PHASE OF THE CELL CYCLE
Contesting the brand: a media analysis of the image of Rio de Janeiro as host of the 2016 Summer Olympics in Dutch language newspapers
Heterozygous de novo variants in <em>CSNK1G1</em> are associated with syndromic developmental delay and autism spectrum disorder.
The gamma-1 isoform of casein kinase 1, the protein encoded byCSNK1G1, is involved in the growth and morphogenesis of cells. This protein is expressed ubiquitously among many tissue types, including the brain, where it regulates the phosphorylation of N-methyl-D-aspartate receptors and plays a role in synaptic transmission. One prior individual with a de novo variant inCSNK1Gpresenting with severe developmental delay and early-onset epilepsy has been reported. Here we report an updated clinical history of this previously published case, as well as four additional individuals with de novo variants inCSNK1G1identified via microarray-based comparative genomic hybridization, exome, or genome sequencing. All individuals (n = 5) had developmental delay. At least three individuals had diagnoses of autism spectrum disorder. All participants were noted to have dysmorphic facial features, although the reported findings varied widely and therefore may not clearly be recognizable. None of the participants had additional major malformations. Taken together, our data suggest thatCSNK1G1may be a cause of syndromic developmental delay and possibly autism spectrum disorder
Changing the Face of Reference: Adapting Biomedical and Health Information Services for the Classroom, Clinic, and Beyond
Heterozygous variants in PRPF8 are associated with neurodevelopmental disorders
The pre-mRNA-processing factor 8, encoded by PRPF8, is a scaffolding component of a spliceosome complex involved in the removal of introns from mRNA precursors. Previously, heterozygous pathogenic variants in PRPF8 have been associated with autosomal dominant retinitis pigmentosa. More recently, PRPF8 was suggested as a candidate gene for autism spectrum disorder due to the enrichment of sequence variants in this gene in individuals with neurodevelopmental disorders. We report 14 individuals with various forms of neurodevelopmental conditions, found to have heterozygous, predominantly de novo, missense, and loss-of-function variants in PRPF8. These individuals have clinical features that may represent a new neurodevelopmental syndrome
Peripheral priming induces plastic transcriptomic and proteomic responses in circulating neutrophils required for pathogen containment
Neutrophils rapidly respond to inflammation and infection, but to which degree their functional trajectories after mobilization from the bone marrow are shaped within the circulation remains vague. Experimental limitations have so far hampered neutrophil research in human disease. Here, using innovative fixation and single-cell-based toolsets, we profile human and murine neutrophil transcriptomes and proteomes during steady state and bacterial infection. We find that peripheral priming of circulating neutrophils leads to dynamic shifts dominated by conserved up-regulation of antimicrobial genes across neutrophil substates, facilitating pathogen containment. We show the TLR4/NF-κB signaling-dependent up-regulation of canonical neutrophil activation markers like CD177/NB-1 during acute inflammation, resulting in functional shifts in vivo. Blocking de novo RNA synthesis in circulating neutrophils abrogates these plastic shifts and prevents the adaptation of antibacterial neutrophil programs by up-regulation of distinct effector molecules upon infection. These data underline transcriptional plasticity as a relevant mechanism of functional neutrophil reprogramming during acute infection to foster bacterial containment within the circulation
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