In this paper a novel clustering algorithm is proposed as a version of the Seeded Region Growing (SRG) approach for the automatic recognition of coastal upwelling from Sea Surface Temperature (SST) images. The new algorithm, One Seed Expanding Cluster (SEC), takes advantage of the concept of approximate clustering due to Mirkin (1996, 2013) to derive a homogeneity criterion in the format of a product rather than the conventional difference between a pixel value and the mean of values over the region of interest. It involves a boundary-oriented pixel labeling so that the cluster growing is performed by expanding its boundary iteratively. The starting point is a cluster consisting of just one seed, the pixel with the cold est temperature. The baseline version of the SEC algorithm uses the Otsu’s thresholding method to fine-tune the homogeneity threshold. Unfortunately, this method does not always lead to a satisfactory solution. Therefore, we introduce a self-tuning version of the algorithm in which the homogeneity threshold parameter is abolished and the similarity threshold derived from the approximation criterion also serves as a homogeneity parameter.
Ribosomal protein S2 is an essential component of translation machinery, and its viable mutated variants conferring distinct phenotypes serve as a valuable tool in studying the role of S2 in translation regulation. One of a few available rpsB mutants, rpsB1, shows thermosensitivity and ensures enhanced expression of leaderless mRNAs. In this study, we identified the nature of the rpsB1 mutation. Sequencing of the rpsB1 allele revealed a G-to-A transition in the part of the rpsB gene which encodes a coiled-coil domain of S2. The resulting E132K substitution resides in a highly conserved site, TKKE, a so-called N-terminal capping box, at the beginning of the second alpha helix. The protruding coiled-coil domain of S2 is known to provide binding with 16S rRNA in the head of the 30S subunit and, in addition, to interact with a key mRNA binding protein, S1. Molecular dynamics simulations revealed a detrimental impact of the E132K mutation on the coiled-coil structure and thereby on the interactions between S2 and 16S rRNA, providing a clue for the thermosensitivity of the rpsB1 mutant. Using a strain producing a leaderless lacZ transcript from the chromosomal lac promoter, we demonstrated that not only the rpsB1 mutation generating S2/S1-deficient ribosomes but also the rpsA::IS10 mutation leading to partial deficiency in S1 alone increased translation efficiency of the leaderless mRNA by about 10-fold. Moderate overexpression of S1 relieved all these effects and, moreover, suppressed the thermosensitive phenotype of rpsB1, indicating the role of S1 as an extragenic suppressor of the E132K mutation.
В статье представлены данные по количественному анализу незаконного, несообщаемого и нерегулируемого промысла (ННН-промысла) осетровых и прилова в браконьерских сетях каспийского тюленя в Дагестане и дельте реки Волга. В основу сбора данных были положены полуструктурированный тип интервью, прямое наблюдение и неформальные беседы. Результаты исследования свидетельствуют, что за 35 поездок, совершённых 15 бригадами рыбаков, специализирующихся на ННН-промысле осетровых, в период с 2013 по 2016 годы было выловлено 10491 кг осетровых и 788 тюленей (как прилов в браконьерских сетях). Результаты показывают, что уловы осетровых и прилов тюленя в браконьерских сетях не изменились за три года исследований (2013-2016 гг.). Однако величина прилова каспийского тюленя при ННН-промысле осетровых увеличилась со времени последнего исследования, проведённого в 2008-2009 годах, и может быть признана одной из самых больших в мире среди приловов, выявленных для ластоногих.
BACKGROUND: World mapping is an important tool to visualize stroke burden and its trends in various regions and countries. OBJECTIVES: To show geographic patterns of incidence, prevalence, mortality, disability-adjusted life years (DALYs) and years lived with disability (YLDs) and their trends for ischemic stroke and hemorrhagic stroke in the world for 1990-2013. METHODOLOGY: Stroke incidence, prevalence, mortality, DALYs and YLDs were estimated following the general approach of the Global Burden of Disease (GBD) 2010 with several important improvements in methods. Data were updated for mortality (through April 2014) and stroke incidence, prevalence, case fatality and severity through 2013. Death was estimated using an ensemble modeling approach. A new software package, DisMod-MR 2.0, was used as part of a custom modeling process to estimate YLDs. All rates were age-standardized to new GBD estimates of global population. All estimates have been computed with 95% uncertainty intervals. RESULTS: Age-standardized incidence, mortality, prevalence and DALYs/YLDs declined over the period from 1990 to 2013. However, the absolute number of people affected by stroke has substantially increased across all countries in the world over the same time period, suggesting that the global stroke burden continues to increase. There were significant geographical (country and regional) differences in stroke burden in the world, with the majority of the burden borne by low- and middle-income countries. CONCLUSIONS: Global burden of stroke has continued to increase in spite of dramatic declines in age-standardized incidence, prevalence, mortality rates and disability. Population growth and aging have played an important role in the observed increase in stroke burden.
Single-point mutations in the transmembrane (TM) region of receptor tyrosine kinases (RTKs) can lead to abnormal ligand-independent activation. We use a combination of computational modeling, NMR spectroscopy and cell experiments to analyze in detail the mechanism of how TM domains contribute to the activation of wild-type (WT) PDGFRA and its oncogenic V536E mutant. Using a computational framework, we scan all positions in PDGFRA TM helix for identification of potential functional mutations for the WT and the mutant and reveal the relationship between the receptor activity and TM dimerization via different interfaces. This strategy also allows us design a novel activating mutation in the WT (I537D) and a compensatory mutation in the V536E background eliminating its constitutive activity (S541G). We show both computationally and experimentally that single-point mutations in the TM region reshape the TM dimer ensemble and delineate the structural and dynamic determinants of spontaneous activation of PDGFRA via its TM domain. Our atomistic picture of the coupling between TM dimerization and PDGFRA activation corroborates the data obtained for other RTKs and provides a foundation for developing novel modulators of the pathological activity of PDGFRA.