331 research outputs found

    Absorption of sunlight in the atmosphere of Venus

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    The profiles of upward, downward and net solar flux on Venus were measured at altitudes from about 62 km to the surface in three spectral bands at a vertical resolution of a few hundred meters. These data measured the penetration and absorption of solar energy in Venus' lower atmosphere quantities that are essential in evaluating the role of the greenhouse mechanism in supporting Venus' remarkably high surface temperature. In addition, the data constrained the vertical structure and optical properties of the Venus clouds

    The single scattering phase functions of Jupiter's clouds

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    The determination of the single scattering phase functions of Jupiter's clouds and a thin upper haze by Tomasko et al. was refined and extended to seven latitudes in blue and red light. The phase function is well-constrained by the Pioneer 10 and 11 photometric data sets. Multiple scattering models were computed to match the limb darkening at each latitude at up to 15 phase angles from 12 deg to 151 deg. Ground-based observations were used for absolute calibration and to extend the data to lower phase angles. The phase functions were parameterized using the double Henyey-Greenstein function. The three Henyey-Greenstein parameters and the single scattering albedo were determined using a non-linear least squares method for the haze and the clouds below. The phase functions derived for the northen zone and belt are remarkably similar to the phase functions of the corresponding regions in the south, with most of the differences in brightness of the northern and southern features resulting from minor differences in single scattering albedo. Analysis of the Equatorial Region is complicated by the presence of numerous small features, but the phase function required is generally similar to that seen in the more homogeneous regions. Details of the phase functions of the haze and clouds are presented, and the differences between the cloud phase functions at low and high latitudes in red and blue light are discussed

    Hydrogen-Bond Driven Loop-Closure Kinetics in Unfolded Polypeptide Chains

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    Characterization of the length dependence of end-to-end loop-closure kinetics in unfolded polypeptide chains provides an understanding of early steps in protein folding. Here, loop-closure in poly-glycine-serine peptides is investigated by combining single-molecule fluorescence spectroscopy with molecular dynamics simulation. For chains containing more than 10 peptide bonds loop-closing rate constants on the 20–100 nanosecond time range exhibit a power-law length dependence. However, this scaling breaks down for shorter peptides, which exhibit slower kinetics arising from a perturbation induced by the dye reporter system used in the experimental setup. The loop-closure kinetics in the longer peptides is found to be determined by the formation of intra-peptide hydrogen bonds and transient β-sheet structure, that accelerate the search for contacts among residues distant in sequence relative to the case of a polypeptide chain in which hydrogen bonds cannot form. Hydrogen-bond-driven polypeptide-chain collapse in unfolded peptides under physiological conditions found here is not only consistent with hierarchical models of protein folding, that highlights the importance of secondary structure formation early in the folding process, but is also shown to speed up the search for productive folding events

    Genome-Wide Copy Number Variation in Epilepsy: Novel Susceptibility Loci in Idiopathic Generalized and Focal Epilepsies

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    Epilepsy is one of the most common neurological disorders in humans with a prevalence of 1% and a lifetime incidence of 3%. Several genes have been identified in rare autosomal dominant and severe sporadic forms of epilepsy, but the genetic cause is unknown in the vast majority of cases. Copy number variants (CNVs) are known to play an important role in the genetic etiology of many neurodevelopmental disorders, including intellectual disability (ID), autism, and schizophrenia. Genome-wide studies of copy number variation in epilepsy have not been performed. We have applied whole-genome oligonucleotide array comparative genomic hybridization to a cohort of 517 individuals with various idiopathic, non-lesional epilepsies. We detected one or more rare genic CNVs in 8.9% of affected individuals that are not present in 2,493 controls; five individuals had two rare CNVs. We identified CNVs in genes previously implicated in other neurodevelopmental disorders, including two deletions in AUTS2 and one deletion in CNTNAP2. Therefore, our findings indicate that rare CNVs are likely to contribute to a broad range of generalized and focal epilepsies. In addition, we find that 2.9% of patients carry deletions at 15q11.2, 15q13.3, or 16p13.11, genomic hotspots previously associated with ID, autism, or schizophrenia. In summary, our findings suggest common etiological factors for seemingly diverse diseases such as ID, autism, schizophrenia, and epilepsy

    a direct encoding for nnc polyhedra

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    We present an alternative Double Description representation for the domain of NNC (not necessarily closed) polyhedra, together with the corresponding Chernikova-like conversion procedure. The representation uses no slack variable at all and provides a solution to a few technical issues caused by the encoding of an NNC polyhedron as a closed polyhedron in a higher dimension space. A preliminary experimental evaluation shows that the new conversion algorithm is able to achieve significant efficiency improvements

    Mutational mechanisms shaping the coding and noncoding genome of germinal center derived B-cell lymphomas

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    B cells have the unique property to somatically alter their immunoglobulin (IG) genes by V(D)J recombination, somatic hypermutation (SHM) and class-switch recombination (CSR). Aberrant targeting of these mechanisms is implicated in lymphomagenesis, but the mutational processes are poorly understood. By performing whole genome and transcriptome sequencing of 181 germinal center derived B-cell lymphomas (gcBCL) we identified distinct mutational signatures linked to SHM and CSR. We show that not only SHM, but presumably also CSR causes off-target mutations in non-IG genes. Kataegis clusters with high mutational density mainly affected early replicating regions and were enriched for SHM- and CSR-mediated off-target mutations. Moreover, they often co-occurred in loci physically interacting in the nucleus, suggesting that mutation hotspots promote increased mutation targeting of spatially co-localized loci (termed hypermutation by proxy). Only around 1% of somatic small variants were in protein coding sequences, but in about half of the driver genes, a contribution of B-cell specific mutational processes to their mutations was found. The B-cell-specific mutational processes contribute to both lymphoma initiation and intratumoral heterogeneity. Overall, we demonstrate that mutational processes involved in the development of gcBCL are more complex than previously appreciated, and that B cell-specific mutational processes contribute via diverse mechanisms to lymphomagenesis
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