Reduced Graphene Oxide-Polycarbonate Electrodes on Different Supports for Symmetric Supercapacitors

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Perspectives on the Trypanosoma cruzi-host cell receptor interaction

Chagas disease is caused by the parasite Trypanosoma cruzi. The critical initial event is the interaction of the trypomastigote form of the parasite with host receptors. This review highlights recent observations concerning these interactions. Some of the key receptors considered are those for thromboxane, bradykinin, and for the nerve growth factor TrKA. Other important receptors such as galectin-3, thrombospondin, and laminin are also discussed. Investigation into the molecular biology and cell biology of host receptors for T. cruzi may provide novel therapeutic targets

HIPK2 and extrachromosomal histone H2B are separately recruited by Aurora-B for cytokinesis

Cytokinesis, the final phase of cell division, is necessary to form two distinct daughter cells with correct distribution of genomic and cytoplasmic materials. Its failure provokes genetically unstable states, such as tetraploidization and polyploidization, which can contribute to tumorigenesis. Aurora-B kinase controls multiple cytokinetic events, from chromosome condensation to abscission when the midbody is severed. We have previously shown that HIPK2, a kinase involved in DNA damage response and development, localizes at the midbody and contributes to abscission by phosphorylating extrachromosomal histone H2B at Ser14. Of relevance, HIPK2-defective cells do not phosphorylate H2B and do not successfully complete cytokinesis leading to accumulation of binucleated cells, chromosomal instability, and increased tumorigenicity. However, how HIPK2 and H2B are recruited to the midbody during cytokinesis is still unknown. Here, we show that regardless of their direct (H2B) and indirect (HIPK2) binding of chromosomal DNA, both H2B and HIPK2 localize at the midbody independently of nucleic acids. Instead, by using mitotic kinase-specific inhibitors in a spatio-temporal regulated manner, we found that Aurora-B kinase activity is required to recruit both HIPK2 and H2B to the midbody. Molecular characterization showed that Aurora-B directly binds and phosphorylates H2B at Ser32 while indirectly recruits HIPK2 through the central spindle components MgcRacGAP and PRC1. Thus, among different cytokinetic functions, Aurora-B separately recruits HIPK2 and H2B to the midbody and these activities contribute to faithful cytokinesis

Inactivation of plant-pathogenic fungus Colletotrichum acutatum with natural plant-produced photosensitizers under solar radiation.

The increasing tolerance to currently used fungicides and the need for environmentally friendly antimicrobial approaches have stimulated the development of novel strategies to control plant-pathogenic fungi such as antimicrobial phototreatment (APT). We investigated the in vitro APT of the plant-pathogenic fungus Colletotrichum acutatum with furocoumarins and coumarins and solar radiation. The compounds used were: furocoumarins 8-methoxypsoralen (8-MOP) and 5,8-dimethoxypsoralen (isopimpinellin), coumarins 2H-chromen-2-one (coumarin), 7-hydroxycoumarin, 5,7-dimethoxycoumarin (citropten) and a mixture (3:1) of 7-methoxycoumarin and 5,7-dimethoxycoumarin. APT of conidia with crude extracts from 'Tahiti' acid lime, red and white grapefruit were also performed. Pure compounds were tested at 50μM concentration and mixtures and extracts at 12.5mgL(-1). The C. acutatum conidia suspension with or without the compounds was exposed to solar radiation for 1h. In addition, the effects of APT on the leaves of the plant host Citrus sinensis were determined. APT with 8-MOP was the most effective treatment, killing 100% of the conidia followed by the mixture of two coumarins and isopimpinellin that killed 99% and 64% of the conidia, respectively. APT with the extracts killed from 20% to 70% of the conidia, and the extract from 'Tahiti' lime was the most effective. No damage to sweet orange leaves was observed after APT with any of the compounds or extracts

Growing at the limit: Reef growth sensitivity to climate and oceanographic changes in the South Western Atlantic

This is the author accepted manuscript. The final version is available from Elsevier via the DOI in this recordWhilst the impacts of climatic and oceanographic change on lower latitude reefs are increasingly well documented, our understanding of how reef-building has fluctuated in higher latitude settings remains limited. Here, we explore the timing and longevity of reef-building through the mid- to late Holocene in the most southerly known reef (24°S) in the Western Atlantic. Reef core data show that reef growth was driven by a single coral species, Madracis decactis, and occurred over two phases since ~6000 calibrated (cal.) yr B.P.. These records further indicate that there was a clear growth hiatus from ~5500 to 2500 cal. yr B.P., and that there is no evidence of reef accretion on the Queimada Grande Reef (QGR) over the past 2000 yrs. It thus presently exists as a submerged senescent structure colonized largely by non-reef building organisms. Integration of these growth data with those from sites further north (18°S and 21°S) suggests that Intertropical Convergence Zone (ITCZ), South Westerlies Winds (SWW) and El Niño-Southern Oscillation (ENSO) variability and shifts during the Holocene drove changes in the position of the Brazil-Falklands/Malvinas Confluence (BFMC), and that this has had a strong regional influence on the timing and longevity of reef growth. Our results add new evidence to the idea that reef growth in marginal settings can rapidly turn-on or -off according to regional environmental changes, and thus are of relevance for predicting high latitude reef growth potential under climate change.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)razilian Research Council (CNPq