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Sökning: WFRF:(Soleimanpour H)

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  • Darabi, H., et al. (författare)
  • Development of a novel hybrid multi-boosting neural network model for spatial prediction of urban flood
  • 2021
  • Ingår i: Geocarto International. - : Taylor and Francis Ltd.. - 1010-6049 .- 1752-0762.
  • Tidskriftsartikel (refereegranskat)abstract
    • In this study, a new hybridized machine learning algorithm for urban flood susceptibility mapping, named MultiB-MLPNN, was developed using a multi-boosting technique and MLPNN. The model was tested in Amol City, Iran, a data-scarce city in an ungauged area which is prone to severe flood inundation events and currently lacks flood prevention infrastructure. Performance of the hybridized model was compared with that of a standalone MLPNN model, random forest and boosted regression trees. Area under the curve, efficiency, true skill statistic, Matthews correlation coefficient, misclassification rate, sensitivity and specificity were used to evaluate model performance. In validation, the MultiB-MLPNN model showed the best predictive performance. The hybridized MultiB-MLPNN model is thus useful for generating realistic flood susceptibility maps for data-scarce urban areas. The maps can be used to develop risk-reduction measures to protect urban areas from devastating floods, particularly where available data are insufficient to support physically based hydrological or hydraulic models.
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  • Soleimanpour, Scott A, et al. (författare)
  • The diabetes susceptibility gene clec16a regulates mitophagy.
  • 2014
  • Ingår i: Cell. - : Elsevier BV. - 1097-4172 .- 0092-8674. ; 157:7, s. 1577-1590
  • Tidskriftsartikel (refereegranskat)abstract
    • Clec16a has been identified as a disease susceptibility gene for type 1 diabetes, multiple sclerosis, and adrenal dysfunction, but its function is unknown. Here we report that Clec16a is a membrane-associated endosomal protein that interacts with E3 ubiquitin ligase Nrdp1. Loss of Clec16a leads to an increase in the Nrdp1 target Parkin, a master regulator of mitophagy. Islets from mice with pancreas-specific deletion of Clec16a have abnormal mitochondria with reduced oxygen consumption and ATP concentration, both of which are required for normal β cell function. Indeed, pancreatic Clec16a is required for normal glucose-stimulated insulin release. Moreover, patients harboring a diabetogenic SNP in the Clec16a gene have reduced islet Clec16a expression and reduced insulin secretion. Thus, Clec16a controls β cell function and prevents diabetes by controlling mitophagy. This pathway could be targeted for prevention and control of diabetes and may extend to the pathogenesis of other Clec16a- and Parkin-associated diseases.
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