Anti-SELE monoclonal antibody, clone 2.3C7 [FITC]

Until now, sedimentary DNA (sedDNA) studies have only focused on cold and temperate regions were DNA is relatively well preserved. Consequently, the tropics, where vegetation is hyperdiverse and natural archives are rare, have been neglected and deserve attention. In this study, we used next-generation sequencing to barcode sedDNA from Lake Sele, localized in the tropical lowlands of Benin (Africa), and compared the taxonomic diversity detected by DNA analyses with pollen assemblages. Plant sedDNA was successfully amplified from 33 of the 34 successfully extracted samples. In total, 43 taxa were identified along the 5000 years spanned by the sediment: 22 taxa were identified at the family level and 21 at the genus level. The plant diversity recovered through sedDNA from Lake Sele showed a specific local signal and limited overlapping with pollen. Introduced plants, grown and cultivated close to the water, such as sweet potato, were also well recorded by sedDNA. It appears, therefore, to be a promising approach to studying past diversity in tropical regions, and could help in tracking the introduction and history of agriculture. This is the first time this method has been used in the field of domestication and dissemination of several specific crops, and the results are very encouraging. (C) 2017 Elsevier Ltd. All rights reserved.

Background: Neuroprotection studies are generally unable to demonstrate efficacy in humans. Our specific hypothesis is that multiple pathophysiologic pathways, of variable importance, contribute to ischemic brain damage. As a corollary to this, we discuss the broad hypothesis that a multifaceted approach will improve the probability of efficacious neuroprotection. But to properly test this hypothesis the nature and importance of the multiple contributing pathways needs elucidation. Our aim is to demonstrate, using functional genomics, in human cardiac surgery procedures associated with cerebral ischemia, that the pathogenesis of perioperative human ischemic brain damage involves the function of multiple variably weighted proteins involving several pathways. We then use these data and literature to develop a proposal for rational design of human neuroprotection protocols. Methods: Ninety-four patients undergoing deep hypothermic circulatory arrest (DHCA) and/or aortic valve replacement surgery had brain damage biomarkers, S100 beta and neurofilament H (NFH), assessed at baseline, 1 and 24 h post-cardiopulmonary bypass (CPB) with analysis for association with 92 single nucleotide polymorphisms (SNPs) (selected by co-author WAK) related to important proteins involved in pathogenesis of cerebral ischemia. Results: At the nominal significance level of 0.05, changes in S100 beta and in NFH at 1 and 24 h post-CPB were associated with multiple SNPs involving several prospectively determined pathophysiologic pathways, but were not individually significant after multiple comparison adjustments. Variable weights for the several evaluated SNPs are apparent on regression analysis and, notably, are dissimilar related to the two biomarkers over time post CPB. Based on our step-wise regression model, at 1 h post-CPB, SOD2, SUMO4, and GP6 are related to relative change of NFH while TNF, CAPN10, NPPB, and SERPINE1 are related to the relative change of S100B. At 24 h post-CPB, ADRA2A, SELE, and BAX are related to the relative change of NFH while SLC4A7, HSPA1B, and FGA are related to S100B. Conclusions: In support of the proposed hypothesis, association SNP data suggest function of specific disparate proteins, as reflected by genetic variation, may be more important than others with variation at different post-insult times after human brain ischemia. Such information may support rational design of post-insult time-sensitive multifaceted neuroprotective therapies.